Mesothelioma Cancer 24

Ocella Lawyer Info News – 2/6/2012:

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Ocella Lawyer Info: The findings from the observational studies that hormone users are at generally lower risk from coronary disease do not necessarily imply cause and effect. Women and their physicians decide on estrogen therapy. Often the health status of the woman will have an important influence on this decision and on the results of studies that examine these women. Thus, some have argued that hormone use is merely a marker rather than a cause of good health. Most of the observational studies reviewed here have provided some in­formation bearing on this critical point. The Nurses’ Health Study tried to evalu­ate whether increased medical care of women using postmenopausal hormones might be responsible for the benefit observed. In an analysis limited to women who reported regular physician visits (50% of the cohort), results were sim­ilar to those found in the larger population of all subjects: the relative risk for major coronary heart disease was 0.52 (95% CI, 0.37-0.74) for current hormone use.

Another approach is to examine the risk profile of estrogen users and non­users to determine whether the differences, if any, are sufficient to explain the large decrease in risk among estrogen users. Barrett-Connor observed that, in a cohort of postmenopausal women, those taking estrogens reported more in­tensive health-care behavior, including frequent screening tests such as blood cholesterol measurement and mammograms. An examination of determinants of estrogen therapy in 9704 women participating in a large, multicenter study of osteoporotic fractures found that hormone users tended to be better educated, less obese, and drank alcohol and participated in sports more often than nonusers. Similarly, in a prospective study of randomly selected premenopausal women, observed a better cardiovascular risk factor profile prior to hormone use among the women who subsequently took hormones at menopause than among women who did not.

For hormone users compared to nonusers and, after further adjustment for high blood pressure, history of angina, MI, or stroke, alcohol use, smoking, body mass index, and age at menopause, the relative risk was virtually the same (RR = 0.79; 95% CI, 0.71-0.88), implying an equivalent risk status for users and nonusers. In addition, to further examine this issue, the Nurses’ Health Study conducted an analysis limited to a subgroup of low-risk women (i.e., those with no diagnosis of hypertension, diabetes, or high serum cholesterol who were nonsmokers and had a Quetelet’s Index below 32 kg/m²). Even with such restrictions, the relative risk for coronary disease was almost 40% lower for current hormone users. In summary, to explain the overall benefit of hormone therapy as a result of con­founding by health status, one would have to presume unknown risk factors which are extremely strong predictors of CHD and very closely associated with estrogen use.

LMWHs, like UFH, bind a cofactor called antithrombin to produce their predominant anticoagulant effect. Binding is mediated through a unique pentasac­charide sequence of the mucopolysaccharide that increases by 1000-fold both the interaction between antithrombin and thrombin (factor II_a), and the interaction between antithrombin and factor Xa. However, a minimum chain length of 15 to 18 saccharides (corresponding to a molecular weight of > 5400 daltons) is required to inactivate thrombin. In contrast, inhibition of factor Xa can occur with short polysaccharide chains. Thus, one potentially important distinc­tion between UFH and LMWH, and among LMWHs themselves, is the varying ratio of factor Xa to factor IIa. The factor Xa:IIa activity for UFH is approxi­mately 1.2, while ratios for the various LMWH preparations vary from 2 to 4. Table 1 lists LMWHs in order of anti Xa:IIa ratio.

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Ocella Lawyer Info: The ESSENCE study was a double-blind, placebo-controlled trial that ran­domly assigned 3171 patients with angina at rest or non-Q-wave myocardial in­farction to receive 2 to 8 days therapy with either 1 mg/kg of enoxaparin subcuta­neously twice daily or continuous intravenous UFH. At 14 days, the risk of death, myocardial infarction, or recurrent angina was significantly lower in the patients assigned to enoxaparin than in those assigned to UFH (16.6% vs. 19.8%; p = 0.019). At 30 days, the risk of this composite endpoint remained significantly lower in the enoxaparin group (19.8% vs. 23.3%; p = 0.016). The need for revas­cularization procedures at 30 days was also significantly less frequent in the pa­tients assigned to enoxaparin (27.1% vs. 32.2%; p = 0.001). The 30-day inci­dence of major bleeding complications was 6.5% in the enoxaparin group and 7.0% in the unfractionated-heparin group, but the incidence of bleeding overall was significantly higher in the enoxaparin group (18.4% vs. 14.2%; p = 0.001), primarily because of ecchymoses at injection sites. Thus, the ESSENCE trial indicates that enoxaparin plus aspirin is more effective than UFH plus aspirin in reducing the incidence of ischemic events in patients with unstable angina or non-Q-wave myocardial infarction in the early phase. This benefit was associated with an increase in minor, but not major, bleeding.

In TIMI-11B, 3910 patients with unstable angina or non-Q-wave MI were randomized to either intravenous UFH for 3 to 8 days followed by subcutaneous placebo injections, or enoxaparin during both the acute phase (initial 30-mg IV bolus followed by injections of 1.0 mg/kg every 12 h for 3 to 8 days) and outpa­tient phase (injections every 12 h for up to 43 days of 40 mg for patients weighing >65 kg and 60 mg for those weighing <65 kg). The primary endpoint (death, myocardial infarction, or urgent revascularization) occurred by 8 days in 14.5% of patients in the UFH group and 12.4% of patients in the enoxaparin group (OR 0.83 [0.69 to 1.00]; p = 0.048) and by 43 days in 19.7% of the UFH group and 17.3% of the enoxaparin group (OR 0.85 [0.72 to 1.00]; p = 0.048). During the first 72 h and also throughout the entire initial hospitalization, there was no differ­ence in the rate of major hemorrhage in the treatment groups. During the outpa­tient phase, major hemorrhage occurred in 1.5% of the group treated with placebo and 2.9% of the group treated with enoxaparin (p = 0.021). Consistent with the ESSENCE findings described above, the results of the TIMI-11B study demon­strate that enoxaparin is superior to UFH in reducing a composite of death and serious cardiac ischemic events during the acute management of patients present­ing with unstable angina, but does not cause a significant increase in the rate of major hemorrhage.

Last, the FRAXIS trial (29) randomized 3468 patients in a double-blind fashion to one of three treatment regimens: UFH (5000 IU bolus, followed by an infusion for 6 ± 2 days); nadroparin for 6 days (nadroparin 86 anti-Xa IU/kg IV bolus, followed by twice-daily subcutaneous injections for 6 ± 2 days); or nadroparin for 14 days (same dose as the prior group for 14 days). No statistically significant differences were observed among the three treatment regimens with respect to the primary outcome (cardiac death, myocardial infarction, refractory angina, or recurrence of unstable angina at day 14). The absolute differences between the groups in the incidence of the primary outcome were: -0.3% (p = 0.85) for the nadroparin 6-day group vs. the UFH group, and +1.9% (p = 0.24) for the nadro- parin 14-day group vs. the unfractionated heparin group. Furthermore, there were no significant intergroup differences regarding any of the secondary efficacy out­comes. However, there was an increased risk of major hemorrhage in the nadro­parin 14-day group compared with UFH (3.5% vs. 1.6%; p = 0.0035). Thus, similar to the FRISC-I trial findings with dalteparin, treatment with nadroparin for 6 days provides similar efficacy and safety to treatment with UFH for the same period. A prolonged regimen of nadroparin (14 days) does not provide any additional clinical benefit and is associated with an increase risk of major hemorrhage.

The use of LMWH as an adjunct to fibrinolytic therapy is actively under investi­gation (33-37). Preliminary results from the HART-II angiographic study (37) demonstrated slightly higher rates of infarct artery patency (80.1% vs. 75.1%; p = NS) and TIMI grade 3 flow rates (52.9% vs. 47.6%; p = NS) at 90 min among 200 patients receiving tPA and enoxaparin (30 mg IV bolus followed by 1 mg/ kg SQ twice daily for >72 h) compared to tPA and UFH. Clinical event rates were similar and reocclusion among patients with a patent artery at 90 min tended to be less frequent in those randomized to enoxaparin (5.9 vs. 9.8%; p = NS). In another angiographic study (36), dalteparin was compared with placebo in patients receiving streptokinase. TIMI grade 3 flow 20 to 28 h later tended to be higher in patients treated with dalteparin (68% vs. 51%; p = 0.10) and the number of ischemic episodes on continuous ECG monitoring was lower (16% vs. 38%; p = 0.04).

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Ocella Lawyer Info: Direct thrombin inhibitors, as indicated by the class name, do not require anti­thrombin or another cofactor to inhibit the function of thrombin. Direct thrombin inhibitors inhibit all the major actions of thrombin, including thrombin-induced generation of fibrin, thrombin-induced platelet activation, as well as thrombin’s autocatalytic reaction. Potential advantages of direct thrombin inhibitors over heparin include: inhibition of clot-bound thrombin lack of inhi­bition by activated platelets; and stable anticoagulant response since no cofactor is required. The prototypic direct thrombin inhibitor is hirudin, a polypeptide consisting of 65 amino acids derived from the leech Hirudo medicinalis. Hirudin selec­tively binds thrombin in a 1:1 fashion at two locations: the carboxy terminus of hirudin binds to the substrate recognition site, the domain of thrombin that recognizes fibrinogen or the platelet and the amino terminus of hirudin binds to the catalytic site of thrombin. Hirudin does not inhibit factor Xa, IX, kallikrein, activated protein C, plasmin, tissue plasminogen activator, or other enzymes in the coagulation or fibrinolytic pathways. Although hirudin does not bind covalently to thrombin, the dissociation rate is extremely slow; thus, hirudin essentially irreversibly inhibits thrombin.

Lepirudin was compared to heparin in the OASIS-2 trial (56). While there were trends toward a reduction in cardiovascular death or MI at 72 h (2.0% vs. 2.6%; p = 0.04) and at 7 days (3.6% vs. 4.2%;p = 0.08), there was an attenuation of this benefit by day 35, in contrast to the sustained superiority of enoxaparin over UFH (30). Furthermore, major bleeding requiring transfusion was more fre­quent with lepirudin (1.2% vs. 0.7% for heparin; p = 0.01). The authors per­formed a metanalysis of all the hirudin trials and observed a modest 10% benefit favoring hirudin, although this was not statistically significant for patients with unstable angina/non-ST-elevation MI at 35 days. The Food and Drug Ad­ministration (FDA) recently reviewed the available clinical data and did not ap­prove hirudin for use in unstable angina/non-ST-elevation MI, citing the lack of sustained benefit and increased risk of bleeding.

In the HIT-3 trial, excess intracranial hemorrhage was observed with lepirudin (0.4 mg/kg bolus, 0.15 mg/kg/h infusion) compared to UFH (3.4% vs. 0%) among 302 patients receiving tPA. In the subsequent HIT-4 trial (71), involv­ing 1208 patients and using a lower dose of lepirudin (0.2 mg/kg bolus, 0.5 mg/ kg subcutaneously b.i.d.) in combination with streptokinase, TIMI flow grade 3 was observed in 40.7% in the lepirudin and in 33.5% in the heparin group (p = 0.16). No difference were seen between lepirudin and heparin in the rate of hemorrhagic stroke (0.2% vs. 0.3%), reinfarction (4.6% vs. 5.1%), or mortality (6.8% vs. 6.4%) at 30 days. Thus, intravenous lepirudin (as administered in HIT- 3) as an adjunct to tPA appears to be unsafe, and lower dose lepirudin in combina­tion with streptokinase does not significantly improve reperfusion or clinical out­comes.

Angiographic trials with other direct thrombin inhibitors in conjunction with fibrinolytic therapy have also been conducted. In a pilot study and the HERO trial, a trend toward improved early (90 to 120 min) TIMI grade 3 flow was observed with the higher dose of Hirulog as compared with heparin in patients receiving streptokinase. Testing with other agents found modest or no improvements compared with heparin. HERO-II, an international phase III trial of approximately 17,000 patients with ST-elevation MI treated with strep­tokinase, is randomizing patients to either Hirulog or UFH and should complete enrollment in the latter half of 2000.

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Ocella Lawyer Info: Despite tremendous initial enthusiasm for the direct thrombin inhibitors, their current role in clinical practice is limited to use as an anticoagulant in patients with heparin allergy, or in the treatment of heparin-induced thrombocytopenia and thrombotic syndrome. Ongoing and future research, particularly as adjunctive therapy in patients receiving fibrinolysis or percutaneous coronary intervention, may identify other clinical situations in which these drugs could play a useful role. However, studies to date have identified a narrow therapeutic window, mar­ginal evidence of incremental, sustained efficacy over UFH, and the possibility of a ‘‘rebound’’ effect. These problems represent challenges to this class of anti­thrombotic drugs.

Because approximately 4 million patients each year are admitted to hospitals worldwide with unstable angina or acute myocardial infarction (MI), and nearly 1 million patients annually worldwide undergo percutaneous coronary intervention (PCI), physicians have focused a great deal of attention on developing new treat­ments for these acute coronary syndromes (ACS). The initiating event of these acute coronary syndromes is rupture of an atherosclerotic plaque followed by local thrombosis. Similar pathophysiology is present during PCI, which is essen­tially a ‘‘planned’’ plaque disruption.

