Impact of active smoking on the immature platelet fraction and its relationship with the extent of coronary artery disease
Impact of active smoking on the immature platelet fraction and its relationship with the extent of coronary artery disease
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DOI：
10.1111/eci.13181
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发表时间：
2020-01-18
影响因子：
5.5
通讯作者：
De Luca, Giuseppe
中科院分区：
文献类型：
--
作者：
Nardin, Matteo;Verdoia, Monica;De Luca, Giuseppe
吸烟是心血管疾病的一个主要危险因素，因为它会诱导氧化应激和低级别、持续的炎症，从而促进动脉粥样硬化血栓形成。然而，导致与吸烟相关的血小板聚集性增加的机制仅部分确定。一个潜在的作用已被假设为未成熟的血小板，一个年轻的和潜在的反应性更强的部分，以前与冠状动脉疾病（CAD）的主要决定因素。因此，我们研究的目的是确定吸烟对未成熟血小板分数（IPF）的影响及其与冠状动脉疾病患病率和程度的关系。方法我们在一个中心招募了一组连续接受冠状动脉造影的患者。严重CAD定义为至少1支血管狭窄> 50%，而严重CAD定义为左主干和/或三支血管病变。入院时通过常规血细胞计数（Sysmex XE-2100）测量IPF。结果我们纳入了2553例患者，根据吸烟状况进行分组（主动吸烟者：512例;非主动吸烟者：2041例）。与非主动吸烟者相比，吸烟者更年轻，更频繁的男性，糖尿病、既往PCI和既往CABG的发生率更低（分别为P < .001），接受ARB、BB、硝酸盐、他汀类药物、阿萨、氯吡格雷、CCB和利尿剂治疗的频率更低（分别为P < .001）。在IPF值较高的患者中观察到吸烟者百分比较高，在多变量分析中，主动吸烟是IPF较高的独立预测因素（校正OR [95% CI] = 1.59[1.03-2.45]，P = 0.035）。在吸烟者中，与IPF较低者相比，IPF较高者的射血分数（P = 0.034）、急性冠脉综合征百分比（P = 0.002）和血小板计数（P <0.001）较低。然而，IPF（根据四分位值）与CAD的患病率和程度无关（第1至第4四分位数分别为82.5%、80.4%、86.1%和80.9%，校正OR[95%CI] = 0.98[0.79-1.23]，P = 0.89）和重度CAD（第1至第4四分位数分别为31%、31.1%、39.1%和35.2%，调整后OR[95%CI] = 1.03[0.86-1.23]，P = 0.76）。结论主动吸烟与冠状动脉造影患者未成熟血小板分数水平存在独立相关性。然而，在主动吸烟者中，IPF不是CAD或重度CAD的独立预测因素。
Introduction Smoking represents a major cardiovascular risk factor, due to the induction of oxidative stress and low-grade, continuous, inflammation that contribute to promote atherothrombosis. However, the mechanisms leading to increased platelet aggregability associated with smoking are only partially defined. A potential role has been hypothesized for immature platelets, a younger and potentially more reactive fraction, previously associated with the main determinants of coronary artery disease (CAD). Therefore, the aim of our study was to define the impact of smoking on the immature platelet fraction (IPF) and its relationship with prevalence and extent of coronary artery disease. Methods We enrolled a cohort of consecutive patients undergoing coronary angiography in a single centre. Significant CAD was defined as at least 1 vessel stenosis >50%, while severe CAD was defined as left main and/or three-vessel disease. IPF was measured at admission by routine blood cell count (Sysmex XE-2100). Results We included in our study 2553 patients who were divided according to smoking status (active smokers: 512; nonactive smokers: 2041). Smokers were younger, more frequent males, with lower rate of diabetes mellitus, previous PCI and previous CABG (P < .001, respectively) and were in treatment less often with ARB, BB, nitrates, statins, ASA, clopidogrel, CCB and diuretics (P < .001, respectively) as compared to nonactive smokers. Higher percentage of smokers was observed in patients with higher IPF values, and at multivariate analysis, active smoking resulted as an independent predictor of higher IPF (adjusted OR [95% CI] = 1.59[1.03-2.45], P = .035). Among smokers, higher IPF was associated with lower ejection fraction (P = .034), percentage of acute coronary syndrome (P = .002) and platelet count (P < .001) compared to ones with lower IPF. However, the IPF (according to quartiles values) was not associated with the prevalence and extent of CAD (82.5%, 80.4%, 86.1% and 80.9%, from 1st to 4th quartile, respectively, adjusted OR[95% CI] = 0.98[0.79-1.23], P = .89) and severe CAD (31%, 31.1%, 39.1% and 35.2%, from 1st to 4th quartile, respectively, adjusted OR[95% CI] = 1.03[0.86-1.23], P = .76). Conclusion The present study shows an independent association between active smoking and the levels of immature platelet fraction in patients undergoing coronary angiography. However, among active smokers, IPF did not result as an independent predictor of CAD or severe CAD.