Key result
Repeated rapid ventricular pacing induced adaptation to myocardial ischemia, evidenced by less pronounced changes in transcardiac pH, K+, ST segment, and wedge pressure during the second period.
Why the study?
Does repeated rapid ventricular pacing induce adaptation to myocardial ischemia in patients with coronary artery disease?
Does repeated rapid ventricular pacing induce adaptation to myocardial ischemia in patients with coronary artery disease?
Repeated rapid ventricular pacing in patients with coronary artery disease induces physiological and metabolic adaptation to myocardial ischemia, demonstrating a preconditioning effect.
Answers are grounded in this paper and cite their sources.
No immediate change to CAD management; leaves open whether repeated pacing induces clinically relevant adaptation.
OBJECTIVE: The purpose of our study was to evaluate whether repeated ventricular pacing is able to induce adaptation against ischemia in coronary artery disease patients. DESIGN: Fifteen patients with documented coronary artery disease were subjected to two successive periods of rapid ventricular pacing (150 bpm) of equal length (295+/-33 s), the first being limited by intolerable anginal pain. The second pacing period, of the same length as the first, was initiated after the disappearance of angina and ST depression, the mean resting time being 433+/-30 s. Blood samples for the determination of transcardiac differences in glucose, lactate, free fatty acids, K+, pCO2, pH, oxygen saturation and noradrenaline were taken from the femoral artery and coronary sinus before and at the end 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, and the observed adaptation in the measured variables during the successive pacing tests was correlated with the duration of angina, severity of coronary artery disease and degree of collateralization. RESULTS: Changes in the transcardiac pH and K+ differences, ST segment and pulmonary capillary wedge pressure were less pronounced during the second pacing period. The subgroup with net lactate production before or after the first pacing period demonstrated metabolic adaptation manifested as improved lactate extraction during the second pacing period. Rate-pressure product and oxygen extraction, and thus presumably also overall oxygen consumption and oxygen delivery, were similar during both tests. The magnitude of adaptation did not correlate with the duration of angina, severity of coronary artery disease or overall 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.
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Keijo Peuhkurinen Kari Ylitalo (2000) studied Coronary artery disease (n=15). Repeated rapid ventricular pacing vs. First pacing period (baseline response) was evaluated on Adaptation to myocardial ischemia (changes in transcardiac pH, K+, ST segment, and pulmonary capillary wedge pressure). Repeated rapid ventricular pacing induced adaptation to myocardial ischemia, evidenced by less pronounced changes in transcardiac pH, K+, ST segment, and wedge pressure during the second period.
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