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  • Title: Myocardial Strain Is Associated with Adverse Clinical Cardiac Events in Patients Treated with Anthracyclines.
    Author: Ali MT, Yucel E, Bouras S, Wang L, Fei HW, Halpern EF, Scherrer-Crosbie M.
    Journal: J Am Soc Echocardiogr; 2016 Jun; 29(6):522-527.e3. PubMed ID: 27068546.
    Abstract:
    BACKGROUND: Anthracycline-induced symptomatic heart failure is often irreversible, underlining the usefulness of pretreatment risk assessment. Global longitudinal strain (GLS) before or after chemotherapy is associated with a later decrease in left ventricular ejection fraction (LVEF); however, whether prechemotherapy GLS is associated with symptomatic heart failure and cardiac death in patients treated with anthracyclines is unknown. METHODS: Patients with hematologic cancers treated with anthracyclines who underwent prechemotherapy echocardiography between November 2006 and June 2011 were retrospectively recruited. Basic demographic data, end-diastolic and end-systolic left ventricular volumes, LVEF, and GLS were measured. Clinical cardiac events (CEs) were defined as cardiac death or symptomatic heart failure. The association of prechemotherapy parameters with CEs was analyzed using proportional hazard analysis. RESULTS: Over a median follow-up period of 1,593 days (range, 13-2,891 days) after the start of chemotherapy, 28 of 450 patients (6%) experienced CEs. Prechemotherapy LVEF and GLS were lower in patients with CEs compared with those without CEs (58 ± 10% vs 62 ± 7% [P = .005] and -15.0 ± 2.8% vs -19.7 ± 2.7% [P < .0001], respectively). Diabetes (hazard ratio [HR], 7.06; P < .0001), hypertension (HR, 2.22; P = .04), LVEF (HR, 0.93; P = .005), and GLS (HR, 1.47; P < .0001) were associated with CEs. After controlling for clinical variables, prechemotherapy GLS remained independently associated with CEs (P < .0001). GLS less than the absolute value of -17.5% was found in 105 patients (23%) and was associated with a sixfold increase in CEs (P < .0001). CONCLUSIONS: Prechemotherapy GLS is an effective tool to stratify patients at high risk for CEs after anthracycline therapy and may help tailor treatments to decrease anthracycline-induced cardiotoxicity.
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