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Platelet activation linked to MI in patients with pneumonia
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MI appears to be an early complication of pneumonia and is associated with in vivo platelet reactivation, according to study data published in the Journal of the American College of Cardiology.
Researchers investigated the relationship between troponin elevation and in vivo biomarkers of platelet activation, including plasma soluble P-selectin, soluble CD40 ligand and serum thromboxane B2, in the early phase of hospitalization. The study included 278 patients with community-acquired pneumonia. Serum high-sensitivity cardiac troponin T levels were obtained every 12 hours and ECGs were taken every 24 hours. Patients were followed until end of hospital stay. The primary endpoint was MI.
Of the 144 patients with elevated high-sensitivity cardiac troponin T levels, defined as >0.14 mcg/L, 31 had signs of MI and 113 did not, Roberto Cangemi, MD, from I Clinica Medica, Sapienza University of Rome, and colleagues reported.
High levels of biomarkers
Compared with patients who did not develop signs of MI, those who developed signs of MI had higher baseline levels of soluble P-selectin (P<.001), soluble CD40 ligand (P<.001) and serum thromboxane B2 (P=.004).
When the researchers performed logistic regression analysis, plasma soluble CD40 ligand (P<.001), soluble P-selectin (P<.001), serum thromboxane B2 (P=.03), mean platelet volume (P=.037), pneumonia severity index score (P=.03) and ejection fraction (P=.001) were identified as independent predictors of MI.
The researchers found no difference in rate of MI between patients taking aspirin (12%) and those not taking aspirin (10%; P=.649). However, among those treated with aspirin, those with MI had higher serum thromboxane B2 compared with those without MI (P=.005).
MI was rarely associated with chest pain in this patient population, so daily monitoring of cardiac troponins and ECG may be necessary, according to the researchers. “Such monitoring should be done immediately after pneumonia diagnosis, as MI generally occurred within 48 [hours] of presentation,” they wrote.
Aspirin 100 mg/day may be insufficient to prevent formation of serum thromboxane B2 in these patients, so a dose of aspirin 100 mg twice a day may be preferable, Cangemi and colleagues wrote.
Risk factor or risk marker
In a related editorial, Carlos G. Santos-Gallego, MD, and Juan J. Badimon, PhD, both from the Atherothrombosis Research Unit of the Cardiovascular Institute of Icahn School of Medicine at Mount Sinai, said it was known that patients with community-acquired pneumonia were at increased risk for MI, but the mechanism of action was not identified, and the present study may have finally provided an explanation.
However, they wrote, “the role of platelet function is not fully understood. Platelet aggregation may be either a risk factor … or a risk marker.” Therefore, if it is a risk marker and not a causal link, antiplatelet therapy would not reduce MI in this patient population, according to Santos-Gallego and Badimon. “Future studies are needed for confirmation of the mechanism and to delineate the best therapy (eg, antiplatelet agents, vaccines) to reduce MI risk,” they wrote.
For more information:
Cangemi R. J Am Coll Cardiol. 2014;64:1917-1925.
Santos-Gallego CG. J Am Coll Cardiol. 2014;64:1926-1928.
Disclosure: The researchers, Badimon and Santos-Gallego report no relevant financial disclosures.