Platelet aggregation and aspirin non‐responsiveness increase when an acute coronary syndrome is complicated by an infection

Abstract

Summary. Background: Epidemiologic studies have shown that there is an association between acute respiratory infection and acute coronary syndrome. The aim of this study was to analyze the thrombotic risk, assessed by platelet aggregation and aspirin non‐responsiveness, in patients with an acute coronary syndrome complicated by an infection. Methods: Patients with an acute coronary syndrome who were admitted to the intensive care unit and hospitalized for at least 3 days in 2002 and 2003 were eligible for the study. Three hundred and fifty‐eight patients were included, of whom 66 had an infection during their hospital stay. Platelet aggregation was analyzed by an aggregometer using laser light (PA‐200, laser light scattering). Aspirin non‐responsiveness was defined as a closure time of ≤193 s measured by PFA‐100. Results: Platelet aggregation was more pronounced during an infectious complication (P < 0.001). The subgroups of patients with persistent fever, urinary tract infection, and pneumonia all had a higher level of aggregates than the group of patients without an infection (P = 0.007, P = 0.04, and P = 0.01, respectively). Aspirin non‐responsiveness was more frequent in the group of subjects with pneumonia compared with those without an infection, 90% vs. 46% (P = 0.006). The CRP levels were independently associated with platelet aggregation and aspirin non‐responsiveness (P < 0.001, P < 0.001, respectively). Conclusion: An infectious complication during the course of an acute coronary syndrome leads to more pronounced platelet aggregation. Aspirin non‐responsiveness is more frequent in severe infections, such as pneumonia. CRP is an independent predictor of platelet aggregation and aspirin non‐responsiveness in the setting of an acute coronary syndrome.

Clinical importance of aspirin and clopidogrel resistance

“…acute coronary syndromes, coronary artery bypass grafting and other surgical procedures, acute or chronic infection and inflammation), a temporary increase of aspirin dose seems reasonable, albeit unproven [38] . Circumstantial evidence for this claim is available as aspirin resistance (as defined by PFA-100) and is twice as common in acute coronary syndromes complicated by pneumonia compared with those cases without infectious complications (90% vs 46%) [41] . In addition, there appears to be an independent association between CRP and aspirin resistance in these patients.…”

Inflammation-related effects of adjuvant influenza A vaccination on platelet activation and cardiac autonomic function

“…Inflammatory stimuli are believed to induce a prothrombotic state [13,14], but there is a relative lack of data about their effects on platelet activation in the clinical setting [15]. Similarly, a relation between ANS activity and inflammation has recently been reported in experimental studies [16][17][18] as well as in several diseases [19][20][21][22], but the exact relation between ANS activity and inflammation in the clinical setting remains unclear.…”

Aspirin resistance in atherosclerosis

“…These cells can release both COX-2-generated TXA 2 and its precursor, PGH 2 , which can be taken up by platelets and converted to TXA 2 through mechanisms downstream of aspirin-inactivated COX-1. Interestingly, aspirin nonresponsiveness has been shown to be more frequent in patients with severe infections, such as pneumonia [40].…”