Although improvements in noninvasive external cardiac pacing have led to a technique with reliable electrical capture and reduced patient discomfort, hemodynamic responses to this pacing mode have not been described previously. Accordingly, this technique was applied to 16 patients with a clinical diagnosis of angina pectoris undergoing cardiac catheterization. Three patients had normal coronary arteries, whereas the remaining 13 had significant coronary artery disease. All patients had noninvasive pacing at increasing heart rates to 85 percent of age-predicted maximal heart rate. At maximal pacing, all patients demonstrated a rise in atrial, pulmonary artery, and mean aortic pressures. Cardiac index remained unchanged, reflecting parallel increases in arteriovenous oxygen difference and oxygen consumption. One minute after cessation of pacing, pulmonary artery pressure and oxygen consumption remained elevated, whereas arteriovenous oxygen difference returned to baseline with a subsequent rise in cardiac index. Angina occurred in eight patients with coronary artery disease at peak pacing and was accompanied by a rise in left ventricular enddiastolic pressure after pacing. In eight patients without pacing-induced angina, including the three patients with normal coronary arteries, there was no significant change in left ventricular end-diastolic pressure after pacing. It is concluded that noninvasive external cardiac pacing produces a rise in both right and left heart filling pressures and in oxygen consumption that persist after pacing, and may provoke angina and hemodynamic abnormalities consistent with myocardial ischemia. This mode of pacing appears hemodynamically safe with maintenance of cardiac index and aortic pressure at 85 percent of maximal agepredicted heart rate.
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