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

The injury-vasospasm hypothesis of IHD was discussed in relation to coronary artery autoregulation and the anoxic-feedback mechanism. Observations in the recent literature, not usually attributed to spasm, were examined in light of this phenomenon. This includes reperfusion models of experimental AMI, the association of AMI with myocarditis, and findings in AMI and SCD as necrotic microlesions, prodromata, and epicardial arterial plaque rupture and hemorrhage. The disparity between the severity of coronary disease and the occurrence of the various types of IHD suggest that atherosclerosis itself does not precipitate attacks of chest pain. It was emphasized that plaque rupture due to spasm might help induce CAT. With exercise, the possible importance of the autoregulatory system was explored in the prevention and induction of AMI and SCD, and the improvement of AP. The role of spasm in IHD should be defined.
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PMID:The injury-vasospasm hypothesis of ischemic heart disease, revisited. 33 91

Latent cytomegalovirus (CMV) infection is not uncommon in the juvenile and adult population. The full blown disease is mostly restricted to immunosuppressed and immunodeficient patients, but may also occur in healthy individuals. The acute CMV-myocarditis often takes a mild course with only transient changes of left ventricular hemodynamics or a pericardial effusion as assessed by echocardiography. In our patient population it was characterized by the presence of anti-interfibrillary antibodies. In acute myocarditis the virus genome can be detected by in-situ hybridization in 42% (40% in the myocytes, 21% in the interstitial cells and 41% in endothelial cells). In patients with perimyocarditis CMV-DNA is found in 24% of patients in the myocytes, in 24% of patients in the interstitial cells and in 50% of patients in the endothelium. In healthy controls CMV-DNA could be assessed only in interstitial and endothelial cells (70% and of the infected 30% of positive cases) but not in the myocytes. In dilated cardiomyopathy (DC) CMV-DNA can be found in 48%. Particularly in myocytes in 45% of cases, in interstitial cells in 50% and in the endothelium of small vessels in 68%. An induction of the disease by a chronic local stimulation of the immune system is a likely pathogenetic explanation of the immuno phenomena observed in parallel to the viral persistence. Additive damage by chronic CMV infection can be caused by the infection of the endothelium and smooth muscle cells of the intima of coronary arteries. There are some reports of CMV-DNA detection in the arterial walls or atherosclerotic plaques of patients with atherosclerosis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Cytomegalovirus associated diseases of the heart]. 131 12

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.
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PMID:The effects of acute and chronic cocaine use on the heart. 134 9

Coronary artery disease has emerged as an important cause of death in young patients with SLE. We report three cases of acute myocardial infarction in young lupus patients who underwent emergent coronary angiography. One patient had a large coronary aneurysm and died five months later from myocarditis. The other two patients underwent coronary angioplasty. The difficulty in distinguishing coronary arteritis from premature atherosclerosis and its relevance to methods of treatment is discussed.
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PMID:Evaluation and treatment of acute myocardial infarction complicating systemic lupus erythematosus. 173 66

With regard to cardiac findings in cocaine abuse, at autopsy the vast majority of patients dying with cocaine toxicity have either no pathologic change in the heart or only minimal changes that could not account for the patient's death. The second most frequent finding is underlying, mild-to-moderate coronary atherosclerosis, with or without coronary thrombosis. There may be acute or healed myocardial infarction or a sudden cardiac death without myocardial changes of ischemia. A high incidence of contraction band necrosis has been reported in the absence of coronary artery disease and may cause a sudden arrhythmic death. Myocarditis also has been described in a few cases as either lymphocytic or lymphocytic and eosinophilic infiltrate in the presence of myocyte necrosis. Usually, the foci are sparse and not always associated with contraction band necrosis. The underlying mechanisms are thought to be either direct effects of norepinephrine on myocytes or through vasospasm of resistance vessels and secondary myocardial ischemia. Cocaine rarely has been associated with aortic dissection, which is probably a result of cocaine's hypertensive effects.
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PMID:Cocaine-associated cardiovascular disease: clinical and pathological aspects. 174 14

