Kai-Hung Cheng1, Mark D Handschumacher2, Bruna Morhy Borges Leal Assuncao2, Igal A Sebag3, Elkan F Halpern4, Marielle Scherrer-Crosbie5. 1. Cardiac Ultrasound Laboratory and Division of Cardiology, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts; Department of Internal Medicine and Faculty of Medicine, College of Medicine, Kaohsiung Medical University Hospital, Kaohsiung, Taiwan. 2. Cardiac Ultrasound Laboratory and Division of Cardiology, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts. 3. Echocardiography Laboratory and Cardiology Division, Department of Medicine, Sir Mortimer B. Davis-Jewish General Hospital and McGill University, Montreal, Quebec, Canada. 4. Institute for Technology Assessment, Massachusetts General Hospital, and Harvard Medical School, Boston, Massachusetts. 5. Cardiac Ultrasound Laboratory and Division of Cardiology, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts; Cardiac Ultrasound Laboratory, University of Pennsylvania, Philadelphia, Pennsylvania. Electronic address: marielle@crosbie.com.
Abstract
BACKGROUND: During the development of heart failure (HF), the changes of contraction timing pattern and temporal heterogeneity of segmental contraction happen early and may precede both symptomatic HF and the decrease in left ventricular ejection fraction (LVEF). In patients treated with anthracyclines, both symptomatic HF and the decrease of LVEF are detected once significant myocardial injury has occurred. The aim of the current study was to investigate whether changes in the timing of contraction can be detected early after anthracyclines therapy. METHODS: Forty-one women (50 ± 11 years old) with newly diagnosed breast cancer were prospectively enrolled in two centers and underwent an echocardiogram before and after anthracyclines. Peak longitudinal myocardial systolic strain was measured on the apical four- and two-chamber views. The time to peak systolic longitudinal strain (TP), ejection time (ET), isovolumic contraction time (IVCT), systolic time, and diastolic time were measured using strain curves and Doppler tracings and compared before and after anthracyclines. The heterogeneity of contraction (dyssynchrony) was measured by the SD of the TP of all segments. RESULTS: Anthracyclines treatment was associated with an increase in heart rate (HR) and a decrease in TP. TP was correlated with HR. TP/ET was independent of HR and inversely correlated to peak strain both at baseline and after anthracyclines. TP/ET increased after anthracyclines (1.26 ± 0.19 to 1.31 ± 0.22; P < .001), and this increase was correlated with the decrease in strain. The increase in TP/ET was due to an increase in IVCT/ET. A similar degree of dyssynchrony was found at baseline and after anthracyclines. CONCLUSIONS: Anthracyclines treatment induces an increase in the duration of contraction, mainly by increasing the IVCT. This increase is correlated to the decrease in strain and may therefore have additional prognostic value.
BACKGROUND: During the development of heart failure (HF), the changes of contraction timing pattern and temporal heterogeneity of segmental contraction happen early and may precede both symptomatic HF and the decrease in left ventricular ejection fraction (LVEF). In patients treated with anthracyclines, both symptomatic HF and the decrease of LVEF are detected once significant myocardial injury has occurred. The aim of the current study was to investigate whether changes in the timing of contraction can be detected early after anthracyclines therapy. METHODS: Forty-one women (50 ± 11 years old) with newly diagnosed breast cancer were prospectively enrolled in two centers and underwent an echocardiogram before and after anthracyclines. Peak longitudinal myocardial systolic strain was measured on the apical four- and two-chamber views. The time to peak systolic longitudinal strain (TP), ejection time (ET), isovolumic contraction time (IVCT), systolic time, and diastolic time were measured using strain curves and Doppler tracings and compared before and after anthracyclines. The heterogeneity of contraction (dyssynchrony) was measured by the SD of the TP of all segments. RESULTS:Anthracyclines treatment was associated with an increase in heart rate (HR) and a decrease in TP. TP was correlated with HR. TP/ET was independent of HR and inversely correlated to peak strain both at baseline and after anthracyclines. TP/ET increased after anthracyclines (1.26 ± 0.19 to 1.31 ± 0.22; P < .001), and this increase was correlated with the decrease in strain. The increase in TP/ET was due to an increase in IVCT/ET. A similar degree of dyssynchrony was found at baseline and after anthracyclines. CONCLUSIONS:Anthracyclines treatment induces an increase in the duration of contraction, mainly by increasing the IVCT. This increase is correlated to the decrease in strain and may therefore have additional prognostic value.