Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Diabetic cardiomyopathy as a distinct entity was first recognized by Rubler et al. in diabetics with congestive heart failure (CHF), who had no evidence of coronary atherosclerosis. The Framingham study showed a 2.4-fold increased incidence of CHF in diabetic men and a 5.1-fold increase in diabetic women over 18 years. Pathological studies show left ventricular hypertrophy and fibrosis with varying degrees of small vessel disease, the functional significance of which is uncertain. Hypertension was recognized as an important cofactor in the development of fatal congestive heart failure in diabetics. On cardiac catheterization, in patients symptomatic of heart failure, either congestive or restrictive patterns have been observed. In contrast, asymptomatic diabetics had decreased left ventricular compliance but normal systolic function on hemodynamic study. Noninvasive studies show alterations in systolic and especially diastolic function, particularly in diabetics with microvascular complications and/or coexistent hypertension. Using load-independent measures of contractility, however, systolic function was generally found to be normal in asymptomatic normotensive diabetics. Experimental studies have focused on the mildly diabetic dog and the severely diabetic rat. Decreased left ventricular compliance and increased interstitial connective tissue were observed in chronically diabetic dogs. In contrast, ventricular myocardium from diabetic rats exhibits a reversible decrease in the speed of contraction, prolongation of contraction, and a delay in relaxation. These mechanical changes are associated with a decreased myosin ATPase, a shift in myosin isoenzyme distribution, alterations in a variety of Ca2+ fluxes, and changes in responses to alpha- and beta-adrenergic and cholinergic stimulation. These biochemical changes may be secondary to alterations in carbohydrate, lipid, and adenine nucleotide metabolism in the diabetic heart.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Diabetic cardiomyopathy. 808 30

From 1988 through 1991, 1663 patients underwent a first reoperation for isolated coronary bypass grafting with 62 (3.7%) in-hospital deaths. At the primary operation, 575 patients had received at least one internal thoracic artery graft and 489 patients had at least one patent internal thoracic artery graft present at the time of reoperation. At reoperation, 1014 patients received at least one internal thoracic artery graft, 10 received an inferior epigastric graft, and 37 received a gastroepiploic graft. Of 489 patients with patent internal thoracic artery grafts at reoperation, the internal thoracic artery was damaged in 17 (3.5%); of 428 patients with a patent internal thoracic artery graft to the left anterior descending coronary artery, 14 (3.3%) had graft damage necessitating regrafting. All patients with damaged internal thoracic arteries survived. Multivariate testing of variables for their association with in-hospital mortality identified no internal thoracic artery graft at either primary surgery or reoperation (p < 0.0001), a history of congestive heart failure (p < 0.0001), advancing age (p = 0.018), female gender (p = 0.029), and emergency operation (p = 0.01) as factors linked to increased risk. Left ventricular function, left main stenosis, extent of native coronary atherosclerosis, and the interval between operations did not influence mortality. Furthermore, the presence of an atherosclerotic vein graft to the left anterior descending coronary artery a factor shown to increase in-hospital risk in previous studies did not increase risk during these years. We attribute the observation that patent internal thoracic artery and atherosclerotic vein grafts do not appear to be factors specifically increasing the risk of reoperation to the use of retrograde cardioplegic solution and increased surgical experience. The use of internal thoracic artery grafts at a primary operation does not increase the risk of a reoperation, and the use of internal thoracic artery grafts at reoperation does not increase in-hospital morbidity or mortality.
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PMID:Influence of arterial coronary bypass grafts on the mortality in coronary reoperations. 812 96

Until recently, only three calcium channel antagonists--verapamil, diltiazem and nifedipine--were available for managing cardiovascular disorders such as hypertension and ischemic heart disease. In the past few years, however, several dihydropyridine calcium channel antagonists, including nicardipine, isradipine, felodipine, nimodipine, and amlodipine, have been marketed. Others are currently awaiting FDA approval. In addition, bepridil, which belongs to a new class of calcium channel antagonists, has recently been marketed for refractory angina pectoris. Clinical uses of calcium channel antagonists have been expanded since the 1970s to include management of cardiovascular disorders such as supraventricular arrhythmias, CHF secondary to diastolic dysfunction, and myocardial reinfarction in selected patients. Calcium channel antagonists are also being investigated for prevention of atherosclerosis. Calcium channel antagonists are a heterogeneous group of pharmacologic agents. Differences in tissue selectivity are largely responsible for the variations in hemodynamic and electrophysiologic properties of these agents. Thus, their clinical uses and side effect profiles differ. These differences must be taken into consideration in the selection of the most appropriate agent for a specific indication. Potential advantages of some of the newer dihydropyridine calcium channel antagonists include less frequent dosing (amlodipine and isradipine) and little or no negative inotropic effect (nicardipine, felodipine, amlodipine, isradipine) compared with the prototype calcium channel antagonists. Additional clinical experience with these newer agents is required, however, before their role in the management of cardiovascular disorders can be fully delineated. The availability of sustained-release formulations of verapamil, diltiazem, nifedipine, felodipine, and nicardipine, as well as the recent marketing of calcium channel antagonists with relatively long half-lives (amlodipine and isradipine), makes once- or twice-daily dosing possible with most calcium channel blockers. However, selection of a particular agent will depend on several factors, including clinical efficacy, side effect profile, cost, and patient characteristics such as concomitant disease states and baseline hemodynamic status.
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PMID:Use of calcium channel antagonists for cardiovascular disease. 821 73

