Left ventricular dyssynchrony in long-term childhood cancer survivors treated with anthracyclines: a retrospective cross-sectional study

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.

Chemotherapy-induced cardiotoxicity: a new perspective on the role of Digoxin, ATG7 activators, Resveratrol, and herbal drugs

“…Different drugs and chemotherapeutic agents lead to various degrees of cardiotoxicity, which could be low, moderate, and high risk according to their potency and targeting of cardiomyocytes (Table 1) [18,19].…”

“…The cardiovascular expressions of toxic sources include heart failure with ventricle diastolic dysfunction (5-Fluorouracil, Capecitabine, Taxanes, Alkaloids, and Bevacizumab), arterial hypertension (Bevacizumab), arrhythmias (anthracyclines and Taxol), and arterial hypotension (Etoposide, Alemtuzumab, Cantuzumab, Rituximab, and Interleukin 2). The formation of reactive oxygen species (ROS), mitochondrial dysfunction, and changes in calcium and iron homeostasis are some of the putative causes of chemotherapy-induced side effects [18]. These modifications cause cardiac cell death, apoptosis, and angiogenesis inhibition [19,20].…”