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Dual antiplatelet therapy is important treatment modality across the spectrum of coronary artery disease manifestations. However, a significant number of patients do not have a completely effective response to clopidogrel. This study assessed the impact of response after clopidogrel with Verify Now device on prognosis on patients undergoing coronary interventions. Consecutive patients following percutaneous coronary intervention were prospectively enrolled. A loading dose of 600 mg of clopidogrel was administered before or during PCI. Blood samples were drawn within 24 h after clopidogrel administration. The effect of clopidogrel was measured using VerifyNow. All patients were evaluated at 6 months. The primary end-point was the combination of death, MI and stroke. 378 patients (69.3 % men and 30.7 % women) were enrolled. The mean age was 67.2 ± 12.8 years, BMI 28.9 ± 17.7, and 116 patients had diabetes (30.7 %). During the 6-months follow-up 30 patients (7.94 %) experienced a monitored end-point: 12 patients (3.17 %) had MI; five patients (1.32 %) strokes and 15 patients (3.97 %) died. The remaining 248 patients (71.26 %) were end-point free. Factors associated with a poor prognosis were: leukocytes (OR 1.7 [1.2-2.4], p < 0.01), creatinine (OR 1.4 [1.1-2.5], p < 0.05) and at a borderline level the presence of AA allele of gene CYP2C19*2 (OR 2.5 [0.99-4.1], p = 0.052). The results using VerifyNow were similar between both groups (Group End-point: 208.5 ± 85.5, group No end-point 203.1 ± 91.3) and failed to show any prognostic value (OR 1.00 [0.992-1.007], p = 0.9). The measurement of clopidogrel efficacy using VerifyNow had no prognostic value for our unselected cohort of patients after PCI.

According to recent trials, a significant number of patients do not have a completely effective response to clopidogrel. The aim of the study was to evaluate the rate of clopidogrel resistance in the context of important clinical characteristics and to specifically determine the relation between clopidogrel efficacy and biomarkers of inflammation. Consecutive non-selected patients following PCI were enrolled into the study. All patients received a loading dose of 600 mg of clopidogrel. The effect of clopidogrel was assessed using the VerifyNow assay 24 h after clopidogrel administration, clopidogrel resistance was defined as PRU ≥ 240. At the same time, standard parameters of biochemistry and hematology, the concentration of anti-inflammatory cytokine interleukin-10 and of soluble CD40 ligand, were measured. 378 patients were enrolled. 243 (64.3%) patients were responders (R) and 135 patients (35.7%) were non-responders (NR). Non-responders were older (R 65.7 ± 13.3, NR 69.8 ± 11.5, P < 0.05), had a higher prevalence of diabetes (R 26.3%, NR 38.5%, P < 0.05), were more often on mechanical ventilation (R 0.8%, NR 4.4%, P < 0.05). The leukocyte count (R 9.8 ± 3.5, NR 11.7 ± 12.8, P < 0.05), and concentration of IL-10 (R 3.1 pg/ml, NR 5.7 pg/ml, P < 0.05) was higher among non-responders. The concentration of CD40L was not significantly different between the groups. In a multivariate logistic regression, older age, higher weight, female gender, mechanical ventilation, and a higher concentration of leukocytes and IL-10 were associated with an increased risk for being a non-responder. Older, obese patients, especially women had a higher risk of high on-treatment-platelet-reactivity. Higher concentrations of leukocytes and interleukin-10 were also an important factor associated with the risk of low clopidogrel responsiveness.