The peptide and peptidomimetic inhibitors (e.g., tirofiban and eptifibatide) are competitive inhibitors of the IIb/IIIa receptor, with very rapid half-lives of dissociation from the IIb/IIIa receptor (10-20 s). Thus, the level of plate­let inhibition is directly related to the drug level in the blood. Since both inhibitors have short half-lives, when the drug infusion is stopped the antiplatelet activity reverses after a few hours, which is a potential benefit for avoiding bleed­ing complications. The third group of GP IIb/IIIa inhibitors are the oral agents. Within this group, there are also the two broad types of agents, those that are competitive inhibitors, and those that bind tightly to the receptor. The oral drugs are usually prodrugs, which are absorbed and then converted to active compounds in the blood. The oral agents all have longer half-lives, such that they can be given once, twice, or three times daily in order to achieve relatively steady levels of IIb/IIIa inhibition.

Abciximab was also found to be beneficial when started 24 h prior to a PCI in the c7E3 Fab Antiplatelet Therapy in Unstable Refractory Angina (CAPTURE) trial: death, MI, or urgent revascularization was reduced by abcix­imab from 15.9 to 11.3% (p = 0.012) (27). In the Evaluation of IIb/IIIa inhib­itor for Stenting (EPISTENT) trial (28), compared with stenting with only aspirin and heparin, the rate of death, MI, or urgent revascularization at 30 days was significantly reduced in both abciximab groups—from 10.8 to 5.3% for stent plus abciximab (p < 0.001) and 6.9% for balloon angioplasty with abciximab (p = 0.007) (28). Benefits were maintained at 6 month and 1 year, with a significant reduction in 1 year mortality in patients treated with stent plus abcix- imab compared with stent alone. In addition, a metanalysis of abciximab trials has shown that there is a significant reduction in mortality when GP IIb/ IIIa inhibition is used.

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Ocella Litigation Info News – 2/6/2012:

Ocella may be linked to serious negative side effects. If you took Ocella and believe you suffered negative side effects as a result, contact us today so that we can make arrangements for a free consultation with a law firm that is investigating cases related to the side effects of Ocella.

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Ocella Litigation Info: An emerging concept of GP IIb/IIIa inhibition, based on evidence from two trials, is that these agents appear to be able to reduce the size of an evolving non-ST-elevation MI, and potentially prevent the development of myocardial ne­crosis. In the troponin substudy of PRISM-PLUS, patients randomized to tiro- fiban plus heparin and aspirin had a significantly lower peak troponin level as compared with patients who received heparin and aspirin alone. This observation was made among patients who had a negative CK-MB on admis­sion. In PURSUIT, using peak CK-MB as a measure of infarct size, it was observed that infarct size, either the index MI or a recurrent MI, was signifi­cantly smaller in patients treated with eptifibatide. Thus, when using these potent antiplatelet therapies early in the course of treatment, there appears to be an immediate reduction of the severity of the presenting illness, which is similar to the beneficial effect of chronic aspirin use in reducing the severity of the pre­senting acute coronary syndrome.

Thrombolytic therapy has dramatically reduced mortality following acute myo­cardial infarction. Its benefit is due to early achievement of infarct-related artery patency, which limits myocardial infarct size, decreases left ventricular dysfunc­tion, and improves survival. While thrombolytic therapy has proved to be a major advance in the treatment of patients with acute myocardial infarction, current regimens are limited by failure of initial reperfusion, inadequate perfusion with delayed flow (TIMI grade 2 flow), reocclusion, and reinfarction in sig­nificant percentages of patients. Because these problems are associated with increased subsequent mortality, and because platelets play a central role in failed reperfusion, reocclusion, and reinfarction, attention has turned to the promising glycoprotein IIb/IIIa inhibitors.

In the setting of ST-elevation MI, IIb/IIIa inhibition was first used following thrombolysis in the Thrombolysis and Angioplasty in Myocardial Infarction (TAMI)-8 trial using abciximab following tissue plasminogen activator (tPA). A consistent dose-dependent inhibition of platelet aggregation was observed and major bleeding was not increased. Eptifibatide was tested in the Integrilin to Manage Platelet Aggregation and Combat Acute Myocardial Infarction (IMPACT-AMI) trial. In addition to accelerated, full-dose tPA, aspirin, and heparin, patients were randomized to ep­tifibatide, at one of six doses, or placebo. The highest dose of eptifibatide ap­peared to improve the 90-min rate of TIMI grade 3 flow (66 vs. 39% for placebo; p = 0.006). More recently, a pilot study combined full-dose streptokinase (1.5 million U/h) and three doses of eptifibatide (180-^g/kg bolus and either 0.75-, 1.33-, or 2.0-^g/kg/min infusion for 24 h) or placebo. Adding the IIb/IIIa inhibitor led to a modest improvement in early complete reperfusion (TIMI grade flow 3 at 90 min) from 38% with placebo to approximately 50% with eptifibatide. The highest dose of eptifibatide was associated with increased bleeding and was discontinued. Further testing of eptifibatide is planned with reduced-dose thrombolytic agents.

The combination of a reduced-dose fibrinolytic agent and a GP IIb/IIIa inhibitor was tested in the TIMI-14 trial, using tPA, streptokinase, and reteplase; in SPEED (Strategies for Patency Enhancement in the Emergency Department) using rete- plase; and in INTRO-AMI and several ongoing trials. In the TIMI-14 trial dose-ranging phase, 681 patients with ST-segment- elevation MI meeting with standard eligibility criteria were randomized within 12 h of onset of chest pain to receive one of four reperfusion regimens (each with several dose levels): accelerated (full-dose) tPA alone (the control arm); reduced-dose tPA plus abciximab; reduced-dose streptokinase plus abciximab; or abciximab alone. All patients received aspirin and heparin, with the initial heparin dosage being 70-U/kg bolus and a 15-U/kg/h infusion in the tPA control arm, and 60-U/kg bolus and a 7-U/kg/h infusion in the abciximab groups.

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Ocella Litigation Info: Abciximab alone was associated with a rate of TIMI grade 3 flow at 90 min of 32% and patency rate of 48% (43). The combination of streptokinase and abciximab produced only slight improvement in 90-min TIMI grade 3 flow: 42% in the 0.5-MU group; 39% in the 0.75-MU group; and 47% in the 1.25-MU group. The 1.5-MU regimen plus abciximab was discontinued after four of six patients developed a major hemorrhage, one of whom had an ICH. Of the various dosing regimens of tPA tested, the best angiographic results were obtained using a 50-mg dose given as a 15-mg bolus and a 35-mg infusion over 60 min. The rate of TIMI grade 3 flow at 90 min was 77% compared with 62% for tPA alone (p = 0.02). Overall patency was achieved in 93% of patients with the combination of abciximab and half-dose tPA compared with 78% for full-dose tPA alone (p = 0.09). An even greater difference was observed at 60 min: accelerated tPA achieved only 43% TIMI grade 3 flow at 60 min compared with 72% for 50-mg tPA plus abciximab (p = 0.0009). Major hemorrhage was similar (approximately 6%) among the tPA plus abciximab and control groups. In-hospital mortality was low in all groups, ranging from 3 to 5%.

The Orbofiban in Patients with Unstable Coronary Syndromes (OPUS-TIMI)-16 trial tested the oral Il/IIIa inhibitor, orbofiban, in patients with acute coronary syndromes. This trial enrolled 10,288 patients at 888 hospitals in 28 countries. The inclusion criteria were onset of an acute coronary syndromes within 72 h, defined as an episode of rest ischemic pain lasting at least 5 min associated with either positive cardiac enzymes (i.e., an acute MI), ECG changes, or a prior his­tory of coronary or vascular disease. Exclusion criteria included renal insuffi­ciency (creatinine >1.6 mg/dL, increased high bleeding risk, or need for oral anticoagulation. All patients received 150 to 162 mg of ASA daily and were randomized, in double-blind fashion, to one of two doses of orbofiban or placebo. In one group, orbofiban was administered as 50 mg twice daily throughout the trial (50/ 50 group); in the other group, 50 mg was given twice daily for the first 30 days (the highest risk period), and was reduced to 30 mg twice daily for the remainder of the trial (50/30 group). Other treatments were at the discretion of the pa­tient’s physician. The primary endpoint was a composite of death, MI, recurrent ischemia leading to rehospitalization or urgent revascularization, or stroke. The planned sample size was 12,000 patients, but the trial was terminated early after an unexpected finding of increased mortality at 30 days in one of the orbofiban groups.

Mortality through 10 months was 3.7% for the placebo group versus 5.1% in the 50/30 group (p = 0.008) and 4.5% in the 50/50 group (p = 0.11). There were no differences in the primary composite endpoint at 10 months (22.9, 23.1, and 22.8%, for the placebo, 50/30, and 50/50 groups, respectively). Major or severe bleeding (but not intracranial hemorrhage) was higher with orbofiban; it occurred in 2.0, 3.7 (p = 0.0004), and 4.5% (p < 0.0001) of patients, respec­tively. Exploratory subgroup analyses did identify that patients who underwent percutaneous coronary intervention had a lower mortality and a significant reduc­tion in the composite endpoint (p = 0.001) with orbofiban. Two substudies from OPUS-TIMI-16 found that orbofiban led to increases in measures of platelet activation, notably P-selectin. These data are con­sistent with observations of other agents, which induced an apparent prothrom- botic effect, with increases in measures of platelet activation and increases in platelet aggregation when drug levels were low. Interestingly, in the TIMI-12 trial, no increase in P-selectin was observed with sibrafiban therapy. Active research is ongoing, but these initial studies suggest that there may be differences among the various oral IIb/IIIa inhibitors with regard to potential prothrombotic effects.

The Evaluation of oral Xemilofiban in Controlling Thrombotic Events (EXCITE) trial studied xemilofiban in 7232 patients undergoing PCI with either stenting or balloon angioplasty without adjunctive intravenous IIb/IIIa inhibition. Patients were randomized in a double-blind fashion to receive one of two doses of xemilofiban or placebo: All the xemilofiban patients received a first 20-mg dose 30 to 90 min prior to PCI, followed by either 10 or 20 mg three times daily for 6 months. The primary endpoint—death, MI, or urgent revascularization at 6 months—occurred in 13.6% of patients in the placebo group, 14.1% of patients in the xemilofiban 10-mg group, and 12.6% of patients in the xemilofiban 20­mg group (p = NS) (78). There was a trend toward fewer periprocedural MIs over the first 48 h following PCI, but this benefit was not sustained at 30 days or 6 months. Mortality at 6 months was 1.0% for placebo, 1.6% for the 10­mg xemilofiban dose group, and 1.1% in the 20-mg dose group. Major bleed­ing was significantly more common in the xemilofiban-treated patients. Thus, xemilofiban did not significantly reduce cardiac events in this patient popu­lation.

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Ocella Litigation Info: The second Symphony trial was terminated prematurely at the time the results from the first Symphony trial were available (and not due to safety issues). It compared the combination of low-dose sibrafiban plus aspirin vs. high-dose si­brafiban (without aspirin) vs. aspirin alone in 6671 patients with stabilized acute coronary syndromes. With an average follow-up of 90 days, the primary endpoint, death, MI, or severe recurrent ischemia, was not different among the three groups: 10.5% in the high-dose sibrafiban group; 9.2% for low-dose sibrafiban plus aspi­rin vs. 9.3% for aspirin alone. In this trial (but not in the larger first Symphony trial), mortality was significantly higher with the high-dose sibrafiban group: 2.4 vs. 1.7% for the low-dose sibrafiban plus aspirin group vs. 1.3% for placebo. Recurrent MI followed a similar pattern: 6.9% for high-dose sibrafiban, 5.3% for the low-dose plus aspirin group, and 5.3% for aspirin. Major bleeding was more common with high-dose sibrafiban (4.6%), and higher still for the combination of low-dose sibrafiban plus aspirin (5.7%) vs. 4.0% for aspirin alone.

It is an exciting time for the practicing physician given the availability of this important new therapy that can significantly reduce death, MI, or refractory ischemia/urgent revascularization. The benefits apply to essentially all patients undergoing PCI, thereby becoming a new standard of care in this setting. For the huge number of patients with unstable angina and non-ST-elevation MI, IIb/ IIIa inhibition will significantly reduce recurrent ischemic events. The trials to date have targeted the higher risk unstable angina patients—those with ECG changes or positive cardiac enzymes, and thus these are the patients in clinical practice who should be targeted for early use of IIb/IIIa inhibitors.

Platelets are integrally involved in the thrombotic complications of atherosclero­sis. Their contribution to thrombosis complicating a ruptured atherosclerotic plaque is well established. Interference with platelet function, therefore, should help to prevent thrombotic occlusion of arteries affected by atherosclerosis. In­deed, numerous studies have demonstrated that antiplatelet agents decrease ad­verse cardiovascular events in patients with atherosclerosis. This chapter will focus on three such antiplatelet agents: aspirin, ticlopidine, and clopidogrel. It will include a brief review of platelet function followed by a discussion of the mechanisms of action of these antiplatelet drugs. Thereafter, clinical evidence supporting the notion that antiplatelet agents reduce adverse cardiovascular events in patients with atherosclerosis will be presented.

The three principal events in the formation of a platelet plug include platelet adhesion, activation, and aggregation. Platelets normally circulate in an inacti­vated state. Vascular injury and disruption of the endothelial lining initiates the process of platelet adhesion, in which platelets are deposited on the intimal surface of blood vessels. Among the most important substances to mediate platelet adhesion to the vascular surface is von Willebrand factor. It binds suben­dothelial collagen to the platelet glycoprotein Ib-IX-V receptor. Binding of plate­lets to the vascular surface prompts an intracellular signaling mechanism, includ­ing the metabolism of arachidonic acid to thromboxane A₂. In addition, the platelets release constituents of their alpha and dense granules such as p-selectin.

