Serial changes in left ventricular (LV) size and function during the adaptation to chronic pressure overload and the transition to pump failure were studied in 16 conscious dogs (aortic bands placed at 8 weeks of age). Echocardiographic data at baseline and at 3, 6, 9, and 12 months after banding revealed a progressive increase in LV mass in all dogs. In six dogs with LV pump failure, there was a progressive decline in circumferential fiber shortening (29+±4% at 12 months); this was significantly less than that seen in five littermate controls (38+±3%, p<0.05). The average LV to body weight ratio in this group was 9.8±2.7 g/kg. In 10 dogs without pump failure (compensated LVH group), shortening exceeded that seen in the controls (43 ±4%, p<0.05); the LV to body weight ratio was 7.7±1.0 g/kg. At 12 months (cardiac catheterization), the LV end-diastolic pressure was higher in the failure (25±+15 mm Hg) than in the compensated group (8±5 mm Hg, p <0.05); mean systolic stress was also higher in the failure group (313 ±67 g/cm2) than in the compensated group (202 ±53 g/cm2, p <0.05). The transmural distribution of myocardial blood flow was measured (at 12 months) with the radioactive microsphere technique; flow data were then related to an index of demand (a stress-time index). There was preferential blood flow to the subendocardial layers in the control (endo/epi= 1.28) and compensated hearts (endo/epi= 1.10), but in the failure group there was a relative decrease in subendocardial flow (endo/epi=0.92). However, the absolute values for subendocardial flow in the normal, compensated, and failure groups were 77±54, 125 ±48, and 113±64 ml/min/100 g; the stress-time indexes in the subendocardial shell were 38+11, 74±19, and 93 +34 g sec 102/cm2/min. Despite what appears to be a marginal balance between blood flow and the stress time index in the failure group, the myocardial high energy phosphates were not depleted and the inoptropic state was not depressed. In this model of LV hypertrophy, the observed differences in fiber shortening can be explained on the basis of the inverse afterloadshortening relation; pump failure was due to an inadequate LV hypertrophy with afterload excess. Pump failure due to afterload excess was associated with adequate subendocardial blood flow at rest; during exercise or other hemodynamic stress, however, these hearts are likely to be especially vulnerable to ischemia and its consequences. (Circulation 1989;79:872-883
Tolerance of the canine heart to prolonged ischemic arrest was studied in 10 hearts from normal control dogs and 15 hearts from dogs with left ventricular hypertrophy (LVH); experiments were performed 1 year after banding the aorta in 8-week-old puppies. At
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.