A 66 year old man with mild hypertension developed congestive cardiac failure of rapid onset associated with a continuous epigastric murmur suggesting an arteriovenous fistula. Doppler ultrasonography, computed tomography, magnetic resonance imaging and abdominal arteriography showed the fistula to arise from a large thrombosed aneurysm of the hepatic artery which had ruptured into the portal vein. Echocardiography and radionuclide angiography showed normal left ventricular systolic function. The patient underwent aneurysmorrhaphy and suture of the portal vein without any complications and the murmur and signs of cardiac failure disappeared. Histological examination showed the arterial lesion to be due to atherosclerosis. The authors underline the rarity of aneurysms of the hepatic artery and, above all, of their rupture into the portal system as there have only been 7 previously reported cases. Fistulae of the portal system are usually well tolerated, the commonest complication being portal hypertension. Cardiac failure is an exceptionally rare occurrence: it may be observed when the fistula develops suddenly and has a high flow rate, and in patients with abnormal myocardial function.
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PMID:[Congestive cardiac failure secondary to hepatico-portal arteriovenous fistula. Apropos of a case and review of the literature]. 821 73

Effective treatment of hypertension in the elderly requires an understanding of both the progressive course of the disease and the impact of aging on the cardiovascular system, including physiological, genetic, lifestyle, and environmental factors. Review of the literature that has attempted to define the impact of an "aging process" on cardiovascular structure and function reveals a diversity of findings and interpretations. However, in general, normotensive elderly subjects exhibit the heart and vascular characteristics of "muted" hypertension, including many features of younger hypertensive patients: cardiac hypertrophy, diminution in resting left ventricular early diastolic filling rate, increased arterial stiffness and aortic impedance, diminution in the baroreceptor reflex, a diminished response to catecholamines and diminished renal blood flow, and an increase in peripheral vascular resistance (PVR). Treatment of elderly hypertensives is more challenging because of the greater likelihood of the presence of concomitant diseases, most importantly, coronary and peripheral atherosclerosis, renal dysfunction, and diabetes mellitus. Isolated systolic hypertension (ISH), the most common form of hypertension in the elderly, has also been clearly shown to be an important predictor of cardiovascular morbidity and mortality, including coronary artery disease, congestive heart failure, and stroke. Treatment of ISH has been shown to lower systolic pressure safely and effectively in the elderly. By reducing PVR, and possibly the arterial stiffness, and thus the early reflected pulse waves, vasodilators, including calcium antagonists, may lower these three components of arterial impedance, and hence lower the arterial load on the heart. The cardiac hypertrophy and reduced left ventricular filling rate associated with hypertension in older individuals can also be ameliorated, to some extent, by calcium channel blockers.
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PMID:Hypertension in the elderly: age- and disease-related complications and therapeutic implications. 824 Oct 7

A 70-year-old man developed hypertension many years previously and had a bout with severe congestive heart failure 4 to 5 years before his death. Autopsy showed congestion and edema characteristic of heart failure, and enlarged heart, and slight focal interstitial left ventricular fibrosis, but only slight to moderate coronary atherosclerosis.
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PMID:Congestive heart failure in a patient with systemic hypertension. 824 13

In the United States, congestive heart failure (CHF) was the underlying cause of death for approximately 38,000 persons in 1990; of those deaths, approximately 92% were among persons aged > or = 65 years. CHF, a clinical syndrome defined as a chronic inadequate contraction of the heart muscle resulting in insufficient cardiac output, is a manifestation of one or more underlying conditions, including systemic or pulmonary hypertension or a history of other heart diseases (e.g., myocardial infarction, atherosclerosis, cardiomyopathy, congenital heart disease, or rheumatic fever). The long-term prognosis of CHF depends on the underlying condition and the response of that condition to treatment. Despite declines in death rates for ischemic heart disease and cerebrovascular disease, improvements in detection and treatment of hypertension, and considerable advances in the diagnosis and management of CHF, mortality from CHF has increased since 1980. This report summarizes trends in CHF mortality in the United States during 1980-1990 and presents state-specific mortality data for 1990 (the most recent year for which such data are available).
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PMID:Mortality from congestive heart failure--United States, 1980-1990. 829 29

