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

BACKGROUND: 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. METHODS AND RESULTS: 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). CONCLUSIONS: 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.