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Ocella Litigation Info: Aspirin inhibits arachidonic acid metabolism and prevents the formation of thromboxane A₂ by irreversibly inhibiting cyclooxygenase via acetylation of a serine moiety. Platelet inhibition occurs approximately 60 min following the oral ingestion of aspirin. The inhibitory effects of platelets last the life of a platelet, which is approximately 10 days. Hemostatic recovery following a single dose of aspirin occurs as new platelets are formed and enter the circulation. Both ticlopidine and clopidogrel are thienopyridines. These inhibit the function of platelet ADP receptors and thereby limit conformational changes in the glycoprotein IIb/IIIa receptor. Inhibition of platelet aggregation occurs ap­proximately 1 to 2 days following administration of these drugs, and 40 to 60% inhibition of ADP-induced aggregation is observed 3 to 5 days following inges­tion. Platelet function is restored approximately 3 to 4 days after discontinua­tion of ticlopidine or clopidogrel.

The beneficial effects of aspirin on cardiovascular outcome in patients with ath­erosclerosis is well established. The Antiplatelet Trialists’ Collaboration per­formed a metanalysis of over 73,000 patients with clinical manifestations of ath­erosclerosis such as acute myocardial infarction, prior myocardial infarction, or prior stroke or transient ischemic attack, in which patients were treated with either antiplatelet therapy or a control. The most widely studied antiplatelet drug was aspirin. Overall, antiplatelet therapy was associated with a 25% odds reduc­tion for the aggregate endpoint of stroke, myocardial infarction, or vascular death. The studies included in this metanalysis, as well as some more recent studies, highlight the efficacy of aspirin in reducing cardiovascular morbidity and mortality in patients with atherosclerosis. Some of the larger studies involving patients with coronary artery disease, cerebrovascular disease, or peripheral arte­rial disease are described below.

In the Antiplatelet Trialists’ Collaboration, antiplatelet therapy, primarily aspirin, was associated with a 29% odds reduction for stroke, myocardial, or vascular death among approximately 20,000 patients with acute myocardial infarction and a 25% odds reduction for these adverse events among approximately 20,000 pa­tients with prior myocardial infarction. The largest trial for acute myocardial infarction included in the Antiplatelet Trialists’ Collaboration was the Second International Study of Infarct Survival (ISIS-2), which randomized over 17,000 patients with acute myocardial infarction to aspirin, streptokinase, both, or neither. Compared to placebo, aspirin was associated with a 23% risk reduction for vascular death, a 50% reduction for nonfatal reinfarction, and a 46% reduction for nonfatal stroke 5 weeks after randomization. The combination of streptokinase and aspirin was more effective than either agent alone in reducing vascular death. The efficacy of aspirin in preventing coronary reocclusion follow­ing thrombolysis for acute myocardial infarction is supported by a metanalysis of 32 studies. Reocclusion occurred in 11% of 419 patients treated with aspirin versus 25% of 513 patients not treated with aspirin, and recurrent ischemic events occurred in 25% of 2977 patients treated with aspirin compared to 41% of 721 patients who were not treated with aspirin.

Several large trials have demonstrated the efficacy of aspirin in preventing myocardial infarction and death in patients with unstable angina. A Veterans Administration Cooperative study randomized 1256 men with unstable angina to aspirin or placebo for 12 weeks. The incidence of fatal or nonfatal myocardial infarction was reduced by 51% in the group treated with aspirin compared to the group treated with placebo. A Canadian multicenter trial randomized 555 patients with unstable angina to aspirin, sulfinpyrizone, both, or neither to 24 months of treatment. The incidence of fatal or nonfatal myocardial infarction was 8.6% in the groups receiving aspirin compared to 17% in the groups not receiving aspirin, resulting in a 51% risk reduction with aspirin. Theroux et al. compared the efficacy of aspirin, intravenous heparin, both, or neither in 479 patients with unstable angina. Approximately 6 days following randomization, myocardial infarction had occurred in 11.9% of patients who received neither aspirin nor heparin, in 3.3% who received any aspirin, in 0.8% of those who received only heparin, and in 1.6% of patients who received both aspirin and heparin. The Research Group on Instability in Coronary Artery Disease in Southeast Sweden (R.I.S.C.) randomized 796 men with unstable angina or non-Q-wave myocardial infarction to aspirin or placebo. After 1 year, myocardial infarction occurred in 21.4% of patients treated with placebo and in 11% of patients treated with aspirin. Thus, aspirin treatment reduced the risk of nonfatal or fatal myocardial infarction by 48%.

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Ocella Settlement Info News – 2/6/2012:

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Ocella Settlement Info: Two recent large trials have studied the efficacy and safety of aspirin in patients with acute ischemic strokes. The International Stroke Trial ran­domized 19,435 patients with acute ischemic stroke to unfractionated heparin, either 5,000 or 12,500 units twice daily, aspirin 300 mg daily, or both heparin and aspirin (11). Among the patients treated with aspirin, there were 2.8% recurrent ischemic strokes within 14 days, compared to 3.9% in the groups not receiving aspirin, and no excess of hemorrhagic strokes. There was a nonsignificant trend for decreased mortality in patients treated with aspirin compared to those not treated with aspirin at 14 days (9% vs. 9.4%). At 14 days, therefore, there was a significant reduction in death or any nonfatal recurrent stroke in the aspirin- treated group (11.3% vs. 12.4%). In patients treated with heparin, there were 2.9% recurrent ischemic strokes within 14 days compared to 3.8% in the groups not receiving heparin, but an increase in hemorrhagic strokes (1.2% vs. 0.4%). As a consequence, there was no significant difference in the incidence of nonfatal recurrent stroke or death between the heparin and nonheparin groups (11.7% vs. 12%, respectively).

Several trials have studied the efficacy of aspirin as primary prevention for myo­cardial infarction, stroke, and death, but the results have not been consistent. The Physicians’ Health Study compared aspirin to placebo in 22,071 male physicians over the age of 40 and followed them for 5 years. Myocardial infarction occurred in 139 persons assigned to aspirin and 239 assigned to placebo. Thus, aspirin was associated with a 44% reduction in the risk of myocardial infarction. Cardiovascular death occurred in 81 persons assigned to aspirin and 83 assigned to placebo. Thus, there was no significant reduction in total cardiovascular mor­tality. The reduction in the risk of myocardial infarction occurred only among men 50 years of age and older. There was a nonsignificant, slightly increased risk of stroke among those taking aspirin compared to those taking placebo. A separate study of 5139 healthy British male physicians compared aspirin to pla­cebo. Total mortality was slightly, but not significantly, less in the control group compared to the aspirin-treated group. There was no significant difference in the incidence of nonfatal myocardial infarction or stroke.

Another British trial, the Thrombosis Prevention Trial, evaluated the effect of low-dose aspirin (75 mg/day) as well as oral anticoagulation with warfarin (average INR = 1.47) in 5499 healthy men aged 45 to 69 years who were random­ized to warfarin, aspirin, both, or neither. The average International Normal­ized Ratio (INR) for those receiving warfarin was 1.47. Warfarin was associated with a 21% reduction in coronary death, fatal, and nonfatal myocardial infarction, and aspirin was associated with a 20% reduction in coronary death and myocar­dial infarction. The risk of hemorrhagic and fatal strokes was increased in the warfarin-treated patients. The principal effect of aspirin was primarily a 32% reduction in nonfatal myocardial infarction; aspirin did not reduce total cardiovas­cular mortality. The effect of aspirin as primary prevention was also evaluated in 87,678 U.S. registered nurses who had been participating in a prospective cohort study. Among women taking one to six aspirin per week, there was a significant, 32% relative risk reduction for myocardial infarction, a nonsignifi­cant, 11% relative risk reduction for cardiovascular death, and no decrease in the risk of stroke.

An analysis of 21 trials included in the Antiplatelet Trialists’ Collaboration found that the odds ratio among persons using aspirin for upper gastrointestinal bleeding was 1.7; for peptic ulcer, 1.3; and for all gastrointestinal bleeding, 1.5 to 2.0. The risk of cerebral hemorrhage is increased by aspirin. A recent metanal- ysis of 16 trials constituting 55,462 persons found that the absolute risk of hemor­rhagic stroke in groups treated with aspirin was 1.2 per thousand individuals accounting for a relative risk of 1.84. Hypersensitivity reactions to aspirin, including nasal congestion, urticaria, and bronchospasm may occur. The frequency of these adverse effects in patients with chronic urticaria is 23%, in patients with asthma is 4 to 19%, and in patients with nasal polyps is approxi­mately 23%.

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Ocella Settlement Info: The Studio della Ticlopidinia nell’Angina Instabile Groupe evaluated the efficacy of ticlopidine in 652 patients with unstable angina. Following treat­ment for 6 months, 7.3% of the patients receiving ticlopidine had a nonfatal myocardial infarction or vascular death compared to 13.6% of patients who did not receive ticlopidine, accounting for a 46.3% relative risk reduction. Several trials have evaluated the efficacy of ticlopidine in preventing throm­bosis or ischemic events subsequent to placement of an intracoronary stent. The Full Anticoagulation versus Aspirin and Ticlopidine (FANTASTIC) study ran­domized patients to aspirin and ticlopidine or to aspirin and conventional antico­agulation with heparin or oral anticoagulants. The primary endpoint of bleed­ing or peripheral vascular complications occurred in 13.5% of patients treated with aspirin and ticlopidine and 21% of patients treated with aspirin and anticoag­ulants. The overall incidence of stent occlusion was similar in each group; yet, acute stent occlusion occurred more frequently in the antiplatelet group (2.4 vs. 0.4%), whereas subacute stent occlusion within 1 week occurred more frequently in the anticoagulant group (3.5 vs. 0.4%).

The Multicenter Aspirin and Ticlopidine Trial after Intracoronary Stenting (MATTIS) study randomized 350 high-risk patients following stent implantation to aspirin and ticlopidine or to aspirin and oral anticoagulation. After 30 days, the primary cardiac endpoint of cardiovascular death, myocardial infarction, or repeated revascularization occurred in 5.6% of the aspirin and ticlopidine group compared to 11% of the aspirin and anticoagulant group, accounting for approximately 50% reduction in the risk of an adverse event with the former compared to the latter group. Schomig et al. randomized 257 patients undergoing placement of coronary artery stents to aspirin and ticlopidine, or to aspirin plus anticoagulation with heparin or phenprocoumon. The primary cardiac endpoint of cardiac death, nonfatal myocardial infarction, coronary artery bypass surgery, or repeat angio­plasty occurred in 1.6% of patients randomized to aspirin plus ticlopidine as compared to 6.2% of those randomized to aspirin plus anticoagulation, account­ing for a relative risk of 0.25 in those randomized to antiplatelet therapy alone. Moreover, hemorrhagic complications occurred in 6.5% of the anticoagulant ther­apy group, but in none of the antiplatelet therapy group.

Two large clinical trials evaluated the efficacy of ticlopidine in patients with symptomatic cerebrovascular disease. The Canadian American Ticlopidine Stud­ies (CATS) randomized 1072 with recent thromboembolic stroke to ticlopidine or placebo and followed them for an average of 24 months. The primary endpoint of stroke, myocardial infarction, or vascular death occurred in 15.3% per year of those treated with placebo and 10.8% per year of those treated with ticlopidine, accounting for a relative risk reduction with ticlopidine of 30.2%. There was no significant difference in the total mortality rate, which was 4.5% per year in those receiving placebo and 4.1% per year in those receiving ticlopidine. The Ticlopidine Aspirin Stroke Study (TASS) randomized 3069 patients with recent transient ischemic attack, amaurosis fugax, or minor stroke to aspirin or ticlopidine.

Several studies have examined the efficacy of ticlopidine in patients with periph­eral arterial disease. Balsano etal. studied 151 patients with intermittent claudica­tion who were randomized to treatment with ticlopidine or placebo. Improve­ment in pain-free and maximal walking distance was greater in the ticlopidine than in the placebo group. The Swedish Ticlopidine Multicenter Study (STIMS) assessed the effect of ticlopidine on cardiovascular events in 687 patients with intermittent claudication followed for a median duration of 5.6 years. The incidence of myocardial infarction, stroke, and transient ischemic attack was 29% in patients treated with placebo compared to 25% among those treated with ticlopidine, accounting for a risk reduction of 11.4% in favor of ticlopidine. Mortality was 26.1% in the placebo group and 18.5% in the ticlopi­dine group, accounting for a relative risk reduction of 29%. A recent metanalysis involving studies of patients with intermittent claudication found that mortality was significantly decreased by ticlopidine compared to placebo, with an odds ratio of 0.68.

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Ocella Settlement Info: Several additional trials that are assessing the efficacy of clopidogrel in preventing cardiovascular events are currently taking place. These include: the Clopidogrel Reduction of Events During Extending Observation (CREDO) trial in which patients undergoing percutaneous revascularization will receive clopido­grel with aspirin for 1 year versus clopidogrel plus aspirin for 1 month followed by aspirin for another 11 months and the Warfarin and Antiplatelet Therapy in Chronic Heart Failure (WATCH) trial in which patients with congestive heart failure will be randomized to warfarin (titrated to an INR of 2.5-3.0), clopidogrel 75 mg/day, or aspirin 160 mg/day, and followed for up to 5 years.

