Abstract 17537: Pathologic Atrophy of the Left Ventricular Myocardium Early After Receipt of Anthracycline-Based Chemotherapy
Background: Aortic stiffening produces systolic hypertension and increases left ventricular (LV) wall stress. Normally this stimulates LV hypertrophy to normalize wall stresses. Previously, we have shown aortic stiffness abruptly increases within 3 to 6 months of anthracycline-based chemotherapy (Anth-bC) initiation, but the effect of this increase on LV mass and remodeling is unknown.
Methods: We performed cardiac magnetic resonance (CMR) on 73 individuals (49 receiving Anth-bC [67% women; 49±14 years] and 24 healthy volunteers [58% women; 52±8 years]) at baseline and 6 months after Anth-bC initiation. In blinded analyses we measured aortic arch stiffness (pulse wave velocity [PWV]) and LV volumes, shape (sphericity index), mass, and wall stress. Paired and two sample t tests were performed to assess differences in cohorts and serial CMR measures. We fit multivariate models to each cohort to examine associations of change in CMR measurements after adjustment for covariates.
Results: In comparison with healthy subjects, those receiving Anth-bC experienced increases in PWV and LV wall stress without LV shape change or a compensatory increase in LV mass (Table 1). In fact, LV mass index decreased upon receipt of Anth-bC relative to healthy subjects (p=0.03). In the cancer cohort models, we found that increased wall stress index was associated with increased PWV (p<0.01) and reduced LV mass index (p<0.001) even after adjusting for age, sex, weight change, and baseline ejection fraction and PWV.
Conclusions: After accounting for overall changes in body weight, we found that early after Anth-bC receipt, increases in PWV and wall stress are associated with an unexpected decrease in LV mass. Early pathologic myocardial atrophy after Anth-bC in the presence of increased afterload leads to inadequate LV mass for wall stress normalization to maintain cardiac output, which can result in chronic afterload excess, contractile deterioration and cardiomyopathies.
- © 2013 by American Heart Association, Inc.