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At least 19 recordsLinked to original sources
PubMed1977

[Perfusion scintigraphy of the myocardium in cardiological diagnosis. Coronary diseases, primary myocardial diseases and rheumatic heart valve diseases].

In 123 patients perfusion scintigrams were compared with the data of clinical investigation, right and left heart catheterisation and coronary arteriography. The intracoronary application of radioactive labelled human-albumin-microspheres and human-microaggregates were without any complications. The patients suffered from coronary heart diseases, primary myocardial diseases and rheumatic valvula heart diseases. There was a good correlation between the myocardial perfusion defect and the degree of coronary artery stenoses. Furthermore an excellent correlation was found between perfusion defects and levocardiographic findings: left ventricular aneurysms, akinetic or hypokinetic areas and the ejection fraction of the left ventricle. All myocardial infarctions were detected by a perfusion defect in the scintigrams. In 16 cardiacsurgery-patients large myocardial perfusion defects were found to be myocardial scars. In primary myocardial diseases perfusion scintigraphy is an effective method of detecting pathological myocardial patterns. The degree of perfusion defects correlates excellently with the levocardiographic findings. It seems that in rheumatic valvular diseases perfusion-scintigraphy is a method to discover rheumatic myocardial abnormalities--probably scar tissue. In comparison with thallium scintigrams it was shown that extensive myocardial failures (aneurysms) can be represented by both nuclear medical procedures but that perfusion scintigraphy is more sensitive and correlates more closely to the levocardiogram findings.

Angiography↗
PubMed1979

Cell-mediated cytotoxicity to cardiac cells of lymphocytes from patients with primary myocardial disease.

The etiology of primary myocardial disease is unknown. With the advent of immunologic technics, an immune process related to primary myocardial disease has been sought, but none has been elucidated as diagnostic or causative. The authors attempted to study the possibility of a cell-mediated component in the etiology of primary myocardial disease. Cell-mediated immunologic injury of cultured, human myocardial cells was studied in cells from patients with primary myocardial disease and controls by means of a 51chromium-release method. Significant lymphocytic cytotoxicity against myocardial cells was detected in cells from 23 (30%) of 73 patients with primary myocardial disease, compared with two (4%) of 49 normal, healthy control subjects. Significant cytotoxicity was also observed in cells from 36 (24%) of 148 patients who had other cardiac diseases, mainly rheumatic and atherosclerotic diseases. No group showed cytotoxicity against a long-term culture of Chang hepatic cells. No clinical correlation between the severity of the disease and increased cytotoxicity could be found. It is concluded that lymphocytic reactivity against myocardial cells probably results from myocardial damage due to a variety of causes, and that it is not specific for primary myocardial disease.

Cardiomyopathies↗
PubMedDate not supplied

Animal models of primary myocardial diseases.

Feline and canine cardiomyopathies (primary myocardial diseases) were reviewed and divided into three groups based on the clinical, hemodynamic, angiocardiographic, and pathologic findings: (1) feline and canine hypertrophic cardiomyopathy, (2) feline and canine congestive (dilated) cardiomyopathy, and (3) feline restrictive cardiomyopathy. All three groups consisted predominantly of mature adult male cats and dogs. Cardiomyopathy in the hamster and turkey was also reviewed. The most common presenting signs were dyspnea and/or thromboembolism in the cat, systolic murmurs with gallop rhythms on auscultation, cardiomegaly with (groups 1 and 3) or without (group 2) pulmonary edema, abnormal electrocardiograms, elevated left ventricular end-diastolic pressures, and angiocardiographic evidence of mitral regurgitation with left ventricular concentric hypertrophy (group 1), left ventricular dilatation (group 2), or midventricular stenosis (group 3). Some cats in groups 1 and 3 also had evidence of left ventricular outflow obstruction. The principal pathologic findings in all of the cats and dogs were left atrial dilation, hypertrophy, increased septal:left ventricular free wall thickness ratio with disorganization of cardiac muscle cells (group 1); dilatation of the four chambers with degeneration of cardiac muscle cells (group 2); and extensive endocardial fibrosis and adhesion of the left ventricle (group 3). Aortic thromboembolism was commonly observed in the cats of all three groups. These clinical and pathologic findings indicate that cardiomyopathy in the cat or dog is similar to the three forms of cardiomyopathy in humans (hypertrophic, congestive, and restrictive).

Animals↗
PubMed1976

The characteristics of diastolic pressure-volume relationships in primary myocardial disease.

