EVALUATION OF DIFFERENT ANTICOAGULATION STRATEGIES DURING PCI IN PAKISTANI PATIENTS
Main Article Content
Keywords
PCI, Anticoagulation, Heparin, Bivalirudin, Glycoprotein IIb/IIIa inhibitors, MACE, Bleeding, Pakistani patients.
Abstract
Background: Percutaneous coronary intervention (PCI) is crucial for treating coronary artery disease (CAD). Anticoagulation during PCI helps prevent clotting, but the best strategy remains uncertain. This is particularly important in Pakistan, where CAD prevalence is high, and patient outcomes vary.
Objective: To evaluate the effectiveness of different anticoagulation strategies during PCI in Pakistani patients.
Methods: This prospective cohort study was conducted at Hayatabad Medical Complex, Peshawar, from January 2021 to December 2022. We included 246 patients undergoing PCI. The sample size was calculated based on a 20% CAD prevalence in Pakistan, resulting in a robust sample of 246. Patients were assigned to one of three groups: heparin monotherapy, bivalirudin, or heparin plus glycoprotein IIb/IIIa inhibitors. The primary outcome was the incidence of major adverse cardiac events (MACE) within 30 days post-PCI. Secondary outcomes included bleeding complications and hospital stay duration. Data were collected from medical records and patient interviews. Statistical analysis was performed using SPSS version 26.0, with ANOVA and Chi-square tests for comparisons.
Results: The mean age of the participants was 63.5 years, with 64.6% being men. MACE occurred in 15.4% of patients, highest with heparin alone (19.2%) and lowest with bivalirudin (8.7%). Bleeding was highest with heparin plus glycoprotein IIb/IIIa inhibitors (18.3%) and lowest with bivalirudin (4.9%). Hospital stays were shortest with bivalirudin (mean ± SD: 3.2 ± 1.4 days) compared to heparin alone (4.8 ± 2.3 days) and heparin plus glycoprotein IIb/IIIa inhibitors (4.1 ± 2.0 days).
Conclusion: Bivalirudin is the best anticoagulation strategy during PCI in Pakistani patients, reducing MACE and bleeding more effectively than heparin alone or heparin with glycoprotein IIb/IIIa inhibitors. These findings suggest revising current anticoagulation protocols to improve patient outcomes.
Objective: To evaluate the effectiveness of different anticoagulation strategies during PCI in Pakistani patients.
Methods: This prospective cohort study was conducted at Hayatabad Medical Complex, Peshawar, from January 2021 to December 2022. We included 246 patients undergoing PCI. The sample size was calculated based on a 20% CAD prevalence in Pakistan, resulting in a robust sample of 246. Patients were assigned to one of three groups: heparin monotherapy, bivalirudin, or heparin plus glycoprotein IIb/IIIa inhibitors. The primary outcome was the incidence of major adverse cardiac events (MACE) within 30 days post-PCI. Secondary outcomes included bleeding complications and hospital stay duration. Data were collected from medical records and patient interviews. Statistical analysis was performed using SPSS version 26.0, with ANOVA and Chi-square tests for comparisons.
Results: The mean age of the participants was 63.5 years, with 64.6% being men. MACE occurred in 15.4% of patients, highest with heparin alone (19.2%) and lowest with bivalirudin (8.7%). Bleeding was highest with heparin plus glycoprotein IIb/IIIa inhibitors (18.3%) and lowest with bivalirudin (4.9%). Hospital stays were shortest with bivalirudin (mean ± SD: 3.2 ± 1.4 days) compared to heparin alone (4.8 ± 2.3 days) and heparin plus glycoprotein IIb/IIIa inhibitors (4.1 ± 2.0 days).
Conclusion: Bivalirudin is the best anticoagulation strategy during PCI in Pakistani patients, reducing MACE and bleeding more effectively than heparin alone or heparin with glycoprotein IIb/IIIa inhibitors. These findings suggest revising current anticoagulation protocols to improve patient outcomes.
References
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2. Bhatt DL, Stone GW, Mahaffey KW, et al. Effect of platelet inhibition with cangrelor during PCI on ischemic events. N Engl J Med. 2013 Jun 20;368(25):2297-2307.
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9. Stone GW, Witzenbichler B, Guagliumi G, et al. Bivalirudin during primary PCI in acute myocardial infarction. N Engl J Med. 2008;358(21):2218-30.
10. Angiolillo DJ, Fernandez-Ortiz A, Bernardo E, et al. Variability in individual responsiveness to clopidogrel: clinical implications, management, and future perspectives. J Am Coll Cardiol. 2007;49(14):1505-16.
11. Stone GW, McLaurin BT, Cox DA, et al. Bivalirudin for patients with acute coronary syndromes. N Engl J Med. 2006;355(21):2203-16.
12. Mega JL, Close SL, Wiviott SD, et al. Cytochrome p-450 polymorphisms and response to clopidogrel. N Engl J Med. 2009;360(4):354-62.
13. Wiviott SD, Braunwald E, McCabe CH, et al. Prasugrel versus clopidogrel in patients with acute coronary syndromes. N Engl J Med. 2007;357(20):2001-15.
14. Mehran R, Pocock S, Nikolsky E, et al. A risk score to predict bleeding in patients with acute coronary syndromes. J Am Coll Cardiol. 2010;55(23):2556-66.
15. Morrow DA, Wiviott SD, White HD, et al. Effect of the novel thienopyridine prasugrel compared with clopidogrel in patients with acute coronary syndromes. Lancet. 2007;369(9560):999-1007.
