Evidence suggesting coronary vasodilation as the principal mechanism in the warm-up phenomenon

Background The mechanisms of the warm-up phenomenon have remained unclear. We hypothesized that, if vasodilatation is the predominant mechanism, use of a highly coronary selective vasodilator, such as nisoldipine, should mask the endogenous protection recruited by exercise testing. Methods and Results Forty-one patients with coronary artery disease were subjected to repeat exercise tests, after which they were randomized to receive a placebo or nisoldipine twice a day for 2 days. On day 2 coronary angiography was performed, and on day 3 the patients underwent another pair of repeat exercise tests. Heart rate, blood pressure, anginal pain, and electrocardiographic signs of ischemia were monitored during the tests. There were no differences in the clinical characteristics of the groups, but the maximal loads achieved during exercise testing were higher in the nisoldipine group. The warm-up phenomenon was observed in both groups on day 1, this being manifested as less significant ST changes in the electrocardiogram, less anginal pain, and a smaller number of patients having ventricular extrasystoles during repeat exercise testing. This was associated with equal or higher double product values during the second exercise test. Two days later the same phenomenon was demonstrable only in the placebo group. Conclusions The fact that nisoldipine, a highly coronary selective vasodilator, masks the protective effects of exercise without affecting double product values supports the hypothesis of coronary vasodilation as being the principal mechanism of the warm-up phenomenon. (Am Heart J 2001;141:e10.)