Effect of Weight Loss on Early Left Atrial Myopathy in People With Obesity But No Established Cardiovascular Disease

Abstract

Background Obesity is associated with left atrial (LA) remodeling (ie, dilatation and dysfunction) which is an independent determinant of future cardiovascular events. We aimed to assess whether LA remodeling is present in obesity even in individuals without established cardiovascular disease and whether it can be improved by intentional weight loss. Methods and Results Forty‐five individuals with severe obesity without established cardiovascular disease (age, 45±11 years; body mass index; 39.1±6.7 kg/m 2 ; excess body weight, 51±18 kg) underwent cardiac magnetic resonance for quantification of LA and left ventricular size and function before and at a median of 373 days following either a low glycemic index diet (n=28) or bariatric surgery (n=17). Results were compared with those obtained in 27 normal‐weight controls with similar age and sex. At baseline, individuals with obesity displayed reduced LA reservoir function (a marker of atrial distensibility), and a higher mass and LA maximum volume (all P <0.05 controls) but normal LA emptying fraction. On average, weight loss led to a significant reduction of LA maximum volume and left ventricular mass (both P <0.01); however, significant improvement of the LA reservoir function was only observed in those at the upper tertile of weight loss (≥47% excess body weight loss). Following weight loss, we found an average residual increase in left ventricular mass compared with controls but no residual significant differences in LA maximum volume and strain function (all P >0.05). Conclusions Obesity is linked to subtle LA myopathy in the absence of overt cardiovascular disease. Only larger volumes of weight loss can completely reverse the LA myopathic phenotype.

Adiposity influences on myocardial deformation: a cardiovascular magnetic resonance feature tracking study in people with overweight to obesity without established cardiovascular disease

“…Increased LA size as an early sign of LA remodeling, as shown in our study, might be an important link between obesity without cardiovascular comorbidities and HF, as deteriorations in LA structure and function of asymptomatic individuals have been shown to precede development of HF [ 61 ]. Our results also imply beneficial effects of dietary-induced weight loss on LA remodeling in healthy obesity suggesting that LA enlargement in early stages is at least partially reversible [ 39 ].…”

“…CMR-FT studies in isolated obesity are rare. Deal, Rayner [ 39 ] observed GLS to be reduced in healthy obesity which was unaffected by dietary-induced weight loss. Likewise, another two studies found in their cross-sectional data a reduction of GLS and GCS in healthy people with obesity compared to healthy normal-weight controls [ 43 , 44 ].…”

“…Some echocardiographic studies analyzing cardiac remodeling in people with obesity without overt cardiovascular disease undergoing dietary or bariatric surgical intervention showed an improvement in diastolic function through intentional weight loss [ 33 – 35 ]. Similarly, CMR studies in healthy people with obesity who intentionally lost weight found concomitant reductions in left ventricular (LV) mass [ 36 – 38 ], and LA volume [ 39 ]. However, reports regarding the effect of dietary intervention on CMR-derived LV strain are scarce in people with overweight to obesity without established cardiovascular disease [ 34 , 39 ].…”

“…Similarly, CMR studies in healthy people with obesity who intentionally lost weight found concomitant reductions in left ventricular (LV) mass [ 36 – 38 ], and LA volume [ 39 ]. However, reports regarding the effect of dietary intervention on CMR-derived LV strain are scarce in people with overweight to obesity without established cardiovascular disease [ 34 , 39 ].…”

Mediating Effect of the NLR on the Relationship Between HbA1c and Left Atrial Stiffness in Overweight Patients With Hypertension

“…According to a study conducted by Deal et al ., 24 obesity resulted in LA myopathy in obese individuals who did not have any obvious cardiovascular conditions. This LA myopathy includes LA enlargement and LA reservoir dysfunction.…”