Obesity-related ventricular remodelling is exacerbated in dilated and hypertrophic cardiomyopathy.
Rayner JJ., Abdesselam I., d'Arcy J., Myerson SG., Neubauer S., Watkins H., Ferreira VM., Rider OJ.
Background:Obesity causes significant cardiac remodelling even in health, and yet the contribution of this maladaptation in the setting of an additional cardiomyopathic process is poorly understood. Cardiovascular magnetic resonance is the gold-standard tool for assessing cardiac geometry, especially in an obese population, and hence perfectly suited to investigate this important question. Methods:Using data from our extensive imaging registry (n=1,554), we documented the relationship between increasing BMI and left ventricular (LV) remodelling in patients with dilated (DCM; n=529) and hypertrophic cardiomyopathy (HCM; n=297), compared to the normal heart (n=728). Results:Regardless of cardiac status, increasing BMI resulted in similar increases in LV stroke volume (P>0.18). However, there was a difference in the degree of LV cavity dilatation associated with this change in stroke volume; when compared to normal hearts [increase in end-diastolic volume of 0.7 mL per unit of rising BMI (mL/kg/m2)], there was a threefold greater LV cavity dilatation in DCM (+2.2 mL/kg/m2) and twofold greater in HCM (+1.9 mL/kg/m2, all P<0.04). Whilst obesity was related to LV hypertrophy in all groups (normal +1.3 g, DCM +2.2g, HCM +2.3 g/kg/m2, all P<0.001), additional obesity-related concentric LV remodelling only occurred in normal hearts and DCM (normal +0.006 vs. +0.003 mass:volume ratio, both P<0.001). Conclusions:In both DCM and HCM, the increase in stroke volume required by obesity appears to be achieved by excessive LV cavity dilatation. The impact of obesity on LV geometry was more pronounced in concomitant cardiovascular disease, and therefore carries potential to become an important therapeutic target in cardiomyopathy.