tetano
Editor, Senior Moderator
PLoS One. 2019 Aug 23;14(8):e0221628. doi: 10.1371/journal.pone.0221628. eCollection 2019.
[h=1]Transient depression of myocardial function after influenza virus infection: A study of echocardiographic tissue imaging.[/h] Ito T[SUP]1[/SUP], Akamatsu K[SUP]1[/SUP], Fujita SI[SUP]1[/SUP], Kanzaki Y[SUP]1[/SUP], Ukimura A[SUP]2[/SUP], Hoshiga M[SUP]1[/SUP].
[h=3]Author information[/h] 1 Department of Cardiology, Osaka Medical College, Takatsuki, Osaka, Japan. 2 Department of General Internal Medicine, Osaka Medical College, Takatsuki, Osaka, Japan.
[h=3]Abstract[/h] [h=4]BACKGROUND:[/h] 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.
[h=4]METHODS AND RESULTS:[/h] 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.
[h=4]CONCLUSIONS:[/h] 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.
PMID: 31442264 DOI: 10.1371/journal.pone.0221628
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[h=1]Transient depression of myocardial function after influenza virus infection: A study of echocardiographic tissue imaging.[/h] Ito T[SUP]1[/SUP], Akamatsu K[SUP]1[/SUP], Fujita SI[SUP]1[/SUP], Kanzaki Y[SUP]1[/SUP], Ukimura A[SUP]2[/SUP], Hoshiga M[SUP]1[/SUP].
[h=3]Author information[/h] 1 Department of Cardiology, Osaka Medical College, Takatsuki, Osaka, Japan. 2 Department of General Internal Medicine, Osaka Medical College, Takatsuki, Osaka, Japan.
[h=3]Abstract[/h] [h=4]BACKGROUND:[/h] 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.
[h=4]METHODS AND RESULTS:[/h] 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.
[h=4]CONCLUSIONS:[/h] 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.
PMID: 31442264 DOI: 10.1371/journal.pone.0221628
Free full text