SEARCH · PubMed Health
Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
The role of endogenous beta-adrenergic activation in the pathogenesis of spontaneous myocardial fibrosis was investigated in male and female Sprague-Dawley (SD) rats. For the purpose of blocking endogenous beta-adrenergic activities, atenolol, a beta-adrenergic blocking a agent, was given at 20, 80 and 320 mg/kg/day mixed in the diet for 12 months. The transverse sections of the ventricles including the vulnerable region for spontaneous myocardial fibrosis was stained by Azan-Mallory method for collagen fibers and examined morphometrically, while being compared with the histological findings from standard hematoxylin-eosin procedure. The fibrosis was graded into 4 classes and compared between nontreated groups and treated groups of both sexes. Fibrous foci developed principally in the subendocardial myocardium. Atenolol failed to produce significant systemic toxic effects not only on weight gains and daily intakes of food but also on death rates. Atenolol did not prevent development of myocardial lesions in both sexes, whereas it significantly promoted fibrosis in the medium and high dose groups of male rats but not at any dose levels in female animals. It is suggested that endogenous beta-adrenergic activation plays no major role in the onset or development of spontaneous myocardial lesions, whereas the adrenergic system may probably control collagen synthesis in myocardial fibrosis.
Explore the source record for details and available documents.
In performing medicolegal autopsies on sudden deaths, there occur a number of cases in which no cause of death can be found. In particular, no evidence of macroscopic cardiac abnormalities can be observed. However, extensive histological screening may reveal isolated areas of myocardial fibrosis. The five cases presented discuss the etiology of this fibrosis and its possible relation to myocarditis. The cases involve white women between the ages of 19 and 25 with no previous medical history. The weight of the heart in all five cases was normal. Macroscopic evidence of fibrosis was visible in four out of five cases. No other macroscopic abnormalities were observed. Histologically, there was evidence of scarring or interstitial fibrosis in all five cases. In four of the cases, additional screening permitted the observation of dispersed inflammatory foci consisting of lymphocytes, plasmocytes and macrophages. Two of the cases demonstrated eosinophil and neutrophil aggregates in the center of necrotic foci. No evidence of vascular inflammatory phenomena was observed in any of the five cases. According to the Dallas criteria, three of the five cases fulfill the requirements for myocarditis and one of the five cases for borderline myocarditis. The Dallas criteria, however, do not take into consideration the possible association between inflammation and myocardial fibrosis since many of the reported series of myocarditis have been from hospital autopsies or endomyocardial biopsies and have not taken into account sudden death from fibrotic sequelae of myocarditis.(ABSTRACT TRUNCATED AT 250 WORDS)
The extent and time course of recovery of left ventricular function were investigated in 29 patients with no previous symptoms who had acute nonischemic congestive cardiomyopathy and left ventricular ejection fraction of 0.22 +/- 0.07. Improvement in left ventricular ejection fraction by at least 0.05 was observed in 24 of the 29 patients and was achieved within 6 months after the initial evaluation. Progressive improvement was seen, with a maximum ejection fraction of 0.45 +/- 0.17 being achieved within approximately 18 months. The degree of ejection fraction recovery was not related to the initial clinical or hemodynamic variables. However, the extent of fibrosis detected on endomyocardial biopsy correlated inversely with subsequent changes in ejection fraction (r = -0.65, p = 0.0003). Thus significant recovery is likely after an acute episode of nonischemic cardiomyopathy and may be progressive during the first year. Recovery is related to the extent of myocardial fibrosis detected on endomyocardial biopsy but cannot be predicted from the initial clinical or hemodynamic presentation.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.