Diastolic function and myocardial structure in patients with myocardial hypertrophy. Special reference to normalized viscoelastic data.

Abstract

Diastolic myocardial stiffness and viscosity were determined in 40 patients with myocardial hypertrophy by combined echo-pressure measurements. These diastolic measurements were compared with left ventricular muscle fiber diameter and interstitial fibrosis obtained from left ventricular endomyocardial biopsies at catheterization. The patients were divided into 4 groups: group 1, eight control patients; group 2, ten patients with moderate-to-severe aortic stenosis; group 3, ten patients with moderate-to-severe aortic insufficiency; and group 4, twelve patients with congestive cardiomyopathy. Myocardial stiffness and viscosity were assessed using a viscoelastic stress-strain model. For the interpatient comparison, a normalization of the stress-strain relationship was performed by calculating a reference midwall circumference (l1) at a transmural stress of 1000 dyn/cm2. The light microscopic evaluation of the left ventricular biopsies included the quantitative assessment of interstitial fibrosis by the point-counting system, and of muscle fiber diameter by direct measurement. The normalized viscoelastic constant of myocardial stiffness (Kn) was slightly, but not significantly, increased in patients with aortic stenosis and insufficiency (13.3 and 13.0), whereas Kn was significantly (P < 0.05) higher in patients with congestive cardiomyopathy (33.8) than in the control subjects (8.8). The constant of myocardial viscosity (Yn) was elevated slightly in patients with aortic valve disease and moderately in patients with congestive cardiomyopathy. In all 3 groups with myocardial hypertrophy, l1 was significantly increased compared with group 1. Left ventricular interstitial fibrosis amounted to 2% in 7 control patients, 15% in patients with aortic stenosis, 11% in patients with aortic insufficiency and 28% in patients with congestive cardiomyopathy. Muscle fiber diameter (control patients 13.7 .mu.) was largest in patients with aortic stenosis (26.8 .mu.) and smaller in patients with aortic insufficiency (21.7 .mu.) or congestive cardiomyopathy (23.6 .mu.). The comparison of functional and structural properties of the left ventricle showed a significant correlation between myocardial stiffness and interstitial fibrosis (r = 0.59; P < 0.001). There was no correlation between myocardial stiffness and angiographic muscle mass or muscle fiber size. Normalized myocardial stiffness is normal in most patients with aortic valve disease, but is significantly higher in patients with congestive cardiomyopathy. Myocardial stiffness appears not to be influenced by left ventricular muscle mass or muscle fiber size, but is increased in the presence of massive left ventricular interstitial fibrosis. Diastolic myocardial stiffness in myocardial hypertrophy evidently is related more to the interstitial than to the muscular tissue.