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

Little is known of the clinical significance of myocardial bridges, which may be recognized angiographically as systolic coronary artery narrowing (SCAN). A retrospective review of a 1 year's experience (313 consecutive coronary arteriograms) revealed 5 patients with SCAN, an incidence of 1.6%. SCAN involved the proximal and/or middle segments of the left anterior descending coronary artery in all patients. It is of particular note that the administration of nitroglycerin noticeably accentuated the SCAN phenomenon in each of 3 patients to whom it was administered. Four of the 5 patients had left ventricular hypertrophy due to hypertrophic cardiomyopathy (2), aortic stenosis (1), and hypertension (1). All 5 patients with the SCAN phenomenon had anginal chest pains, and critical obstructive coronary atherosclerosis was observed in only 2 cases. The other 3 patients showed, otherwise normal coronary arteriograms. Thus, myocardial bridges appear to be angiographically manifest predominantly in patients with cardiac hypertrophy. Nitroglycerin, which accentuates SCAN, might be useful as a provocative test to enhance the angiographic recognition of this phenomenon. The possible role of myocardial bridges in the production of myocardial ischemia warrants further investigation.
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PMID:Myocardial bridges in man: clinical correlations and angiographic accentuation with nitroglycerin. 40 19

Clinical and morphologic features of transmural myocardial infarction (associated with insignificant or absent atherosclerosis of the extramural coronary arteries) are described in seven patients with hypertrophic cardiomyopathy. Marked chronic congestive heart failure associated with supraventricular arrhythmias occurred in six of the seven patients, each of whom had no or mild left ventricular outflow tract obstruction under basal conditions. No patient had typical angina pectoris, and only one patient had clinically evident acute myocardial infarction. Infarction may have caused cardiac arrest in one other patient, but was "silent" in the remaining five patients. At necropsy, six of the seven patients had extensive myocardial scarring involving the ventricular septum, left ventricular free wall and one or both left ventricular papillary muscles; in four patients portions of the right ventricular wall were also scarred. Six patients had dilated ventricular cavities, including two who were known to have nondilated ventricular cavities earlier in their clinical course. It is concluded that transmural myocardial infarction in the absence of significant coronary atherosclerosis is a not uncommon finding (prevalence rate 15 percent) in a population of patients who had died from hypertrophic cardiomyopathy. Although transmural infarction is possibly a secondary event, it more likely contributes causally to the clinical deterioration of some patients with hypertrophic cardiomyopathy, leading to ventricular dilatation and progressive fatal cardiac failure.
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PMID:Hypertrophic cardiomyopathy and transmural myocardial infarction without significant atherosclerosis of the extramural coronary arteries. 57 70

The incidence of sudden death in athletes is low. Some pathologic conditions, such as hypertrophic cardiomyopathy, coronary artery anomalies, and right ventricular dysplasia may predispose to sudden death during exercise in young athletes. In older individuals, exercise may trigger terminal arrhythmias in patients with atherosclerosis. Screening programs for young individuals undertaking athletic regimens are currently recommended only for those with a suggestive clinical or family history. For older individuals, caution should be advised for patients with known or suspected atherosclerotic disease.
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PMID:Causes of sudden death in athletes. 153 67

Sports-related sudden cardiac deaths were compared with non-sports-related sudden cardiac death in individuals (14 to 40 years old) who were autopsied from 1981 to 1988 at the Maryland Medical Examiner's Office. Thirty-four of 690 total cases of sudden cardiac death were sports-related, which represents 5% of sudden cardiac death in this age group. Causes of death were severe atherosclerosis (nine), hypertrophic cardiomyopathy with asymmetry (eight), coronary artery anomalies (four), idiopathic concentric left ventricular hypertrophy (three), myocarditis (two), arrhythmogenic right ventricle (one), Kawasaki disease (one), and unknown (six); two of the cases with unknown causes had tunnel arteries. Exercise-related deaths were more likely due to hypertrophic cardiomyopathy (p = 0.0007) compared with 102 age-, sex-, and race-matched controls in the non-exercise group; there was no difference in the incidence of severe atherosclerosis (p = 0.4). The mean age of individuals with hypertrophic cardiomyopathy with asymmetry was less than that of those with severe atherosclerosis (24 vs 32 years, p = 0.03). Thus exercise precipitates sudden cardiac death in younger individuals with hypertrophic cardiomyopathy.
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PMID:Sports-related and non-sports-related sudden cardiac death in young adults. 182 9

