Impact of Cigarette Smoking on Triglyceride-rich Lipoprotein Cholesterol Levels: An observational study

Abstract Background: Cigarette smoking is a well-established modifiable cardiovascular risk factor that adversely affects lipid metabolism. Despite growing evidence linking triglyceride-rich lipoprotein cholesterol (TRL-C) to atherosclerotic cardiovascular disease, its specific relationship with cigarette smoking in the setting of acute myocardial infarction (AMI) including both ST-segment elevation myocardial infarction (STEMI) and non-ST-segment elevation myocardial infarction (NSTEMI) remains poorly characterized in Indian populations. Methods: A hospital-based cross-sectional, observational study was conducted at Dr. D.Y. Patil Medical College, Hospital and Research Institute, Pimpri, Pune. A total of 125 enrolled patients were stratified by smoking status, and lipid parameters including total cholesterol, triglycerides, High-Density Lipoprotein Cholesterol (HDL-C), Low-Density Lipoprotein Cholesterol (LDL-C); directly measured), TRL-C, and the Triglyceride (TG)/HDL-C ratio ratio) were analyzed. Results: A total of 125 patients (63 NSTEMI and 62 STEMI) were enrolled over 3 years. Smoking prevalence was 39.7% in NSTEMI and 40.3% in STEMI patients, representing approximately 40% of the total cohort. TGs were significantly higher in NSTEMI patients (216.43 ± 77.89 mg/dL, P = 0.004), and the TG levels (TG/HDL-C ratio) were significantly elevated in NSTEMI (5.43 ± 2.25; P = 0.05). Mean TRL-C was 27.05 ± 63.82 mg/dL in NSTEMI and 44.84 ± 93.46 mg/dL in STEMI ( P = 0.216). The cardiac biomarkers (CPK-MB and troponin-I) were markedly elevated in STEMI patients (both P < 0.001). STEMI patients had a significantly longer hospital stay ( P < 0.001), while in-hospital complications and outcomes were similar between the groups. Conclusion: Cigarette smoking contributes to an atherogenic lipid environment characterized by elevated TRL-C and TG/HDL-C ratio in patients with AMI. Smoking was uniformly prevalent across both MI subtypes, suggesting its pervasive role in promoting atherogenic dyslipidemia. Future adequately powered studies with direct TRL subfractionation stratified by smoking status are warranted.