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