Abstract

BackgroundIt is unclear whether obesity and type 2 diabetes (T2D), either alone or in combination, induce left ventricular hypertrophy (LVH) independent of hypertension. In the current study, we provide clarity on this issue by rigorously analysing patient left ventricular (LV) structure via clinical indices and via LV geometric patterns (more commonly used in research settings). Importantly, our sample consisted of hypertensive patients that are routinely screened for LVH via echocardiography and normotensive patients that would normally be deemed low risk with no further action required.MethodsThis cross sectional study comprised a total of 353 Caucasian patients, grouped based on diagnosis of obesity, T2D and hypertension, with normotensive obese patients further separated based on metabolic health. Basic metabolic parameters were collected and LV structure and function were assessed via transthoracic echocardiography. Multivariable logistic and linear regression analyses were used to identify predictors of LVH and diastolic dysfunction.ResultsMetabolically healthy normotensive obese patients exhibited relatively low risk of LVH. However, normotensive metabolically non-healthy obese, T2D and obese/T2D patients all presented with reduced normal LV geometry that coincided with increased LV concentric remodelling. Furthermore, normotensive patients presenting with both obesity and T2D had a higher incidence of concentric hypertrophy and grade 3 diastolic dysfunction than normotensive patients with either condition alone, indicating an additive effect of obesity and T2D. Alarmingly these alterations were at a comparable prevalence to that observed in hypertensive patients. Interestingly, assessment of LVPWd, a traditional index of LVH, underestimated the presence of LV concentric remodelling. The implications for which were demonstrated by concentric remodelling and concentric hypertrophy strongly associating with grade 1 and 3 diastolic dysfunction respectively, independent of sex, age and BMI. Finally, pulse pressure was identified as a strong predictor of LV remodelling within normotensive patients.ConclusionsThese findings show that metabolically non-healthy obese, T2D and obese/T2D patients can develop LVH independent of hypertension. Furthermore, that LVPWd may underestimate LV remodelling in these patient groups and that pulse pressure can be used as convenient predictor of hypertrophy status.

Highlights

  • It is unclear whether obesity and type 2 diabetes (T2D), either alone or in combination, induce left ventricular hypertrophy (LVH) independent of hypertension

  • There are three LV geometric patterns that can identify the type of LVH present, eccentric hypertrophy, concentric remodelling [increased relative wall thickness (RWT) of the LV posterior wall diameter (LVPWd), normal LV mass] and concentric hypertrophy

  • The co‐existence of obesity and T2D in Normotensive patients had additive effects on the prevalence of LVH The presence of LVH was determined by assessing the clinical hypertrophy indices LVPWd and LV mass, which were derived from M-Mode measurements (Table 2)

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Summary

Introduction

It is unclear whether obesity and type 2 diabetes (T2D), either alone or in combination, induce left ventricular hypertrophy (LVH) independent of hypertension. There are three LV geometric patterns that can identify the type of LVH present, eccentric hypertrophy (increased LV mass), concentric remodelling [increased relative wall thickness (RWT) of the LVPWd, normal LV mass] and concentric hypertrophy (increased LV mass and increased RWT). These changes in cardiac structure are often accompanied by diastolic dysfunction (DD, impaired LV relaxation) and can be detected in obese patients via transthoracic echocardiography (TTE) [3]. Monitoring risk in obese and/or T2D patients this way presumes that without hypertension, obesity and T2D are insufficient stresses to induce LVH

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