Smoking, as a clear risk factor for coronary heart disease, can induce endothelial damage, inflammatory response, plaque erosion and rupture, leading to endothelial dysfunction and vasodilatation, and ultimately atherosclerosis progression, increasing the risk of myocardial infarction [9-11]. The finding of a survival benefit from smoking in patients with acute myocardial infarction has led to the introduction of the smoker's paradox [3], with speculation that possible mechanisms including the relatively younger age of smokers, fewer risk factors, better clopidogrel responsiveness and therefore better platelet suppression[12],the high pre-hospital mortality in smokers may lead to biased findings [13]and an increased incidence of deep vein thrombosis after smoking cessation [14], etc.
A recent meta-analysis showed that the mortality rate was lower in smokers with ACS at 30 days (2.3% vs. 3.3%, OR=0.54, 95%CI: 0.39-0.76, p<0.001), 12 months (2.3% vs. 3.6%, OR=0.54, 95%CI:0.30-0.70, p<0.001) , and this decrease is associated with younger age, lower incidence of diabetes, less severe coronary lesions, and male sex ratio [15]. However, most of the studies supporting this paradox originated in the thrombolytic and early PCI era. Few studies were based on the post-PCI era, which was recently supplemented by Parasuraman et al. In a cohort study including 12,656 patients with non-elective PCI, smokers underwent PCI at an earlier age and were more likely to undergo PCI for acute coronary syndromes and had an increased 30-day mortality rate compared to non-smokers[16].
Ndrepepa et al. observed a lower incidence of no-reflow in smokers than in nonsmokers in the population undergoing emergency PCI for STEMI [17], but this can be explained by the younger age of the smokers, fewer cardiovascular risk factors comorbid and a higher thrombotic component in the study. Shemirani et al. further showed that after adjusting for confounding factors such as age, no significant differences were observed between smokers and nonsmokers in the no-reflow phenomena and short-term complications[18], consistent with the findings of Sherif's team [19]. In the non-ST-segment elevation myocardial infarction population, Feistritzer demonstrated that smoking status had no effect on infarction size, microcirculatory obstruction, or MACE development [20] by Magnetic Resonance Imaging, which challenged the smoker's paradox to varying degrees.
LM lesions used to be considered off-limits to PCI, but with the increasing development of interventional techniques, PCI has become the main treatment for LM lesions[21,22].The EXCEL study included 1,905 patients with LM lesions, randomized to PCI and CABG, showed an increased incidence of the 5-year composite endpoint in current smokers compared with nonsmokers, with no increased risk seen in ex-smokers[23]. The SYNTAX study was also performed in patients with more complex coronary artery disease and dynamically observed the smoking status of patients during the follow-up period, and similar conclusions were yield with further analysis [24].
In our study, smoking did not affect the incidence of MACE or TLF in this population, only that the incidence of myocardial infarction and target vessel-related myocardial infarction was lower in current smokers. According to the baseline data, the younger of current smokers, the higher incidence of previous myocardial infarction and the more history of PCI all suggested that this population had an earlier onset of coronary heart disease and fewer co-existing high-risk factors, and the creatinine clearance rate was higher than the other two groups, which can also partially explain the lower incidence of postoperative myocardial infarction, target vessel-related myocardial infarction and hemorrhage in current smokers. In addition, smoking status can change over the course of follow-up, with the possibility of relapse in ex-smokers and gradual smoking cessation in current smokers, but the vast majority of studies have just examined smoking status at baseline and were performed with post-hoc analysis, limiting the accuracy of the results to some extent.
Although the impact of smoking on long-term prognosis is still not completely clear, there is no doubt that adherence to smoking cessation is important.A meta-analysis including 12,603 smokers with coronary artery disease showed that smoking cessation after acute myocardial infarction or cardiac surgery significantly decreased the mortality rate(RR=0.64, 95%CI:0.58-0.71) [26], and after PCI treatment, compared to smoking cessation patients ,those who continue to smoke have worse health-related quality of life and a higher frequency of angina attack symptoms [8]. However, the rate of smoking cessation in patients undergoing PCI and pharmacotherapy is lower than that of in CABG [7], so there is still much work to be done to promote smoking cessation and manage patients in clinical practice.
Although this study is a large-scale study of the population undergoing PCI for LM lesions, there are still certain limitations in the following aspects: 1) the study is a retrospective observational study; 2) the study is a single center study, with a small sample size and only male patients, and the ex-smoking group is significantly smaller than the other two groups, which reduces the statistical efficiency; 3) the smoking status is only evaluated before enrollment, and the cigarette consumption and duration is missing,which limits the quantitative analysis of the impact of smoking on long-term prognosis. In the future, a multicenter study on smoking status can be conducted to further expand the sample size, adequately match the population of three groups, extend the follow-up time, continue to improve the observation of smoking status during the follow-up period, and conduct quantitative statistics on the cigarettes consumption and the duration of smoking, so as to better verify the predictive ability of smoking as an important risk factor for the long-term prognosis of patients undergoing PCI for LM lesions.