Exercise time: A possible source of misleading results during long‐term pharmacological studies by multiple stress testing in coronary artery disease

Abstract

inimary:The assessment of chronic phannacological atnient of stable angina requires serial exercise stress ;rings. It is well known that exercise tolerance can be ,proved by the training effect of performing repeated ;tings. Our study investigated the values of heart rate, stolic blood pressure, rate-pressure product, and duratn of exercise at 0.1 mV ST depression during exercise d the same parameters plus the maximal ST-segment pression at peak exercise, collected from three differt tests. The first and second werc performed at one-week ervals before, and the third (75 days after the first), was rformed after a double-blind study with a drug versus tcebo. We found a significant increase of exercise duion at 0.1 mV ST depression and at peak exercise, while if 12 patients increased exercise duration from the send to the third test. Individual variability of exercise ration showed increasing values, ranging from 0 to 7 1 % rst vs. third test). In contrast, the ratio of heart rate and rtolic blood pressure did not differ between the tests. ir data criticized the use of mean values of exercise time -phamiacological studies; moreover, individual variaity could affect results independently of drug or placebo ministration. These findings should be taken into acunt in order to exclude misleading results. . dc Arcangelis is presently a medical student.

Chelation Therapy for Ischemic Heart Disease

“…In the absence of studies confirming such effects and, more importantly, confirming a definite clinical benefit of chelation therapy, it remains possible that anecdotally reported improvements are simply due to the spontaneous fluctuations in symptoms frequently seen in ischemic heart disease. [24][25][26][27] In our trial, the 1-minute increase in exercise time to ischemia and the improvement in the exertional capacity component of the Seattle Angina Questionnaire in both groups is consistent with a combination of placebo [24][25][26][27] and training effects [28][29][30] commonly seen in studies of angina patients. Another potential explanation for improvement is that both groups were treated with optimal risk reduction therapy.…”

Effects of KATPchannel blockade by glibenclamide on the warm-up phenomenon

“…It is well established that while, on the one hand, the rate-pressure product at 1·5 mm ST-segment depression represents a reliable, non-invasive index of myocardial oxygen consumption at the ischaemic threshold, which can be improved by ischaemic preconditioning, on the other, time to 1·5 mm ST-segment depression and to pain onset are global indexes of exercise tolerance [15][16][17] , which can be improved by ischaemic preconditioning and, more importantly, by the training effect. The latter, in turn, is unlikely to be affected by glibenclamide, thus explaining why K ATP channel blockade failed to significantly affect these global indexes of exercise tolerance.…”

“…These considerations may explain, at least in part, the apparent conflicting results between our study and that of Correa and Schaefer [18] , who showed that glibenclamide has no significant negative effect on indexes of demand ischaemia. In fact, they did not assess the ischaemic threshold, but only end-points reflecting exercise tolerance, which are influenced by the peripheral response, and the ratepressure product at maximal ST-segment depression, which is likely to be influenced by the subjective attitude of both the physician and the patient [4,[15][16][17] . The chain of events responsible for ischaemic preconditioning and the mechanisms by which K ATP channels produce their cardioprotective actions are only partially understood and cannot be deduced by the results of the present study.…”