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Digoxin did not reduce overall mortality, but it reduced the rate of hospitalization both overall and for worsening heart failure. These findings define more precisely the role of digoxin in the management of chronic heart failure.

Abstract-Numerous studies have used a J-shaped or U-shaped curve to describe the relationship between alcohol use and total mortality. The nadir of the curves based on recent meta-analysis suggested optimal benefit at approximately half a drink per day. Fewer than 4 drinks per day in men and fewer than 2 per day in women appeared to confer benefit. Reductions in cardiovascular death and nonfatal myocardial infarction were also associated with light to moderate alcohol intake. Although some studies suggested that wine had an advantage over other types of alcoholic beverages, other studies suggested that the type of drink was not important. Heavy drinking was associated with an increase in mortality, hypertension, alcoholic cardiomyopathy, cancer, and cerebrovascular events, including cerebrovascular hemorrhage. Paradoxically, light-to-moderate alcohol use actually reduced the development of heart failure and did not appear to exacerbate it in most patients who had underlying heart failure. Numerous mechanisms have been proposed to explain the benefit that light-to-moderate alcohol intake has on the heart, including an increase of high-density lipoprotein cholesterol, reduction in plasma viscosity and fibrinogen concentration, increase in fibrinolysis, decrease in platelet aggregation, improvement in endothelial function, reduction of inflammation, and promotion of antioxidant effects. Controversy exists on whether alcohol has a direct cardioprotective effect on ischemic myocardium. Studies from our laboratory do not support the concept that alcohol has a direct cardioprotective effect on ischemic/reperfused myocardium. Perhaps the time has come for a prospectively randomized trial to determine whether 1 drink per day (or perhaps 1 drink every other day) reduces mortality and major cardiovascular events. Key Words: alcohol Ⅲ arrhythmia Ⅲ cardiomyopathy Ⅲ heart failure Ⅲ myocardial infarction A lcohol is an old drug that has attracted human interest for thousands of years. Evidence of wine making was depicted on the walls of the temples of the pharaohs in Egypt and the Sumerians of Mesopotamia. Scientific debate about the risks and benefits of alcohol started in Europe several centuries ago and continues today. How much alcohol should people drink, what should they drink, and who should be doing the drinking are important questions that need definitive answers. This article provides an in-depth analysis of the effect of alcohol on the human heart and its clinical relevance to patient care.A recurring theme is that although high doses of alcohol are harmful to the heart (cardiomyopathy, arrhythmias, and hypertension), mild to moderate alcohol consumption has been associated with reductions in coronary artery disease and even total mortality.When we reviewed the literature, it became very evident that definitions describing how much alcohol is in a drink vary remarkably by article and country, and terms such as light, moderate, and heavy drinking are variably defined. Table 1 provides some of the definitions we could...

It is clear that cocaine has cardiotoxic effects. Acute doses of cocaine suppress myocardial contractility, reduce coronary caliber and coronary blood flow, induce electrical abnormalities in the heart, and in conscious preparations increase heart rate and blood pressure. These effects will decrease myocardial oxygen supply and may increase demand (if heart rate and blood pressure rise). Thus, myocardial ischemia and/or infarction may occur, the latter leading to large areas of confluent necrosis. Increased platelet aggregability may contribute to ischemia and/or infarction. Young patients who present with acute myocardial infarction, especially without other risk factors, should be questioned regarding use of cocaine. As recently pointed out by Cregler, cocaine is a new and sometimes unrecognized risk factor for heart disease. Acute depression of LV function by cocaine may lead to the presence of a transient cardiomyopathic presentation. Chronic cocaine use can lead to the above problems as well as to acceleration of atherosclerosis. Direct toxic effects on the myocardium have been suggested, including scattered foci of myocyte necrosis (and in some but not all studies, contraction band necrosis), myocarditis, and foci of myocyte fibrosis. These abnormalities may lead to cases of cardiomyopathy. Left ventricular hypertrophy associated with chronic cocaine recently has been described. Arrhythmias and sudden death may be observed in acute or chronic use of cocaine. Miscellaneous cardiovascular abnormalities include ruptured aorta and endocarditis. Most of the cardiac toxicity with cocaine can be traced to two basic mechanisms: one is its ability to block sodium channels, leading to a local anesthetic or membrane-stabilizing effect; the second is its ability to block reuptake of catecholamines in the presynaptic neurons in the central and peripheral nervous system, resulting in increased sympathetic output and increased catecholamines. Other potential mechanisms of cocaine cardiotoxicity include a possible direct calcium effect leading to contraction of vessels and contraction bands in myocytes, hypersensitivity, and increased platelet aggregation (which may be related to increased catecholamine). The correct therapy for cocaine cardiotoxicity is not known. Calcium blockers, alpha-blockers, nitrates, and thrombolytic therapy show some promise for acute toxicity. Beta-Blockade is controversial and may worsen coronary blood flow. In patients who develop cardiomyopathy, the usual therapy for this entity is appropriate.

At the conclusion of a primary percutaneous coronary intervention for ST-segment elevation myocardial infarction, and after the cardiologist makes certain that there is no residual stenosis following stenting, assessment of coronary flow becomes the top priority. The presence of no-reflow is a serious prognostic sign. No-reflow can result in poor healing of the infarct and adverse left ventricular remodeling, increasing the risk for major adverse cardiac events, including congestive heart failure and death. To achieve normal flow, features associated with a high incidence of no-reflow must be anticipated, and measures must be undertaken to prevent its occurrence. In this review, the authors discuss various preventive strategies for no-reflow as well as pharmacological and nonpharmacological interventions that improve coronary blood flow, such as intracoronary adenosine and nitroprusside. Nonpharmacological therapies, such as induced hypothermia, were successful in animal studies, but their effectiveness in reducing no-reflow in humans remains to be determined.

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Coronary no-reflow occurs commonly during acute percutaneous coronary intervention, particularly in patients with acute myocardial infarction and those with degenerated vein grafts. It is associated with a guarded prognosis, and thus needs to be recognized and treated promptly. The pathophysiology originates during the ischemic phase and is characterized by localized and diffuse capillary swelling and arteriolar endothelial dysfunction. In addition, leukocytes become activated and are attracted to the lumen of the capillaries, exhibit diapedesis and may contribute to cellular and intracellular edema and clogging of vessels. At the moment of perfusion, the sudden rush of leukocytes and distal atheroemboli further contributes to impaired tissue perfusion. Shortening the door-to-balloon time, use of glycoprotein IIb/IIIa platelet receptor inhibitors and distal protection devices are predicted to limit the development of no-reflow during percutaneous interventions. Distal intracoronary injection of verapamil, nicardipine, adenosine, and nitroprusside may improve coronary flow in the majority of patients. Hemodynamic support of the patient may be needed in some cases until coronary flow improves.