Comparative effects of ischemia and hypoxemia on left ventricular systolic and diastolic function in humans

During the initial phase of an ischemic insult, left ventricular (LV) performance depends on the complex interaction between oxygen deprivation, vascular turgor, and accumulation of metabolites. In experimental preparations, low-flow ischemia decreases systolic shortening and increases diastolic LV distensibility, whereas pacing-induced ischemia or hypoxic perfusion produces smaller decreases in systolic shortening but decreases LV diastolic distensibility. The purpose of this study was to investigate the different effects of low-flow ischemia, pacing-induced ischemia, and hypoxemic perfusion on LV performance in humans.

In 20 patients with a significant stenosis in the left anterior descending coronary artery, micromanometer-tip LV pressure recordings (n = 20), LV angiography (n = 18), and coronary sinus blood sampling (n = 11) were obtained at rest and during the following conditions: pacing-induced ischemia (PI) (n = 11), low-flow ischemia of balloon coronary occlusion (CO) (n = 20), and hypoxemia induced by balloon coronary occlusion with hypoxemic perfusion distal to the occlusion (CO+P) (n = 11). LV stroke work index fell from 75 +/- 17 g.m at rest to 43 +/- 14 g.m at the end of CO (n = 18; P < .001). In addition, LV stroke work index was lower at the end of CO than during PI (50 +/- 11 vs 77 +/- 15 g.m; n = 11; P < .002) and was lower at the end of CO than at the end of CO+P (35 +/- 7 vs 46 +/- 9 g.m; n = 9; P < .02). LV end-diastolic pressure rose from 16 +/- 5 mm Hg at rest to 23 +/- 6 mm Hg at the end of CO (n = 20; P < .001). However, LV end-diastolic pressure was lower at the end of CO than during PI (20 +/- 5 vs 30 +/- 5 mm Hg; n = 11; P < .002) and was lower at the end of CO than at the end of CO+P (26 +/- 5 vs 34 +/- 7 mm Hg; n = 11; P < .01). LV end-diastolic volume index increased from 75 +/- 14 mL/m2 at rest to 79 +/- 15 mL/m2 at the end of CO (n = 18; P < .05). Left ventricular end-diastolic volume index increased to values similar to those for CO during PI (79 +/- 13 mL/m2; n = 11; P = NS) and at the end of CO+P (78 +/- 14 mL/m2; n = 9; P = NS). Higher values of LV end-diastolic pressure and unchanged values of LV end-diastolic volume index for PI and CO+P, compared with CO, suggested a lower end-diastolic LV distensibility during PI and during hypoxemia, as compared with low-flow ischemia. Upward shifts of individual diastolic LV pressure-volume curves during PI (9 of 11 patients) and at the end of CO+P (7 of 9 patients), compared with CO, were also consistent with lower LV diastolic distensibility during pacing-induced ischemia and during hypoxemia, compared with low-flow ischemia. Coronary sinus lactate, H+, and K+ levels increased after balloon deflation (CO and CO+P) and during pacing (PI).

Thus, during low-flow ischemia, LV systolic performance was lower and LV diastolic distensibility larger than during pacing-induced ischemia or hypoxemia. The variable response of the human myocardium to different types of ischemia was probably related to the degree of vascular turgor and accumulation of tissue metabolites.