Experimental Subendocardial Ischemia in Dogs with Normal Coronary Arteries

TLDR

Subendocardial ischemia can arise without coronary obstruction when metabolic demand exceeds supply, particularly because subendocardial flow is largely diastolic and depends on coronary driving pressure and diastolic duration. In anesthetized open‑chest dogs, the authors measured aortic and left‑ventricular pressures, coronary flow, and subendocardial/epicardial perfusion, then varied the diastolic pressure‑time index by creating arteriovenous fistulas, constricting the ascending aorta, and pacing, while estimating myocardial oxygen demand with the tension‑time index. These interventions reduced the endocardial‑to‑epicardial flow ratio to 0.1:1, nearly eliminated diastolic flow fraction and post‑ischemic hyperemia, yet mean and systolic coronary flow rose 300–500 %, and the ratio of diastolic pressure‑time index to tension‑time index best predicted the altered flow ratios.

Abstract

Subendocardial ischemia without anatomic coronary artery obstruction may result from a discrepancy between metabolic needs and available blood supply. We studied this in open-chest anesthetized dogs and measured pressures in aorta and left ventricle (LV), phasic left coronary arterial blood flow (CBF) by electromagnetic flowmeter, total CBF and LV subendocardial (endo) and subepicardial (epi) flow with radioactive microspheres 8-10µ, in diameter. Since LV Subendocardial flow is mainly or entirely diastolic, it should depend on coronary driving pressure and duration of diastole (i.e., the area between aortic and left ventricular diastolic pressures). This diastolic pressure time index (DPTI) was varied by opening arteriovenous fistulas to lower aortic diastolic pressure, constricting the ascending aorta to raise LV diastolic pressure and pacing to shorten diastole. Myocardial oxygen needs were estimated from the tension time index (TTI). Normal endo-epi flow ratios per gram (1:1) fell to 0.1:1 with these procedures and paralleled a fall in diastolic flow fraction (often nearly zero) and postischemic coronary reactive hyperemic responses. These changes occurred despite normal or raised mean CBF and 300-500% increase in systolic CBF. The altered flow ratios were best predicted by relating them to the ratio of DPTI (supply) to TTI (demand).