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

A 64-year-old man underwent cardiac transplantation for long-standing severe dilated cardiomyopathy. Postoperative complications included primary cytomegalovirus (CMV) infection with several episodes of moderate acute rejection and severe pneumonia. Six months after transplantation, an endomyocardial biopsy specimen revealed focal necrotizing myocarditis with intranuclear inclusions consistent with CMV. The patient subsequently developed fulminant pneumonia and died 7 months after transplantation. Postmortem examination revealed that the cause of death was acute necrotizing bronchopneumonia due to Staphylococcus aureus, with underlying CMV pneumonitis. The transplanted heart had left ventricular hypertrophy with multiple organizing myocardial infarcts, moderate coronary atherosclerosis, and organizing thrombi of the left atrium. Characteristic inclusions of CMV were identified, predominantly within endothelial cells, in the left coronary artery, left ventricular endocardium, and myocardium. With in situ hybridization, the presence of CMV was verified in the inclusions, as well as in many fibroblasts without inclusions. In situ hybridization is warranted in myocardial biopsy specimens when suspicious inclusions or infiltrates are present, to confirm CMV infection, so that appropriate therapy can be initiated.
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PMID:Cytomegalovirus endomyocarditis in a transplanted heart. A case report with in situ hybridization. 185 May 89

Over the last 10 years, our knowledge of immunologically mediated processes involving the myocardium appears to have made quantum leaps. New and important disease entities such as AIDS have appeared and the cardiologist now becomes an important member of the "AIDS team." Our understanding of "older diseases" such as sarcoidosis, Lyme disease, systemic lupus and other connective tissue syndromes has significantly increased. The concept of high-dose steroid therapy for these processes may, in fact, turn out to be futile and more selective, as less dangerous immunosuppression is being introduced. This concept has significantly advanced in the field of cardiac transplantation where immunosuppression has now been usurped by specific immunotherapy aimed at selective aspects of the immune sequence. New and exciting concepts will emerge from the molecular biology laboratory that will have direct bearing on the management of patients with cardiovascular disorders. This information explosion will force the cardiovascular physician to become more in tune with the world of immunology and molecular biology. Many obvious, significant problems remain, such as accelerated atherosclerosis in the transplant patient and the role of myocarditis in the patient with heart failure. However, it will truly be an exciting decade in which to work and watch the unraveling of these mysteries and hopefully, the study of today's problems will give way to solutions and a clearer understanding of the heart as a target of immune injury.
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PMID:The heart as a target organ of immune injury. 191 12

Kawasaki disease is an acute vasculitis characterized by mucosal inflammation, rash, cervical adenopathy, indurative edema of the hands and feet, and late membranous desquamation of the fingertips. Early cardiac effects include myocarditis (occasionally with congestive heart failure), pericardial inflammation, and, rarely, valve involvement. Coronary artery aneurysms are a long-term concern because coronary thrombosis with myocardial infarction can be a late manifestation. The origin of Kawasaki disease is unknown, but an infectious agent is most likely. Management consists of aspirin for control of fever and inflammatory manifestations and intravenous gamma globulin for the prevention of coronary aneurysm formation. Careful late follow-up is required, especially for patients with persistent coronary abnormalities. Giant aneurysms (greater than 8 mm) are more likely to progress to coronary obstructive disease, and coronary bypass grafts have been required for some patients. Late coronary artery manifestations in patients with mild early coronary dilatation have not been described. However, since long-term epidemiologic studies have not yet been performed, it is prudent to consider childhood Kawasaki disease to be a potential risk factor for coronary disease, especially in atherosclerosis-prone Western societies.
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PMID:Diagnosis and management of Kawasaki disease. 202 52

Genetically determined resistance to the lethal effects of infection with murine cytomegalovirus (MCMV) has been reported previously in adult and newborn mice. We examined the pathogenesis of MCMV infection in resistant (CBA, H-2k) and susceptible (BALB/c, H-2d) mice infected intraperitoneally on the day of birth. BALB/c mice developed a severe interstitial pneumonitis and myocarditis 10 days post-infection. Their pulmonary and tissues contained high MCMV titres and large numbers of MCMV-antigen positive cells. MCMV also infected the endothelial and myointimal cells of the coronary arteries in newborn BALB/c mice. Only limited infection and pathological changes were seen in CBA mice. Since the severe disease in BALB/c mice resembles the pneumonitis and less frequently reported myocarditis observed after perinatal HCMV infection, the newborn mouse model will be useful for studying the consequences and treatment of such infections, the influence of the host genotype on disease severity and the possible association between perinatal HCMV infection and atherosclerosis.
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PMID:Cytomegalovirus-induced pneumonitis and myocarditis in newborn mice. A model for perinatal human cytomegalovirus infection. 217 34


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