American heart journal
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American heart journal · Oct 1999
Review Comparative StudySafety of glycoprotein IIb-IIIa inhibitors: A heart surgeon's perspective.
Platelet-mediated coronary thrombosis is the primary pathophysiologic mechanism of acute coronary syndromes (ACS) and acute ischemic complications of percutaneous coronary intervention (PCI). The final common pathway of platelet aggregation that leads to thrombotic occlusion of coronary arteries involves cross-linking of receptor glycoprotein (GP) IIb-IIIa on adjacent platelets by adhesive plasma proteins, primarily fibrinogen. Clinical trials of several GP IIb-IIIa inhibitors have demonstrated an unequivocal clinical benefit of this potent antithrombotic therapy in patients with ACS as well as in those undergoing PCI. ⋯ Therefore, among patients requiring CABG after treatment with GP IIb-IIIa inhibitors, eptifibatide and tirofiban may be associated with fewer bleeding episodes than is abciximab. With recent approval of eptifibatide for patients with ACS and those scheduled for PCI and of tirofiban for patients with ACS, the number of patients receiving GP IIb-IIIa inhibitor therapy who subsequently undergo CABG is expected to increase significantly. Strategies for improved management of bleeding complications in these patients, including the choice of a GP IIb-IIIa inhibitor, are clearly needed and are discussed in detail.
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American heart journal · Sep 1999
Randomized Controlled Trial Clinical TrialPulmonary function, cardiac function, and exercise capacity in a follow-up of patients with congestive heart failure treated with carvedilol.
Chronic heart failure causes disturbances in ventilation and pulmonary gas transfer that participate in limiting peak exercise oxygen uptake (VO(2p )). The beta-adrenergic receptor blocker carvedilol improves left ventricular (LV) function and not VO(2p). This study was aimed at investigating the pulmonary response to changes in LV performance produced by carvedilol in patients with chronic heart failure. ⋯ In chronic heart failure carvedilol ameliorates LV function at rest and does not significantly affect ventilation and pulmonary gas transfer or functional capacity. These results suggest that improvement in cardiac hemodynamics with carvedilol does not reverse pulmonary dysfunction. Persistent lung impairment might have some role in the failure of carvedilol to improve exercise performance.
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American heart journal · Aug 1999
ReviewOptimal treatment of patients with acute coronary syndromes and non-ST-elevation myocardial infarction.
Non-ST-elevation myocardial infarction is usually indistinguishable from unstable angina at the initial presentation. The diagnosis is made subsequently when cardiac enzymes are found to be elevated either at admission or within 18 hours. Our understanding of the pathophysiology of acute coronary syndromes has advanced dramatically, and coupled with this understanding has been the introduction of new antiplatelet and antithrombotic treatments. ⋯ Patients at intermediate risk should be treated with aspirin, unfractionated or low-molecular-weight heparin and, if unfractionated heparin is chosen, an adjunctive IIb/IIIa receptor antagonist. Patients at high risk should be treated with the same therapies and considered for expeditious angiography and revascularization as appropriate. A long-term secondary prevention strategy should be implemented.
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American heart journal · Aug 1999
Randomized Controlled Trial Clinical TrialShort-term and long-term hemodynamic and clinical effects of metoprolol alone and combined with amlodipine in patients with chronic heart failure.
Initiation of beta-blocker therapy is often limited by worsening congestive heart failure, which may manifest as worsening hemodynamics. Deleterious hemodynamic effects might be mitigated with the vasodilation of combined calcium channel/beta-blocker therapy. ⋯ There was no further measurable benefit with the addition of amlodipine to metoprolol compared with the effects of metoprolol alone. Therapy with metoprolol alone and the combination of metoprolol and amlodipine was well tolerated in patients with mild to severe heart failure, as evidenced by a lack of adverse effects on hemodynamic parameters over the short term and clinical and hemodynamic improvement with long-term treatment.