The response of the myocardial metabolism to atrial pacing in patients with coronary slow flow

The pathophysiology of angina pectoris is not precisely known yet in patients who have no coronary lesion but slow coronary flow by angiography. In this study we aim to display metabolic ischemia via atrial pacing to determine the difference of lactate production and arterio-venous O2 content difference (AVO2). Thirty-four patients with slow coronary flow detected by coronary angiography via the TIMI 'frame count' method were included in this study. The resting and stress images from the patients undergoing myocardial perfusion tomography were recorded, pre and postpacing lactate extraction and AVO2 content difference values were calculated. Patients were classified according to their metabolic responses to atrial pacing stress. Group I consisted of 28 patients (18 male, 10 female, mean age 54.42 +/- 9.61) who did not demonstrate metabolic ischemia and group II consisted of six patients (four male, two female, mean age 60 +/- 5.76) who had metabolic ischemia after the procedure. There was no statistically significant difference between prepacing AVO2 content difference in group I (57.38+/-2.05%) and group II (58.23 +/- 2.11%) (P = NS). However postpacing AVO2 content difference of group I and group II was statistically significant (respectively, 57.96+/-2.65 vs. 68.35 +/- 2.15%, P < 0.001). In other words, postpacing AVO2 content difference was unchanged from the basal AVO2 content difference level in group I (respectively, 57.38 +/- 2.05 vs. 57.96 +/- 2.65%; P = NS) in contrast to the postpacing AVO2 content difference which increased significantly in group II (58.23 +/- 2.11 vs. 68.35 +/- 2.15%; P < 0.028). Although basal lactate extraction rates were similar in groups I and II (respectively, 0.24 +/- 0.1 vs. 0.23 +/- 0.18; P = NS), postpacing lactate extraction rates were decreased significantly in the two groups, prominently in group II (0.154 +/- 0.15 vs. -0.471 +/- 0.27; P < 0.0001) which indicated that lactate extraction converted to lactate production. Metabolic ischemia was detected in only 17.6% of patients included in this study and 83.4% of these six patients with proven metabolic ischemia had perfusion defects in scintigraphy. Our data confirmed that angina pectoris was not originated from myocardial ischemia in most of the patients with slow coronary flow. We conclude that perfusion scintigraphy is a reliable and accurate method for detection of true ischemia in this group of patients.