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)

The cardiological examination of 22 patients (pts) with suspected heart sarcoidosis (histologically established lung sarcoidosis, heart rhythm disturbances, cardiomegaly) has revealed thallium scan defects in 20 pts at rest and during exercise. In 19 pts we found pathologic left heart wall motions established by laevocardiography by applying the half axis method. The number of pathologic half axis shortenings correlated with ejection fraction, but not with left ventricular enddiastolic pressure and left ventricular enddiastolic volume index. IHD could not be found in coronarography in any case. Myocardial biopsy did not show myocarditis. Cardiomyopathies, other specific heart muscle diseases or rheumatic myocarditis could not be excluded as causes of the results mentioned above. The follow-up examinations of the patients will give more detailed information on the etiology of the pathologic cardiac findings.
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PMID:[Thallium myocardial scintigraphy, hemodynamics and left ventricular wall kinetics in patients with suspected myocardial sarcoidosis]. 293 10

We studied one hundred consecutive patients with rheumatoid arthritis from the cardiological point of view through non invasive methods to detect the frequency of cardiovascular complications. Seventy three (73%) were females and twenty seven (27%) males. Mean age, 48.6 years. Mean age of presentation of the disease, 34.2 years. Mean age of duration of the illness, 21.8 years. Fifty seven per cent had some type of cardiopulmonary complication. Clinically 52 per cent referred some type of cardiopulmonary symptoms. The physical examination was abnormal in 27 per cent. Rheumatoid factor (Waaler-Rose) was positive in 82 per cent. The cardiac X ray series was abnormal in 33 per cent, the resting electrocardiogram in 48 per cent and the M mode echocardiogram in 52 per cent of the cases. The complications detected were: pericardial effusion (21%); pleural effusion (9%); pulmonary fibrosis (6%) which represents a higher incidence of previously reported in the literature; congestive heart failure (10%); valvular lesion (9%) among those are included six patients with valvular heart disease of non detectable etiology; ischemic heart disease (8%); myocarditis (6%); rythm disturbances (22%) and conduction defects (20%) including a 46 year old female patient who developed a complete AV block during an exacerbation of her illness, requiring the insertion of definitive pacemaker. Our results showed that some of the detected lesions are in part more frequent and severe than those reported in the literature, probably due to, that on one hand their search was intentional and on the other, our group was constituted by with severe and long standing rheumatoid arthritis.
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PMID:[The heart and rheumatoid arthritis. Prospective study of 100 cases]. 295 63

Twenty-seven patients (15 men, 12 women; mean age 48.9 years) suffering from ventricular tachycardia (VT) (n = 30) were studied by radionuclide angiocardiography with Fourier phase analysis, both in sinus rhythm and during tachycardia. VT was spontaneous, electrically inducible, sustained, haemodynamically stable and monomorphous, with a mean rate of 174 beats/min (range: 115-260 beats). Heart diseases responsible for VT were: non-obstructive cardiomyopathy (n = 7), hypertrophic cardiomyopathy (n = 1), ischaemic heart disease (n = 5), probable right ventricular arrhythmogenic dysplasia (n = 4), congenital left ventricular aneurysm (n = 2), sequela of myocarditis (n = 2) and aortic valve regurgitation (n = 1); no heart disease was detectable in 5 patients. On surface electrocardiogram there was good concordance between the initial radionuclide site of VT activation and the configuration and electrical axis of QRS. At Fourier phase analysis all 17 VT of the right lag type originated in the left ventricle, arising from the apical septum (n = 7) or lateral segment (n = 2) in case of left axis, from the basal segment (n = 6) or the lateral segment (n = 1) in case of vertical or right axis, and from the middle left septum (n = 1) in case of normal axis. Nine VT of the left lag type originated in the right ventricle, arising from the basal septum or the latero-basal region in case of vertical or right axis (n = 6), from the apical septum or the inferior-apical region in case of left axis (n = 2) and from the middle septum in case of normal axis (n = 1). Four of our patients (3 with coronary disease and 1 with congenital left ventricular aneurysm) had VT of the left lag type and an initial radionuclide site of activation in the middle part of the left septum in case of left axis (n = 2) and in the basal part of that septum in case of right axis (n = 2). Seven patients were operated upon for recurrent VT: 4 had intra-operative mapping which in every case confirmed the results of radionuclide angiocardiography, a method which in the other 3 patients was the only surgeon's guide. Correlations between the site of origin of VT at radionuclide mapping and kinetic abnormalities visualized at radiological angiography and gamma-ray angiocardiography were common in our study. In one of our patients the same lesion gave birth to 2 VT of different morphologies.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Isotope angiocardiographic study of 30 cases of ventricular tachycardia with Fourier phase analysis]. 313 7

