Abstract 15436: Silent Myocardial Infarction Complicates the Acute Phase of Pneumonia: Relationship With Platelet Thromboxane B2 Production
Background: Myocardial infarction may complicate the clinical course of pneumonia. The role of platelets is still unclear.
Methods: Two-hundred-fifty consecutive patients hospitalized for community-acquired pneumonia were included and followed-up until discharge. Upon admission serum thromboxane (Tx) B2, a stable metabolite of platelet TxA2, was measured; serum high-sensitivity Troponin T and ECG were measured every 12 and 24 hours, respectively. Myocardial infarction during the hospitalization phase was the primary end-point of the study.
Results: Thirty-five patients (14%) experienced myocardial infarction, which occurred within 48 hours from pneumonia presentation. Myocardial infarction was not associated with chest pain in all patients except one. Logistic regression analysis showed pneumonia severity index (p<0.001), history of coronary heart disease (p=0.006) and serum TxB2 (p=0.002) as independent predictors of myocardial infarction. Patients in the highest quartile of TxB2 (>200ng/ml) had a higher relative risk of myocardial infarction compared to patients in the other quartiles (OR 4.595; 95% CI: 1.958-10.785; p<0.001). Among 110 patients (44%) taking aspirin (100 mg/day), myocardial infarction rate was not significantly different compared to aspirin-untreated ones (18 vs. 11%; p=0.132). Aspirin-treated patients with myocardial infarction had higher serum TxB2 compared to those without myocardial infarction (p<0.001).
Conclusions: Silent myocardial infarction is a frequent and early complication of pneumonia; daily monitoring of serum troponins and ECG is, therefore, essential to detect it.
Platelet TxB2 over-production increases the risk of myocardial infarction; 100 mg/day aspirin seems to be insufficient to blunt it.
- © 2013 by American Heart Association, Inc.