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Results for “ENDOMYOCARDIAL FIBROSIS”

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At least 1,243 records · Page 69Linked to original sources
PubMed1987

Pathogenesis and preventive and therapeutic trials in an animal model of dilated cardiomyopathy induced by a virus.

An animal model of dilated cardiomyopathy following encephalomyocarditis (EMC) virus has been developed. Virus was isolated from mouse hearts and viral antigens were detected in the myocardium until the second week of infection, but neither was found thereafter. Differences were found among different strains of mice in the frequency of occurrence and severity of myocarditis, and even in the character of the pathologic lesions. Thus, genetic factors may play an important role in the pathogenesis. Autoantibodies against heart developed and the distribution of cardiac myosin isoenzymes was altered during the course of myocarditis. Virus, vaccine, maternal vaccination, recombinant interferon alpha A/D and ribavirin were effective in protecting the mice from developing myocarditis. This animal model is suitable for studying the pathogenesis of viral myocarditis and evaluating preventive and therapeutic interventions of the condition.

Animals↗
PubMed1987

Dilated cardiomyopathy: clinical significance of possible related factors.

The present study investigates the clinical significance of several possible causative or conditioning factors which have been proposed to be involved in the pathogenesis of dilated cardiomyopathy (DCM). By reviewing the medical records of 68 patients with DCM, we found a definite, and suggestive family history in 16%, and 28%, respectively, and antecedent flu-like symptoms in 43%. A history of hypertension was observed in 35%, habitual alcoholism in 49% and diabetic pattern on glucose tolerance test in 37%. We then classified the study patients into three groups; familial, myocarditic and acquired groups. The familial group showed advanced myocardial damage with the poorest prognosis. Abnormal T-cell subsets in this group suggested that genetically determined abnormal immune response is involved in the development of DCM. In the myocarditic group, endomyocardial biopsy demonstrated mononuclear cell infiltration in 53% and the myocardial damage and prognosis were of intermediate severity. The acquired group showed significantly more frequent histories of hypertension, habitual alcoholism or diabetes than their age- and sex-matched controls, suggesting that they developed the disease in association with these factors. The severity of hemodynamic impairment and myocardial damage was the least extensive and prognosis was relatively favorable in this group. These different clinical features in the three groups may provide evidence that these factors actually contribute to the development of myocardial damage in DCM and that the condition is a clinical syndrome associated with heterogeneous etiologies or conditioning factors. Determination and management of these factors would be of practical value in treating patients with DCM that has no established therapy against underlying etiologies.

Adult↗
PubMed1989

Mechanism of development of asymmetric septal hypertrophy in patients with essential systemic hypertension.

In order to understand the mechanism of development of asymmetric septal hypertrophy (ASH) in hypertension, 290 patients with essential hypertension (HT) were examined echocardiographically. Out of them 84 cases of advanced left ventricular hypertrophy (LVH) [37 cases of symmetric hypertrophy (HT-SH group) and 47 cases of ASH (HT-ASH group)] were compared in their clinical and echocardiographic findings with hypertrophic cardiomyopathy (HCM). In the 290 HT cases, the highest systolic pressure in each patient's history was found to correlate with left ventricular (LV) posterior wall thickness (PWT), but not with the septal wall thickness (IVST). There were no differences in LV thickness (IVST + PWT) among patients in the HT-ASH, HT-SH and HCM groups. While the HCM group patients showed no significant differences in IVST and PWT from those in the HT-ASH group, they did have greater IVST and smaller PWT than HT-SH group patients. The rapid filling rate (RFR) was also not much different in the HCM and HT-ASH groups, but was significantly lower in the HCM group than in the HT-SH group. Furthermore, HT-ASH group patients has a milder degree of hypertension and a higher incidence of familial occurrence of HCM than did those in the HT-SH group. After treatment for HT, the HT-SH group showed a significant decrease in wall thickness during long-term observation, while the HT-ASH and HCM groups, failed to exhibit such changes. Moreover, the degree of myocardial disarrangement in the HT-ASH group did not differ significantly from that in the HCM group. These results suggested that LVH in HT is related not only to pressure load but also to genetic factors similar to that in HCM.