In the CAPRIE trial, bleeding occurred with comparable frequency in the patients receiving clopidogrel compared to aspirin (9.27% vs. 9.28%, respectively). In patients receiving clopidogrel, intracranial hemorrhage occurred in 0.35% and gastrointestinal hemorrhage in 1.99%, the latter being less frequent than in pa­tients receiving aspirin. In patients receiving clopidogrel, diarrhea occurred in 4.46% and rash occurred in 6.02%. Of patients receiving clopidogrel, neutro­penia (<1200/|J.L) was present in 0.1%, severe neutropenia (<450/|J.L) in 0.05%, thrombocytopenia (<100 X 10³/|J.L) in 0.26%, and severe thrombocytopenia (<80 X 10³/|J.L) in 0.19% of patients receiving clopidogrel. A recent report high­lighted the potential association of thrombotic thrombocytopenic purpura with clopidogrel (41). Eleven patients who had been treated with clopidogrel, 10 of whom had been treated for 14 days or less, were identified over a 2-year period by active surveillance of medical directors of blood banks, hematologists, and a surveillance overseen by pharmaceutical manufacturers. At the time of this report, the authors estimated that more than 3 million people had received clopidogrel. Idiopathic thrombotic thrombocytopenic purpura has been estimated to occur in approximately 3.7 per million.

Heart failure was the first major area in which ACE inhibitors have proven their undisputed role in improving clinical outcomes, indeed, survival. In the early 1980s, the ‘‘vasodilator era,’’ then pioneering acute studies revealed that favor­able hemodynamic improvements could be obtained by ACE inhibitors in patients with severe heart failure. The first demonstration of a survival benefit with the use of an ACE inhibitor in any cohort of patients can be attributed to the Cooperative North Scandinavian ENalapril SUrvival Study (CONSENSUS), which randomized patients with severe heart failure. In this trial, despite the use of digitalis, diuretics, and other vasodilators, the placebo mortality rate was exceedingly high, approaching 50% at 6 months. Those randomized to the active therapy (enalapril) had a pronounced reduction in the risk of death. Indeed, the combination of the high placebo event rate and the relative effectiveness of ther­apy led to conclusive results in a population of approximately 500 patients.

The Studies of Left Ventricular Dysfunction (SOLVD) greatly expanded the indications for ACE inhibitors as a consequence of their results in two parallel randomized trials collectively involving over 6000 patients. In the treatment arm, symptomatic heart failure patients with left ventricular dysfunction (ejection fraction <35%) of all etiologies were randomized to placebo or enalapril. Despite background therapy with digitalis or diuretics or both, the enalapril group experi­enced a 16% reduction in the risk of death and clear reductions in the need for rehospitalization for heart failure. The same screening procedures identified and randomized over 4000 patients who also had left ventricular dysfunction. However, the study investigators did not feel that these patients had sufficient symptoms to warrant therapy—the Prevention Arm. In this unique group, the randomization to enalapril showed a favorable trend for a reduction in fatal events with a clear reduction in the development of heart failure during the ap­proximately 4 years of follow-up. As a consequence of these and other smaller studies, ACE inhibitors had proven themselves as an essential, indeed, ‘‘corner­stone’’ therapy for the management of patients with heart failure. In some respects, the V-HeFT-II study put the icing on the cake for the use of ACE inhibi­tors in heart failure. It showed that, in a group of symptomatic heart failure pa­tients randomized to either the combination of hydralazine and nitrates (the first life-sustaining therapy for heart failure) versus enalapril, the ACE inhibitor re­sulted in superior survival even compared to a previously proven therapy for heart failure. Taken together, we now had clear evidence that the morbidity and mortality of heart failure could be effectively reduced by the use of an ACE inhibitor.

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Ocella Settlement Info: The rationale for the treatment of patients with myocardial infarction with an ACE inhibitor stems from the pioneering work of the late Dr. Janice Pfeffer, beginning when she was a fellow in the Braunwald laboratory. Experimental models of infarctions were readily utilized to determine whether infarct size could be favorably modified by pharmacological therapy. Pfeffer explored the relation­ship between infarct size and ventricular function and incorporated important lessons from her doctoral training in hypertension at Edward Frohlich’s labora­tory to determine the long-term consequences of abrupt loss of myocardium from coronary ligation. Indeed, she demonstrated in the animal model that the loss of myocytes should be viewed as the beginning of an insidious phase of progressive ventricular enlargement (remodeling), which is related both to the extent of the histological damage as well as to the duration of time from the infarct. In­deed, the enlargement itself is a central component in the progressive worsening of dysfunction. Ventricular remodeling could also involve the normal remaining myocardium, which, as a consequence of unfavorable geometry and wall stress, could suffer an abnormal hemodynamic burden.

These observations of ventricular remodeling provided a new therapeutic target for a novel use of ACE inhibition—to attenuate time-dependent ventricular enlargement following infarction. The use of ACE inhibitors was a natural exten­sion of her work in hypertension, where these agents were particularly effective in preventing hypertrophy and left ventricular chamber enlargement. In the myocardial infarction model, long-term administration of an ACE inhibitor did indeed attenuate ventricular enlargement as treated animals had smaller left ven­tricular cavities and more preserved ventricular pump function. In a subse­quent study, a prolongation of survival was demonstrated with ACE inhibitor treatment.

These animal studies provided the rationale for initially small mechanistic studies, which confirmed both the process of progressive enlargement post-myo­cardial infarction and the attenuation of enlargement with the use of an ACE inhibitor. These mechanistic studies were soon followed by an extensive series of international multicenter randomized trials testing the hypothesis that administration of an ACE inhibitor to patients in the acute and chronic phases of myocardial infarction would lead to improved survival. The Survival and Ven­tricular Enlargement (SAVE) study, as suggested by the trial’s acronym, tested the hypothesis that attenuation of ventricular enlargement in high-risk patients post-myocardial infarction would lead to improved survival. The SAVE study demonstrated that the addition of captopril to a conventionally treated pa­tient who survived a myocardial infarction with an ejection fraction less than 40% without overt heart failure would lead not only to a reduction in the risk of death, but also to a reduced risk of developing heart failure and experiencing a recurrent myocardial infarction. A detailed quantitative echocardiographic study did confirm an attenuation in remodeling in the ACE inhibitor group and, more­over, these investigators were able to demonstrate linkage between progressive enlargement, risk of an adverse cardiovascular event, and the favorable benefit of the ACE inhibitor therapy.

The Acute Infarction Ramipril Efficacy (AIRE) study administered the ACE inhibitor ramipril to patients starting in the acute phase of the infarct and continuing long term. The AIRE investigators identified high-risk patients based on clinical signs or symptoms of pulmonary congestion or transient heart failure. The long-term administration of the ACE inhibitor resulted in a 26% reduction in the risk of death and comparable reductions in other nonfatal cardiovascular endpoints. The TRandolapril Cardiac Evaluation (TRACE) investigators employed echocardiographic assessment of wall motion to identify higher risk acute infarct patients. Here, again, the randomization to the ACE inhibitor resulted in an im­portant reduction in the risk of death. In the Survival of Myocardial In­farction Long-term Evaluation (SMILE), the ACE inhibitor zofenopril was ad­ministered to patients with anterior myocardial infarction who had not received thrombolytic therapy. This randomized trial demonstrated a reduction in risk of death or development of heart failure during only 6 weeks of therapy. The TRACE and AIRE investigators have extended their observations beyond the formal trial period and demonstrated that the survival benefits persisted.

Our use of the term or terms Ocella Settlement Info is for descriptive purposes only. There is no relationship between the owners of this website and the maker of the product discussed in this post. Our use of the words Recall, Class Action Lawsuit and other similar words related to an event do not necessarily mean that this event has occurred. Refer to the website of the United States Food and Drug Administration for information on drug or medical device recalls. If a Class Action Lawsuit is formed in relation to the product discussed in this post we will provide that information at the time the Class Action is formed. A Class Action Lawsuit is not required to exist for you to file a lawsuit if you have been injured by the product discussed in this post.

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Ocella Side Effect Info News – 2/6/2012:

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Ocella Side Effect Info: An overview of this selective approach to the use of ACE inhibitors for higher risk myocardial infarction patients indicates that approximately 20 to 30 lives are saved in the first month of treatment and that, with continued therapy, approximately 60 to 80 lives are saved per 1000 patients treated. It is impor­tant to underscore that the benefits of the use of an ACE inhibitor in myocardial infarct patients could be considered as additive to conventional therapy with thrombolytics, beta-blockade, and even aspirin. Therefore, it is fair to conclude that use of an ACE inhibitor in these patient populations results in a new and complementary modality to reduce risk of death and other major cardiovascular events.

The only ‘‘fly in the ointment’’ in the field of ACE inhibitors and acute myocardial infarction was from the CONSENSUS II study, which showed a nega­tive trend when ACE inhibitor therapy was started intravenously in the first day of the infarct and then continued orally for the projected study duration of 6 months. With over 100,000 patients in randomized, placebo-controlled trials of different designs, agents and durations, the consensus of international experts strongly recommends the use of an ACE inhibitor starting early and continued long term for patients at higher risk. These authoritative guidelines do indi­cate that there are sufficient rationale and data for clinicians to adopt a more global approach for the use of ACE inhibitors in an even broader population.

Additional mechanisms to explain the ACE inhibitor influence on coronary events soon came from novel experimental studies that revealed an important interface between the renin-angiotensin system and the balance between throm­bolysis and thrombosis. An infusion of angiotensin-II raised plasminogen activa­tor inhibitor-1 (PAI-1), which would alter the fibrinolytic balance toward throm­bosis. The randomized use of ACE inhibitors in patients with acute myocardial infarction did indeed lower PAI-1 levels and, particularly, the balance of PAI-1 to intrinsic tPA. Augmented PAI-1 levels had been associated with greater risk of infarct and others had speculated that reduced PAI-1 may be an indication of restoration of endothelial function. In the TREND study, the long-term treatment with the ACE inhibitor quinipril led to a better restoration of coronary endothelial function. Along these lines, it has been postulated that lowering angiotensin-II with an ACE inhibitor would reduce superoxide anions, promote nitric oxide, and limit further vascular damage.

In the mid-to-late 1990s, three major trials were initiated to determine whether an ACE inhibitor would reduce atherosclerotic events. The Heart Out­comes Prevention Evaluation (HOPE) study selected patients for clinical evi­dence of vascular disease with prior myocardial infarction, stroke, peripheral vas­cular disease, or diabetes plus another risk factor and randomized to conventional therapy plus placebo or ramipril. Patients with heart failure or known depressed ejection fraction were excluded. The Prevention of Events with Angiotensin Converting Enzyme Inhibition (PEACE) study, specifically designed as a follow- up of SAVE, included patients with documented coronary disease and an ejection fraction over 40% randomized to conventional therapy plus either trandolapril or placebo. The EUropean trial on Reduction Of cardiac events with Perindo­pril in stable coronary Artery disease (EUROPA) randomized patients with coro­nary disease regardless of their ejection fraction to either perindopril or placebo.

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Ocella Side Effect Info: HOPE was the first of these major studies to be completed. Randomization to ramipril resulted in a convincingly consistent 20% and greater reduction in ath­erosclerotic events, such as cardiovascular death, myocardial infarction, and stroke. The HOPE study results are based on a substantial number of clinical events and consistent findings were present in all predefined subgroups. Again, the small reduction in blood pressure with the ACE inhibitor in and of itself could not explain the magnitude of the clinical benefits in this patient population. Within the HOPE study, a mechanistic trial evaluating carotid arterial thickness as a surrogate marker of the atherosclerotic process did demonstrate a dose-dependent reduction in ca­rotid thickness with the use of an ACE inhibitor. Other important mechanistic observations such as the reduction in the development of diabetes and diabetic complications may provide additional key insights. Indeed, the hemoglobin A1C levels in the subpopulation evaluated was reduced by chronic therapy with the ACE inhibitor. The HOPE study expands both the patient population who will receive benefits from ACE inhibitor therapy as well as the potential mechanisms that can be evoked to explain these impressive beneficial actions.

With the obvious broad overlap in patients who would benefit from both of these agents, a negative interaction with the concomitant use of these two agents would have major public health implications. At the outset, it must be acknowledged that there is yet to be a two- by-two trial of aspirin and ACE inhibitors as there was of thrombolytics and aspirin in ISIS-2. Indeed, with the now established benefits of both of these agents, such a trial in which patients would have either of these life-saving thera­pies withheld would be deemed unethical. Decisions will have to be based on the experience of prior trials. Since most of the major aspirin trials were con­ducted prior to the knowledge of the survival benefit of ACE inhibitors, there are few data on concomitant use. On the other hand, there is extensive experience in the ACE inhibitor trials with patients on aspirin.

The initial hypothetical question of a possible interaction, whereby the con­comitant use of both drugs offsets the potential benefits of an ACE inhibitor, was proposed by Donald Hall and his colleagues. A mechanistic study of patients with severe heart failure and marked neurohormone activation observed that the vasodilating effect of enalapril was offset by the concomitant use of aspirin. Since one of the important actions of an ACE inhibitor, aside from reducing the production of angiotensin-II, is to impede the breakdown of bradykinin, which also enhances the production of prostaglandins, it was reasoned that an aspirin effect on inhibiting prostaglandin synthesis could offset some of the hemody­namic benefits of administering an ACE inhibitor. Indeed, their work on the he­modynamics of severe heart failure was confirmed by others. This is similar to the use of nonsteroidal anti-inflammatory agents that had long been known to exacerbate signs and symptoms of heart failure, impairing renal function, and even offsetting antihypertensive effects of a variety of therapeutic compounds. Hall provided mechanistic underpinning and focus for important questions regarding a potential for aspirin to offset some of the clinical benefits of ACE inhibitor use in patients with severe heart failure.

