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European Heart Journal 1985 6(3):239-246;
Copyright © 1985 by the European Society of Cardiology.
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© 1985 The European Society of Cardiology

Effects of cold stimulation on coronary haemodynamics during exercise in patients with coronaryartery diseas

S. DE SERVI, A. MUSSINI, L. ANGOLI, M. FERRARIO, E. BRAMUCCI, A. GAVAZZI, S. GHIO, D. ARDISSINO and G. SPECCHIA

Divisione di Cardiologia, Policlinico S. Matteo, Istituto di Ricovero e Cura a carattere scientifico Pavia (Italy)

Received 1 July 1984; revised 29 November 1984; accepted 1 February 1984.

Stefano de Servi, M.D., Divisione Cardiologia, Policlinico s. Matteo, 27100 PAVIA (Italy).

Abstract

To assess if cold-induced vasoconstriction may persist during exercise and contribute to the development myocardial ischaemia, we studied 11 patients with exertional angina and angiographically proven coronary artery disease, in all cases involving the proximal portion of the leftanterior descending artery. Great cardiac vein flow (GCVF) was measured by the thermodilution technique and the coronary resistance of abnormally perfused anterior region (ARCR) was calculated as the quotient of mean arterial pressure and GCVF. All patients performed a supine bicycle exercise test (ET1) until angina occurred. After recovery, they underwent a cold pressor test (CPT) and then performed a second exercise test (ET2) while cold stimulation was continued. During ET1, ARCR decreased (from 1.53± 0.43 to 12.04± 0.35 mmHg ml1––1, P<0.001) as a result of the metabolic vasodilation, while it rose, although non significantly, during CPT despite the increase in double product (P<0.001), reflecting the augmented myocardial oxygen consumption. However, such abnormal response to CPT did not persist during ET2, because ARCR decreased to a value non significantly different from that achieved at peak ET1. In five patients, who showed a reduced exercise tolerance during ET2, ARCR dropped by 22% during ET2 compared with 34% decrease during ET1. However, such a difference was unlikely to account for the reduction in exercise tolerance, because double product at peak ET2 was never lower than the corresponding value at peak ET1. Our data show that the inappropriate vasoconstriction induced by CPT in an abnormally perfused myocardial region does not persist during exercise, when metabolic vasodilation occurs. The more rapid achievement of critical levels of myocardial oxygen consumption seems the most likely mechanism by which cold stimulation lowers angina threshold during exercise.

Key Words: Angina pectoris • cold pressor test • exercise testing


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