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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 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

The work is based on the analysis of 206 patients with myocarditis of whom 168 had infectious allergic myocarditis and 38 had idiopathic myocarditis. A wide variety of clinical laboratory and instrumental methods of examination was used and intravital puncture biopsy of the myocardium was conducted. The article discusses the criteria of differential diagnosis which make it possible to distinguish the form of myocarditis from a large group of cardiovascular diseases following a similar course, i.e. primary rheumatic carditis, ischemic heart disease, valvular diseases, pericarditis and others.
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PMID:[Differential diagnosis of myocarditis from a number of cardiovascular system diseases]. 45 25

A working classification of noncoronarogenic damage to the cardiac muscle is suggested in which 4 general-pathology groups are considered: myocardial dystrophies, myocarditis, cardiomyopathy, and neoplasms. The main principles are presented for grouping diseases of the myocardium not associated with ischemic heart disease, hypertension or rheumatic fever. Certain problems of the clinical picture and differential diagnosis of dystrophic, inflammatory, and idiopathic damages to the heart muscle are discussed.
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PMID:[Classification of non-coronarogenic myocardial damage]. 67 84

Five term and two premature newborn infants were referred for respiratory distress and congestive heart failure, and were found to have electrocardiographic Q or ST-T abnormalities suggesting ischemia. Echocardiographic and/or hemodynamic assessment excluded anatomic heart disease in six infants. In three infants, moderate or severe hemodynamic impairment within 36 hours of age was suggested by these studies. Myocardial perfusion images in all patients showed very poor myocardial uptake of thallium 201, compatible with global myocardial ischemia. Infants of similar age with myocarditis, or with congenital heart disease and congestive failure, had normal myocardial uptake. Rapid clinical improvement occurred within three to seven days. Two to five months later, all infants were well. Two had persistent electrocardiographic abnormalities but repeat thallium 201 imaging in six demonstrated almost normal myocardial uptake. These data provide further evidence that perinatal respiratory distress may be associated with myocardial dysfunction and congestive heart failure in some infants without anatomic heart disease, and suggest that myocardial dysfunction in these infants is associated with global myocardial ischemia, most of which is transient. The timing and nature of the insult causing the ischemia are unclear.
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PMID:Transient myocardial ischemia of the newborn infant demonstrated by thallium myocardial imaging. 76 22

Based on the experience gained in examining over 3000 patients with various cardiovascular diseases (hypertensive, ischemic heart disease, myocarditis, heart failures of different etiology, etc) and upon literature sources a clinical grouping of bloodless methods of exploring the heart and vessels is given. At the root of the grouping is laid an investigation into the parameters of the cardio-vascular activity. Attention is called to widely employed and well-approved methods, such as electrocardiography, echocardiography and to the ones holding good promise (magnitocardiography, contactless investigations of the arterio-venous pulsation, etc). The authors believe the most informative bloodless methods of examination to be the ones that reflect the parameters of the cardio-vascular activity in a direct way, whereas methods reposing on the study of secondary manifestations produced by the work of the heart and vascular system (ballisto-, dynamo-, cardiovectorography and others) appear to them less promising with their significance for the clinical practice being of minor importance. The "bloody" and bloodless graphic methods of examining the heart and vessels do not compete with each other, but are mutually complementary. The diagnostic merit of the methods in recognizing circulatory insufficiency increases by using functional load and pharmacological tests.
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PMID:[Diagnostic value of bloodless graphic methods of studying the heart and vessels in the early detection of circulatory insufficiency]. 123 13

