Myocardial Balance of Inorganic Phosphate and Enzymes in Man
Effects of Tachycardia and Ischemia
The effects of atrial pacing on the cardiac balance of inorganic phosphate (Pi) were studied during control, atrial pacing, and recovery periods in 29 patients. Group A (n = 18) who had roentgenographically demonstrated coronary artery disease (CAD) developed angina during pacing, and showed mean myocardial lactate (L) production, abnormal left ventricular end-diastolic pressure (LVEDP) and ST segment depression. Group NA (n = 11), composed of six patients with CAD and five subjects with no demonstrable cardiac disease, had normal lactate metabolism, LVEDP, and ST segments during pacing. In addition, blood levels of two enzymes were determined: creatine phosphokinase (CPK) in nine patients of Group A and six patients of Group NA, and glutamic oxaloacetic transaminase (GOT) in eight patients of each group.
During control, small uptake of Pi was observed in both groups. During pacing, Group A showed first a fall and then abolition of mean Pi uptake, and during the early recovery period, a small loss of this ion was observed. Although there was a good correlation between L and Pi uptakes (r = 0.86, P < 0.001) throughout the study, Pi loss, which occurred in 55% of patients in Group A, appeared to be a less reliable index of myocardial anaerobiosis than L production, which occurred in 72%. No consistent changes in Pi balance were observed in Group NA. The only significant enzymatic change was the small but sudden and significant rise of mean CPK levels in coronary sinus (CS) blood above the arterial levels in five patients of Group A during the first 6 min of pacing. These data show that during pacing-induced angina the human heart loses Pi. In addition, these preliminary observations on the CS CPK levels during pacing in the angina patients suggest that the stress of tachycardia and ischemia may facilitate the escape of this enzyme from the heart.
- Atrial pacing
- Creatine phosphokinase
- Left ventricular end-diastolic pressure
- Coronary artery disease
- ST segments
- Myocardial anaerobiosis
- Glutamic oxaloacetic transaminase
- Received July 2, 1973.
- Accepted September 4, 1973.
- © 1974 American Heart Association, Inc.