title: Morphometric investigation of human myocardium in arterial hypertension and valvular aortic stenosis.
abstract: Both arterial hypertension and aortic stenosis lead to pressure overload of the left ventricle. As intramyocardial vasculature is confronted with pressure overload in hypertension but not in aortic stenosis, structural differences are to be expected in both forms of left ventricular hypertrophy. With the aid of morphometry, we investigated human myocardium from autopsied hearts from six patients with arterial hypertension and 10 controls, as well as myectomy specimens from cardiac surgery from 14 patients with aortic stenosis. Mean left ventricular myocytic diameter was significantly (P less than 0.05) increased compared with controls (12.4 +/- 1.5 microns) during hypertension (+27%) as well as aortic stenosis (+65%) (P less than 0.05). This was combined with a greater volume density of perimyocytic fibrosis (controls = 0.8 +/- 0.4 V upsilon %) during hypertension (+250%) and aortic stenosis (+587%) (P less than 0.05). Walls of intramyocardial arterioles (external diameter 20-40 and 40-80 microns) were thickened to 32% and 44% (P less than 0.05) during hypertension, but not during aortic stenosis. Compared with controls, perivascular fibrosis of these arterioles was increased by +215% and 61% (P less than 0.05), respectively, during hypertension, but not during aortic stenosis.
  
  
  CONCLUSIONS
  Myocytic hypertrophy and increased perimyocytic fibrosis accompany intraventricular pressure overload (hypertension and aortic stenosis) in human hearts. Myocardial structure as a result of arterial hypertension, but not aortic stenosis, is also characterized by intramyocardial arteriole wall-thickening and increased perivascular fibrosis. Thus, distinct structural reaction patterns are noted in the cardiac hypertrophy associated with hypertension and aortic stenosis.
authors.affiliation: Department of Cardiology, Heinrich Heine University of Düsseldorf, Germany.
authors.forename: B
authors.initials: B
authors.lastname: Schwartzkopff
authors.forename: H
authors.initials: H
authors.lastname: Frenzel
authors.forename: J
authors.initials: J
authors.lastname: Dieckerhoff
authors.forename: P
authors.initials: P
authors.lastname: Betz
authors.forename: M
authors.initials: M
authors.lastname: Flasshove
authors.forename: H D
authors.initials: HD
authors.lastname: Schulte
authors.forename: M
authors.initials: M
authors.lastname: Mundhenke
authors.forename: W
authors.initials: W
authors.lastname: Motz
authors.forename: B E
authors.initials: BE
authors.lastname: Strauer
mesh_terms: D000368:Aged; D001024:Aortic Valve Stenosis / Q000473:pathology*; D001794:Blood Pressure / Q000502:physiology*; D005260:Female; D005355:Fibrosis; D006333:Heart Failure / Q000473:pathology*; D006346:Heart Septum / Q000473:pathology; D006352:Heart Ventricles / Q000473:pathology; D006801:Humans; D006973:Hypertension / Q000473:pathology*; D017379:Hypertrophy, Left Ventricular / Q000473:pathology*; D008297:Male; D008875:Middle Aged; D009131:Muscle, Smooth, Vascular / Q000473:pathology; D009206:Myocardium / Q000473:pathology*; D012016:Reference Values