Abstract
Calcium channel blockers (CCBs) do not reduce the risk of initial or recurrent myocardial infarction (MI) in patients diagnosed with stable coronary artery disease (CAD). The aim of this current study was to evaluate the association between CCBs and aspirin resistance in patients with CAD. Patients with stable CAD who were regularly taking aspirin (75-100 mg qd) for at least 1 month prior to enrollment in the study were included. The VerifyNow system was used for platelet function testing with high on-aspirin platelet reactivity (HAPR) defined as aspirin reaction units (ARU) >550. We compared patients treated with CCBs versus control group. Five hundred three patients with CAD were included in this study, and 88 were treated with CCBs. Mean age (67.9±9.7 in the CCB group vs. 66.5±11.4 in the control group), gender (77.3 male vs. 82.9%), rates of diabetes mellitus (34.7 vs. 36.9%), rates of CKD (23.5 vs. 23.5%), dyslipidemia (85.1 vs. 85.3%), and statin therapy (89.5 vs. 90.7%) were similar. The mean ARU was 465.4±70.0 for patients treated with CCBs versus 445.2±60.0 in controls (p=0.006). Similarly, 15.9% of CCB patients demonstrated HAPR compared to 7.0% (p=0.006). The administration of CCBs was independently associated with HAPR in a multivariate analysis (OR 1.72, 95% CI: 1.04-8.91, p=0.047) as well as in propensity score matched analysis (OR 1.56; CI: 1.22-1.93; p<0.001). Usage of CCBs is positively correlated with aspirin resistance. These findings may suggest an adverse pharmacologic effect of CCBs among patients with stable CAD treated with aspirin.
Highlights
In platelets, one of the pivotal activating factors that leads to aggregation occurs through the messaging cascade initiated by calcium influx [1]
The administration of Calcium channel blockers (CCBs) was independently associated with high on-aspirin platelet reactivity (HAPR) (OR- 1.72, 95% CI 1.04 – 8.91, p=0.047)
Usage of CCBs is positively correlated with aspirin resistance
Summary
One of the pivotal activating factors that leads to aggregation occurs through the messaging cascade initiated by calcium influx [1]. As the calcium concentration rises within the cell, the signaling cascade leads to both actin cytoskeleton reorganization and degranulation, which are essential for platelet aggregation [1,2,3] Aspirin prevents these steps and halts platelet aggregation. A quarter of patients who have been prescribed aspirin for prevention of cardiac or cerebral vascular events have an inadequate response to the drug [5,6]. This decreased response may stem from many sources, including increased levels of epinephrine, which can inhibit aspirin’s effectiveness and reverse its anti-thrombotic effect [7,8]. Previous studies have demonstrated that patients with increased HAPR have increased risk of experiencing recurrent ischemic events [11,12]
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