Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Since 1984, 122 orthotopic heart transplants have been performed at the University of Ottawa Heart Institute. Of the 114 adult patients, 100 (87.8%) were males and 14 (12.2%) females, with mean ages of 45.8 and 47.9 yr, respectively. The hearts of these adults were pathologically diagnosed as chronic ischemic heart disease (CIHD) in 55 (48.2%), acute ischemic heart disease (AIHD) in 17 (14.9%), dilated cardiomyopathy (DC) in 30 (26.3%), valvular heart disease in five (4.4%), congenital heart disease in three (2.6%), myocarditis in three (2.6%), and other in one (0.9%) of the cases. The adult hearts (94) among the first 100 transplants were studied morphologically, to look for differences among the three major groups with clinical "end-stage" heart failure. The mean heart weights were 435, 356, and 463 gm in the CIHD, AIHD, and DC groups, respectively, with AIHD less than CIHD or DC (p less than 0.01). The ventricular wall thicknesses were similar in CIHD and DC, but the left ventricular (LV) wall thicknesses in AIHD were more than in CIHD or DC (p less than 0.01). The ventricular diameters were greater in DC than in CIHD or AIHD (p less than 0.01) and greater in CIHD than in AIHD (p less than 0.01). The mean LV cavity volumes were 158, 94, and 200 ml in CIHD, AIHD, and DC, respectively, with DC greater than in CIHD or AIHD (p less than 0.01) and CIHD greater than in AIHD (p less than 0.01). The relative differences in AIHD compared to CIHD and DC are referrable to the shorter duration of disease in the acute ischemic group.2+ off
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PMID:The University of Ottawa Heart Institute Cardiac Transplant Program: the first 100 transplants. A pathologic study of the explanted hearts. 157 94

Cardiovascular complications are among the most common and dangerous complications of cocaine abuse, ranging from episodic arrhythmias to myocardial infarction, strokes, cardiomyopathy, and sudden death. The central nervous system-mediated action of cocaine triggers an increase in circulating catecholamines, resulting in arterial vasoconstriction, increase in myocardial oxygen demand, myocardial ischemia, tachycardia, and other arrhythmias. The peripheral cardiovascular action of cocaine involves the inhibition of reuptake of catecholamines at adrenergic nerve terminals, with local release of epinephrine, direct stimulation and vasospasm of the coronary arteries, coronary intimal hyperplasia, inhibition of baroreceptors, interference with the electrical conduction through the myocardium, and direct myocardial toxicity. The cardiovascular complications of cocaine include cardiac dysrhythmias and hypertension, acute myocardial infarction, myocarditis, infectious endocarditis, ventricular dysfunction, dilated cardiomyopathy, hypotensive shock, and cerebral strokes. Cocaine-related vascular changes in the pregnant woman and fetus have been related to an increased incidence of abortion, abruptio placentae, and congenital anomalies of the fetus.
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PMID:Cardiovascular complications of cocaine abuse. 158 6

Beta-blockers were initially given to patients with chronic heart failure due to ischemic heart disease and resting tachycardia. The prompt effect on severe backward heart failure was directly associated with an immediate fall in heart rate. This observation led to long-term administration to patients with idiopathic dilated cardiomyopathy and, later, to patients with ischemic cardiomyopathy and secondary cardiomyopathies as well. Due to marked down-regulation of beta receptors, patients with heart failure are extremely sensitive to beta blockade. A test dose of metoprolol 5 mg b.i.d. for 2 days is recommended to select patients for long-term beta-blockade, followed by careful titration with increment in dose over 6 weeks. One important effect of beta-blockade in the early phase of treatment is a reduction in the myocardial energy demand early after the onset of long-term treatment. After 1 month of treatment with beta-blockers, marked improvement of diastolic function is observed. This effect might be attributed to inhibition of calcium overload. After 3 months of treatment, an increase in ejection fraction can be observed, which might be attributed to upregulation of beta receptors. The withdrawal of long-term treatment was followed by a deterioration of heart function in 61% of patients and improvement was seen after reinstitution of beta-blockade. There was an increase in cardiac index and stroke work index at rest as well as during supine exercise. A marked fall in left ventricular filling pressure at rest and unchanged filling pressure during supine exercise was noted, while exercise capacity increased by 25%. A similar pattern was seen in patients with ischemic cardiomyopathies and other secondary cardiomyopathies. However, the increase in ejection fraction in the ischemic cardiomyopathy group was lower (0.06) compared to the groups with dilated cardiomyopathy and other secondary cardiomyopathies (0.18).
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PMID:Beta-adrenergic blockade in dilated cardiomyopathy, ischemic cardiomyopathy, and other secondary cardiomyopathies. 168 23