Utilizing the pressure-volume relationship, the indices of left ventricular diastolic compliance, SV/EDP-DP, dV/dP, and dV/VdP, ventricular stiffness index, I/P(dV/dP), and myocardial stiffness index, I/S(dD/dS) were evaluated of seven patients with normal left ventricle, eleven patients with hypertrophic and seven with congestive type of primary myocardial disease. Myocardial stiffness index was obtained from the equation of S = aekD, where S is a wall stress, a; a constant, D; a length of short axis, K; a stiffness constant. The mean values and standard errors of the means of SV/EDP DP, dV/dP, dV/VdP, I/P(dV/dP), and I/S(dD/dS) for normal group are 16.7 +/- 8.7 (ml/mmHg), 16.03 +/- 6.98 (ml/mmHg), 0.1259 +/- 0.0447 (mmHg-1), 0.0059 +/- 0.0032 (ml-1) and 0.603 +/- 0.153 (cm-1), for hypertrophic type are 10.5 +/- 5.5 (ml/mmHg), 7.23 +/- 7.42 (ml/mmHg), 0.0599 +/- 0.0736 (mmHg-1), 0.0174 +/- 0.0097 (ml-1) and 1.3555 +/- 0.3395 (cm-1), and for congestive type are 17.5 +/- 3.4 (ml/mmHg), 3.91 +/- 2.13 (ml/mmHg), 0.0250 +/- 0.0239 (mmHg-1), 0.0308 +/- 0.0126 (ml-1), and 3.287 +/- 1.272 (cm-1). There were highly significant differences between normal and primary myocardial disease in each indices except SV/EDP-DP. I/P(dV/dP), and I/S(dD/dS) had highly significant differences between hypertrophic and congestive type, the latter is stiffer than the former. The compliance index was not sensitive enough to separate two types of primary myocardial disease.

Adult↗
PubMed1980

Effect of procainamide on left ventricular performance in patients with primary myocardial disease.

The effect of procainamide (P) on left ventricular function as measured by the systolic time intervals (STI) was studied in 14 patients with primary myocardial disease. P, 7.5 mg/kg body weight, was given intravenously at a rate of 100 mg per minute. Administration of P produced a decrease in left ventricular performance as manifest by a significant prolongation of the pre-ejection period corrected for heart rate (PEPI) and an increase of the PEP to the left ventricular ejection time (LVET) ratio. The peak effect on PEPI and PEP/LVET occurred at 2 minutes after P administration (delta PEPI + 14 +/- 1.9 ms, p < 0.001, delta PEP/LVET + 0.052 +/- 0.007, p < 0.001) with values returning towards baseline by 60 min. In 6 of the patients P blood levels were measured simultaneously with the STI measurements. Changes in PEPI and PEP/LVET directly parallel changes of P blood levels. It is concluded that P given intravenously at the usual therapeutic doses decreases left ventricular performance in patients with primary myocardial disease. These changes in left ventricular performance directly parallel procainamide blood levels.

Adult↗
PubMed1986

Chronic afterload reduction in infants and children with primary myocardial disease.

The purpose of this study was to determine the long-term effects of chronic afterload reduction with oral hydralazine therapy in patients with primary myocardial disease (PMD). Twenty-six children aged 3 to 48 months with the diagnosis confirmed by M-mode and two-dimensional echocardiograms and angiograms were given digitalis and diuretics. Fourteen of these patients also received hydralazine orally in doses up to 4.0 mg/kg/day in four divided doses. Echocardiograms were initially repeated at 1- to 3-month intervals and subsequently at 6-month intervals. Long-term follow-up data were available in 10 patients given hydralazine and eight control patients; the follow-up interval ranged from 3 to 48 months. In the hydralazine group the shortening fraction rose from 14.5 +/- 4.9 to 23.2 +/- 7.5 (P less than 0.01), and the ratio of pre-ejection period to ejection time (0.52 +/- 0.05 to 0.35 +/- 0.06, P less than 0.001) and left ventricular size, normalized to body surface area (116 +/- 7 to 87 +/- 21, P less than 0.01), decreased. Significant improvement was demonstrated by echocardiography after 12 months of hydralazine therapy. There was no significant change in any of these values in the control group. We conclude that hydralazine therapy is a useful adjunct in the management of primary myocardial disease in infancy and childhood.

Administration, Oral↗
PubMed1977

Primary myocardial disease in the cat. A model for human cardiomyopathy.

Thirty-four cats with primary myocardial disease were studied. The cats were divided into two groups, depending on the clinical, hemodynamic, angiocardiographic, and pathologic findings. Group A consisted of those cats with hypertrophic cardiomyopathy and Group B consisted of those cats with congestive cardiomyopathy. Similarity in the characteristics of cardiomyopathy in the human cat was found. Both Group A and Group B consisted predominantly of mature adult male cats. The most common presenting signs were dyspnea and/or thromboembolism, systolic murmurs with gallop rhythms on auscultation, cardiomegaly with (Group A) or without (Group B) pulmonary edema, abnormal electrocardiograms, elevated left ventricular end diastolic pressures, and angiocardiographic evidence of mitral regurgitation with left ventricular concentric hypertrophy (Group A) or left ventricular dilatation (Group B). Some cats in Group A also had evidence of left ventricular outflow obstruction. The principal pathologic findings in these cats were left atrial dilatation, symmetric hypertrophy or asymmetric septal hypertrophy of the left ventricle (Group A), and dilatation of the four cardiac chambers (Group B). Aortic thromboembolism was commonly observed in both groups. These clinical and pathologic findings indicate that cardiomyopathy in the cat is similar to the two most common forms of cardiomyopathy in the human (hypertrophic cardiomyopathy, with and without obstruction, and congestive cardiomyopathy).

Age Factors↗