Subsequently, a subgroup analysis from the SOLVD studies did indicate that there was a trend for less of a survival benefit in patients randomized to the ACE inhibitor who were reported to be on aspirin at baseline. Proponents of an important negative interaction whereby aspirin offsets some of the benefits of an ACE inhibitor could also turn to the CONSENSUS-II acute myocardial infarction study to bolster these positions. Conversely, subgroup analyses from other large studies appear to refute these observations. With the proven benefits of both of these agents independently and the overlapping clinical profile of pa­tients that should be receiving these therapies simultaneously, this becomes a critical question to resolve.

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Ocella Side Effect Info: In the short term, broad-inclusion analysis of 96,712 patients, aspirin was used at baseline in 86,884 (89.4%) and not in 10,228 patients (10.6%). Aspirin use was not randomized and, as it turns out, there was a marked disparity in risk profile with respect to use of aspirin. Patients who did not receive aspirin were less likely to receive thrombolytics or beta-blockers, were older, and were more likely to have had pulmonary congestion as is manifested by Killip Class 2 and 3. Not surprisingly, regardless of ACE inhibitor status, the non-aspirin-treated patients had more than twice the mortality rate (14.4 vs. 6.5%, no aspirin vs. aspirin) in these short-term studies. The test for heterogeneity between the reductions in risk of death produced by randomization to the ACE inhibitor in the presence or absence of aspirin use at baseline was not significantly different. This analysis is inclusive of CONSENSUS-II, which is frequently cited as an example of an aspirin-ACE interaction where no benefit of the ACE inhibitor was observed in the presence of aspirin.

Since we have not had (and are unlikely to have) a direct two-by-two test of these two proven agents, interpretation of the information from the existing studies must suffice to generate our clinical conclusions. Along these lines, it is fortunate that use of ACE inhibitors for reduction of cardiovascular events is an extremely well-studied area. Particularly so in patients with myocardial in­farction, with over 100,000 patients in randomized trials and the majority on aspirin, providing a good data set from which to draw these conclusions. Just as the antiplatelet trialists have formed a collaboration to collectively extract more data from their individual studies, so have the ACE inhibitor myocardial infarction investigators. Representatives from eight major trials have pooled their individual data to provide more precise point estimates and to particularly probe prospective subgroup analyses for both efficacy and safety. The ACE Inhibitor Myocardial Infarction Collaborative group prospectively determined that the broad-inclusion, short-term studies should be analyzed separately from the elec- tive-inclusion, long-term studies. Both of these systematic overviews (metanal- ysis) have been completed and recently published.

Symptomatic arterial occlusive disease generally occurs when the artery lumen is reduced to half normal. Atherosclerosis is by far the most common cause of peripheral arterial occlusive disease. Other etiologies must be considered in individuals who do not have risk factors for atherosclerosis or in those who have an unusual distribution of arterial occlusive disease. These etiologies include Ta­kayasu arteritis and giant cell arteritis. Both of these arteritides may result in stenosis of any extremity vessel, visceral vessels, or the aorta. Other forms of vasculitis also result in symptomatic arterial occlusive disease. Thromboangiitis obliterans should be suspected if the distal arteries of the upper and lower extrem­ities are involved, particularly in those who smoke cigarettes. Acute arterial occlusion occurs as a consequence of embolism or thrombosis in situ. Thrombosis can develop acutely in atherosclerotic arteries or it can occur in locations such as the renal arteries in the presence of antithrombin-III deficiency.

Symptomatic lower extremity atherosclerosis is reported in 3% of those individuals over age 50. In individuals greater than 70, over 25% have evi­dence of peripheral arterial occlusive disease by noninvasive testing. The preva­lence of peripheral arterial disease is threefold greater when determined by nonin­vasive testing for arterial stenosis rather than by questionnaires regarding symptoms, consistent with the observation that two-thirds of affected individuals are asymptomatic by traditional history. Yet, in a recent community screening program, these asymptomatic individuals had lower functional capacity than those without peripheral arterial disease, as well as an increased risk of cardiovas­cular death.

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Ocella Side Effect Info: Noninvasive testing for lower extremity arterial occlusive disease provides objec­tive information that, together with the history and physical examination, is used to make decisions regarding further evaluation and treatment. These tests can be used for screening, for physiological assessment of hemodynamically signifi­cant stenosis, and to follow-up after revascularization procedures. The most sim­ple and widely used noninvasive test of extremity arterial occlusive disease is measurement of systolic pressure using a sphygmomanometric cuff and a Doppler device to detect arterial flow. Duplex scanning extends the capabilities of nonin­vasive testing by identifying anatomical and physiological information at the sites of arterial stenoses.

Three-dimensional arterial reconstruction using magnetic resonance im­aging (MRI) arteriography and spiral CT arteriography can provide non­invasive assessment of the distal aorta and iliac vessels, but presently with less clarity than is available with invasive arteriography. Contrast arteriography is necessary to completely evaluate the anatomical extent of disease in the distal aorta and lower extremity arteries. It is generally performed only in order to determine the optimal revascularization procedure because of its invasive nature and risk. The functional significance of the arterial occlusive disease can be confirmed by invasive pressure measurements proximal and distal to the stenosis, and can be determined before and after administration of a vasodilator.

The combination of B-mode ultrasound scanning and pulsed Doppler interrogation allows noninvasive assessment of the anatomy and hemodynamic abnormalities in the arterial segments from the distal aorta to the popliteal trifurcation. For exam­ple, soft plaque and thrombi may have similar acoustic properties to blood and, therefore, may not be detected by B-mode imaging, but they will result in a flow disturbance that can be detected by Doppler evaluation. Equipment for peripheral arterial testing includes a linear array transducer, operating at a gray-scale fre­quency of 4 to 10 MHz, and capable of providing frequencies above 3 MHz for Doppler signal analysis. Gray-scale imaging is used to examine the arteries and the presence of detectable atherosclerotic plaque or thrombus. The pulsed Doppler spectral analysis is used to document the presence of blood flow and to determine blood flow velocity. Normal Doppler waveforms in the lower extremity will be triphasic, with a peak velocity less than 120 cm/s. Color Doppler flow mapping allows for a rapid survey of the arteries in order to identify those sites where more labor-intensive and precise Doppler spectral analysis is needed. Still, full evaluation of the lower extremity arteries takes from 1 to 2 h.

Duplex examination can be combined with exercise testing to detect disproportionate velocity increases with exercise and therefore identify the le­sions responsible for a patient’s symptoms. The duplex scan is potentially supe­rior to angiography in the evaluation of iliac artery, and in determining the hemo­dynamic status of ostial lesions in the profunda and superficial femoral arteries. Peripheral artery bypass grafts can be followed serially with duplex ultrasonogra­phy. The first month after surgery and every 1 to 2 years following surgery are key times to identify early changes consistent with stenosis within the graft. The criteria for discrete stenosis in bypass grafts is similar to that in native ves­sels. In addition, a peak systolic velocity that is decreased to 45 cm/s indicates a dramatically increased likelihood of graft failure and provides a rationale for early intervention. In addition, duplex evaluation is likely to be similarly useful in the follow-up of peripheral arteries following percutaneous revascularization.

Our use of the term or terms Ocella Side Effect Info is for descriptive purposes only. There is no relationship between the owners of this website and the maker of the product discussed in this post. Our use of the words Recall, Class Action Lawsuit and other similar words related to an event do not necessarily mean that this event has occurred. Refer to the website of the United States Food and Drug Administration for information on drug or medical device recalls. If a Class Action Lawsuit is formed in relation to the product discussed in this post we will provide that information at the time the Class Action is formed. A Class Action Lawsuit is not required to exist for you to file a lawsuit if you have been injured by the product discussed in this post.

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Pradaxa Lawsuit News – 2/9/2012:

If you were prescribed Pradaxa and have suffered negative side effects, please contact us today so that we can put you in touch with an attorney to advise you of your legal rights.

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Pradaxa Lawsuit: There are over 795,000 new and recurrent strokes each year. Someone in the United States has a stroke every 40 seconds. Stroke is the third leading cause of Leath in America today— and a leading cause of long-term akult disability. Approximately 160,000 people die from stroke every year— and 5.5 million survivors continue to suffer its aftermath. One out of every ten families is touched by stroke.

The American Stroke Association’s definition says it all: “A stroke occurs when blood flow to the brain is interrupted by a blocked or burst blood vessel.” Period. But this sudden disruption can be years in the mak-ing. It can be the result of clogged blood vessels in the brain, the buildup over time of the fatty cholesterol deposits that translate into atherosclerosis. This disruption also can be created from a blood clot that travels to the brain from another part of the body, a clot that can become lodged in the blood vessels and, acting like a dam, stop”ping the blood supply from getting through to hungry cells.

Or, less commonly, a stroke can be caused by a weakness in blood vessel walls. This vulnerability, present from birth or from uncontrolled high blood pressure, eventually can cause a blowout in the vessel. The blood then will hemorrhage, or leak out, into the brain. But whatever the disruption, the result is the same: the area beyond the clogged blood vessel, beyond the clot, beyond the hem”orrhaging blowout, is not getting the blood supply that it needs. Like a lawn that isn’t watered in a drought, this area of the brain begins to dry up, to shrivel. The brain cells that aren’t “watered” will die very quickly.

TIA is a name to remember. It stands for transient ischemic at”tack and it can save your life. Sudden blurred vision, numbness or weakness, or difficulty in speaking that lasts only a few min”utes or less than twenty-four hours can be a sign that things are amiss—and that it’s time to take immediate care of yourself. In fact, if you experience these transient symptoms, you should call 911, immediately go to the emergency room, and hopefully pre”vent a stroke.

Whoever coined “There’s more here than meets the eye” could very well have been a neurologist. Frankly, it’s not much to look at. A brain looks like a well-used sponge. But appearances lie. The brain is bursting with energy. It consists of billions of nerve cells called neurons. And these neu”rons are settled in specific locales that are responsible for every”thing from the way we eat to the food we like. And this so-called “sponge” can soak up so much information that nothing, not even the most sophisticated computer in the world, can compare to it. Nothing. As with most things, organization, delegation, and record keeping are crucial factors in its success. Despite its lumpy ap”pearance, the brain is very active and very well organized—and in touch with all its “employees.”

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Pradaxa Lawsuit: Veins, arteries, and nerves—all are intertwined, all are intricately spread throughout our bodies. When we touch a hot plate with our fingers, when we step on a nail, when we bang into the corner of a table, when we sip an ice-cold glass of champagne, when”ever our senses are involved, so is our peripheral nervous system, sending our sensations, or stimuli, to our brain for responses. In normal brain functioning, the brain sends messages back down to those nerve endings, telling us to move our fingers from the hot plate or feel the pain of the nail, the table corner, the ice-cold ache of sipping a drink. The peripheral nervous system is like a vast messenger service, the adjunct staff so important to any suc”cessful organization.

The brain feeds on oxygen, which is extracted from red blood cells. It’s assured a constant supply from the high-speed pumping action of the heart, which, despite the soul-searching words of poets and philosophers, is actually a “hard-body” muscle that is about the size of a fist. This “fist,” however, can squirt a jet of life-sustaining blood several feet. You can feel this jet of blood surging through your body by taking your pulse. Each beat of your pulse pushes out about one cup of blood into your bloodstream. But quality is more important than quantity. Believe it or not, our bodies contain only about twelve pints—or twenty-four cups—of blood. This is equivalent to approximately six quarts of milk or the weight of one Thanksgiving turkey.

The twelve pints of blood pumped by the heart are, in effect, used over and over again. They go around and around in an endless circle throughout our bodies, delivering the blood’s oxygen to all our organs and taking away their wastes. This process is called circulation. Briefly, here’s how it works: The heart is divided into four chambers, the. right and left atrium and the right and left ventricle. The oxygen-filled blood from the lungs comes into the left atrium of the heart. It moves into the left ventricle and is pumped out into the bloodstream through the aorta, the “king” of all arteries. From the aorta, blood, carrying our body’s fuel and food, travels through its passageways called arteries. The walls of the arteries are very elastic; they are muscular tubes that branch out, becom”ing smaller and smaller, until they are only one cell thick.

Fuel and oxygen can pass through them. These tiny arteries are called capillaries. The hungry cells in the body, from the muscles to the brain, from the kidneys to the liver, “eat” their fill and deposit carbon dioxide through their cell walls. The depleted, waste-carrying blood now begins its journey home through the veins. The blood is now more sluggish. The heart has used most of its energy to pump oxygen-rich blood into the body; it has less “oomph” for the return trip. Thus, the veins have little “pockets” or valves that catch any “back”flow” to make sure the blood keeps moving toward the heart and doesn’t get backed up. The veins get bigger and bigger until they reach the right atrium of the heart. As the heart pumps and clenches, this blood is pushed into the right ventricle, where it travels to the lungs and fills up once again with oxygen. This oxygen-rich blood journeys back to the left side of the heart, and the cycle begins anew.

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Pradaxa Lawsuit: Like the water in your house, circulation needs pressure to keep moving. Your blood pressure is what keeps your blood flowing and moving in a rhythmic way through your arteries. When you get your blood pressure taken, the upper num”ber in the reading, called the systolic pressure, reflects how hard your heart has to squeeze and contract to push the blood through your arteries. A high reading means that your heart is having to squeeze too hard to keep your blood moving. The lower number, or the diastolic pressure, reflects the pressure in your arteries while the heart rests between beats. A high number here means that the pressure remains elevated even when your heart is resting between beats.