In Leeds in hospital populations of patients with angina the maximal ST/HR slope was found to be a reliable index of myocardial ischemia as assessed by coronary angiography. Subsequent studies in Leeds and elsewhere in populations of patients with cardiac enlargement or following myocardial infarction have shown that the slope is affected by myocardial scarring, ventricular enlargement and aneurysm. These findings implied that the slope had features in common with other usual exercise tests; studies in Leeds and elsewhere, however, have shown a superior diagnostic reliability using the maximal ST/HR slope in patients with angina. The present report involves the use of the slope in asymptomatic populations. Trials are being undertaken in two factory populations, which respectively comprised all volunteers or asymptomatic men over the age of 30 who were randomly chosen by computer. Subjects with slope values indicating, according to previous experience, myocardial ischemia equivalent to coronary heart disease were referred for cardiological investigations which included angiocardiography; blind comparisons were performed between results of investigations and the slope. So far 1194 subjects have been examined. In 68 subjects the maximal ST/HR slope indicated myocardial ischemia, and in 24 of these cardiological investigations were completed. In nine of the 24 subjects the slope corresponded to the number of significantly narrowed coronary arteries (greater than 75% reduction in luminal diameter); in 12 of the remaining 15 subjects who had no coronary narrowing, there were cardiac lesions which included cardiac enlargement, aortic valve disease, myocarditis, pericarditis, myocardial bridging and conduction defects.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Diagnostic value of the maximal ST segment/heart rate slope in asymptomatic factory populations. 332 Feb 57

The immune cytotoxic mechanism of myocardial lesion was studied in 15 patients with non-specific myocarditis (NM) and in 10 patients with idiopathic congestive cardiomyopathy (ICC). In addition, 10 control patients having ischaemic heart disease (IHD) with congestive heart failure (CHF) and a control group of blood donors were examined. The following parameters were examined: anti-heart antibodies (by indirect enzyme-linked immunosorbent assay), lymphocyte sensibilization (by leucocyte migration inhibition test; the antigen used was cardiomyocyte membrane protein), and killer cells (K-cells) activity in the course of antibody-dependent cell-mediated cytotoxicity. Anti-heart antibodies were found in 73% of patients with NM, 50% patients with ICC and 33% patients with CHF. Lymphocyte sensibilization to the myocardium was found in 87% of patients with NM, and in more than half of the patients with ICC. Cardiospecific cytotoxic immune reaction was reproduced in vitro in 9 patients with NM and in 4 patients with ICC. It is assumed that an analogical mechanism of myocardial lesion functions in vivo.
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PMID:Immune cytotoxic mechanism of myocardial lesion in non-specific myocarditis and idiopathic congestive cardiomyopathy. 339 Oct 36

Five patients with acquired immune deficiency syndrome (AIDS) developed clinical evidence of mild to severe cardiac dysfunction confirmed by nuclear angiography and echocardiography. In 4 patients who were studied postmortem there was no evidence of myocarditis, valvular, or ischemic heart disease. Cardiac involvement in patients with AIDS may include pericardial and myocardial involvement by opportunistic pathogens or Kaposi's sarcoma, subclinical myocardial dysfunction, or an as-yet unexplained cardiomyopathy.
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PMID:Cardiac dysfunction associated with the acquired immunodeficiency syndrome (AIDS). 339 44

Although vasodilators and new inotropic agents have been shown to improve ventricular function and reduce symptoms, their effect on mortality is uncertain. In view of our failure to reduce mortality in patients with congestive heart failure (CHF), the identification and amelioration of potentially reversible factors that might alter survival are crucial before initiating therapy. The first step is to establish the diagnosis of CHF and the presence or absence of dilated congestive cardiomyopathy. The extent of myocardial dysfunction, both right and left, must also be evaluated. In post-myocardial infarction patients, left ventricular ejection fraction is an important indicator of prognosis during the first 1 to 2 years. However, in patients with chronic CHF and dilated cardiomyopathy, right ventricular ejection fraction may be a more effective predictor of survival. The presence, frequency and complexity of ventricular arrhythmias must be determined, because these arrhythmias may independently increase the risk of sudden cardiac death in patients with ischemic cardiomyopathy. Their role in patients with idiopathic cardiomyopathy is less certain. In addition, myocardial ischemia, left ventricular dyskinesis or aneurysm, occult myocarditis and neurothrombosis formation must be ruled out. Detection and correction of serum electrolyte and neurohumeral abnormalities are essential. Our failure to reduce mortality in patients with CHF may not entirely lie in the lack of effective therapeutic agents but rather in our failure to apply properly the diagnostic and therapeutic approaches now available.
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PMID:Evaluation of the patient with congestive heart failure and ventricular arrhythmias. 351 59

