Harsha V Erathi1, Rajasekhar Durgaprasad2, Vanjakshamma Velam1, Sarma Pvgk3, Madhavi Rodda1, Kapil C1, Sreedhar N Kanavath1. 1. Department of Cardiology, Sri Venkateswara Institute of Medical Sciences, Tirupati, Andhra Pradesh, India. 2. Department of Cardiology, Sri Venkateswara Institute of Medical Sciences, Tirupati, Andhra Pradesh, India - cardiologysvims@gmail.com. 3. Department of Biotechnology, Sri Venkateswara Institute of Medical Sciences, Tirupati, Andhra Pradesh, India.
Abstract
BACKGROUND: The aim of this paper was to investigate the variability of On-clopidogrel platelet reactivity overtime, the association between HTPR, gene polymorphism and Syntax Score (SS) for risk prediction of MACE in patients with ST-Elevation Myocardial Infarction (STEMI) undergoing percutaneous coronary intervention (PCI). Platelet function testing may be used to optimize antiplatelet therapy in high-risk patients, but identification of this subset of patients remains a challenge. High on-treatment platelet reactivity (HTPR) has emerged as a risk factor for major adverse cardiovascular events (MACE). Genetic polymorphisms play key role in clopidogrel hypo-responsiveness. METHODS: This prospective, observational study includes 151 consecutive STEMI patients who underwent PCI and treated with clopidogrel. Platelet Activity Index (PAI) was measured at two different time points post-PCI. Patients were stratified by the presence of HTPR (PAI≥5) and by upper SS (SS≥15). Allele-specific polymerase chain reaction for identifying CYP2C19*2, CYP3A5*3, PON1, P2Y12 gene polymorphisms was done. The end point at one year follow up was MACE. RESULTS: There was a significant increase in mean platelet reactivity and the total number of non-responders over a period of three months (9.9% vs. 23.8% P=0.05). Patients with SS≥15 in the presence of HTPR during follow-up had highest rates of MACE, especially among diabetics compared to non-diabetics (P=0.024). The prevalence of CYP2C19*2 polymorphism was 49%%, was associated with HTPR during follow-up but unassociated with MACE. CONCLUSIONS: In STEMI patients undergoing PCI, the presence of SS≥15, HTPR during follow-up were associated with high MACE rates especially among diabetics. Hence, such high-risk groups shall require sequential testing for HTPR and optimize therapy accordingly.
BACKGROUND: The aim of this paper was to investigate the variability of On-clopidogrel platelet reactivity overtime, the association between HTPR, gene polymorphism and Syntax Score (SS) for risk prediction of MACE in patients with ST-Elevation Myocardial Infarction (STEMI) undergoing percutaneous coronary intervention (PCI). Platelet function testing may be used to optimize antiplatelet therapy in high-risk patients, but identification of this subset of patients remains a challenge. High on-treatment platelet reactivity (HTPR) has emerged as a risk factor for major adverse cardiovascular events (MACE). Genetic polymorphisms play key role in clopidogrel hypo-responsiveness. METHODS: This prospective, observational study includes 151 consecutive STEMI patients who underwent PCI and treated with clopidogrel. Platelet Activity Index (PAI) was measured at two different time points post-PCI. Patients were stratified by the presence of HTPR (PAI≥5) and by upper SS (SS≥15). Allele-specific polymerase chain reaction for identifying CYP2C19*2, CYP3A5*3, PON1, P2Y12 gene polymorphisms was done. The end point at one year follow up was MACE. RESULTS: There was a significant increase in mean platelet reactivity and the total number of non-responders over a period of three months (9.9% vs. 23.8% P=0.05). Patients with SS≥15 in the presence of HTPR during follow-up had highest rates of MACE, especially among diabetics compared to non-diabetics (P=0.024). The prevalence of CYP2C19*2 polymorphism was 49%%, was associated with HTPR during follow-up but unassociated with MACE. CONCLUSIONS: In STEMI patients undergoing PCI, the presence of SS≥15, HTPR during follow-up were associated with high MACE rates especially among diabetics. Hence, such high-risk groups shall require sequential testing for HTPR and optimize therapy accordingly.