Blood flow, its rhythm and pressure, can be affectedby hered”itary factors, kidney disease, weight gain, and cholesterol, a waxy substance that is carried through the bloodstream. As it builds up, cholesterol is deposited on the arterial walls. Eventually, the walls of the arteries thicken to the point where blood may not get through. If these deposits occur in the arteries feeding the heart, this can result in a heart attack. If they accumulate in the arteries feeding the brain, this can result in a stroke.

The brain has a hungry man’s appetite. It needs 20 percent of the total blood supply to get the oxygen and food that it needs. The crucial arteries through which the heart pumps blood up to the hungry brain are called the carotid arteries. Both the right and the left carotid arteries are all-important, branching out into a series of arteries in the front of the neck and into the brain. These arteries grow smaller and smaller as they travel, allowing all the areas of the brain, from the thalamus to the hippocam”pus, from the frontal to the temporal lobes, to get “served” with oxygen-rich blood.

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Pradaxa Lawsuit: Blood. We can be upset by the sight of it or donate it to save a life. But whatever the “gut feeling,” blood is literally a carrier—of life. Think of it as a highly reputable moving van, a transporter that carries necessary food to our cells. And there is much more than meets the eye in its red color. If you put a drop of blood under a microscope, you’d see all of the following: Plasma is the liquid that holds the blood cells; it gives the blood its consistency. The red blood cells (or corpuscles) hold the food. They con”tain the oxygen and the other nutrients (in the chemical form of glucose) that the body needs to survive. After the various organs finish their “meal,” these red blood cells head for the veins, carry”ing back the “empty plates” to the heart. Red blood cells also give the blood its red color.

The white blood cells are the “superheroes.” They respond to “foreign invaders/’ both by fighting infection and by increasing in number when infection or inflammation threatens the body. The platelets are responsible for clotting. When you cut yourself, platelets “rush in” and begin to create a web, a micro”scopic gauze of fiber, that traps other blood cells to stop the flow of blood. Problems can arise, however, in the most well-oiled ma”chine—and the human body is no exception. Clotting is crucial if you fall and hurt your knee, if you step on that ever-present nail. However, especially as we get older, our arteries can narrow and develop rough areas, which draw the attention of the platelets.

Our use of the term or terms Pradaxa Lawsuit is for descriptive purposes only. There is no relationship between the owners of this website and the maker of the product discussed in this post. Our use of the words Recall, Class Action Lawsuit and other similar words related to an event do not necessarily mean that this event has occurred. Refer to the website of the United States Food and Drug Administration for information on drug or medical device recalls. If a Class Action Lawsuit is formed in relation to the product discussed in this post we will provide that information at the time the Class Action is formed. A Class Action Lawsuit is not required to exist for you to file a lawsuit if you have been injured by the product discussed in this post.

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Pradaxa Lawyers News – 2/9/2012:

If you were prescribed Pradaxa and have suffered negative side effects, please contact us today so that we can put you in touch with an attorney to advise you of your legal rights.

Pradaxa Lawyers: The year is 1890. A jowl-faced gentleman is enjoying his mutton and ale at a local pub. His pipe sits nearby, an after-dinner treat. He is laughing at something his companion is saying. They are talking loudly; smoke fills the crowded, hot room; steam covers the small, high windows. Suddenly, without warning, the

gentleman starts to cough. He can’t stop. His face turns red. His head falls into his food. It’s a few weeks later. The gentleman is alive, but he’s a stranger. He babbles. He can’t move his right arm. He forgets things. The doctor calls it apoplexy. The priest calls it possession. The family is bereft. They wait for him to heal or die. As each day passes with no change, they hope for the latter.

Turn now to 1940. A different man, a salesperson, is trying to convince a customer to buy his company’s widgets. He smokes, his cigarette a counterpoint to his almost nonstop sales pitch. It’s no go. The salesperson, disgusted, leaves the office building and grabs some lunch at a local greasy spoon. On the way back to his car, he suddenly feels light-headed and dizzy. He collapses. A few months later, this same man is back on the beat, put­ting even more hours into his workdays to make up for lost time. His doctor calls his recovery luck. His family calls it a miracle. The salesperson doesn’t know what it means, but he’s glad that everything is back to normal. Sitting on a stool in a different greasy spoon, he orders extra butter on his toast and lights an­other cigarette.

Today, we know better. Thanks to the biomedical and scien­tific inroads made in the past few decades, now not only can we diagnose stroke, but we can determine why it hit and where. And even more important, unlike the stroke victim a cen­tury ago or the uninformed modern man of the 1940s, we can take steps to prevent stroke from striking—again.

When we first see a stroke patient, we determine who he is and if there was a predisposition to the condition. This involves a de­tailed history, including any individual risk factors that may or may not be present: hypertension, a lifetime of smoking, diabetes, a prior TIA. If any of these are present, they can help determine who this stroke patient is. Background clues also are helpful in coming up with a diag­nosis and subsequent treatment plan. These include work habits, gender, and race.

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The physician-detective also must determine exactly what hap­pened and exactly what the event was that took place. A stroke is a general term. Physicians need to know more than “She sud­denly fainted” or “He fell down in midspeech.” They will ask questions to pinpoint the event in more specific terms. What was the patient doing? Did you feel your heart skip beats? Had he just complained about a headache or a numb feeling in his limbs? Then there are the more technical questions. As we have seen, knowing the type of stroke is crucial. Did it occur from an embolism traveling from the heart? Or was it thrombotic in nature, the result of a clogged-up artery in the brain?

But, in general, the more questions physicians ask, the more they can flesh out the event and the more accurately the stroke can be diagnosed. In some cases, even with good information, your doctor may not be able to determine with certainty whether an embolic or thrombotic stroke occurred. Where is a powerful word. As we now know, the type of stroke is one thing and its location in the brain quite another. Where is the damage? What part of the brain is involved? In addition to sophisticated x-rays, CT scans, and MRI scans, this question also is answered through language, motor, cognitive, and emotional evaluations, which we also will be go­ing over later in this chapter. These tests not only help determine the extent of the damage, but also the functions that still are pre­served. The rehabilitation team will immediately start to build on what skills remain intact.

Look beyond the surface and there’s always a “why.” Whether it’s a family argument, an office problem, or a physical condi­tion, understanding why something has occurred can go far in preventing it from happening again. And even more important, understanding the disease process that caused a patient’s stroke also can help prevent it from recurring. Examining who, what, where, and why will help determine the action needed—whether it is treatment with medication, sur­gery, or rehabilitation.

Echocardiogram, or ultrasound. A step beyond an elec­trocardiogram (EKG), this uses sound as a detector. It is useful for detecting the heart as a source of an embolus. A device, con­nected to a computer, is placed on a patient’s chest or neck and bounces sounds waves off the heart’s walls and the arteries of the neck. These sound-wave echoes (or ultrasound) are recorded and analyzed by the connected computer. If a blood clot is present in the heart or the carotid artery in the neck is narrowed, sound waves bouncing back to the ultrasound machinery can draw a picture of the problem. Your doctor may request a transesopha­geal echocardiogram (TEE) to get a better look at your heart and aorta. By painlessly swallowing a small probe, the sound waves can get closer to their desired target.

CT scan. Often this is the first test administered to obtain specific information, outlining the severity, the type, and the location of the stroke. This is particularly important in light of some of the newer “clot-busting” medicine we use to treat stroke. Although a “dry” stroke (where a plugged-up artery creates a “drought” in the brain past the blockage) may not show up for a few days, it is important to rule out bleeding in the brain before using these medications.

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Pradaxa Lawyers: During the CT scan itself, a patient lies down inside what has been described as a giant white doughnut; the CT scan, hooked up to a computer, then takes sophisticated pictures of the inside of his brain, “peeling” off slices, layer after layer, of tissue. MRI. Magnetic resonance imaging (MRI) provides a much more detailed picture of the size and location of a stroke than a basic CT scan. An MRI is, in simple terms, a superconducting magnet, creating a powerful magnetic force that, with the aid of radio frequencies, can take pictures of the brain. Because its images are based on molecular principles, an MRI is not bound by the same constrictions as a CT scan. It can take pictures of the brain past any skeletal structures; it can depict extraordinary details of specific, minute areas within the brain. An MRI can show areas of the brain that have had previous damage during a “silent” stroke. An MRI is particularly good at looking at the brain stem and cerebellum.

SPECT and PET scans. Although PET scans may sound like x-rays performed on your favorite cat or dog, both PET scans, and their “cousin” SPECT scans, are diagnostic tools that take imaging one step further. A combination of chemistry and tech­nology, positron emission tomography (or PET) and single pho­ton emission computed tomography (or SPECT) actually map the metabolic activity of the various chemicals in the brain via an injection of a “tagged” radioactive liquid. They take pictures of the biochemical reactions that occur in the liquid message’s journey through the brain’s blood vessels. Their exquisite detail actually can show the inactivity caused by a stroke.

In the future, these scans may be an excellent tool to monitor the effects of medicines on blood flow in the brain. Angiography. This still is the test of choice for visualiz­ing the cerebral arteries—-and, subsequently, any pathological changes caused by stroke. Pictures of the blood vessels in the neck and brain are obtained in one of two ways: Magnetic resonance angiography (MRA) is performed with an MRI machine; it safely produces pictures of the larger arteries in the brain and neck. Higher-quality images are obtained with a conventional angiogram; it requires a liquid dye to be injected directly into the artery. Doctors can see if there is any narrowing caused by clots or lesions as the dye speeds along. Unfortu­nately, an angiogram is an invasive test. And there are risks. People can develop allergies from the dye that is injected to make the arteries visible. Fortunately, new technology and improved dyes have greatly decreased these risks.

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Pradaxa Lawyers: Today, thanks to the advances made in neurology, pharma­cology, science, and technology, medication therapy is more ef­fective than ever. We now know the anatomy of the brain. We now know the intricate maneuvers of blood and its substances as it surges through the passageways of the body. We now know how blood coagulates—and its biological, neurological, and emo­tional aftermath. To help you understand the action behind the words, we have described the most common medications used in treating stroke. But please note that the following lists are meant only as a brief introduction to medication therapy. None of these are a substitute for your doctor. Nor should any of these medications be administered without your doctor’s supervision.

Almost everyone today has heard of the medicine that helps dis­solve blood clots in the heart’s arteries and stop heart attacks dead in their tracks. But it is only since June 1996 that the clot-busting drug tPA (Tissue Plasminogen Activator) has been approved by the FDA for use in ischemic strokes. In an ideal situation, tPA dissolves the clot, blood returns to the oxygen-starved brain, and the patient’s paralysis goes away. Overall, the use of tPA reversed the effects of stroke in 12 percent of patients and significantly improved functional outcomes. But there is a real downside: bleeding into the brain with worsening of the stroke occurred in patients 6 percent of the time.

It makes sense. Because most infarctions occur from clotted blood clogging an artery, a medication that can prevent blood from clot­ting should go far in preventing stroke. Thus, the anticoagulants were born. Although most people say these medications “thin” blood, this is not really true. Rather, anticoagulants prevent clot formation. The anticoagulant Heparin is administered through a vein directly into a blood vessel and its use is restricted to the in­patient setting. Patients may be started on Heparin in the hospital and then are switched to Coumadin®, an oral anticoagulant, for outpatient use.

Aspirin seems to work best in those patients who have had a TIA or a stroke. It can prevent additional, more severe attacks and also can decrease death from other vascular causes, such as heart attack. Many physicians will tell patients with multiple risk factors (diabetes, heart disease, high cholesterol) to take aspirin even though they have not had a stroke or TIA.

Our use of the term or terms Pradaxa Lawyers is for descriptive purposes only. There is no relationship between the owners of this website and the maker of the product discussed in this post. Our use of the words Recall, Class Action Lawsuit and other similar words related to an event do not necessarily mean that this event has occurred. Refer to the website of the United States Food and Drug Administration for information on drug or medical device recalls. If a Class Action Lawsuit is formed in relation to the product discussed in this post we will provide that information at the time the Class Action is formed. A Class Action Lawsuit is not required to exist for you to file a lawsuit if you have been injured by the product discussed in this post.

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Pradaxa Recall – 2/9/2012: If you were prescribed Pradaxa and have suffered negative side effects, please contact us today so that we can put you in touch with an attorney to advise you of your legal rights.

Pradaxa Recall: Before the clot or deposit disappears, symptoms may appear. As with a completed stroke, the symptoms of TIA also depend on the area of the brain where the blood supply was inter­rupted. Unfortunately, because these symptoms disappear, some­times within minutes, they are often ignored. Furthermore, be­cause they are often vague or mild, we quickly ignore them. After all, who wants to believe that they could be having a stroke? But therein lies the danger of TIA. Yes, its symptoms fade, but the underlying mechanisms that created it still are hidden within our bodies. Blood still can be filled with cholesterol. Artery walls still can be vulnerable. Clots still can be forming.

Temporary weakness, numbness, or paralysis of the hand, arm, leg, or face on one or both sides of the body. These are the most crucial “red flag” symptoms. They are not only the most common characteristics of TIA, but if immediately brought to your physician’s attention, they can save your life. One note: this weakness or numbness is not the same thing as the “pins and nee­dles” you feel when, for example, your foot falls asleep. It comes on quickly and leaves just as fast. Sudden blurred, dimmed, or complete loss of vision in one or both eyes that lasts longer than a few seconds. Sudden loss of vision in one eye can signal an embolus to the main artery to the eye, and the loss of vision in both eyes can be the result of inadequate blood flow to the occipital lobes.

