Myocardial Infarction Unstable Angina Research Articles

GW26-e0235 Lipid among Patients Presented with Acute Myocardial Infarction Unstable Angina and Stable Angina Pectoris

GW26-e0235 Lipid among Patients Presented with Acute Myocardial Infarction Unstable Angina and Stable Angina Pectoris

Dynamic Use of B-Type Natriuretic Peptide–Guided Acute Coronary Syndrome Therapy

BackgroundVery few studies have evaluated the potential of using B-type natriuretic peptide (BNP) and N-terminal pro-B-type natriuretic peptide (NT-proBNP) as surrogate markers to guide clinical interventional or conservative therapy decisions. AimThe aim of the current study was to evaluate the potential of using BNP and NT-proBNP as surrogate markers to guide clinical interventional or conservative therapy decisions. MethodsWe identified randomized controlled trials that randomized patients with acute coronary syndrome (ACs) of unstable angina and myocardial infarction without sT-segment elevation ACs to early invasive therapy versus a more conservative approach by systematic search of articles and databases. ResultsFive randomized controlled trials with a total of 8125 patients and with a mean duration of 11.2months were included in the meta-analysis. At a mean follow-up of 11.2months, the incidence of all-cause mortality was 5.9% in the early invasive group, compared with 6.8% in the conservative group (risk ratio = 0.74; 95% confidence interval, 0.59-0.86; P = 0.001). Conclusionsin summary, BNP/NT-proBNP-guided management of ACs is significantly improved by early invasive therapy by improving long-term survival and reducing nonfatal myocardial infarction for unstable angina. However, there does not seem to be a clear benefit of using such a strategy over existing clinical recommendations.

Recent advances in the management of unstable angina and non-Q-wave myocardial infarction

Recent advances in the management of unstable angina and non-Q-wave myocardial infarction

Activation of blood coagulation by plaque rupture: Mechanisms and prevention

Inhibition of thrombosis is proving to be an important treatment goal in many clinical situations, including coronary thrombolysis, angioplasty, and unstable angina. Heparin is a potent inhibitor of thrombin and thrombin generation, but its ability to accelerate thrombolysis, prevent acute reocclusion after vascular injury in angioplasty, and prevent myocardial infarction in unstable angina is relatively limited, possibly because clot-bound thrombin plays an important role in these clinical situations. Thus, when thrombin binds to fibrin, it remains enzymatically active and relatively impervious to inactivation by heparin or other fluid-phase inhibitors. However, direct thrombin inhibitors—such as d-Phe- l-Pro- l-Arg-CH 2CI (PPACK), hirudin, hirugen, and hirulog—inhibit free and clot-bound thrombin with equal efficacy, presumably because their sites of interaction are not masked when thrombin binds to fibrin. Advanced clinical trials suggest that the direct thrombin inhibitors and 7E3, an inhibitor of platelet glycoprotein IIb/IIIa, will soon be incorporated into the armamentarium against arterial thrombosis.

Drugs or Diet

Early observations that the regular use of aspirin (acetylsalicylic acid, ASA), a nonsteroidal anti-inflammatory agent, seemed to protect against myocardial infarction and reduce platelet aggregation made this substance the most frequently used drug in large clinical trials. The objectives of these studies were to reduce thromboembolic complications in arterial cardiovascular diseases (prevention of myocardial infarction in unstable angina, secondary prevention of acute myocardial infarction, and increased patency of aortocoronary bypass grafts) and to reduce platelet deposition on artificial surfaces (artificial heart valves and hemodialysis shunts). Despite the recent synthesis of more selective inhibitors of arachidonic acid metabolism in blood platelets, and a multitude of questions concerning optimal dose, schedule, and mode of action that still remain open, ASA continues to be the most frequently used drug in arterial vascular disorders. Because of the frequent and potentially serious side effects of aspirin, mainly on the gastrointestinal tract, less toxic ways of inhibiting eicosanoid metabolism in blood platelets are attracting more and more interest. Among these, the alimentary substitution of omega-3 fatty acids for a competitive inhibition of the omega-6-arachidonic acid metabolism seems the most promising. Results with fish-oil diet raise the question of whether substitution of polyunsaturated lipid acids influence only platelet metabolism, or whether the action of "anti-platelet" drugs or diet in cardiovascular disorders is mediated primarily by leukocytes or monocytes. This new dietary principle, which possibly corrects only a poor alimentary habit of civilization, could open simple and adequate ways for even a primary prophylaxis of vascular disease by diet alone or, at least for therapeutic aims, in combination with drugs.