Clinical Characteristics and Outcomes of Acute Coronary Syndrome in Pakistani Smokers ACS Outcomes in Pakistani Smokers
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Abstract
Background: Acute coronary syndrome (ACS) is a major global health issue, contributing significantly to morbidity and mortality. Smoking is a well-established risk factor for the development and progression of coronary artery disease (CAD) and ACS, leading to increased platelet aggregation, endothelial dysfunction, and accelerated atherosclerosis. This study focuses on ACS's clinical characteristics and outcomes in Pakistani smokers.
Objective: The primary objective of this study was to evaluate the incidence of major adverse cardiac events (MACE) within 12 months post-ACS in Pakistani smokers. Secondary objectives included assessing improvements in left ventricular ejection fraction (LVEF), reduction in angina episodes, and changes in lipid profiles.
Methods: This prospective observational study was conducted at Hayatabad Medical Complex, Peshawar, from January 2022 to December 2023. A total of 300 adult patients with ACS and a history of smoking were included. The intervention involved standard care for ACS, including pharmacological management with dual antiplatelet therapy, statins, beta-blockers, ACE inhibitors, and lifestyle modifications such as smoking cessation counseling. Data were collected during hospital stays and follow-up visits at 1, 6, and 12 months post-ACS. Primary outcomes measured were the incidence of MACE, including myocardial infarction (MI), stroke, and cardiac death. Secondary outcomes included improvements in LVEF, reduction in angina episodes, and changes in lipid profile parameters. Statistical analyses were conducted using SPSS version 26.0.
Results: The mean age of the participants was 55 ± 10 years, with 70% being male. The overall incidence of MACE was 20%, with MI occurring in 10%, stroke in 5%, and cardiac death in 5% of patients. LVEF improved from 45% ± 7% pre-procedure to 52% ± 6% post-procedure (p < 0.001). The frequency of angina episodes per week decreased from 3.5 ± 1.2 to 1.2 ± 0.7 (p < 0.001). Significant improvements were observed in lipid profiles, with total cholesterol reducing from 200 ± 30 mg/dL to 180 ± 25 mg/dL, LDL cholesterol from 130 ± 20 mg/dL to 110 ± 18 mg/dL, and triglycerides from 150 ± 40 mg/dL to 130 ± 35 mg/dL (all p < 0.01).
Conclusion: This study demonstrates that standard ACS treatment significantly improves clinical outcomes in Pakistani smokers, evidenced by reduced MACE incidence and enhanced secondary outcomes. These findings underscore the importance of continuous monitoring and tailored therapeutic strategies to optimize patient outcomes.
Keywords: Acute coronary syndrome, smoking, major adverse cardiac events, left ventricular ejection fraction, angina, lipid profile, dual antiplatelet therapy, Pakistan
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References
Libby P, Theroux P. Pathophysiology of coronary artery disease. Circulation. 2005;111(25):3481-3488.
Ambrose JA, Barua RS. The pathophysiology of cigarette smoking and cardiovascular disease: an update. J Am Coll Cardiol. 2004;43(10):1731-1737.
Fagerström K. The epidemiology of smoking: health consequences and benefits of cessation. Drugs. 2002;62 Suppl 2:1-9.
Levine GN, Bates ER, Bittl JA, et al. 2016 ACC/AHA guideline focused update on duration of dual antiplatelet therapy in patients with coronary artery disease. J Am Coll Cardiol. 2016;68(10):1082-1115.
Yusuf S, Hawken S, Ôunpuu S, et al. Effect of potentially modifiable risk factors associated with myocardial infarction in 52 countries (the INTERHEART study): case-control study. Lancet. 2004;364(9438):937-952.
Jafar TH, Jafary FH, Jessani S, Chaturvedi N. Heart disease epidemic in Pakistan: women and men at equal risk. Am Heart J. 2005;150(2):221-226.
Benowitz NL. Cigarette smoking and cardiovascular disease: pathophysiology and implications for treatment. Prog Cardiovasc Dis. 2003;46(1):91-111.
Teo KK, Ounpuu S, Hawken S, et al. Tobacco use and risk of myocardial infarction in 52 countries in the INTERHEART study: a case-control study. Lancet. 2006;368(9536):647-658.
Hasdai D, Garratt KN, Grill DE, et al. Effect of smoking status on the long-term outcome after successful percutaneous coronary revascularization. N Engl J Med. 1997;336(11):755-761.
Jha P, Ramasundarahettige C, Landsman V, et al. 21st-century hazards of smoking and benefits of cessation in the United States. N Engl J Med. 2013;368(4):341-350.
Mottillo S, Filion KB, Bélisle P, et al. Behavioural interventions for smoking cessation: a meta-analysis of randomized controlled trials. Eur Heart J. 2012;33(24):3147-3157.
Critchley JA, Capewell S. Mortality risk reduction associated with smoking cessation in patients with coronary heart disease: a systematic review. JAMA. 2003;290(1):86-97.
Tanuseputro P, Manuel DG, Leung M, et al. Risk factors for cardiovascular disease in Canada. Can J Cardiol. 2003;19(11):1249-1259.
Rigotti NA. Strategies to help a smoker who is struggling to quit. JAMA. 2012;308(15):1573-1580.
Stead LF, Lancaster T. Combined pharmacotherapy and behavioural interventions for smoking cessation. Cochrane Database Syst Rev. 2012;(10).
Buxbaum SG, Elston RC, Tishler PV, et al. Genetic mediation of smoking habits and lung function. Am J Hum Genet. 2002;71(3):518-529.