May 1, 1974Open Access

Release of Adenosine from Human Hearts during Angina Induced by Rapid Atrial Pacing

AFArthur C. FoxColumbia University Irving Medical Center GRGeorge E. ReedIsland Health EGEphraim GlassmanColumbia University Irving Medical Center

Structured PICO

Does rapid atrial pacing-induced angina cause the release of adenosine into coronary sinus blood in patients with severe coronary atherosclerosis?

Population

33 patients undergoing diagnostic cardiac catheterization, divided into 4 groups: 15 with anginal syndrome and severe coronary atherosclerosis (≥75% obstruction) who developed angina on pacing, 9 with similar disease who did not develop angina on pacing, 5 with normal coronaries and no myocardial disease, and 4 with severe heart failure and normal coronaries. (Preliminary studies also included 6 dogs).

Intervention

Rapid atrial pacing (ventricular rate accelerated by increments of 10 beats/min until definite anginal pain or AV block appeared) or exercise to induce temporary myocardial ischemia.

Comparator

Resting state, recovery state (10 min after angina), and control groups (patients not developing angina, patients with normal coronaries, and patients with heart failure) undergoing similar pacing or exercise.

Outcome

Concentration of adenosine in coronary sinus blood.surrogate

Human hearts release significant amounts of adenosine during severe regional myocardial ischemia, suggesting it may serve as an index of ischemia and influence regional coronary flow.

Abstract

This study was designed to determine whether human hearts release adenosine, a possible regulator of coronary flow, during temporary myocardial ischemia and, if so, to examine the mechanisms involved. Release of adenosine from canine hearts had been reported during reactive hyperemia following brief coronary occlusion, and we initially confirmed this observation in six dogs hearts. Angina was then produced in 15 patients with anginal syndrome and severe coronary atherosclerosis by rapid atrial pacing during diagnostic studies. In 13 of these patients, adenosine appeared in coronary sinus blood, at a mean level of 40 nmol/100 ml blood (SE = +/-9). In 11 of these 13, adenosine was not detectable in control or recovery samples; when measured, there was concomitant production of lactate and minimal leakage of K(+), but no significant release of creatine phosphokinase, lactic acid dehydrogenase, creatine, or Na(+). THERE WAS NO DETECTABLE RELEASE OF ADENOSINE BY HEARTS DURING PACING OR EXERCISE IN THREE CONTROL GROUPS OF PATIENTS: nine with anginal syndrome and severe coronary atherosclerosis who did not develop angina or produce lactate during rapid pacing, five with normal coronaries and no myocardial disease, and three with normal coronaries but with left ventricular failure. The results indicate that human hearts release significant amounts of adenosine during severe regional myocardial ischemia and anaerobic metabolism. Adenosine release might provide a useful supplementary index of the early effects of ischemia on myocardial metabolism, and might influence regional coronary flow during or after angina pectoris.

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