16. Bhatt DL, Scheiman J, Abraham NS, et al. ACCF/ACG/AHA 2008 expert consensus document on reducing the gastrointestinal risks of antiplatelet therapy and NSAID use: a report of the American College of Cardiology Foundation Task Force on Clinical Expert Consensus Documents. J Am Coll Cardiol. 2008;52(18):1502-17.
17. Yusuf S, Zhao F, Mehta SR, et al. Effects of clopidogrel in addition to aspirin in patients with acute coronary syndromes without ST-segment elevation. N Engl J Med. 2001;345(7):494-502.
18. Sabatine MS, Cannon CP, Gibson CM, et al. Addition of clopidogrel to aspirin and fibrinolytic therapy for myocardial infarction with ST-segment elevation. N Engl J Med. 2005;352(12):1179-89.
19. Fox KA, Mehta SR, Peters R, et al. Benefits and risks of the combination of clopidogrel and aspirin in patients undergoing surgical revascularization for non–ST-elevation acute coronary syndrome: the Clopidogrel in Unstable angina to prevent Recurrent Events (CURE) trial. Circulation. 2004;110(10):1202-8.
20. Steinhubl SR, Berger PB, Mann JT 3rd, et al. Early and sustained dual oral antiplatelet therapy following percutaneous coronary intervention: a randomized controlled trial. JAMA. 2002;288(19):2411-20.
2. Bhatt DL, Stone GW, Mahaffey KW, et al. Effect of platelet inhibition with cangrelor during PCI on ischemic events. N Engl J Med. 2013 Jun 20;368(25):2297-2307.
3. Jolly SS, Cairns JA, Yusuf S, et al. Radial versus femoral access for coronary angiography and intervention in patients with acute coronary syndromes (RIVAL): a randomised parallel group multicentre trial. Lancet. 2011 Apr 23;377(9775):1409-20.
4. Zubaid M, Rashed WA, Thalib L, et al. Comparison of diabetes, hypertension, and smoking as coronary risk factors in Asian patients with acute coronary syndrome. J Cardiovasc Risk. 2002 Oct;9(5):287-94.
5. Khan SS, Nasir K, Rahman R, et al. High prevalence of metabolic syndrome among Pakistani patients with coronary artery disease. Asian Cardiovasc Thorac Ann. 2007 Apr;15(2):107-12.
6. Steg PG, Bhatt DL, Hamm CW, et al. Stent thrombosis with drug-eluting stents: An appraisal of the FDA reports. Eur Heart J. 2009 Sep;30(22):2723-9.
7. Muhammad A, Saqib M, Abdullah A, et al. Prevalence of coronary artery disease in Pakistan: A single-center experience. J Pak Med Assoc. 2020;70(1):40-45.
8. Giugliano RP, White JA, Bode C, et al. Early vs. delayed, provisional eptifibatide in acute coronary syndromes. N Engl J Med. 2009;360(21):2176-90.
9. Stone GW, Witzenbichler B, Guagliumi G, et al. Bivalirudin during primary PCI in acute myocardial infarction. N Engl J Med. 2008;358(21):2218-30.
10. Angiolillo DJ, Fernandez-Ortiz A, Bernardo E, et al. Variability in individual responsiveness to clopidogrel: clinical implications, management, and future perspectives. J Am Coll Cardiol. 2007;49(14):1505-16.
11. Stone GW, McLaurin BT, Cox DA, et al. Bivalirudin for patients with acute coronary syndromes. N Engl J Med. 2006;355(21):2203-16.
12. Mega JL, Close SL, Wiviott SD, et al. Cytochrome p-450 polymorphisms and response to clopidogrel. N Engl J Med. 2009;360(4):354-62.
13. Wiviott SD, Braunwald E, McCabe CH, et al. Prasugrel versus clopidogrel in patients with acute coronary syndromes. N Engl J Med. 2007;357(20):2001-15.
14. Mehran R, Pocock S, Nikolsky E, et al. A risk score to predict bleeding in patients with acute coronary syndromes. J Am Coll Cardiol. 2010;55(23):2556-66.
15. Morrow DA, Wiviott SD, White HD, et al. Effect of the novel thienopyridine prasugrel compared with clopidogrel in patients with acute coronary syndromes. Lancet. 2007;369(9560):999-1007.
16. Bhatt DL, Scheiman J, Abraham NS, et al. ACCF/ACG/AHA 2008 expert consensus document on reducing the gastrointestinal risks of antiplatelet therapy and NSAID use: a report of the American College of Cardiology Foundation Task Force on Clinical Expert Consensus Documents. J Am Coll Cardiol. 2008;52(18):1502-17.
17. Yusuf S, Zhao F, Mehta SR, et al. Effects of clopidogrel in addition to aspirin in patients with acute coronary syndromes without ST-segment elevation. N Engl J Med. 2001;345(7):494-502.
18. Sabatine MS, Cannon CP, Gibson CM, et al. Addition of clopidogrel to aspirin and fibrinolytic therapy for myocardial infarction with ST-segment elevation. N Engl J Med. 2005;352(12):1179-89.
19. Fox KA, Mehta SR, Peters R, et al. Benefits and risks of the combination of clopidogrel and aspirin in patients undergoing surgical revascularization for non–ST-elevation acute coronary syndrome: the Clopidogrel in Unstable angina to prevent Recurrent Events (CURE) trial. Circulation. 2004;110(10):1202-8.
20. Steinhubl SR, Berger PB, Mann JT 3rd, et al. Early and sustained dual oral antiplatelet therapy following percutaneous coronary intervention: a randomized controlled trial. JAMA. 2002;288(19):2411-20.