Verdoia Monica, Secco Gioel G, Cassetti Ettore, Schaffer Alon, Barbieri Lucia, Perrone-Filardi Pasquale, Marino Paolo, Suryapranata Harry, Sinigaglia Fabiola, De Luca Giuseppe
aDivision of Cardiology, Azienda Ospedaliera-Universitaria 'Maggiore della Carità', Eastern Piedmont University, Novara, Italy bDivision of Cardiology 'Azienda Ospedaliera Marche Nord', Pesaro, Italy cDepartment of Medicine, Cardiovascular and Immunological Sciences, University Federico II, Naples, Italy dDepartment of Cardiology, UMC St Radboud, Nijmegen, The Netherlands eBiochemistry, Department of Translational Medicine, Eastern Piedmont University, Novara, Italy.
Blood Coagul Fibrinolysis. 2014 Mar;25(2):107-13. doi: 10.1097/MBC.0b013e3283650717.
Acute coronary syndromes (ACSs) represent a high-risk condition, as enhanced platelet reactivity importantly influences myocardial perfusion and procedural results after percutaneous coronary intervention (PCI). In fact, higher rate of periprocedural myocardial infarction (PMI) and reduced event-free survival have been reported in these patients. The single nucleotide polymorphism Leu33Pro of platelet glycoprotein IIIa has been related to an increased platelet reactivity, a lower response to antiplatelet agents and higher risk of stent restenosis. Therefore, our aim was to evaluate the impact of this polymorphism on PMI in patients undergoing PCI for non-ST-segment elevation MI (NSTEMI). Our population is represented by 478 consecutive patients undergoing coronary angioplasty for NSTEMI. Cardiac biomarkers were monitored at intervals from 8 to 48 h after the procedure. Genetic analysis was performed to assess the presence of Leu33Pro polymorphism. A total of 156 patients (32.6%) were polymorphic. Clinical features did not differ according to genetic status, neither pharmacological treatment pre and during angioplasty. PlA carriers had lower rate of calcifications (P = 0.01) and higher coronary tortuosity (P = 0.03) at angiography and underwent more frequently to thrombectomy (P = 0.05). PCI-related complications did not differ according to genotype. Leu33Pro polymorphism was not associated with increased risk of periprocedural myonecrosis and PMI even after correction for baseline differences, [odds ratio (OR) (95% confidence interval (CI) = 0.70 (0.44-1.13), P = 0.15 for PMI and OR (95% CI) = 0.77 (0.53-1.11), P = 0.17 for myonecrosis, respectively]. Results were confirmed in high-risk subgroups of patients. In conclusion, among patients undergoing PCI for ACS, the polymorphism Leu33Pro of platelet glycoprotein IIIa is not associated with increased risk of PMI.
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