Maximum contractility of the experimentally hypertrophied heart in situ and survival of the acute coronary occlusion

Summary

Studies were carried out in dogs with significant moderate left ventricular hypertrophy (LVH) induced by artifical coarctatio aortae to reveal the reserve of performance and the behavior in response to acute ligation of the LCA (left circumflex artery). The hemodynamic data at rest and during catecholamine stimulation were not essentially different, whereas the maximal inotropic state was a little enhanced in LVH dogs (LVH₁ = 12; CG₁ = 6). The acute maximal pressure rise of the left ventricle — obtained by acute clamping of the aorta ascendens — was nearly the same in both groups (LVH₂ = 6; CG₂ = 6) when related to 100 g left ventricular wet weight. The LVH hearts react to a rapid volume overload with a slightly higher increase of HR and LVEP indicating a minor adaption to an acute volume overload explained by diminished compliance. In consequence to acute ligation of the LCA (LVH₃ = 13; CG₃ = 11) LVH hearts showed a higher (p < 0.05) survival rate (69%) than controls with comparable collateral status of the coronary collateral vessels because 91% of these developed ventricular fibrillation. To explain this phenomenon we determined the catecholamine-concentration in each part of the heart in a further group (LVH₄ = 5; CG₄ = 6). Unexpectedly a significant diminution was seen in the non-hypertrophied right ventricle, but the other compartments also showed a decrease of the catecholamine concentration. Subsequent studies have to be done to explore the better electrophysiologic protection of the LVH heart in consequence to acute ligation of the LCA.