The presence and properties of serum autoantibodies against beta-adrenergic receptors in patients with idiopathic dilated cardiomyopathy were studied using synthetic peptides derived from the predicted sequences of the human beta-adrenergic receptors. Peptides corresponding to the sequences of the second extracellular loop of the human beta 1- and beta 2-adrenergic receptors were used as antigens in an enzyme immunoassay to screen sera from patients with dilated cardiomyopathy (n = 42), ischemic heart disease (n = 17), or healthy blood donors (n = 34). The sera of thirteen dilated cardiomyopathy patients, none of the ischemic heart disease patients, and four of the healthy controls monospecifically recognized the beta 1-peptide. Only affinity-purified antibodies of these patients had a inhibitory effect on radioligand binding to the beta 1 receptor of C6 rat glioma cells. They recognized the receptor protein by immunoblot and bound in situ to human myocardial tissue. We conclude that a subgroup of patients with idiopathic dilated cardiomyopathy have in their sera autoantibodies specifically directed against the second extracellular loop of the beta 1-adrenergic receptor. These antibodies could serve as a marker of an autoimmune response with physiological and/or pathological implications.
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PMID:Mapping of a functional autoimmune epitope on the beta 1-adrenergic receptor in patients with idiopathic dilated cardiomyopathy. 170 Jul 98

Cardiovascular complications have occurred in clinical trials of interferon. We review herein experience to date of cardiotoxicity with all types of interferons in cancer patients. The most common presentations of cardiotoxicity were cardiac arrhythmia, dilated cardiomyopathy, and symptoms of ischemic heart disease, including myocardial infarction and sudden death. The cardiac effects were not related to the daily dose, cumulative total dose, or period of therapy. Some of the patients in whom interferon has caused cardiovascular sequelae have had a history of coronary heart disease or have previously been given chemotherapy with drugs known to be cardiotoxic. In most of the patients, cardiac toxicity was reversible following the cessation of the drug therapy.
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PMID:Cardiotoxicity of interferon. A review of 44 cases. 170 26

Ten healthy (aged 28 to 39) and ten heart failure NYHA II (aged 19 to 49) male subjects were prospectively studied under no drugs, under furosemide (40 mg/day), under captopril (150 mg/day) and under their association. Arterial compliance (ml/mmHg) was measured in all subjects at rest and supine. Heart failure etiology was dilated cardiomyopathy or ischemic heart disease without significant regurgitation. Arterial compliance was significantly higher in healthy than in heart failure patients in all studied conditions (p less than 0.001) (healthy = 2.2 + 0.29 vs. heart failure = 0.79 + 0.14). Neither single drug nor their association induced any change in healthy subjects. Arterial compliance progressively increased in heart failure with furosemide, captopril, and their association (no drug = 0.79 + 0.14; furosemide = 0.87 + 0.15; captopril = 0.94 + 0.15 and furosemide + captopril = 0.99 + 0.14). Captopril induced a higher increment than furosemide (p less than 0.001) and their association even a higher increment (p less than 0.001) than any single drug. Thus captopril and/or furosemide increased arterial compliance in heart failure but not in healthy subjects, possibly through changes in arterial wall edema and smooth muscle contraction.
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PMID:Effect of drugs on a noninvasive index of arterial compliance in healthy and heart failure patients. 174 91

Cocaine-related cardiovascular events escalated during the 1980s as cocaine became purer, cheaper, and easier to obtain. Cocaine abuse is a risk factor for myocardial ischemia and/or infarction, cardiac arrhythmias, pulmonary edema, ruptured aortic aneurysm, cerebral infarction, infective endocarditis, vascular thrombosis, myocarditis, and dilated cardiomyopathy. As medical and social complications of cocaine have become evident, and with the growing negative image of cocaine, the number of first-time users has begun to decline. Cocaine abuse is seen on all levels of our society and has emerged as an issue of significant medical and public health importance. All routes and forms of cocaine abuse are potentially cardiotoxic and can be lethal. Fatal cardiac complications can occur in a first-time user. All physicians should be alert for cocaine abuse when confronted with unexplained cardiac symptoms. Cocaine is the newest and sometimes unrecognized risk factor for cardiovascular disease in young individuals otherwise free of cardiovascular risk factors.
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PMID:Cocaine: the newest risk factor for cardiovascular disease. 181 Jun 80

