Does long-term hypertension and LVH in a dog model lead to proportional coronary angiogenesis?
In a canine model of long-term hypertension and LVH, coronary angiogenesis occurs in proportion to the increase in left ventricular mass, maintaining normal minimal coronary vascular resistance and arteriolar density.
Many studies have documented that during the development of left ventricular hypertrophy (LVH) coronary vascular growth lags behind that of cardiac muscle. To ascertain whether significant growth of coronary resistance vessels occurs with long-standing hypertension and LVH, we studied dogs with Goldblatt (one-kidney, one-clip) hypertension seven months after surgery. Left ventricular minimal coronary vascular resistance (LV MCVR) was derived from adenosine-induced maximal flow measured with 15 microns microspheres. Morphometric data were based on perfuse-fixed hearts arrested in diastole. Hypertension and LVH were associated with a 46% increase in left ventricular weight/body weight ratio (LVH, 6.73 +/- 0.31; control, 4.62 +/- 0.30), no significant change in LV MCVR/100 g, and a reduction in total LV MCVR (LVH, 0.11 +/- 0.02 mm Hg/ml/min; control, 0.15 +/- 0.02 mm Hg/ml/min). Arterial and arteriolar wall/lumen ratios were virtually identical in the two groups. Arteriolar (lumen diameter less than 200 microns) numerical densities (arteriolar profiles/mm2) were also similar for the two groups even when analyzed according to lumen diameter size class and by ventricular location (epimyocardium, midmyocardium, and endomyocardium). Moreover, the relative frequency distribution of any arteriolar size class was similar for both groups. Because MCVR and arteriolar density were normal, this study provides new evidence that angiogenesis during long-term LVH in this model is of sufficient magnitude to enable the cross-sectional area of the coronary resistance vessels to increase in proportion to the increase in left ventricular mass.
Tomanek et al. (1989) studied this question.