Carvedilol is a cardiovascular drug currently used for the treatment of hypertension. Clinical studies have recently demonstrated efficacy in angina and congestive heart failure. Recently, carvedilol has been shown to attenuate oxygen free radical-initiated lipid peroxidation and to inhibit vascular smooth muscle mitogenesis induced by a wide variety of growth factors. These findings are of interest since smooth muscle proliferation and abnormal lipid metabolism are proposed to play an important role in the pathogenesis of atherosclerotic plaque formation and in development of stenotic lesions following vascular injury by balloon angioplasty and coronary artery bypass grafting. On the basis of these observations, the antiproliferative actions of carvedilol have been explored in detail. In human cultured pulmonary artery vascular smooth muscle cells, carvedilol (0.1-10 microM) produced a concentration-dependent inhibition of the mitogenesis stimulated by platelet-derived growth factor, epidermal growth factor, thrombin, and serum, with IC50 values ranging from 0.3 to 2.0 microM. Carvedilol also produced a concentration-dependent inhibition of vascular smooth muscle cell migration induced by platelet-derived growth factor, with an IC50 value of 3 microM. The extensive neointimal formation that occurs following balloon angioplasty of rat carotid arteries was markedly attenuated by carvedilol (1 mg/kg, i.p.; twice daily starting 3 days before angioplasty and continuing until 14 days after angioplasty). Quantitative image analysis demonstrated that carvedilol reduced the neointimal growth following angioplasty by 84% without altering either medial or adventitial cross-sectional areas. These observations indicate that carvedilol may also be effective in the treatment of pathological disorders principally associated with abnormal vascular smooth muscle growth, such as atherosclerosis and acute vascular wall injury induced by angioplasty or coronary artery bypass grafting.
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PMID:Carvedilol, a cardiovascular drug, prevents vascular smooth muscle cell proliferation, migration, and neointimal formation following vascular injury. 832 99

In 103 hearts with various forms of cardiac muscle hypertrophy the following parameters were estimated: diameter, length, volume, density and number of myocytes, and density of myocyte nuclei. The values of all histometric parameters correlated well with left ventricular (LV) weight up to 350 g. In heavier hearts these parameters remained approximately of the same magnitude. The number of myocytes was significantly higher in hearts with LV weight above 250 g. The influence on LV weight of age, coronary artery diameters, degree of atherosclerosis, weight and percent of fibrous tissue was also evaluated. On the basis of a linear discriminant function, hearts were divided into three classes: (1) LV weight < or = 250 g (absence of hyperplasia, hypertrophy only); (2) LV weight 251-350 g (hypertrophy+signs of hyperplasia); (3) LV weight > 350 g (marked signs of hyperplasia). The percent of fibrosis increased proportionally to LV weight. Where LV weight was above 250 g there was a subsequent increase in the mean percent of fibrosis (approx. 26%). This phenomenon (plateau of percent fibrosis) is the result of an increased number of myocytes (myocyte hyperplasia). We suggest that, independent of aetiology, in all hearts above 350 g (patients with congestive heart failure) hyperplasia phenomenon exists.
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PMID:Hypertrophy or hyperplasia in cardiac muscle. Post-mortem human morphometric study. 843 76

Preexisting cardiovascular conditions (angina pectoris, intermittent claudication, stroke or transient ischemic attack, and congestive heart failure) were evaluated in relation to long-term prognosis after an initial MI in 828 subjects from the Framingham Heart Study. Preexisting angina pectoris and intermittent claudication in men were associated with increased risk of coronary mortality and recurrent MI, whereas congestive heart failure increased coronary mortality. In women, prior angina pectoris increased the risk of recurrent MI and congestive heart failure increased the coronary mortality. Adjusting for the major cardiovascular risk factors measured before MI, these results held for men but no significant adverse effects persisted in women. Among subjects who survived to return for subsequent examinations, only prior congestive heart failure in men increased the risk after adjusting for post-MI risk factors. In women who returned, angina pectoris and intermittent claudication were associated with poor post-MI prognosis. These results suggest that atherosclerosis is a diffuse disease of the circulatory system, and one in which post-MI prognosis is influenced by the presence of other preexisting cardiovascular conditions. Hence a patient who has an MI after prior expression of cardiovascular disease requires more vigorous preventive management.
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PMID:Preexisting cardiovascular conditions and long-term prognosis after initial myocardial infarction: the Framingham Study. 843 16


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