Abstract

The purpose of this study was to investigate left ventricular contraction patterns in asymptomatic Childhood cancer survivors (CCS) using two-dimensional speckle tracking echocardiography (2DSTE). Left ventricular longitudinal and circumferential myocardial parameters were assessed using 2DSTE, in asymptomatic CCS and age matched healthy controls. Time to peak (T2P) systolic strain was quantified. Dyssynchrony index (DI) was measured by calculating the standard deviation of T2P systolic strain of six segments in each view. Difference between T2P systolic longitudinal strain of septal and lateral wall was also assessed as a parameter for dyssynchrony. We included 115 CCS with a median age of 17.2 years (range 5.6–39.5) and a median follow up of 11.3 years (range 4.9–29.5) and 119 controls. Conventional echocardiographic parameters and global longitudinal strain were significantly decreased in CCS compared to controls (p < 0.01 and p = 0.02, respectively). Dyssynchrony index did not differ between CCS and controls. There was a clinically insignificant smaller absolute difference between T2P systolic longitudinal of septal and lateral wall in CCS compared to controls. We showed no difference in longitudinal or circumferential left ventricular dyssynchrony in CCS compared to controls using 2DSTE. Future research should focus on assessing dyssynchrony in more segments and a larger CCS population, using both 2D and 3DSTE.

Highlights

  • Long-term survival of children with cancer has improved over the last decades to approximately 70–80%

  • The study was approved by the local ethical committee and informed consent was obtained from all survivors

  • Except for a significantly lower blood pressure and a higher heart rate in the cancer survivors (CCS) group, characteristics were similar for both groups

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Summary

Introduction

Long-term survival of children with cancer has improved over the last decades to approximately 70–80%. Anthracyclines are used in many cancer treatment protocols and have a known cardiotoxic effect. Mechanisms of anthracycline-induced cardiotoxicity have been studied extensively. Cardiac extracellular matrix remodeling (cardiac fibrosis) may represent an additional important mechanism contributing to impaired Left ventricular (LV) function and adverse cardiac outcome [3,4,5]. This fibrosis is measurable by calculating extracellular volume fraction by cardiac magnetic resonance and has been found in CCS [6, 7]. Fibrosis has been shown in myocardial biopsies from patients with anthracycline cardiomyopathy [8]. Fibrosis of the myocardial wall has been correlated to dyssynchronous myocardial contraction

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