STRUCTURAL-ANALYSIS OF ARTERIOLAR AND MYOCARDIAL REMODELING IN THE SUBENDOCARDIAL REGION OF PATIENTS WITH HYPERTENSIVE HEART-DISEASE AND HYPERTROPHIC CARDIOMYOPATHY

Citation
M. Mundhenke et al., STRUCTURAL-ANALYSIS OF ARTERIOLAR AND MYOCARDIAL REMODELING IN THE SUBENDOCARDIAL REGION OF PATIENTS WITH HYPERTENSIVE HEART-DISEASE AND HYPERTROPHIC CARDIOMYOPATHY, Virchows Archiv, 431(4), 1997, pp. 265-273
Citations number
58
Categorie Soggetti
Pathology
Journal title
ISSN journal
09456317
Volume
431
Issue
4
Year of publication
1997
Pages
265 - 273
Database
ISI
SICI code
0945-6317(1997)431:4<265:SOAAMR>2.0.ZU;2-5
Abstract
Left ventricular hypertrophy is a risk factor for cardiovascular morbi dity and mortality. In arterial hypertension and in hypertrophic cardi omyopathy it may be accompanied by clinical signs of myocardial ischae mia resulting from microcirculatory dysfunction in the absence of coro nary macroangiopathy. Structural changes of the vascular and interstit ial compartment of the heart are involved in the pathogenesis of impai red microcirculation. We investigated patients with hypertensive heart disease (III-ID, n=12) and hypertrophic cardiomyopathy (HCM; n=19) wi thout coronary macroangiopathy but with signs of myocardial ischaemia. Right septal endomyocardial biopsies were evaluated to quantify the s tructure of intramyocardial arterioles, collagen content and myocytic diameter by morphometric rules. Nine normotensive subjects served as c ontrols. The groups differed significantly (P<0.05) in myocytic diamet er and total collagen content. The myocytic diameter correlated with t he thickness of the interventricular septum. Arterioles in HHD showed a significant increase in cross-sectional medial area and in I-II-ID p atients the periarteriolar collagen area increased both in absolute te rms and when standardized to medial area. Arteriolar density was signi ficantly reduced in HCM. In a multivariate discriminant analysis the p ositive predictive value for differentiation of the groups by non-myoc ytic variables was 72.5% (P=0.013). HI-ID and HCM differ in the struct ural alterations in the arteriolar bed. Medial hypertrophy and periart eriolar fibrosis prevail in HHD, and reduced arteriolar density is fou nd in HCM. Different microvascular remodelling at the level of arterio les indicates distinct pathophysiologic processes that may contribute to the clinically observed disturbance of coronary microperfusion in t hese two diseases.