Objectives Smoking has been associated with increased angiogenesis in experimental animal models. We hypothesized that smokers undergoing enhanced external counterpulsation would have increased benefit due to recruitment of a larger number of coronary collaterals in regions of ischemia.
Methods We studied current smokers (C), non-smokers (N), and past smokers (P) enrolled in the International EECP registry who had one year follow-up. Angina symptoms and major cardiac events were examined at baseline, immediately after a course of EECP, and at one year.
Results C were younger (59 years vs. 67 years for P and 68 years for N, p<0.001) and more likely to be male (75% vs. 81% for P and 59% for N, p<0.001). They were more likely to have a prior MI (78% vs. 71% for P and 65% for N, p<0.001). Angina symptoms were similar, however, with 86% reporting CCS class 3 or 4 angina vs. 87% for P and 85% for N (p = NS). C were not able to augment as well as other patients (last peak ratio 0.93 vs. 1.05 for P and 1.15 for N, p<0.001 and only 76% completed the standard course treatment (vs. 83% for N and P, p<0.05). C showed similar reduction in angina status (73% down at least one CCS class, vs. 74% for P and 77% for N, p = NS), and there was no difference in the maintenance of this angina reduction at one year (74% vs. 78% vs. 76%, p = NS). Major cardiac events (death, MI, CABD, PCI) were identical in all three groups at 20% at one year.
Conclusion There is no evidence to support the hypothesis that smoking improves the benefit of enhanced external counterpulsation in angina patients.
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