Key result
Increasing BMI caused greater left ventricular cavity dilatation in dilated (+2.2 mL/kg/m2) and hypertrophic cardiomyopathy (+1.9 mL/kg/m2) compared to normal hearts (+0.7 mL/kg/m2; P<0.04).
Why the study?
Obesity causes cardiac remodelling in health, but the contribution of this maladaptation in the setting of an additional cardiomyopathic process is poorly understood.
Does increasing BMI exacerbate left ventricular remodelling in patients with dilated and hypertrophic cardiomyopathy compared to normal hearts?
Observational (n=1,554)
Does increasing BMI exacerbate left ventricular remodelling in patients with dilated and hypertrophic cardiomyopathy compared to normal hearts?
Obesity exacerbates left ventricular cavity dilatation and hypertrophy in patients with dilated and hypertrophic cardiomyopathy more profoundly than in normal hearts.
May amplify LV remodelling with rising BMI in cardiomyopathy; hypothesis-generating and requires prospective trials.
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.
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Rayner et al. (2020) conducted an observational in Dilated and hypertrophic cardiomyopathy (n=1,554). Increasing BMI (Obesity) vs. Normal hearts was evaluated on Left ventricular cavity dilatation per unit increase in BMI (p=<0.04). Increasing BMI caused greater left ventricular cavity dilatation in dilated (+2.2 mL/kg/m2) and hypertrophic cardiomyopathy (+1.9 mL/kg/m2) compared to normal hearts (+0.7 mL/kg/m2; P<0.04).
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