Journal of cardiovascular pharmacology · 2015
Body Mass Index and Platelet Reactivity During Dual Antiplatelet Therapy With Clopidogrel or Ticagrelor.
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Nardin Matteo, Verdoia Monica, Sartori Chiara, Pergolini Patrizia, Rolla Roberta, Barbieri Lucia, Schaffer Alon, Marino Paolo, Bellomo Giorgio, Suryapranata Harry, De Luca Giuseppe, Novara Atherosclerosis Study Group
Аннотация
INTRODUCTION: Dual antiplatelet therapy (DAPT) is considered essential in clinical management of patients undergoing percutaneous coronary revascularization or acute coronary syndromes. However, the optimal platelet inhibition is not always obtained, with high residual platelet reactivity (HRPR) increasing stent thrombosis and recurrent ischemic events. Aim of this study was to investigate the impact of body mass index (BMI) on platelet reactivity in patients on DAPT.
METHODS: We included patients treated with acetylsalycilic acid (ASA) (100-160 mg) and clopidogrel (75 mg) or ticagrelor (90 mg twice a day) for acute coronary syndromes or drug-eluting stent implantation. Platelet reactivity was assessed at 30-90 days postdischarge by multiple-electrode aggregometry. HRPR for adenosine diphosphate (ADP) antagonists was defined as ADP test results >417 AU*min. HRPR for ASA was considered for ASPI test >862 AU*min.
RESULTS: Our population is represented by 498 patients, 308 (61.8%) were treated with clopidogrel and 190 (38.2%) with ticagrelor. Overall, higher BMI was related with younger age (P = 0.003), higher prevalence of diabetes mellitus (P < 0.001), hypercholesterolemia (P = 0.017), hypertension (P < 0.001), chronic therapy with angiotensin-receptor blockers (P = 0.019), calcium channel blockers (P = 0.003). Higher values of BMI directly related with hemoglobin (P = 0.02), triglycerides (P < 0.001), glycemia (P = 0.035), HbA1c (P < 0.001), and inversely related with high-density lipoprotein cholesterol (P = 0.01). BMI did not influence the effectiveness of ASA, whereas it was associated to a nonsignificant trend for higher platelet reactivity (r = 0.08, P = 0.08) for ADP antagonists. In fact, 111 patients (22.3%) displayed HRPR at ADP test (>417 AU*min) with no statistically significant difference according to BMI {20.3% vs. 27.1% vs. 25.7%, P = 0.28; adjusted odds ratio [OR] [95% confidence interval (CI)] = 1.19 [0.86-1.64], P = 0.30}. However, results were different when considering separately patients receiving clopidogrel or ticagrelor. In the clopidogrel-treated subgroup, significantly higher ADP-mediated aggregation values were found in patients with higher BMI (r = 0.14, P = 0.023) that emerged as an independent predictor of HRPR with clopidogrel [OR (95% CI), 1.45 (1.01-2.12), P = 0.049]. On the contrary, no impact of BMI was observed in the ticagrelor-treated subgroup for platelet reactivity (r = -0.036, P = 0.62) or the prevalence of HRPR [adjusted OR (95% CI), 0.73 (0.39-1.36), P = 0.32].
CONCLUSIONS: This study shows that among patients treated with DAPT for coronary artery disease, higher BMI is related to increased platelet reactivity and a higher prevalence of HRPR in clopidogrel-treated patients while not significantly influencing the effectiveness of ticagrelor or ASA.
METHODS: We included patients treated with acetylsalycilic acid (ASA) (100-160 mg) and clopidogrel (75 mg) or ticagrelor (90 mg twice a day) for acute coronary syndromes or drug-eluting stent implantation. Platelet reactivity was assessed at 30-90 days postdischarge by multiple-electrode aggregometry. HRPR for adenosine diphosphate (ADP) antagonists was defined as ADP test results >417 AU*min. HRPR for ASA was considered for ASPI test >862 AU*min.
RESULTS: Our population is represented by 498 patients, 308 (61.8%) were treated with clopidogrel and 190 (38.2%) with ticagrelor. Overall, higher BMI was related with younger age (P = 0.003), higher prevalence of diabetes mellitus (P < 0.001), hypercholesterolemia (P = 0.017), hypertension (P < 0.001), chronic therapy with angiotensin-receptor blockers (P = 0.019), calcium channel blockers (P = 0.003). Higher values of BMI directly related with hemoglobin (P = 0.02), triglycerides (P < 0.001), glycemia (P = 0.035), HbA1c (P < 0.001), and inversely related with high-density lipoprotein cholesterol (P = 0.01). BMI did not influence the effectiveness of ASA, whereas it was associated to a nonsignificant trend for higher platelet reactivity (r = 0.08, P = 0.08) for ADP antagonists. In fact, 111 patients (22.3%) displayed HRPR at ADP test (>417 AU*min) with no statistically significant difference according to BMI {20.3% vs. 27.1% vs. 25.7%, P = 0.28; adjusted odds ratio [OR] [95% confidence interval (CI)] = 1.19 [0.86-1.64], P = 0.30}. However, results were different when considering separately patients receiving clopidogrel or ticagrelor. In the clopidogrel-treated subgroup, significantly higher ADP-mediated aggregation values were found in patients with higher BMI (r = 0.14, P = 0.023) that emerged as an independent predictor of HRPR with clopidogrel [OR (95% CI), 1.45 (1.01-2.12), P = 0.049]. On the contrary, no impact of BMI was observed in the ticagrelor-treated subgroup for platelet reactivity (r = -0.036, P = 0.62) or the prevalence of HRPR [adjusted OR (95% CI), 0.73 (0.39-1.36), P = 0.32].
CONCLUSIONS: This study shows that among patients treated with DAPT for coronary artery disease, higher BMI is related to increased platelet reactivity and a higher prevalence of HRPR in clopidogrel-treated patients while not significantly influencing the effectiveness of ticagrelor or ASA.