Morphometric Study for Muscular and Microvascular Remodeling of Left Ventricular Free Wall and Interventricular Septum in Hypertrophic Cardiomyopathy.
- Author:
Young Jik LEE
;
Hyung Suk KIM
;
Jong Tae PARK
;
Chang Soo PARK
- Publication Type:Original Article
- Keywords:
Hypertrophic cardiomyopathy;
Heart;
Microvasculature;
Morphometric study;
CD34
- MeSH:
Adult;
Cardiomyopathy, Hypertrophic*;
Fibrosis;
Heart;
Heart Failure;
Heart Ventricles;
Humans;
Hypertrophy;
Microvessels;
Myocardial Ischemia;
Vasodilation
- From:Korean Journal of Pathology
1999;33(9):675-683
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Hypertrophic cardiomyopathy (HCMP) is characterized myofiber hypertrophy and structural remodeling with changes in the proportion of the muscular, vascular, and interstitial compartments. A study was done to determine the structural remodeling patterns and the role of microvasculature of hearts in HCMP. Forty-two postmortem hearts were analyzed including 14 from patients who died of HCMP (group 1), 8 patients with HCMP but who died from extracardiac causes (group 2), 10 patients with ischemic heart disease (group 3), and 10 normal adult hearts (group 4). Macro- and microscopic examination, immunohistochemical study using CD34 antibody, and morphometric studies using image analyzer were performed. Mean cardiac weight and wall thickness were significantly higher in the HCMP group. Myocardial hypertrophy, and a variety of myocardial disarray and fibrosis involved the whole area of the left ventricles with HCMP. The percentage areas of microvessels were 6.40 0.7 in group 1, 5.90 0.6 in group 2, 4.98 0.3 in group 3, 4.85 0.4 in group 4, respectively, and the numbers of microvessels were 198.0 20.7 in group 1, 230.0 22.3 in group 2, 211.7 11.2 in group 3, and 236.4 11.4 in group 4, respectively (mean SE). The percentage area of microvessels was significantly higher in group 1 than in other groups. However, the number of microvessels in that group was lower than in the other groups, although it was statistically insignificant. Since flow-dependent vasodilation is preserved in HCMP, we considered flow-dependent vasodilation the cause of the discrepancy between the area and the number of microvessels. Ischemic changes observed in chronic HCMP and related heart failure were considesed to be due to the relative deficiency of the coronary flow compared to the increasing cardiac mass.