Speech, and language difficulties. This can involve having trouble actually speaking and understanding the spoken word (aphasia) or the written word (alexia). Slurred or “thick” speech (dysarthria) is a sign of a vertebrobasilar TIA, which is a TIA in the arteries at the back of the brain. Lack of coordination or balance. Technically, this condi­tion is yet another A term: ataxia. It can involve arms or legs— resulting in difficulty holding a glass or walking. It is a sign of vertebrobasilar insufficiency.

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Pradaxa Recall: Dizziness is one of the most common symptoms of vertebrobasilar TIA, affecting the back of the brain where the vertebral and basal arteries reside. Seventy percent of all people who have this type of TIA experience this dizziness. But vertigo must be combined with other symptoms for it to signify an at­tack. For example, dizziness without numbness, weakness, or speech problems is rarely a sign of TIA. Nausea or vomiting or both. Alone, these symptoms are too vague to point to TIA, but in combination with vertigo, speech problems, or loss of balance, they can signal a possible attack.

A transient ischemic attack is reversible. Heeding its warn­ing signs can go far in preventing a stroke. But sometimes the “dreaded impossible” occurs, despite our best intentions and our best care. Sometimes a stroke will strike—and in the next section, we’ll see exactly what symptoms it creates and, most important, how it can be treated. The location of the stroke is the other crucial element. It’s a fact: most strokes occur in only one side, or hemi­sphere, of the brain. And their symptoms will appear on only one side of the body, the side opposite the affected hemisphere in the brain. In other words, when a stroke strikes the right hemisphere of the brain, it will affect the left side of the body. When a stroke strikes the left hemisphere of the brain, it will affect the body’s right side.

The most common symptom of stroke is paralysis on one side of the body. This phenomenon can be total or partial, affecting, for example, the fine motor movements of our hands and feet or cre­ating a numbness or paralysis in our entire leg or arm. Further, it is not unusual to have total paralysis of a hand or foot but still be able to move a shoulder or hip. Numbness or paralysis, however, is only one part of the story. Each hemisphere also controls different thinking, speaking, and infor- mation-processing functions. A stroke in the right hemisphere can affect, for example, memory, attention span, and impulse control. A stroke in the left side of the brain can affect language skills and cognition, which is, literally, the act of knowing.

But not every stroke is found in the right or left hemisphere of the brain. As with most situations, there are exceptions to every rule. Although less common than their “right-left” counterparts, some strokes occur in the brain stem or in the cerebellum. Strokes here may affect movement, balance, and basic body functions, such as swallowing and breathing. Of course, we usually don’t see every symptom in every per­son who suffers a stroke. Nor are every person’s symptoms the same. But when stroke strikes a specific area, there are enough similarities to make pinpointing the location a help in diagnosis and, ultimately, in the rehabilitation outcome.

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Pradaxa Recall: As we have seen, the right and left hemispheres of the brain con­trol different functions. But like most things in life, they aren’t divided neatly in two. They work in concert, one adding dimen­sion to the other, one overlapping the other within every aspect of our personality—from thinking to speaking, from performing to perceiving. But depending on the specific function, one side does domi­nate the other. The right hemisphere is more in control of our visual organi­zation, perception, and attention. It adds meaning and substance to what we see. The right brain also is responsible for nonverbal communi­cation, for the slang, inflection, style, and gestures that go along with our conversations with others. Furthermore, our right hemisphere also is involved in our ability to perceive space, to understand where we are, what we are looking at, what we are doing, and why various objects are placed where they are.

Neglect can mean many things. It can mean a failure to focus on the outside world. Or a lack of attention. Or, in its extreme, an inability to recognize that one has even had a stroke. In 1981, Dr. M. Mesulam isolated the attention network in the brain. He found that the small reticular formation, found deep within the brain stem, is responsible for general arousal and wakefulness. The parietal lobes concern themselves with sensory cues, and the frontal lobes help coordinate our actual activities. The limbic system provides the necessary desire and motivation to interact with our environment.

Although the left hemisphere controls most of our basic language skills, from vocabulary to pronunciation, the right hemisphere provides its color. Indeed, studies have shown that to rebuild lan­guage skills, rehabilitation teams must include nonverbal, right- brain-oriented programs. Patients who have suffered a right- brain stroke might lose their speech inflection; their words might come out flat. Similarly, they might not be able to pick up the inflection, emotion, or meaning of someone else’s conversation. In scientific terms, prosody is the color that we add to our state­ments that make them questions or exclamations. Aprosody is its loss, a result of right-brain stroke.

It makes sense. Sensory impairment, memory loss, neglect, lack of attention—these separate symptoms of stroke can, unfortu­nately, culminate in other symptoms, such as time disorientation, impaired abstract thinking, and, ultimately, poor judgment. This inability to judge and decipher events and situations is particular­ly dangerous because, more times than not, it shows itself when it comes to safety measures. Walking out of the house in a bathrobe and slippers; getting behind the wheel of a car without a license, glasses, or a sense of direction; preparing lunch in the kitchen without recognizing the difference between dishwasher powder and salt—all these are hazardous to a stroke patient’s health.

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Pradaxa Recall: It’s also true, as we have seen, that the left hemisphere works in concert with the right, and that language and comprehension skills are found in both. But, here, in the left hemisphere, speech disturbances come out in different ways: words might not be un­derstood nor physically produced. Depression, too, is more common in left-hemisphere stroke than when stroke strikes the supposedly more emotional right side.

Left-hemisphere language difficulties, or aphasia, can take other forms. In fact, approximately 85,000 of those Americans who are stricken by stroke every year suffer aphasia. Mary had a nonfluent aphasia with an ability to say only a few words. Other people might have a fluent aphasia where they have many words available and they can also make up phrases. One of our patients would say “spoof ” instead of “spoon” and “prazum” instead of “please.”

Repeat phrases over and over again. A former stroke pa­tient of ours would, at one time, declare, “Hallo, hallo, hallo,” at any time and at any place, despite the situation. When a nurse would come in to change his linen, he’d say, “Hallo, hallo, hal­lo.” When a visitor would get up from a chair to leave, he’d say, “Hallo, hallo, hallo.” When he first went home, he found himself repeating this phrase over and over again—in the supermarket, on the street, and over dinner. Hear something other than what you said. Another patient of ours could pronounce his words just fine. But he couldn’t un­derstand much of what we said. To him, our conversations were gobbledygook, a foreign language that he couldn’t penetrate. Instead of “Good morning, Mr. Smith. How are you today?” he heard something else—the gist of which we may never know.

Suffer from Broca’s (nonfluent) aphasia. These patients will, like Mary, have problems speaking. Their conversations will be slow, full of effort, and ungrammatical. Initially, they will not be able to write or be able to read more than a few words. Have trouble picking out individual words. One of our pa­tients, a middle-aged woman, could speak just fine. She could understand what others said to her. But put a book, a magazine, or a newspaper in front of her and, without directions, she was at a loss.

Our use of the term or terms Pradaxa Recall is for descriptive purposes only. There is no relationship between the owners of this website and the maker of the product discussed in this post. Our use of the words Recall, Class Action Lawsuit and other similar words related to an event do not necessarily mean that this event has occurred. Refer to the website of the United States Food and Drug Administration for information on drug or medical device recalls. If a Class Action Lawsuit is formed in relation to the product discussed in this post we will provide that information at the time the Class Action is formed. A Class Action Lawsuit is not required to exist for you to file a lawsuit if you have been injured by the product discussed in this post.

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Pradaxa Side Effects News – 2/9/2012:

Did you take Pradaxa? Please contact us today if you took Pradaxa and later experienced harmful side effects. We will connect you with a lawyer that is experienced in complex litigation that may be able to help you recover monetary damages.

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Pradaxa Side Effects: If there is one single highest risk factor in stroke, it is high blood pressure, or hypertension. A national survey found that between 40 percent and 70 percent of the people who had strokes also had high blood pressure. The groundbreaking Framingham study, which has followed more than 5,000 men and women for more than fifty years, continues to find that people with hypertension are two to four times more likely to have a stroke than those with normal pressure. And the Systolic Hypertension in Europe Study showed that even moderately high blood pressure can cause a stroke.

In addition, the blood vessels themselves are getting extra wear and tear and weakening to the point where a stroke is possible. And finally, high blood pressure can accelerate atherosclerosis, or hardening of the arteries, and increase the risk of heart disease, both of which are additional risk factors in stroke. Yes, there is no doubt that hypertension is deadly. What makes it worse is the fact that there are no symptoms. It is com-pletely silent, carrying on its destruction quietly over time, un”til the buildup of pressure and weakened artery walls result in a stroke.

In the past, people did not know they had hypertension until it was too late, until they had a stroke or a heart attack. Today, more and more adults, are becoming savvy. They get their blood pressure checked at least annually. Indeed, studies have found that the successful treatment of hypertension can dramatically reduce the risk of stroke by more than 40 percent.

High blood pressure can be regulated. You are in control. But some of the risk factors of stroke are beyond your powers. They are simply a fact of life. Aging is one of them. As you age, your arteries become more fragile. They are less elastic and flexible. They become brittle. This hardening of the arteries is called atherosclerosis. The more the buildup of athero”sclerosis, the more likely these arteries are to clog or close off. If this occurs in the brain, it will result in stroke.

At first glance, diabetes seemingly has nothing to do with stroke. After all, it is a disease that impairs the body’s ability to control the level of sugar. But below the surface of that definition is a very strong—-and dangerous—connection. Diabetes can affect circulation. And poor circulation can affect the blood vessels, es-pecially the small capillaries in the eyes. Here, because of weak”ened, impaired blood vessels, diabetes can cause hemorrhages and blindness. Likewise, similar hemorrhages within the brain.

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Pradaxa Side Effects: We all talk about it. We check labels for it. We get our blood checked for it. But many of us are not quite sure what cholesterol is—or its connection to disease. Basically, cholesterol is a waxy material that the body manu”factures, and, believe it or not, it’s natural and necessary for many of our functions. But today, there can be too much of a good thing. Not only does the body manufacture cholesterol, but cholesterol also is found in many of the foods we eat, such as steak and eggs. And saturated fats found in such foods as meat, cheese, milk fat, shortening, and even margarine contribute even more to higher blood cholesterol levels than does dietary intake of cholesterol.

Cholesterol is carried in the bloodstream by lipoproteins, a “shopping cart” substance of fat and protein produced by the liver. The lipoprotein that does most of the work is low-density lipoprotein (LDL) cholesterol. All well and good, but once the body has taken what it needs, the LDL is still floating around, all dressed up with nowhere to go. Eventually, this floating LDL cholesterol settles on the artery walls, clogging passageways or causing clots that could break off and travel to the brain. This is why LDL is called “bad cholesterol.” But LDL does not travel alone.

The risk of high cholesterol comes from the amount of LDL in the bloodstream. Cholesterol has received most of its press from its relationship with heart attacks. Indeed, until recently, cholesterol has not been considered a risk for stroke. But new re”search has shown that lowering cholesterol is important in stroke prevention. A recent study of the new “statin” drugs showed that by lowering LDL cholesterol by 23 percent to 42 percent, the risk of stroke was decreased by 29 percent. In short, cholesterol levels, especially LDL cholesterol, must be watched. The current recommendation is keep your choles”terol below 200MG/DL, and if your LDL is more than 100MG/ DL you should be on a statin medication. High-risk patients with multiple risk factors should try to get their LDL down to 70MG/ DL. And if your levels are high, help decrease the numbers by eating a low-fat diet, taking cholesterol-lowering medication, and exercising regularly. You are never too young to know your cho”lesterol level and to start working on a healthy lifestyle.

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Pradaxa Side Effects: It is a fact—-smoking doubles the risk of having a stroke. That’s right, you are twice as likely to have a disabling stroke if you smoke. Smoking has a major distinction: it is the most pre”ventable of all the risks for stroke. Simple. But, as anyone who has ever smoked knows, quit”ting is easier said than done. Even though studies have found that smokers are one and one-half to three times more at risk for stroke than nonsmokers, even though smoking adversely affects circulation and blood supply, and even though the risk of smok”ing is high with or without taking into account high blood pres”sure, heart disease, and age, many people continue to smoke.

Birth control pills have helped shape the way we think, the way we act, and, obviously, the way we conceive. They helped give birth to women’s rights. They influenced an entire generation of young adults. But as the years pass, studies have found that there are some side effects with oral contraceptives. One of these is the risk of stroke, especially in women over the age of thirty who .have a history of hypertension and smok”ing. One study of stroke in young women discovered that certain women who used birth control pills were at an increased risk for stroke compared to women who did not. This risk increased in women who have hypertension. And other studies show there is also a connection between oral contraceptives, heavy cigarette smoking, and stroke. The overall risk is quite small, so you need to weigh it against the fact that pregnancy itself carries a risk. The decision is difficult, but women who are older, hypertensive, and smoke should consult their doctors regarding the risks of taking birth control pills.

