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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cigarette smoking is the most preventable cause of cardiovascular morbidity and mortality. Smoking has been associated with a two-to fourfold increased risk of coronary heart disease, a greater than 70% excess rate of death from coronary heart disease, and an elevated risk of sudden death. These risks are compounded in the presence of hypertension, hypercholesterolemia, glucose intolerance, and diabetes, all of which exhibit a synergistic effect with smoking. The relationship between smoking and the risk of peripheral vascular disease has also been well documented. Smokers account for approximately 70% of patients with atherosclerosis obliterans and virtually all those with thromboangiitis obliterans. An association between smoking and cerebrovascular disease remains a matter of debate, although a higher risk of stoke and stroke-related mortality has been observed in smokers than in nonsmokers. Smoking has also been implicated in the development of cor pulmonale, but a direct association with congestive heart failure has not been established. Nicotine and carbon monoxide appear to play major roles in the cardiovascular effects of smoking. Both components adversely alter the myocardial oxygen supply/demand ratio and have been shown to produce endothelial injury, leading to the development of atherosclerotic plaque. Adverse effects on the lipid profile have been noted as well, but the relationship between these changes and the risk of cardiovascular disease remains to be confirmed. Notably, smoking cessation results in a dramatic reduction in the risk of mortality from both coronary heart disease and stroke. In light of the fact that the incidence of smoking has declined primarily among educated sectors of the U.S. population, future efforts must focus on providing effective education, including smoking cessation techniques, to the less-educated groups.
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PMID:Smoking and cardiovascular disease. 149 5

Nitroglycerin and the long-acting nitrates are widely used in all of the anginal syndromes and have proven effectiveness in relieving or preventing myocardial ischemia. Recent developments into nitrate mechanisms of action provide new insights as to the many anti-ischemic effects of these agents. Important concepts relating to coronary arterial endothelial function are germane to nitrate therapy. Endothelial-derived relaxing factor (EDRF) is presently believed to be nitric oxide (NO), which exerts vasodilatory and/or antiplatelet actions by increasing intracellular cyclic guanosine monophosphate as a result of activation of the enzyme guanylate cyclase. In the setting of coronary atherosclerosis, or even hyperlipidemia without histologic vascular disease, endothelial dysfunction may be present, promoting a vasoconstrictor/proplatelet aggregatory milieu. Nitroglycerin and the organic nitrates are NO donors; NO is the final product of nitrate metabolism, and in the vascular smooth muscle NO induces relaxation, resulting in vasodilation of arteries and veins. In the presence of inadequate EDRF production and/or release, it appears that nitroglycerin may partially replenish EDRF-like activity. Nitrates have long been known to have major peripheral circulatory actions resulting in a marked decrease in cardiac work. Venodilation and arterial relaxation result in a decrease in intracardiac chamber size and pressures, with a resultant decrease in myocardial oxygen consumption. In addition, a variety of direct coronary circulatory actions of the nitrates have been documented. These include not only epicardial coronary artery dilation, but the prevention of coronary vasoconstriction, enhanced collateral flow, and coronary stenosis enlargement. Recent work suggests that the nitrates may also act by preventing distal coronary artery or collateral vasoconstriction, which can reduce blood flow downstream from a total coronary obstruction. Thus, there are many anti-ischemic mechanisms of action by which nitroglycerin and the organic nitrates may be beneficial in both acute and chronic ischemic heart disease syndromes. The unique salutory effects of the nitrates in subjects with left ventricular dysfunction or congestive heart failure make these drugs particularly attractive for patients with abnormal systolic function and intermittent myocardial ischemia. Finally, the emergent role of intravenous nitroglycerin in acute myocardial infarction offers new prospects that nitrate therapy may prove to be beneficial in acute myocardial infarction as well as postmyocardial infarction for the reduction of left ventricular remodeling.
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PMID:Mechanisms of action of the organic nitrates in the treatment of myocardial ischemia. 152 24

Graft arteriosclerosis is the major limitation to long-term survival after heart transplantation. In this study, myocardial pathologic changes, especially those that might permit early diagnosis, were characterized in endomyocardial biopsy specimens and hearts obtained at retransplantation or autopsy from nine orthotopic heart transplant recipients. All had severe diffuse proliferative arterial stenoses without plaque rupture or coronary thrombi. Eight patients died with and one underwent retransplantation because of graft arteriosclerosis less than 12 months (six patients) or greater than 46 months (three patients) after operation. Six patients had antecedent symptoms of congestive heart failure and six had angiographically demonstrated epicardial coronary artery graft arteriosclerosis; four had both. Myocardial ischemic lesions included subendocardial myocyte vacuolization (seven patients) and microfocal to regional coagulation necrosis and granulation tissue or scar, or both (seven patients). Subendocardial myocyte vacuolization (indicative of sublethal ischemic injury) was diagnosed at prior right ventricular biopsy in two patients and was noted at autopsy in areas accessible to right-sided biopsy in three additional patients. Three patients had pathologic changes diagnostic of acute infarction on right or left ventricular biopsy, or both. Thus, all nine patients had lesions, of which five had biopsy-identified myocardial abnormalities caused by graft arteriosclerosis. It is concluded that graft arteriosclerosis yields not only myocardial pathologic changes similar to those associated with typical coronary atherosclerosis, but also lesions resulting from focal or diffuse ischemia caused by small vessel obstructions. This is manifest as subendocardial myocyte vacuolization or microfocal infarction. Recognition of these biopsy-accessible myocardial changes associated with graft arteriosclerosis may allow early recognition and appropriate therapeutic intervention.
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PMID:Myocardial changes in cardiac transplant-associated coronary arteriosclerosis: potential for timely diagnosis. 153 14

