Platelet Activation Is Associated With Myocardial Infarction in Patients With Pneumonia

Study Questions:

What is the interplay between platelet overactivation and cardiovascular events during pneumonia?

Methods:

The investigators included 278 consecutive patients hospitalized for community-acquired pneumonia, who were followed up until discharge. At admission, platelet activation markers such as plasma soluble P-selectin (sP-selectin), soluble CD40L (sCD40L), and serum thromboxane (Tx) B2 were measured. Serum high-sensitivity cardiac troponin T (hs-cTnT) levels and electrocardiograms (ECGs) were obtained every 12 hours and 24 hours, respectively.

Results:

Among 144 patients with elevated hs-cTnT, 31 had signs of myocardial infarction (MI) and 113 did not. Baseline plasma levels of sP-selectin and sCD40L and serum TxB2 were significantly higher in patients who developed signs of MI. Logistic regression analysis showed plasma sCD40L (p < 0.001) and sP-selectin (p < 0.001), serum TxB2 (p = 0.030), mean platelet volume (p = 0.037), Pneumonia Severity Index (PSI) (p = 0.030), and ejection fraction (p = 0.001) as independent predictors of MI. There were no significant differences in MI rate between the 123 patients (45%) taking aspirin (100 mg/day), and those who were not aspirin-treated (12% vs. 10%; p = 0.649). Aspirin-treated patients with MI had higher serum TxB2 compared to those without MI (p = 0.005).

Conclusions:

The authors concluded that MI is an early complication of pneumonia and is associated with in vivo platelet activation and serum TxB2 overproduction.

Perspective:

This study reports that in the early phase of pneumonia (within 48 hours of presentation), patients showed elevated hs-cTnT, which may either be isolated or may be MI-associated and that severity of pneumonia, as assessed by PSI and ejection fraction, was independently associated with MI. In vivo platelet activation and overproduction of serum TxB2 formation were independently associated with MI, and furthermore, 100 mg/day aspirin seemed insufficient for preventing serum TxB2 overproduction. Future studies should be done to identify a more appropriate aspirin dosage or the use of other antiplatelet agents to fully block COX1, thus preventing serum TxB2 overproduction in patients with pneumonia.

Clinical Topics: Dyslipidemia, Heart Failure and Cardiomyopathies, Lipid Metabolism, Heart Failure and Cardiac Biomarkers

Keywords: Myocardial Infarction, Pneumonia, P-Selectin, Platelet Aggregation Inhibitors, Thromboxane B2, Troponin T, Mean Platelet Volume, Electrocardiography, Aspirin, Platelet Activation, Patient Discharge, CD40 Ligand


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