As many as 40 men suffering from essential hypertension (EH) and left ventricular hypertrophy (LVH) or hypertrophic cardiomyopathy (HCMP) were examined. All the patients exercised on a treadmill according to the Cornell protocol taking into consideration the ST/HR slope and the ST/HR index, underwent echocardiography with measurements of the left ventricular mass (LVM), and coronary ventriculography. Coronary insufficiency was revealed in all the patients. Of these, 11 patients suffered from it due to associated EH and coronary heart disease (CHD), 31 had relative coronary insufficiency in the presence of associated EH and LVH phenomena with no stenosis of coronary vessels, and 7 patients showed up relative coronary insufficiency in the presence of HCMP. The ST/HR slope and the ST/HR index correlated well with the LVM and the asymmetry index of the left ventricle but in patients with associated relative coronary insufficiency and EH. In patients with associated EH and CHD, the ST-dependent parameters correlated well neither with the degree of atherosclerosis spreading nor with the LVM. This may indicate that both factors influence the gravity of coronary insufficiency at a time. In case a patient suffering from associated EH and coronary insufficiency phenomena has the ST/HR slope greater than or equal to greater than or equal to 4.5 microV/stroke/min and/or the ST/HR index greater than or equal to greater than or equal to 2.5 microV/stroke/min, it is more likely that myocardial ischemia is provoked by concomitant atherosclerosis of coronary arteries (sensitivity 28%, specificity 71%).
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PMID:[The ST-segment-dependent indices of patients with left ventricular hypertrophy and coronary failure]. 183

Most ischemic heart disease in associated with severe coronary atherosclerosis. A small subset of patients, however, had angina pectoris despite angiographically normal coronary arteries and absence of inducible coronary spasm. Coronary microcirculation (i.e. arteries too small to be visualized by current angiographic techniques) has been identified as the weak point of these patients. Small coronary vessel involvement may be due to organic conditions (such as diabetes, vasculitis, systemic collagen-vascular diseases, infectious processes) that act through coronary thrombosis or embolism and related alteration in coronary vasomotion; alternatively, the vascular abnormality appears to be entirely functional (no ultrastructural myocardial changes) such as the case of hypertension, hypertrophic cardiomyopathy and syndrome X. Whatever the cause(s) and mechanism(s) of the small coronary artery involvement, this leads to myocardial ischemia and to the related complications as in classic atherosclerotic heart disease. Syndrome X is characterized by effort-induced angina pectoris, ST-segment changes during exercise testing, negative ergonovine test and reduced coronary reserve. A pre-arteriolar hypersensitivity to vasoconstrictor influences (elicited by cold pressor test or ergonovine) and a reduced vasodilator capacity (unmasked by metabolic and pharmacological studies) have been proposed as potential pathogenetic substrate. This dynamic alteration in vasomotion would answer for both symptoms and signs of myocardial ischemia, that, however, appear to be contemporarily elicitable in a minority of patients. Treatment with beta-blockers and calcium-antagonists has been found to be effective. The long-term follow-up shows favorable outcome with a high survival rate and a low incidence of cardiovascular events.
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PMID:[Angina due to microvascular pathology]. 184 63

Heart muscle perfusion was studied by exertion scintigraphy Tal-201 in 24 patients, 16M and 8F, aged 16-45 years, means--28 +/- 7.4 years with hypertrophic cardiomyopathy. The relationship between perfusion disturbances and sudden death risk factors occurring in this group of patients was evaluated. Disturbances of heart muscle perfusion were found in 20 pts (83%); 2 pts had permanent perfusion defects, in 18 pts these defects were completely or partially reversible at rest. Only 4 pts (17%) had normal heart muscle perfusion. In patients with perfusion disturbances there was found a significantly more frequent occurrence of the following sudden death risk factors: 1. syncope (p less than .01) 2. ventricular arrhythmia of IV b class according to Lown (p less than .01) 3. advanced hypertrophy of intraventricular septum (p less than .01) 4. sudden death in patients families (p less than .05) The evaluation of the heart muscle perfusion confirmed the occurrence of myocardial ischemia in most of the examined patients. Normal coronaro-angiography in all the patients over 35 years as well as the young age of the other patients exclude atherosclerosis as the cause of myocardiac ischemia in the group under study. This is a confirmation of nonatherosclerotic etiology of myocardiac ischemia in hypertrophic cardiomyopathy patients. The correlation between perfusion disturbances and sudden death risk factors points to the role of ischemia in the natural course of disease and the value of exertion scintigraphy TI-201 in prognosing patients with hypertrophic cardiomyopathy.
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PMID:[Disturbances of myocardial perfusion by exertion scintigraphy in patients with hypertrophic cardiomyopathy and their relationship with sudden death risk factors]. 194 60