Among dialysis patients, only 23% have a normal echocardiogram, about 10% have recurrent or chronic congestive heart failure, and 17% have asymptomatic ischemic heart disease. The predisposing factors for congestive heart failure are dilated cardiomyopathy, hypertrophic hyperkinetic disease, and ischemic heart disease. Dilated cardiomyopathy, a disorder of systolic function, includes among its risk factors age, hyperparathyroidism, and smoking. Hypertrophic disease results in diastolic dysfunction, and its predictors include age, hypertension, aluminum accumulation, anemia, and, perhaps, hyperparathyroidism. Ischemic heart disease is due to the presence of coronary artery disease and also to nonatherosclerotic disease caused by the reduction in coronary vasodilator reserve and altered myocardial oxygen delivery and use. The clinical outcome of congestive heart failure is comparable to that of nonrenal patients with medically refractory heart failure. Left ventricular hypertrophy is an important independent determinant of survival. A subset have hyperkinetic disease with severe hypertrophy and have a bad survival, as low as 43% have a 2-yr survival after the first admission to hospital with cardiac failure. The prognosis for those with dilated cardiomyopathy is less severe but is worse than those with normal echocardiogram. The survival of patients with symptomatic ischemic heart disease was little different from that of patients without symptoms, suggesting that the underlying cardiomyopathies had an adverse impact on survival independent of ischemic disease. Much research needs to be undertaken on the risk factors, natural history, and therapy of the various types of cardiac disease prevalent in dialysis patients.
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PMID:The natural history of myocardial disease in dialysis patients. 183 84

The long-term prognosis and prognostic factors were assessed in patients with left ventricular dilatation with impaired function secondary to idiopathic dilated cardiomyopathy (DCM) or to heart diseases of various pathogeneses masquerading as DCM (DCM-like). The echocardiographic criteria for DCM-like disease were 1) left ventricular end-diastolic dimension exceeding 60 mm and 2) fractional shortening less than 15%. Those who showed improvement in either of these 2 parameters within 3 months were excluded from this study. One hundred and fifty-eight of 35,250 serially examined patients fulfilled the definitions. The pathogeneses of diseases were valvular heart disease (VHD) in 30 patients, ischemic heart disease (IHD) in 37, alcoholic cardiomyopathy (AC) in 12, hypertensive heart disease (HHD) in 31 and DCM in 48. All of the survivors were followed for more than 24 months; an average of 40 months. During this period, there were a total of 75 deaths, 18 (27%) of whom were judged as sudden death. Five-year survival rates calculated using the Kaplan-Meier method in AC and HHD were 86% and 77%, respectively, which were significantly higher than those in DCM (48%; p < 0.05); whereas, patients with VHD and IHD had lower values (60% and 46%, respectively) which were nearly equal to those in DCM. Factors that contributed to the increase in total cardiac mortality were advanced age, higher NYHA functional class, larger cardiac size on chest radiograph and history of heavy alcohol intake. Each of these factors were closely related to the specific pathogeneses as follows: age to IHD, cardiac size to VHD, and NYHA functional class to DCM. Long-term prognosis of DCM-like heart diseases, especially those of IHD and VHD, seemed to be as bad as those of DCM.
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PMID:[Long-term prognosis in patients with echocardiographic left ventricular dysfunction masquerading as dilated cardiomyopathy]. 184 21

The diagnosis of the origin of a broad complex tachycardia may be difficult, especially in the absence of a 12-lead electrocardiogram of the tachycardia. This study investigates the value of signal averaging in the differential diagnosis of broad complex tachycardia. Signal averaging during sinus rhythm was performed in 102 consecutive patients who presented with broad complex tachycardia (QRS width greater than 110 ms), in whom a definitive electrophysiological diagnosis was made. The presence of late potentials was determined on the basis of two definitions, the second including total QRS duration. The patients studied included 75 with ventricular tachycardia; 33 of these patients had suffered previous myocardial infarction, five had dilated cardiomyopathy, and 37 had a 'normal' heart. Of the 27 patients with supraventricular tachycardia, 22 had an atrioventricular accessory pathway (seven with a delta wave in sinus rhythm), three had atrioventricular nodal tachycardia and two had atrial tachycardia. The sensitivity of late potentials for the diagnosis of ventricular tachycardia was low utilizing both definitions (28% and 45%) although specificity was high (96% and 95%). The sensitivity for the diagnosis of ventricular tachycardia was higher for patients with ischaemic heart disease (43% and 70%) but very low for patients with ventricular tachycardia and a normal heart (16% and 22%). In conclusion, signal averaging in the remote diagnosis of broad complex tachycardia is specific but not sensitive for ventricular tachycardia, which limits its usefulness in selecting patients for electrophysiological study.
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PMID:Signal averaging of the electrocardiogram in the remote differential diagnosis of broad complex tachycardias. 188 42


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