Hypertension is a major risk factor for cardiovascular diseases, including coronary artery disease (CAD), stroke, left ventricular hypertrophy (LVH), congestive heart failure, peripheral vascular disease, renal failure, and aortic aneurysms. It is also a potent promoter of atherosclerosis. Observational studies have shown a linear relationship between a wide range of blood pressures and the risk for CAD and stroke. Clinical trials have indicated that hypertension reduction leads to the predicted reduction in stroke incidence, but that CAD incidence is affected to a lesser extent than predicted. The modest effect of traditional antihypertensive drugs on CAD may be due to several factors, including failure to reverse well-established coronary atherosclerosis, particularly if multiple risk factors are not reduced as well. Metabolic side effects of antihypertensive drugs or excessive lowering of blood pressure leading to inadequate myocardial perfusion, especially in patients with increased left ventricular (LV) mass, also may play important roles. Hypertension is a major cause of renal failure, particularly in black males, but control of the hypertension does not necessarily prevent deterioration of renal function. Increased glomerular pressure is thought to play a causative role in the development of renal failure in hypertensive and diabetic patients. Antihypertensive drugs may have a direct effect on the arterial wall, which may be independent of their antihypertensive action. Beta-adrenergic blockers, calcium antagonists, and angiotensin-converting enzyme (ACE) inhibitors inhibit the development of vascular lesions in response to hypercholesterolemia or to iatrogenic balloon injury, but the clinical importance of these observations remains to be determined.
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PMID:Vascular effects of systemic hypertension. 157 75

Hypertension should be detected and treated early in diabetic patients. It markedly affects the morbidity and mortality of diabetic individuals as a result of both atherosclerosis and microvascular disease. Antihypertensive treatment is an effective tool in slowing the progression of early and advanced diabetic nephropathy. No prospective studies have addressed the effects of antihypertensive regimens on the incidence of congestive heart failure, stroke, and coronary artery disease in large groups of diabetic patients. Such studies are urgently needed. Special consideration should be given to the effects of antihypertensive drugs on glycemic control and the lipid profile of the diabetic patient. Because hyperinsulinemia (and insulin resistance) have been advocated as hypertensive and atherosclerotic risk factors, the effects of antihypertensive drugs on insulin action and plasma insulin levels may become an important element in the selection an antihypertensive agent. More information, however, is needed in these areas. ACE inhibitors, calcium channel blockers, and alpha-adrenergic blockers probably offer a more favorable metabolic profile as compared with diuretics and beta-blockers. The former agents should be used as initial drugs in most clinical settings.
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PMID:Management of hypertension in diabetes. 161 71

The most important step in the management of toxicity due to any of the cardiac glycosides is its recognition. Despite the development of an accurate clinical assay for serum levels of digoxin greater than 20 years ago, digitalis toxicity remains common and difficult to confirm, even if suspected, due primarily to 2 factors. First, the signs and symptoms of digitalis toxicity, most commonly an abnormal electrocardiogram showing ventricular or atrial arrhythmias, with or without some degree of concurrent atrioventricular block, often also occur in patients with congestive heart failure (CHF) and underlying coronary atherosclerosis who are not receiving a cardiac glycoside. Second, due to digoxin's narrow therapeutic ratio, the marked degree of variability in the sensitivity of individual patients to its toxic effects, and the common problem of obtaining blood samples inappropriately during the early distribution phase following dosing, a serum digoxin concentration often does not serve as a reliable indicator of toxicity. Despite these difficulties in diagnosis, the management of digoxin toxicity has been made much more effective with the widespread availability of F(ab) fragments of anti-digoxin antibodies. This drug provides the clinician with a rapidly acting, safe antidote for all commonly used digitalis preparations. Conventional therapy for digoxin toxicity remains the maintenance of serum potassium levels greater than or equal to 4 mEq/liter, reversal of decompensated CHF or overt myocardial ischemia, attention to serum magnesium levels and the patient's acid-base status, appropriate antiarrhythmics in the event of ventricular arrhythmias, and a temporary pacemaker for high-grade atrioventricular block. Nevertheless, the high specificity and documented safety of the antibody preparation provides a needed safety net for the continuing use of cardiac glycosides as first-line inotropic agents in the modern therapy of chronic CHF.
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PMID:Recognition and management of digitalis toxicity. 162 85