Although death during exercise is rare, vigorous physical activity is associated with increased risk for fatality, particularly in individuals with overt cardiac disease or a high coronary risk profile. The mechanism of death is usually a lethal ventricular arrhythmia, but this may vary depending on the underlying cardiac condition. Cardiac disease is present in the great majority of individuals who die during exercise. In young persons, hypertrophic cardiomyopathy and congenital coronary anomalies are most frequent, whereas older victims usually have coronary artery atherosclerosis. Cardiac disease is typically unrecognized before the fatal event in young individuals; in the older group, most have overt coronary disease or identifiable risk factors. Screening asymptomatic subjects to identify increased cardiac risk during exercise is problematical in terms of logistics, expense and accuracy. However, careful evaluation, including exercise testing, is mandatory before a program of increased physical activity is initiated in cardiac patients. For other individuals, firm guidelines are lacking, and the extent of the evaluation must be determined on an individual basis.
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PMID:Sudden death during exercise. 207 59

Calcium antagonists are now widely used for the treatment of clinical hypertension and angina pectoris. They are efficacious for the treatment of vasospastic, fixed atherosclerotic and mixed angina; they reduce the incidence of silent ischemia; and they have been shown to reduce postmyocardial infarct angina. Experimental data suggest that they may have certain cardioprotective properties in cases of acute myocardial ischemia and infarction, stunned myocardium, diastolic dysfunction, left ventricular hypertrophy and atherosclerosis. Moreover, they have been shown to improve exercise performance, as well as the diastolic abnormalities in patients with hypertrophic cardiomyopathy. In animals, they may delay or reduce the extent of myocardial necrosis after coronary occlusion or coronary occlusion followed by reperfusion, and in low doses that do not alter the hemodynamic profile, they have been shown to enhance the return of ventricular function in animals with stunned myocardium. However, the early first-generation calcium antagonists (nifedipine, verapamil, diltiazem) have not been shown to reduce myocardial infarct size or to enhance survival in patients with acute myocardial infarction. There now are clinical studies that suggest that, unlike beta blockers or nitrates, nifedipine may slow the development of atherosclerotic progression in humans over a 2-year period, and it seems likely that in the 1990s there will be further expansion of the use of calcium antagonists for not only angina and hypertension but also for aspects of cardioprotection. That calcium antagonists may delay, prevent or possibly regress atherosclerotic lesions is an exciting possibility.
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PMID:Progress in cardioprotection: the role of calcium antagonists. 214 58

Among 144 patients with hypertrophic cardiomyopathy, eight (58.3 +/- 7.0 years, M:F = 7:1) had complicating myocardial infarction, which was diagnosed clinically and by elevated cardiac enzymes or new Q-waves on electrocardiography. Coronary occlusion or stenosis evidenced by coronary angiography and nuclear cardiological findings were investigated. In six of the eight patients, coronary atherosclerosis caused infarction. These patients had many coronary risk factors compared to the other two patients. Sixteen of the 144 patients (11%) with hypertrophic cardiomyopathy had coronary atherosclerosis, the rate of which is reportedly 10 to 20%. Two of the eight patients had no coronary atherosclerosis. One patient had a diffusely spastic diathesis provoked by the intravenous administration of ergonovine maleate during coronary angiography, suggesting that coronary spasm caused myocardial infarction. The other patient had recurrent episodes of supraventricular tachyarrhythmia and no evidence of spasm during coronary angiography, suggesting coronary embolism as a cause of myocardial infarction. Myocardial infarction in patients with hypertrophic cardiomyopathy and normal coronary arteries as advocated by Maron et al. may have such pathogenesis. We conclude that coronary angiography may be mandatory in patients with hypertrophic cardiomyopathy, especially those who have many coronary risk factors and anginal symptoms. In these patients, ST-T changes and abnormal Q-waves on electrocardiography sometimes may be misleading when diagnosing the occurrence of acute myocardial infarction by electrocardiography alone. In such cases, infarct-avid scintigraphy with 99 m-Tc pyrophosphate is preferable.
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PMID:[Clinical diagnosis and pathogenesis of myocardial infarction complicated by hypertrophic cardiomyopathy: review of eight cases]. 256 22


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