Abstract
Acute infection is suspected of involvement in the onset of acute myocardial infarction (MI). We aimed to assess the incidence, pathogenesis and prognosis of post-infectious MI. All consecutive patients hospitalized for an acute MI in coronary care units were prospectively included. Post-infectious MI was defined by a concurrent diagnosis of acute infection at admission. Type 1 MI (acute plaque disruption) or Type 2 MI (imbalance in oxygen supply/demand) were adjudicated according to the universal definition of MI. From the 4573 patients admitted for acute MI, 466 (10%) had a concurrent acute infection (median age 78 (66–85) y, 60% male), of whom 313 (67%) had a respiratory tract infection. Type 2 MI was identified in 72% of post-infectious MI. Compared with other MI, post-infectious MI had a worse in-hospital outcome (11 vs. 6% mortality, p < 0.01), mostly from cardiovascular causes. After adjusting for confounders, acute infections were no more associated with mortality (odds ratio 0.72; 95% confidence interval 0.43–1.20). In the group of post-infectious MI, Type 1 MI and respiratory tract infection were associated with a worse prognosis (respective odds ratio 2.44; 95% confidence interval: 1.12–5.29, and 2.89; 1.19–6.99). In this large MI survey, post-infectious MI was common, accounting for 10% of all MI, and doubled in-hospital mortality. Respiratory tract infection and Type 1 post-infectious MI were associated with a worse prognosis.
Highlights
Acute infections are known to be associated with an increased risk of myocardial infarction (MI), especially respiratory tract infection, including pneumonia, bronchitis and influenza, and digestive and urinary tract infections [1,2]
The mechanisms underlying the triggering of post-infectious MI by acute infection could include both coronary endothelial dysfunction [5] and platelet activation, and subsequent coronary thrombosis [6], and a sepsis-related increase in myocardial oxygen consumption leading to functional MI
Considering a causal link has already been established between acute infection and MI, our findings strongly suggest a new nosological entity: post-infectious MI
Summary
Acute infections are known to be associated with an increased risk of myocardial infarction (MI), especially respiratory tract infection, including pneumonia, bronchitis and influenza, and digestive and urinary tract infections [1,2]. Experimental data supports a causal relation between acute respiratory tract infection and acute coronary syndromes [1]. Despite the identification of acute infection as a causal factor, diagnosis of post-infectious MI is not usually individualized in clinical practice, and there is a disconcerting lack of prospective observational data in cardiology units for this frequent condition. The mechanisms underlying the triggering of post-infectious MI by acute infection could include both coronary endothelial dysfunction [5] and platelet activation, and subsequent coronary thrombosis [6], and a sepsis-related increase in myocardial oxygen consumption leading to functional MI. Type 2 MI, is an emerging pathophysiological concept corresponding to a mismatch between myocardial oxygen supply and demand, leading to ischemic myocardial injury [8]. The respective frequency of these two pathophysiological mechanisms in post-infectious MI remains unclear
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