The Journal of Thoracic and Cardiovascular Surgery, Vol 92, 931-935, Copyright © 1986 by The American Association for Thoracic Surgery and The Western Thoracic Surgical Association
Effects of acute tachycardia on left ventricular adenine nucleotide levels and subsequent tolerance to ischemia
HF Tripp Jr, W Lewis, C Veronee, RJ Damiano, LD German and JE Lowe
Electrophysiologically guided surgical procedures for the ablation of
supraventricular and ventricular dysrhythmias often require prolonged
periods of tachycardia to complete intraoperative mapping studies. It is
unknown whether tachycardia depletes the myocardium of high-energy
compounds or alters subsequent tolerance to ischemia. In the present study,
12 anesthetized dogs were paced from the right ventricle at a cycle length
of 250 msec for 60 minutes. In seven animals, drill biopsy specimens were
taken from the left ventricular free wall for analysis of adenine
nucleotide levels and their breakdown products before and after pacing and
after 20 minutes of recovery from pacing. In the remaining five animals,
the heart was made totally ischemic immediately after tachycardia and the
time to the onset of ischemic contracture was determined and compared to
that of five nonpaced control dogs. Acute tachycardia resulted in no
significant reduction in adenine nucleotide levels compared to control
values. Furthermore, in hearts rendered totally ischemic after tachycardia,
the mean time to ischemic contracture was 65.6 +/- 1.3 minutes versus 63.6
+/- 2 minutes in nonpaced control animals (no significant difference).
These data show that pacing-induced tachycardia in the normal heart does
not decrease adenine nucleotide levels or affect subsequent tolerance to
ischemia. These results may be clinically relevant to patients without
coronary artery disease who undergo operative procedures necessitating
prolonged periods of tachycardia for intraoperative mapping to identify the
site of arrhythmogenesis.