In this review we have attempted a comprehensive compilation of the cardiac morphologic changes that occur in spontaneous and experimental myocardial diseases of animals. Our coverage addresses diseases of mammals and birds and includes these diseases found in both domesticated and wild animals. A similar review of the myocardial diseases in this broad range of animal species has not been attempted previously. We have summarized and illustrated the gross, microscopic, and ultrastructural alterations for these myocardial diseases; and, whenever possible, we have reviewed their biochemical pathogenesis. We have arranged the myocardial diseases for presentation and discussion according to an etiologic classification with seven categories. These include a group of idiopathic or primary cardiomyopathies recognized in man (hypertrophic, dilated, and restrictive types) and a large group of secondary cardiomyopathies with known causes, such as inherited tendency; nutritional deficiency; toxicity; physical injury and shock; endocrine disorders, and myocarditides of viral, bacterial, and protozoal causation. Considerable overlap exists between each of the etiologic groups in the spectrum of pathologic alterations seen in the myocardium. These include various degenerative changes, myocyte necrosis, and inflammatory lesions. However, some diseases show rather characteristic myocardial alterations such as vacuolar degeneration in anthracycline cardiotoxicity, myofibrillar lysis in furazolidone cardiotoxicity, calcification in calcinosis of mice, glycogen accumulation in the glycogenoses, lipofuscinosis in cattle, fatty degeneration in erucic acid cardiotoxicity, myofiber disarray in hypertrophic cardiomyopathy, and lymphocytic inflammation with inclusion bodies in canine parvoviral myocarditis. The myocardial diseases represent the largest group in the spectrum of spontaneous cardiac diseases of animals. Pericardial and endocardial diseases and congential cardiac diseases are seen less frequently; and, in contrast to man, coronary artery disease and myocardial ischemia are rather infrequent in animals. The present review shows clearly that the spectrum of myocardial diseases in animals is enlarging and that many newly recognized diseases are emerging and assuming considerable importance. For example, various heritable cardiomyopathies have recently been described in the KK mouse, cattle, and rats. Increasingly recognized myocardial diseases include cardiomyopathies in cats, dogs, and birds; anthracycline cardiotoxicity; furazolidone cardiotoxicity; ionophore cardiotoxicity; myocardial damage associated with central nervous system injuries; myocardial hypertrophy in
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PMID:Myocardial diseases of animals. 352 54

Between March 1981 and March 1986, 200 orthotopic heart transplantations were performed at the University of Pittsburgh. Fourteen of those procedures were carried out in children 2 to 16 years of age. Two children received combined liver and heart transplants; one because of familial hypercholesterolemia with associated ischemic heart disease, and the other because of dilated cardiomyopathy associated with intrahepatic biliary atresia. Eight patients had dilated cardiomyopathy, and two had myocarditis. Two had heart transplantations for congenital heart disease: one had multiple muscular ventricular septal defects repaired in infancy and had an associated cardiomyopathy, and the other developed a cardiomyopathic ventricle from a congenital right coronary artery to right atrial fistula. Chronic immune suppression consisted 0.2 to 0.5 mg/kg/d of prednisone and 5 to 50 mg/kg/d cyclosporine, with the addition of antithymocyte globulin for unresolved moderate or severe acute rejection. There were three early postoperative deaths: one from intracranial bleeding, one from Pseudomonas mediastinitis, and one from ischemic injury to transplanted organs. Early postoperative complications included reversible renal failure, hypertension, and seizures. Late problems were related to allograft rejection and side effects of cyclosporine and corticosteroids. Significant rejection episodes occurred in all patients surviving longer than 2 weeks, with seven requiring antithymocyte globulin. Two patients died 8 months following transplantation of severe acute and chronic rejection; another patient required retransplantation for ischemic cardiomyopathy resulting from chronic rejection but subsequently died of recurring rejection 3 months after the second transplantation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Experience with heart transplantation in children. 354 Aug 34

Prolongation of the PR interval is a nonspecific condition. Etiologies include normal physiologic variance, idiopathic bundle branch fibrosis, calcific valvular heart disease, ischemic heart disease, cardiomyopathies, infections resulting in myocarditis, drugs (especially type I antidysrhythmic medications), collagen vascular diseases, tumors, trauma, electrolyte imbalances, and many other miscellaneous causes. Isolated first degrees atrioventricular block is generally not associated with an increased risk of sudden death, syncope, or progression to higher degrees of atrioventricular block. Exceptions include patients with intra-atrial conduction delays prone to atrial fibrillation, acute myocardial infarction, or bundle branch disease where higher degrees of atrioventricular block may develop. Treatment consists of correction of the underlying disorder or discontinuation of the offending medication.
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PMID:First degree atrioventricular block. 358 15


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