The hypothesis that diabetes mellitus provokes a specific cardiomyopathy is supported by numerous clinical, epidemiological and anatomopathological studies. However, the frequent association of diabetes mellitus with other conditions, such as hypertension and coronary atherosclerosis, both capable of causing the dysfunction of the cardiac muscle, makes it difficult to interpret many of the data reported in the literature and contributes to the continuing debate regarding the effective existence of diabetic cardiomyopathy and its possible pathogenetic mechanisms. In clinical terms, diabetic cardiomyopathy is manifested both as an altered diastolic and/or systolic phase, assessed using various non-invasive techniques, or as congested cardiac decompensation. The pathogenesis of diabetic cardiomyopathy is still not altogether clear. The alteration of the smallest coronary vessels might be responsible for the increased interstitial fibrosis found in the heart of diabetic patients. In this paper numerous data from the literature on this argument are reported and the authors advance the hypothesis that endothelial dysfunction may play a pathogenetic role in the development of cardiopathy.
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PMID:[Diabetic cardiomyopathy: possible pathogenetic role of coronary microcirculation]. 163 Jun 65

Adrenaline, noradrenaline and dopamine excretion was investigated in essential hypertension (n = 20), atherosclerotic heart failure (n = 20, NYHA class II and III), chronic angina (n = 10) and in healthy controls, in four time intervals: between 600-1200, 1200-1800, 1800-2400, 2400-600. Fluorimetric method of Anton and Sayre was employed. In patients with essential hypertension the circadian rhythm of adrenaline, noradrenaline and dopamine excretion was maintained but in all time intervals excretion of dopamine was decreased. In individuals with congestive heart failure due to atherosclerosis and in patients with ischemic heart disease, physiological circadian rhythm of adrenaline and noradrenaline excretion was found to be abolished. This was not the case with dopamine excretion which was undisturbed.
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PMID:[Hypertension, heart failure and angina pectoris. Diurnal rhythm of urinary excretion of catecholamines]. 164 Jun 65

Antihypertensive therapy has been used for almost 35 years to reduce blood pressure and prevent morbidity and mortality related to the hypertensive state. Malignant, severe, and moderate hypertension have all been shown to be worthy of drug treatment, but controversy remains as to the degree of benefit that is achievable by treating milder hypertension. A variety of clinical trials have demonstrated that antihypertensive therapy reduces the incidence of stroke, congestive heart failure, and left ventricular hypertrophy and the progression in severity of hypertension. The benefits with respect to prevention of coronary heart disease (CHD) have been much less impressive. Thiazide diuretics have been the base therapy for the bulk of the hypertensive subjects studied to date who have not demonstrated reduced incidence of CHD. Therapy with beta-blockers has the potential for reducing CHD, but an analysis of four studies finds only two with positive results. On the other hand, since that study found reduced total mortality as well as CHD compared with thiazide diuretic, its findings cannot be ignored. Other questions deserving further investigation include how other antihypertensive therapies compare with respect to the risk reduction found with thiazide diuretics and beta-blockers, the optimal posttreatment blood pressure, whether persons with mild hypertension benefit from therapy, whether women should be treated differently, and whether atherosclerosis may be affected by specific antihypertensive therapies.
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PMID:Are some antihypertensive therapies more efficacious than others in preventing complications and prolonging life? 167 54

Cardiovascular medicine has evolved steadily over the past two decades. Inspired by progressive declines in the overall incidence and mortality rates from cardiovascular diseases, emphasis has been placed on 3 specific areas: prevention, early diagnosis, and aggressive intervention. During the decade spanning the 1980s, impressive strides were made in many areas--diagnostic and therapeutic alike. However, an observed reduction in patient mortality stemming from acute myocardial infarction was particularly gratifying. Clearly, the large scale use of thrombolytic therapy and postinfarction strategies designed to prevent reinfarction, limit ventricular dilation, and reduce cardiac death figured prominently. Despite these encouraging facts, however, coronary heart disease remains the leading cause of death in Western society, and thrombolytic therapy is still not being utilised by the medical community to its full potential. Furthermore, adjuvant therapy, during both the early and the late phases of acute myocardial infarction, is being instituted inconsistently, and at times haphazardly. Arrhythmia management and the prevention of sudden cardiac death require further investigation, as does the treatment of chronic congestive heart failure, and the prevention of coronary atherosclerosis. This overview provides a state-of-the-art review and look into the future of 5 critical areas: acute myocardial infarction, adjuvant treatment strategies for acute myocardial infarction, cardiac arrhythmias, chronic congestive heart failure, and hyperlipidaemias.
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PMID:Cardiovascular therapies in the 1990s. An overview. 171 42


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