Left ventricular function and collagen content after regression of hypertensive hypertrophy
Motz, W.; Strauer, B.E.
Hypertension 13(1): 43-50
1989
ISSN/ISBN: 0194-911X PMID: 2521332 Document Number: 347484
To determine whether regression of hypertensive hypertrophy through blood pressure control also involves left ventricular collagen and consecutive alterations in left ventricular diastolic and systolic function, antihypertensive treatment with the calcium channel blocker nifedipine (30 mg/kg.day) was employed in 20-week-old spontaneously hypertensive rats (n=15) for a period of 20 weeks. Age-matched (40 weeks old) untreated (n=13) and 20-week-old spontaneously hypertensive rats representing the state before therapy (n=14) were used for comparison. Myocardial stiffness was described by the tangent modulus Km of the elastic stiffness-stress relation. Left ventricular collagen was determined by means of hydroxyproline (OH-proline) concentration. Myocardial working capacity of the left ventricle was measured as the peak developed systolic pressure per weight unit muscle mass and systolic peak pump function as the maximum achievable cardiac output under volume loading. After the 20-week course of nifedipine treatment, systolic aortic pressure dropped from 287.+-.11 to 144.+-.6 mm Hg (p<0.001). Regression of hypertrophy was shown to be a left ventricular muscle/body weight ratio of 2.13.+-.0.18 mg/g (p<0.01) in the 40-week-old nifedipine-treated hypertensive rats, whereas the ratios of the 20-week-old and 40-week-old untreated spontaneously hypertensive rats were 2.3.+-.0.30 and 2.34.+-.0.18 mg/g, respectively. In proportion with hypertrophy reversal, total OH-proline content of the left ventricle was lower than in the nifedipine-treated group compared with the untreated controls (1.89.+-.0.20 mg vs. 2.37.+-.0.23 mg, p<0.01). Left ventricular OH-proline content per weight unit myocardium was also lower in the nifedipine-treated hearts (2.66.+-.0.17 mg/g) compared with the untreated ones (2.92.+-.0.26 mg/g, p<0.01). Myocardial stiffness constant Km remained unchanged after reversal of hypertrophy (19.8.+-.2.6 vs. 20.3.+-.2.6). Because of the unchanged elastic material properties of the myocardium, myocardial working capacity remained unaltered after regression of hypertrophy. Since preload, heart rate, and myocardial working capacity remained unchanged, the enhanced left ventricular pumping function in the nifedipine-treated group (left ventricular ejection fraction: 82.+-.9 vs. 63.+-.13%, p<0.05) was caused by the pronounced decrease inleft ventricular systolic wall stress, that is, left ventricular aferload under nifedipine treatment (166.+-.44 vs. 210.+-.37.9 [103 dyn/cm2], p<0.05).