ISSN:
1432-2307
Keywords:
Key words Microangiopathy
;
Arteriolar density
;
Fibrosis
;
Remodelling
;
Cardiac hypertrophy
Source:
Springer Online Journal Archives 1860-2000
Topics:
Medicine
Notes:
Abstract Left ventricular hypertrophy is a risk factor for cardiovascular morbidity and mortality. In arterial hypertension and in hypertrophic cardiomyopathy it may be accompanied by clinical signs of myocardial ischaemia resulting from microcirculatory dysfunction in the absence of coronary macroangiopathy. Structural changes of the vascular and interstitial compartment of the heart are involved in the pathogenesis of impaired microcirculation. We investigated patients with hypertensive heart disease (HHD; n=12) and hypertrophic cardiomyopathy (HCM; n=19) without coronary macroangiopathy but with signs of myocardial ischaemia. Right septal endomyocardial biopsies were evaluated to quantify the structure of intramyocardial arterioles, collagen content and myocytic diameter by morphometric rules. Nine normotensive subjects served as controls. The groups differed significantly (P〈0.05) in myocytic diameter and total collagen content. The myocytic diameter correlated with the thickness of the interventricular septum. Arterioles in HHD showed a significant increase in cross-sectional medial area and in HHD patients the periarteriolar collagen area increased both in absolute terms and when standardized to medial area. Arteriolar density was significantly reduced in HCM. In a multivariate discriminant analysis the positive predictive value for differentiation of the groups by non-myocytic variables was 72.5% (P=0.013). HHD and HCM differ in the structural alterations in the arteriolar bed. Medial hypertrophy and periarteriolar fibrosis prevail in HHD, and reduced arteriolar density is found in HCM. Different microvascular remodelling at the level of arterioles indicates distinct pathophysiologic processes that may contribute to the clinically observed disturbance of coronary microperfusion in these two diseases.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1007/s004280050098
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