Adult↗
PubMed2000

Association of matrix metalloproteinase expression and left ventricular function in idiopathic dilated cardiomyopathy.

Myocardial remodeling is an important predictor for the development of dilated cardiomyopathy (DCM). Matrix metalloproteinases (MMPs) are the family of proteins responsible for extracellular remodeling, and tissue inhibitors of metalloproteinases (TIMPs) tightly control their activity. In the present study, the expression of MMP-2, MMP-9, TIMP-1 and TIMP-2 was determined by immunohistochemistry in right ventricular endomyocardial biopsy samples from 16 patients with idiopathic DCM, and its clinical significance was evaluated by comparison with parameters of cardiac function. To obtain a semi-quantitative assessment of MMP and TIMP expression, the average number of positive cells per high power field was counted. The left ventricular ejection fraction (LVEF) significantly correlated with the expression of both MMP-2 (r=-0.68) and TIMP-2 (r=-0.58). Patients were classified into 2 groups according to the degree of MMP-2 expression: strongly positive and weakly positive. LVEF, left ventricular (LV) end-diastolic pressure, right ventricular end-diastolic pressure, pulmonary capillary wedge pressure and the plasma norepinephrine level were significantly greater in the strongly positive group (p<0.05). In conclusion, the expression of MMPs and TIMPs in the cardiac matrix of patients with idiopathic DCM is closely associated with myocardial remodeling and subsequent deterioration of LV performance. These findings suggest new therapeutic targets for patients with idiopathic DCM.

Adult↗
PubMed1993

Treatment of presumed arrhythmogenic right ventricular dysplasia in an adolescent.

Familial arrhythmogenic right ventricular dysplasia is a rare cardiomyopathy that is usually diagnosed on postmortem examination or on presentation with progressive congestive heart failure. We present a patient in whom an automatic implantable cardioverter-defibrillator was inserted prophylactically. A review of the condition and possible therapies is included.

Adolescent↗
PubMed2006

DNA microarray analysis for human congenital heart disease.

Right ventricular hypertrophy and failure are prominent features in cyanotic congenital heart disease, tetralogy of Fallot (TF). Patients with TF require primary cardiac surgery at a very young age. To gain insight into the underlying molecular mechanisms of right ventricular hypertrophy and to identify gene(s) involved in TF, differential gene expression profile was assessed using expression-based microarray technology on right ventricular biopsies from young TF patients who underwent primary correction. By using quantitative immuno histochemistry, expression of vascular endothelial growth factor (VEGF), flk-1, and extracellular matrix (ECM) proteins (collagens and fibronectin) as well as vessel counts and myocyte cell size was evaluated in TF patients in relation to age-matched controls. Among 236 genes showing altered expression pattern in TF patients, VEGF (1.8-fold) and ECM markers were clearly upregulated (fibronectin, 2.4-fold; collagen Ialpha, 7.5-fold; and collagen III, 4.4-fold); flk-1 and most matrix metalloproteinases (MMPs) remained unchanged, except the levels of MMP-13 and -17 declined. Tissue inhibitors of metalloproteinases showed a downregulated pattern. Staining of VEGF in cardiomyocytes and of ECM proteins (fibronectin, collagen I and III) in interstitial as well as in perivascular area was increased (p < 0.01) in TF patients. Morphometric analysis revealed enhanced vascular density (p < 0.05) with unchanged wall thickness and enlarged myocyte cross-sectional areas (p < 0.01) with linear correlation (p < 0.01) with the age in TF-1 patients. We conclude that the upregulation of genes encoding VEGF and ECM proteins are the key events contributing to right ventricular hypertrophy and stunted angiogenesis in patients with TF.

Adult↗
PubMed2004

The role of aldosterone in heart failure and the clinical benefits of aldosterone blockade.

Aldosterone has a variety of detrimental effects on the heart and vasculature and is increasingly recognized as an important target in chronic heart failure, as illustrated by the Randomized Aldactone Evaluation Study. In this article, the evidence supporting the cardiovascular effects of aldosterone in humans and the proven benefits of aldosterone-receptor antagonists in heart failure shall be discussed.

Aldosterone↗