Intracoronary papaverine induced myocardial lactate production in patients with angiographically normal coronary arteries.

Abstract

Although intracoronary papaverine has been widely used for the measurement of coronary flow reserve, little is known concerning whether papaverine may produce deleterious metabolic changes in humans. We investigated the effect of papaverine on lactate metabolism in 28 patients with normal coronary arteries. We continuously monitored phasic coronary flow velocity in the proximal left anterior descending coronary artery using Doppler guidewire. We also obtained paired samples of arterial and coronary sinus blood for the measurement of lactate at control and at 1 min after administration of 10 mg of intracoronary papaverine. There were no serious side effects during papaverine infusion. Sixteen patients showed ST-T abnormalities after papaverine. The QTc interval increased from 450 +/- 42 msec to 571 +/- 58 msec (P < 0.001). Average peak velocity increased significantly (% increase: 198.5 +/- 87.8%, range: 27.8-374.1%) after papaverine. Although intracoronary papaverine produced no significant change in arterial lactate levels (8.5 +/- 4.0-8.8 +/- 5.0 mg/ml), it induced a significant increase in coronary sinus lactate levels (5.4 +/- 3.2-15.3 +/- 8.2 mg/ml, P < 0.001). Lactate extraction ratio decreased significantly (36.4 +/- 18.4--82.2 +/- 58.4%, P < 0.001), and all patients showed net lactate production (-3.9--198.0%) after papaverine. There was weak but significant correlation between lactate extraction ratio after papaverine and coronary flow reserve (R2 = 0.15, P < 0.05). There was no correlation between lactate extraction ratio and QTc interval after papaverine. The mean value of lactate extraction ratio was not different in patients with ST-T abnormalities induced by papaverine compared to those without. These results demonstrate that intracoronary papaverine induces myocardial lactate production irrespective of the degree of coronary flow reserve and electrocardiographic changes in patients with normal coronary arteries. A safer and more reliable agent is needed for the measurement of coronary flow reserve.