K. Ylitalo et K. Peuhkurinen, Adaptation to myocardial ischemia during repeated ventricular pacing in patients with coronary artery disease, SC CARDIOVA, 34(2), 2000, pp. 134-141
Objective: The purpose of our study was to evaluate whether repeated ventri
cular pacing is able to induce adaptation against ischemia in coronary arte
ry disease patients. Design: Fifteen patients with documented coronary arte
ry disease were subjected to two successive periods of rapid ventricular pa
cing (150 bpm) of equal length (195 +/- 33 s), the first bring limited by i
ntolerable anginal pain. The second pacing period, of the same length us th
e first. was initiated Lifter the disappearance of angina and ST depression
, the mean resting lime being 433 +/- 30 s. Blood samples Tur the determina
tion of transcardiac differences in glucose, lactate, free fatty acids, K+,
pCO(2), FH, oxygen saturation and noradenaline were taken from the femoral
artery and coronary sinus before and at the rad of each pacing period. The
mechanical performance of the hearts was followed by continuous monitoring
of intra-arterial blood pressure and pulmonary capillary wedge pressure, a
nd the observed adaptation in the measured variables during the successive
pacing tests was correlated with the duration of angina, severity of corona
ry artery disease and degree of collateralization. Results: Changes in the
transcardiac pH and K+ differences, ST segment and pulmonary capillary wedg
e pressure were less pronounced during the second pacing period. The subgro
up with net lactate production before or after the first pacing period demo
nstrated metabolic adaptation manifested as improved lactate extraction dur
ing the second pacing period. Rate-pressure product and oxygen extraction,
and thus presumably also overall oxygen consumption and oxygen delivery, we
re similar during both tests. The magnitude of adaptation did not correlate
with the duration of angina, severity of coronary artery disease or overal
l collateral score. Conclusion: Rapid ventricular pacing is able to induce
adaptation to myocardial ischemia. but the exact mechanisms in this process
remain to be elucidated.