Coronary flow limitation during the development of ischemia: Effect of atrial pacing in patients with left anterior descending coronary artery disease

Atrial pacing-induced tachycardia causes increased myocardial oxygen demand and leads to the development of angina in patients with significant coronary arterial narrowing, when the ability to augment coronary flow is limited. This study evaluated the response of coronary flow in a single coronary bed as that bed was rendered ischemic by progressive increases in oxygen demand. Thermodilution measurements of great cardiac vein flow, representing the efflux from the territory of the left anterior descending coronary artery, were obtained in 20 patients as heart rate was increased by incremental atrial pacing until the maximal heart rate was reached or angina developed. Ten of the 20 patients had no significant coronary narrowing on angiography, and 10 had a lesion obstructing more than 50 percent of the diameter of the left anterior descending coronary artery but no other significant coronary narrowing. No significant difference was found between the two groups in resting heart rate, aortic pressure, left ventricular end-diastolic pressure or great cardiac vein flow. With each increment in heart rate throughout the pacing test, the patients without significant coronary stenosis showed a steady increase in great cardiac vein flow. During all submaximal pacing increments, the increase in great cardiac vein flow per increment in heart rate was similar in those with and without significant stenosis (mean ± standard deviation 1.05 ± 0.48 ml/beat versus 0.79 ± 0.31 ml/beat, respectively). However, over the final pacing increment, the patients with coronary stenosis had no increase in great cardiac vein flow, whereas those without disease continued to have increased flow ( Δ = 0.10 ± 0.19 ml/beat versus 1.3 ± 0.69 ml/beat, respectively, p < 0.001). This flow limitation phenomenon was observed in all 10 patients with coronary stenosis and was accompanied by angina or S-T segment changes, or both, in all 10. This striking difference in coronary flow patterns between patients with and without significant left anterior descending coronary artery disease may prove useful in (1) further studies of the pathophysiology and therapy of myocardial ischemia in human beings, and (2) clinical evaluation of the hemodynamic importance of left anterior descending coronary arterial lesions in selected patients.