English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Plus monthly

Global: Zendy Tools annual

Global: Zendy Tools monthly

Global: Zendy Free Plan

Obesity is associated with the development of left ventricular (LV) hypertrophy. Whether obesity in in the absence of comorbidities can cause LV hypertrophy to an extent which could create diagnostic uncertainty with pathological states (such as hypertrophic cardiomyopathy) is unknown. We used cine cardiovascular magnetic resonance imaging to precisely measure LV wall thickness in the septum and lateral wall in 764 people with body mass indices ranging from 18.5 kg/m 2 to 59.2 kg/m 2 in the absence of major comorbidities. Obesity was related to LV wall thickness across the cohort (basal septum r 0.30, P &lt; 0.001 and basal lateral wall r 0.18, P &lt; 0.001). Although no participant had hypertension, these associations remained highly significant after controlling for systolic blood pressure (all P &lt; 0.01). Each 10 kg/m 2 increase in BMI was associated with an increase in basal septal wall thickness of 1.0 mm males and 0.8 mm in females, with no statistically significant difference between genders (P = 0.1). Even in class 3 obesity (BMI &gt; 40 kg/m 2 ), no LV wall thickness &gt; 13.4 mm in males or &gt; 12.7 mm in females was observed in this cohort. We confirm that obesity in the absence of comorbidities is associated with LV hypertrophy, and establish that the magnitude of this change is modest even in severe obesity. LV hypertrophy &gt; 14 mm cannot safely be attributed to obesity alone and alternative diagnoses should be considered.

Obesity in the absence of comorbidities is not related to clinically meaningful left ventricular hypertrophy