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Impaired Left Ventricular Reserve in Childhood Cancer Survivors Treated With Anthracycline Therapy
Author(s) -
Kaneko Sachie,
Tham Edythe B.,
Haykowsky Mark J.,
Spavor Maria,
Khoo Nee S.,
Mackie Andrew S.,
Smallhorn Jeffrey F.,
Thompson Richard B.,
Nelson Michael D.
Publication year - 2016
Publication title -
pediatric blood and cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.116
H-Index - 105
eISSN - 1545-5017
pISSN - 1545-5009
DOI - 10.1002/pbc.25933
Subject(s) - medicine , supine position , cardiology , diastole , anthracycline , ejection fraction , heart rate , heart failure , cancer , blood pressure , breast cancer
Background Childhood cancer survivors show evidence of diffuse myocardial fibrosis that is related to exercise capacity. The mechanism of reduced exercise tolerance in anthracycline cardiotoxicity remains unclear. We explored the determinants of exercise intolerance by evaluating left ventricular (LV) distensibility and functional reserve. Methods Patients (n = 22) and healthy controls (n = 10) underwent two‐dimensional echocardiography while supine, upright, and during cycle exercise. LV distensibility was measured as the change in end‐diastolic cavity area (EDCA) from supine to the upright position. LV functional reserve was assessed during peak exercise, and measured as the exercise‐induced change in systolic circumferential strain rate (SR) and early‐diastolic SR (EDSR). The peak rate of oxygen consumption was measured by indirect calorimetry. Results Median age of patients was 16 years (range 8–19) and controls 14 years (range 8–19). Median time since anthracycline therapy was 6 years (range 2–16). Peak oxygen consumption was significantly lower in patients compared to controls (35 ml/kg/min [28–60] vs. 45 ml/kg/min [44–53], P = 0.005). Transitioning from the supine position to the upright position caused a similar reduction in LV EDCA, suggesting similar LV distensibility between patients (–22% [–46 to –4]) and controls (–20% [–46 to –3], P = 0.3). However, during exercise, both systolic SR and EDSR reserve were significantly impaired in patients (∆SR: 93% [14–308], ∆EDSR: –4.5% [–88 to 121]) compared to controls (∆SR: 128% [54–230], P = 0.046; ∆EDSR: 74% [22–234], P = 0.02). Conclusions Our findings suggest that impaired LV contractility and functional reserve play a role in the reduced exercise capacity in anthracycline cardiotoxicity rather than LV distensibility.