Aging and hypertension additively impaired coronary circulation in rats, with cardiac fibrosis rather than hypertrophy correlating with progressive deterioration of coronary hemodynamics.
Does cardiac fibrosis or hypertrophy drive the progressive deterioration of coronary flow reserve associated with hypertension and aging in rats?
Cardiac fibrosis, rather than hypertrophy, correlates with progressive deterioration of coronary hemodynamics in aging and hypertension, potentially explaining diastolic dysfunction in older hypertensive patients.
OBJECTIVE: To delineate hypertension-related and age-related changes in coronary hemodynamics and to assess the role of myocardial (i.e. left ventricular) hypertrophy and cardiac fibrosis in inducing progressive deterioration of coronary flow reserve associated both with hypertension and with aging. METHODS: Systemic and coronary hemodynamics (using radionuclide-labeled microspheres), right ventricular, left ventricular, and aortic mass indexes, and ventricular hydroxyproline concentrations (an estimate of collagen) in normotensive Wistar-Kyoto and spontaneously hypertensive rats aged 22, 35, and 65 weeks were determined. RESULTS: Spontaneously hypertensive rats of all ages had greater left ventricular and aortic masses, greater collagen concentrations in both ventricles, a lower coronary flow reserve, and greater minimal coronary vascular resistance after administration of dipyridamole than did Wistar-Kyoto rats. Despite spontaneously hypertensive rats having only left ventricular hypertrophy, coronary hemodynamics were impaired to the same extent in both ventricles. Progressive increases in myocardial collagen concentration, decreases in coronary flow reserve, and increases in minimal coronary vascular resistance were observed in rats of both strains with aging. A positive correlation and linear regression between myocardial collagen concentration and minimal vascular resistance were found for both ventricles of rats of both strains. CONCLUSIONS: Both aging and hypertension adversely affected the coronary circulation; furthermore, these effects appeared to be additive. Cardiac fibrosis, but not hypertrophy, might play a role in progressive deterioration of coronary hemodynamics in aging and hypertension and could provide an explanation for the diastolic dysfunction encountered clinically in older patients with hypertension.
Sušić et al. (Sun,) conducted a other in Hypertension and aging. Hypertension and aging vs. Normotensive Wistar-Kyoto rats was evaluated on Systemic and coronary hemodynamics, ventricular and aortic mass indexes, and ventricular hydroxyproline concentrations. Aging and hypertension additively impaired coronary circulation in rats, with cardiac fibrosis rather than hypertrophy correlating with progressive deterioration of coronary hemodynamics.