Single cardiac myocytes were isolated from the ventricles of failing and non-failing human hearts. The contraction amplitude, time-to-peak shortening and time to 50% and 90% relaxation were measured in cells stimulated at 0.2 Hz at 32 degrees C. The effects of increasing extracellular calcium and isoproterenol were investigated using cumulative concentration/response curves. Maximum contraction amplitude in high calcium or velocities of contraction or relaxation were not impaired in cells from failing hearts. Beta-adrenoceptor function in a single cell was assessed by the maximum contraction amplitude in the presence of isoproterenol relative to that with high calcium in the same cell (isoproterenol/calcium ratio). A decrease in the isoproterenol/calcium ratio correlated positively with an increase in the isoproterenol EC50 (concentration for half-maximal effect) for a cell (P less than 0.02, n = 39). The isoproterenol/calcium ratio in left ventricular myocytes decreased with increasing severity of disease, correlating with failure as defined by New York Heart Association class (P less than 0.001, n = 26 patients), left ventricular ejection fraction (P less than 0.001, n = 24), left ventricular end diastolic pressure (P less than 0.05, n = 21) and amount of diuretics prescribed (P less than 0.001, n = 26). In right ventricular myocytes, only increasing NYHA class correlated with decreasing isoproterenol/calcium ratios. There was a correlation of the isoproterenol/calcium ratio between right and left ventricular cells from patients with ischemic heart disease (P less than 0.05), n = 11). Beta-adrenoceptor subsensitivity occurred in mitral valve disease, ischemic heart disease, congenital abnormalities and congestive cardiomyopathy, but not in the right ventricle of patients with myocarditis. The isoproterenol/calcium ratio correlated negatively with the age of the patient (P less than 0.001, n = 26, left ventricle). Multiple regression indicated that the maximum contraction amplitudes in either high isoproterenol or high calcium declined significantly with age only, but that both age and severity of disease contributed to the decrease in isoproterenol/calcium ratio. Time-to-peak tension in isoproterenol, as well as relaxation times in high calcium also decreased with the age of the patient. Analysis of variance showed that between-patient variation was significantly greater than between-cell for most of the parameters measured. Beta-adrenoceptor desensitisation may be detected in individual myocytes from failing hearts, and this relates more to the severity of disease and the age of the patient rather than the etiology of heart failure. A decline in absolute contractility of muscle cells with age was detected.
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PMID:Isolated ventricular myocytes from failing and non-failing human heart; the relation of age and clinical status of patients to isoproterenol response. 132 14

Patients with different heart diseases, dilated cardiomyopathy, valvular heart disease, hypertension, ischemic heart disease or myocarditis showed manifestations of autoimmunity and down-regulation of beta-adrenergic receptors. Autoantibodies against beta-adrenergic receptors in these patients were detected with radioligand binding inhibition assay. The results suggested that the down-regulation of cardiac beta-adrenergic receptors in these patients may be mediated by autoimmunity. Autoantibodies against beta-adrenergic receptor were not related to any specific heart diseases, but to the severity of heart failure irrespective of its etiology. The significance of these autoantibodies in heart failure was discussed.
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PMID:[Circulating autoantibodies against beta-adrenergic receptors in patients with heart diseases]. 133 2

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

Cocaine abuse may lead to serious cardiac complications, including myocardial ischemia and infarction, myocarditis, cardiomyopathy and arrhythmias. With concomitant use of alcohol and cocaine, cocaethylene is produced by hepatic transformation. Cocaethylene is now thought to be primarily responsible for the deaths that occur among cocaine abusers. Treatment of cardiovascular complications focuses on cocaine-induced ischemia, hypertension and arrhythmias. The use of thrombolytic agents in myocardial infarction remains controversial. Concurrent detoxification with bromocriptine and norepinephrine is recommended.
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PMID:Cardiovascular complications of cocaine abuse. 846 3

Serum cardiac myosin light chain I (LCI) levels were quantitated using a radioimmunoassay kit in patients suspected of dilated cardiomyopathy (DCM). In this study, 55 patients were evaluated between 1986 and 1991. They were composed of 40 males and 15 females, and their age was 27-75 years (51 +/- 11 years). The patients with renal dysfunction were excluded due to their serum creatinine levels (greater than 2.0 mg/dl). 1) After cardiac catheterization, endomyocardial biopsy and echocardiography, 44 patients were diagnosed as DCM, 2 as ischemic heart disease, 2 as chronic myocarditis, 1 as restrictive cardiomyopathy, 1 as dilated hypertrophic cardiomyopathy, 1 as cardiac amyloidosis, 2 as myopathy, 1 as polymyositis and 1 as hypothyroidism. 2) Only two patients with DCM had elevated LCI. Besides, two patients with myopathy or hypothyroidism had elevated LCI. 3) In the follow-up, one patient died suddenly 6 months later and another showed normal value of LCI four years later. 4) LCI elevation in DCM was not related to either the severity of heart failure or cardiac function and it showed no finding of 201Tl myocardial defect or elevated CPK. 5) The mechanism for elevated LCI in myopathy is related to a cross-reaction with myosin light chain in the skeletal muscle. In hypothyroidism, it may be related to decreased clearance of normal LCI concentration or increased myosin light chain from damaged skeletal muscle. In conclusion, it is evident that the measurement of LCI is not helpful in clinical assessment of patients with DCM, but may be useful in detection of secondary cardiomyopathy.
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PMID:[Clinical assessment of serum myosin light chain I in patients with dilated cardiomyopathy]. 143 84


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