吸烟增加有心肌梗死危险因素的老年患者的平均血小板体积

Virendra Kumar, Sanjay Melhotra, A. R.C, K. ViashA.
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摘要

本研究旨在探讨吸烟与心肌梗死对血小板大小的影响。本研究共纳入298例(18岁以上)在印度乔治国王医科大学心内科冠状动脉监护室就诊的心脏病急诊成人疑似急性冠状动脉综合征患者。248例患者有肌钙蛋白I升高或不升高的心电图改变(st段抬高、st段降低、t位倒置、q波出现),并接受抗血小板药物治疗。其余50例心电图正常,心肌肌钙蛋白I正常,未接受抗血小板治疗。他们被视为对照组(第二组)。临床病史、医疗报告、检查结果和信息记录在预先设计的数据表中,并得到知情和书面同意。冠状动脉造影前在导管实验室采集平均血小板体积(MPV)血样,用自动分析仪测定。对照组平均年龄40.9±17.9岁,病例平均年龄59.2±11.9岁。病例组吸烟者占72.2%,对照组不吸烟者占60%。病例组平均血小板301.01±177.1,对照组平均血小板304.7±132.5。病例组平均MPV为8.5.0±1.2 fl,对照组为7.8±0.4 fl (p < 0.05)。观察到,在所有这些组中,吸烟病例组的平均值均高于其他组(307.6±192.72)。在商务;吸烟状况(吸烟或不吸烟两组,病例与对照组)差异有统计学意义(p值< 0.05)。观察发现,吸烟病例组的平均值(8.58±1.41)高于其他组。这些结果表明,吸烟可能会增加动脉粥样硬化血管中的血小板消耗,随后巨核细胞被激活,产生更大、更活跃的血小板。因此,吸烟引起的MPV升高也可能加速动脉粥样硬化,应被视为动脉粥样硬化疾病的危险因素
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Cigarette smoking increases the mean platelet volume in elderly patients with risk factors for mi
This study was proposed to study the effects of cigarette smoking and myocardial Infarction on platelet size. A total of 298 adults (18 years above) patients with clinically suspected acute coronary syndrome who attended in cardiac emergency and admitted in coronary care unit in the department of Cardiology, King George’s Medical University, India were enrolled in this study. Among them 248 patients had ECG changes (ST-elevation, STdepression, T-inversion, appearance of Q-wave) with or without elevated troponin I and treated with anti-platelet drugs. They were considered as cases (group I). The rest 50 Patients had normal ECG findings, normal cardiac troponin I and did not receive anti-platelet therapy. They were considered as controls (group II). Clinical history, medical reports, findings and information were documented in a pre-designed data sheet with informed and written consent. Blood samples for mean platelet volume (MPV) were obtained in the catheterization laboratory before coronary angiography and determined by automated analyzer. The mean age of controls was 40.9±17.9 and that in cases was 59.2±11.9. Among them 72.2% were smokers in cases groups while 60% were nonsmokers in control group. The mean platelet in case group was 301.01±177.1 and in control group 304.7±132.5. While the mean MPV in case group was 8.5.0±1.2 fl and in control group 7.8±0.4 fl (p<0.001). In Platelet; statistically no significant difference was observed between smoking status (smoker or nonsmoker for both groups cases and controls) (p value > 0.05). It was observed that at all these groups higher mean was observed in smoker in cases groups than other groups i.e. 307.6±192.72. In MPV; statistically significant difference was observed between smoking status (smoker or nonsmoker for both groups cases and controls) (p value < 0.05). It was observed that at all these groups higher mean was observed in smoker in cases groups than other groups i.e. 8.58±1.41. These results suggest that smoking may increase platelet consumption in atherosclerotic vessels and that subsequently megakaryocytes are activated to produce larger platelets, which are more active. Thus, an increase in MPV due to smoking may also contribute to the acceleration of atherosclerosis and should be considered as a risk factor for atherosclerotic disease
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