Key result
Myocardial function was transiently depressed 2 weeks after influenza virus infection compared to 4 weeks, with significant improvements in LV early diastolic strain rate (1.43 to 1.59 1/s) and myocardial performance index (0.52 to 0.38).
Why the study?
Influenza virus infection is associated with minor cardiac changes, but the characteristics of myocardial involvement remain poorly understood.
Observational (n=20)
Single-blind
No
Echocardiographic tissue imaging reveals transient, subclinical depression of myocardial function during early recovery from influenza virus infection, even in the absence of overt myocardial injury.
May warrant short-term cardiac monitoring after influenza; hypothesis-generating and leaves open need for prospective confirmation.
BACKGROUND: Influenza virus infection (IVI) was reported to be associated with minor cardiac changes, mostly those detected on electrocardiogram with and without elevated blood markers of myocardial injury; however, the characteristics of myocardial involvement in association with IVI are poorly understood. This study used echocardiographic tissue imaging (tissue Doppler, strain, and strain rate) to evaluate changes in left atrial (LA) and left ventricular (LV) myocardial function after IVI. METHODS AND RESULTS: We examined 20 adult individuals (mean age, 43 years) at 2 and 4 weeks after diagnosis of IVI. For myocardial functional variables, we obtained LV global longitudinal strain (GLS), LV early diastolic strain rate (e'sr), LA strain, and LA stiffness (E/e'/LA strain), in addition to data on tissue Doppler (s', e', and a') and myocardial performance index. Blood markers of myocardial injury were also examined. During follow-up, there were no significant changes in global chamber function such as LV ejection fraction, E/e', and LA volume. However, significant changes in myocardial function were observed, namely, in s' (8.0 ± 1.6 cm/s to 9.3 ± 1.5 cm/s; p = 0.01), e' (10.2 ± 2.8 cm/s to 11.4 ± 3.0 cm/s; p < 0.001), e'sr (1.43 ± 0.44 1/s to 1.59 ± 0.43 1/s; p = 0.005), and LA strain (35 ± 8% to 40 ± 12%; p = 0.025), and the myocardial performance index (0.52 ± 0.20 to 0.38 ± 0.09; p = 0.009), but not in a', LA stiffness, or GLS. Cardiac troponin T and creatinine kinase isoenzyme MB were not elevated significantly at any examination. CONCLUSIONS: Myocardial dysfunction during IVI recovery appeared to be transient particularly in the absence of myocardial injury. Echocardiographic tissue imaging may be useful to detect subclinical cardiac changes in association with IVI.
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Ito et al. (2019) conducted an observational in Influenza virus infection (n=20). Influenza virus infection (2 weeks post-diagnosis) vs. 4 weeks post-diagnosis was evaluated on LV early diastolic strain rate (e'sr) (p=0.005). Myocardial function was transiently depressed 2 weeks after influenza virus infection compared to 4 weeks, with significant improvements in LV early diastolic strain rate (1.43 to 1.59 1/s) and myocardial performance index (0.52 to 0.38).
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