Unfortunately, this decline has plateaued recently, which further shows that other risk factors must be treated as well. A lower-fat diet that is also lower in salt, exercise, weight loss, no smoking, even taking one drink of alcohol a day (but don’t forget that heavy drinking increases the risk of stroke!)—all these can help reduce the risk of stroke. And reducing one risk factor can have a favorable outcome on the others. As we have seen, many conditions are related: high cholesterol and hypertension, obesity and diabetes. Treating one of these factors can help treat another.

Pradaxa Side Effects: Information and News

Pradaxa Side Effects: It’s called a thrombosis, the most common form of stroke. In fact, 80-85 percent of all strokes are ischemic in nature. Here, the blood flow in the brain, either deep in its interior or in the less deep carotid artery in the neck, is blocked because of a clot that forms in the artery. Atherosclerosis is its greatest influence. Think of it. Either through cholesterol deposits or aging, the in”side walls of the arteries become less flexible; thick deposits of fat form, and passageways become too narrow for blood to flow through smoothly. Instead, the blood forms a clot around these thick deposits as it tries to get past.

Ironically, these clots usually begin as a healthy measure. The deposits or rough places on the artery wall are seen by the body as a “call to arms,” a need to stave off infection. The blood, thinking these areas need repair, clots around them. Platelets send out their thin clotting fibers. Red and white blood cells join in the action. Soon, the clotting has a life of its own, acting like a net as it pulls platelets, red blood cells, even bits of floating cholesterol into its web. A scab can form, making the mass of cholesterol and blood even thicker.

This type of stroke, too, is caused by a clot. These embolic strokes are less common than their thrombotic cousin. But these clots, called emboli, are the traveling salespeople of stroke, a mass of tissue, blood, and cholesterol that originates somewhere else in our body, usually in the heart or the neck’s carotid artery, only to end up in the brain. Here, when the clotting action occurs, a piece of clot eventually breaks off. This clot, or embolism, is carried by the bloodstream to the brain, where the arteries are smaller. Soon, the clot gets stuck, literally plugging up the passageway beyond it. Blood simply cannot get past the embolism.

Our use of the term or terms Pradaxa Side Effects is for descriptive purposes only. There is no relationship between the owners of this website and the maker of the product discussed in this post. Our use of the words Recall, Class Action Lawsuit and other similar words related to an event do not necessarily mean that this event has occurred. Refer to the website of the United States Food and Drug Administration for information on drug or medical device recalls. If a Class Action Lawsuit is formed in relation to the product discussed in this post we will provide that information at the time the Class Action is formed. A Class Action Lawsuit is not required to exist for you to file a lawsuit if you have been injured by the product discussed in this post.

To keep up to date on Pradaxa Side Effects visit our site often.

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Cymbalta Withdrawal Lawsuit News – 2/21/2012: Did you take Cymbalta? Please contact us today if you took Cymbalta and later experienced harmful side effects. We will connect you with a lawyer that is experienced in complex litigation that may be able to help you recover monetary damages.

Cymbalta Withdrawal Lawsuit: When a pregnant woman fails to eat enough vital nutrients, birth defects can also develop. Good nutrition during pregnancy helps a fetus to grow and develop normally. Calcium is needed for bones to grow. Brain cells cannot develop correctly without ade­quate protein. Nerve cells need folic acid, a B vitamin, to develop normally. Indeed, lack of folic acid is linked to spina bifida, a birth defect in which the neural tube that connects the brain to the spinal cord does not develop properly. As a result, the spinal cord is exposed and nerves that go from the spinal cord to the legs, bowels, and bladder do not function normally.

Some birth defects are the result of fetal exposure to infectious agents that cause sexually transmitted dis­eases. During birth, such exposure can occur in the birth canal. Exposure to genital warts in this manner can cause warts to grow on the baby’s vocal cords, causing the baby to have problems making sounds. Exposure to gen­ital herpes can cause the baby to have skin and mouth sores, brain damage, mental retardation, and blindness.

Other sexually transmitted diseases also cause dam­age. Syphilis can cause brain damage, cerebral palsy, blindness, and hearing loss, as well as death. Chlamydia, which is one of the most common of all sexually trans­mitted diseases, causes a blinding eye infection, while gonorrhea can cause a life-threatening blood infection, as well as problems in a baby’s joints. There are many birth defects that are believed to have un­known multifactorial causes. A clubfoot, in which the joints, bones, and muscles in the foot and ankle malform, and a cleft lip or palate, in which the mouth or lip malforms, are two examples.

Birth defects can occur in any baby. However, some babies are at greater risk. These include babies born to women exposed to dangerous substances and infections, babies that do not receive adequate prenatal nutrition, and babies born to families with a history of inherited diseases. Even when a family does not have a history of an inherited disease, members of certain ethnic groups are more likely to carry the gene for a particular inherited disease than members of other groups. For example, people of African descent are at a greater risk of developing sickle-cell anemia than individuals of other ethnicities. An estimated 1 in every 375 African Americans has the disease compared to 1 in every 72,000 Non-African Amer­icans. And about 8 percent or 3.5 million African Americans are carriers of the sickle-cell gene.

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Cymbalta Withdrawal Lawsuit: A pregnant woman’s age can also put a baby at risk. Babies with Down syndrome are more likely to be bom to older mothers. Ac­cording to the March of Dimes, the chance of a woman in her twenties having a baby with Down syndrome is 1 in 1,230. At age thirty-five the chance is 1 in 270. At forty the risk rises to 1 in 78, and at forty-five the chance increases to 1 in 22. Scientists do not know why this is so. Other problems arise because older mothers are likely to give birth to more than one baby per pregnancy. This is often because many older women have difficulties becoming pregnant and use fertility treatments, which encourage multiple gestations.

For a woman of any age, multiple births put a baby at risk of birth defects. One reason is that multiple fetuses must share nutrients, oxygen, and blood. Therefore, they receive less of these vital sub­stances than a single fetus. It is not surprising then that almost 60 percent of twins, 90 percent of triplets, and almost all higher multi­ple births are born prematurely, putting them at risk of developing cerebral palsy and other birth defects linked to premature births. Identical twins face an extra risk. Because identical twins form from one egg that divides and forms two fetuses, only one pla­centa connects both of them to the mother. Fifteen percent of iden­tical twins develop a problem called twin-to-twin transfusion syndrome, in which the shared placenta contains abnormal blood vessels that send too much blood to one fetus and not enough to the other. If not corrected through surgery, both babies can die.

Obesity also raises the risk of birth defects. Obese and over­weight women have an increased risk of having babies with heart abnormalities, spina bifida, and omphalocele, a defect in which the baby’s intestines protrude through the navel. Accord­ing to the Centers for Disease Control, 9 to 15 percent of babies born to obese women have a serious birth defect compared to 3 to 5 percent of babies born to women of normal weight. Scientists have not determined why obesity raises the risk of birth defects. The)’’ theorize that many obese women have poor eating habits. They often consume nutrient-poor junk food rather than more nourishing foods. This may lead to the fetus not get­ting adequate protein, calcium, and B vitamins.

About 250 birth defects can be identified before a baby is bom, including Down syndrome, spina bifida, heart defects, gastroin­testinal and kidney malformations, and missing and malformed limbs. Tests administered to expectant mothers detect these prob­lems. When a pregnant woman first visits a doctor, she is given a blood test. The test determines the mother’s blood type and whether she does or does not have a protein in her blood known as the Rh factor. There is no problem if the mother’s blood con­tains this protein. If her blood does not, however, but the father’s blood does, the fetus’s blood will also contain it. This makes the mother’s and the fetus’s blood incompatible. When this occurs, the mother’s immune system produces antibodies that attack the fetus, causing cerebral palsy and heart problems. To prevent this, a series of injections are given to the mother. These prevent the production of the destructive antibodies.

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Cymbalta Withdrawal Lawsuit: An ultrasound test is administered in the same time frame as the triple-marker test. It allows the doctor to see how the fetus is de­veloping and how fetal organs are forming and functioning. Struc­tural defects are often, but not always, detected with ultrasound. During an ultrasound test the health care professional rubs a special sound-conducting gel on the pregnant woman’s abdomen. Then, a small handheld device similar to a scanning wand is passed across the pregnant woman’s internal organs. It produces sound waves that bounce off the woman’s abdomen back to the wand. The reflected sound waves form a pattern, which a com­puter program translates into an image of the fetus on a com­puter monitor.

Some birth defects like fragile X syndrome, muscular dystrophy, and cerebral palsy are not evident at birth, nor are they recogniz­able in infants, A child with cerebral palsy may never develop the ability to walk without assistance. However, since all infants are unable to walk, an infant with cerebral palsy appears to be nor­mal. As the baby grows, a birth defect is suspected if he or she fails to acquire intellectual, motor, or speech skills on par with his or her peers. It is usually the parent who first notices a problem.

When parents suspect a problem, a developmental evaluation is done. First the pediatrician compares the baby’s progress to nor­mal developmental milestones such as sitting by seven months and walking by fourteen months. Then, specialists evaluate the child. These specialists often include a neurologist who looks for nerve damage, an orthopedic specialist who examines the pa­tient’s bones and muscles, an audiologist who checks for hearing loss, and an ophthalmologist who looks for visual problems. Fetal surgery poses risks for both the mother and the fetus. Fe­tal surgery can cause death or premature birth of the fetus. The mother faces excess bleeding and infection. Therefore, fetal surgery is usually reserved for severe lung abnormalities, along with meningocele, a type of spina bifida that surgery can cure. When these defects are corrected before birth they are less damaging than when the defect is corrected after the baby is bom.

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Cymbalta Withdrawal Lawsuit: In most cases birth defects are not treated until after birth. When a newborn baby is diagnosed with a serious birth defect such as heart, kidney, or lung problems the infant is placed in the neona­tal intensive care unit (NICU) of the hospital. Like the intensive care unit of a hospital, the NICU has a specially trained staff and special equipment designed to treat and monitor ill newborns. Most babies in the NICU are kept in isolettes, small heated beds enclosed by clear plastic. Isolettes provide newborns with a warm quiet environment. Wires and tubes connect each baby to a variety of instruments that measure its heart rate, breathing, oxygen level, and blood pressure. For instance, wires attached to three electrodes placed on the baby’s chest connect to a car­diorespiratory monitor, a machine that records the newborn’s heart and breathing rates.

Babies that need help breathing may be attached to a ventila­tor. This machine pushes air in and out of the baby’s lungs via a tube placed in the infant’s windpipe and connected to the venti­lator. Other tubes deliver medicine and food. Some newborns are administered medication intravenously. Among other things, such medication may be needed to help the baby’s heart work, fight infection, or stimulate breathing. If the baby cannot take food normally, he or she is fed intravenously.

Sometimes the only way to save an infant’s life is with surgery to correct a birth defect. For example, infants born with hydro­cephalus, a birth defect related to spina bifida, can die if the defect is not treated. When individuals have hydrocephalus, dangerous amounts of fluid gather in the blood vessels of the brain, causing the head to swell. But surgery, in which a tube called a shunt is placed in a blood vessel, moves the excess fluid out of the brain to the baby’s abdomen. Sometimes a baby is bom with a heart, kidney, liver, or other or­gan that is so impaired that the only way to save the baby’s life is through an organ transplant. At other times, damage from cys­tic fibrosis can cause a child’s lungs to fail later in life, making an organ transplant necessary.

Vital organs are taken from organ donors—people who had agreed that, upon their death, their organs were to be donated to others. Permission to take organs may also be granted by the fam”ilies of the deceased. Unfortunately, there are many more people in need of donated organs than there are organs available. So, sick children are put on a waiting list until a suitable organ is found. Yvette, whose daughter Bianka had a heart transplant, recalls: “The doctors told me it could take a week or months for a match to come in. They also told me she could die waiting.”

Our use of the term or terms Cymbalta Withdrawal Lawsuit is for descriptive purposes only. There is no relationship between the owners of this website and the maker of the product discussed in this post. Our use of the words Recall, Class Action Lawsuit and other similar words related to an event do not necessarily mean that this event has occurred. Refer to the website of the United States Food and Drug Administration for information on drug or medical device recalls. If a Class Action Lawsuit is formed in relation to the product discussed in this post we will provide that information at the time the Class Action is formed. A Class Action Lawsuit is not required to exist for you to file a lawsuit if you have been injured by the product discussed in this post.

To keep up to date on Cymbalta Withdrawal Lawsuit News visit our site often.

Cymbalta Withdrawal

Journalist Mark Bonokoski, recently featured in the London Free Press, has stirred up a lot of controversy in a recent article. While discussing a letter sent by activists to Zimbabwe Dictator Robert Mugabe requesting that he does not reopen the country’s asbestos mines, Bonokoski recommended that the mines indeed be opened to save the economy of the struggling nation. While the opening of this mine may mildly stimulate the nation’s economy, it will also greatly increase the number of serious and fatal diseases found in the region. Exposure to asbestos has been linked toasbestosis, lung cancer and mesothelioma, and is estimated to kill more than 107,000 people globally every year.

In the same article, Bonokoski weighed-in on Canada blocking an international agreement to restrict the sale of chrysotile asbestos. He said of Canada’s pro-asbestos actions: “Quite simply because it was the right thing to do.” Bonokoski defended his statement by saying that since the government of Quebec awarded a $58-million loan to the owners of the Jeffrey Mine in Asbestos, Quebec, they couldn’t simply just throw their money away. Apparently Bonokoski believes that two wrongs will make a right.

It is time to ban asbestos throughout the world to prevent exposing any more people to this deadly mineral. Bolstering the global asbestos trade by mining and manufacturing this silent killer should be the last idea on the minds’ of our leaders and journalists.

Asbestos