Toward a therapeutic window for antiplatelet therapy in the elderly

Abstract

This editorial refers to ‘High on-thienopyridine platelet reactivity in elderly coronary patients: the SENIOR-PLATELET study’†, by J. Silvain et al. , on page 1241 Pathophysiological changes reported in the elderly include increased platelet activation and reactivity, elevated levels of coagulation factors and plasminogen activator inhibitor type-1, and decreased bleeding time—all consistent with an increased risk for thrombosis.1 However, elderly patients with coronary artery disease (CAD) also encounter an increased risk of bleeding during antiplatelet therapy. Thus, we face a challenging treatment dilemma in these patients that is further complicated by frequent co-morbid diseases and polypharmacy. Guideline recommendations for antiplatelet therapy in the elderly are fuzzy due to a lack of dedicated pharmacodynamic and clinical outcome studies in this population. Since the first description of clopidogrel response variability and resistance, much has been learned about numerous factors influencing the metabolism of clopidogrel that directly translate into the pharmacodynamic response ( Figure 1 ).2,3 Non-responsiveness to the world's second most widely used antiplatelet agent, now de facto , has fuelled the development of and widespread interest in new and more pharmacodynamically predictable P2Y12 receptor blockers and laid the cornerstone for personalized antiplatelet therapy.3 Figure 1 Various factors influencing platelet reactivity and clinical events during clopidogrel therapy. ADP, adenosine diphosphate; BMI, body mass index; CAD, coronary artery disease; CCB, calcium channel blocker; CYP, cytochrome P450; DDI, drug–drug interaction; HPR, high on-treatment platelet reactivity; LPR, low on-treatment platelet reactivity; PPI, proton pump inhibitor; SJW, St. John's wort; SNP, single …