Beyond BMI: why waist measures matter more in patients with reduced cardiac function

The End of the Obesity Paradox? 

Although the concept of an "obesity paradox" has historically influenced the interpretation of body weight in patients with established cardiovascular disease, accumulating evidence now challenges this paradigm. Recent Mendelian randomization analyses in heart failure suggest that the apparent survival benefit of higher BMI is largely attributable to index-event bias rather than a true protective biological effect (2), while contemporary imaging studies increasingly indicate that the distribution of adipose tissue, rather than total body mass, determines cardiovascular risk. Against this background, the study by Khanna and colleagues provides timely evidence that measures of central adiposity outperform BMI in predicting mortality among patients with left ventricular(LV) systolic dysfunction. Using data from 5,615 community-dwelling participants in the UK Biobank Imaging Enhancement Programme, all with cardiac magnetic resonance (CMR)-defined LV systolic impairment (LVEF <50%) but without prevalent heart failure at baseline, the authors evaluated five adiposity measures: body mass index (BMI), waist circumference (WC), waist-to-hip ratio (WHR), body fat percentage, and total fat mass. Over a median follow-up of 13.5 years, 290 all-cause and 76 cardiovascular (CV) deaths occurred. (1)

Waist Circumference Emerges as a Stronger Predictor 

The principal finding is both clinically straightforward and methodologically important: central adiposity measures, WC and WHR, outperformed BMI in predicting both all-cause and CV mortality. In fully adjusted Cox regression models, each one-standard-deviation increase in WHR was associated with a 30% higher risk of all-cause death and a 52% higher risk of CV death — compared with 19% and 37%, respectively, for BMI. WC performed similarly. To translate these findings into practical terms: each additional ~13 cm of waist circumference was associated with a 49% higher CV mortality risk, and each 0.09-unit increase in WHR with ~52% higher risk. These are clinically meaningful values , particularly in a cohort enriched for subclinical or early-stage LV dysfunction. 

A More Accurate Way to Assess Risk 

Importantly, adding WC or WHR to a BMI-based model resulted in modest but statistically significant improvements in risk discrimination (ΔC-statistic up to +0.012 for CV mortality). In contrast, body composition measures, including body fat percentage and total fat mass, did not provide similar incremental prognostic value. The associations were consistent regardless of LV dysfunction aetiology (ischaemic vs. non-ischaemic) and across LVEF strata, strengthening the generalizability of the findings. 

The Biology Behind Central Adiposity 

Why would fat distribution matter more than overall weight? The authors draw on well-established biological reasoning: visceral and ectopic adipose tissue including epicardial and pericardial fat depots are metabolically active, pro-inflammatory, and linked to insulin resistance, myocardial fibrosis, and adverse cardiac remodelling (3). In their cohort, greater central adiposity was indeed associated with larger LV volumes, increased LV mass, and lower right ventricular ejection fraction, consistent with a more adverse structural phenotype. Peripheral subcutaneous fat, in contrast, may exert a partially protective metabolic role. These mechanistic distinctions go literally to the heart of why BMI, which cannot distinguish fat compartments, may be an inadequate prognostic tool in this population. 

New Opportunities for Targeted Treatment 

The study also may have therapeutic implications. GLP-1 receptor agonists and SGLT-2 inhibitors, cardiometabolic pharmacotherapy, disproportionately reduce visceral adiposity. If central fat is indeed the more relevant prognostic target in patients with LV systolic impairment, these agents may offer benefits that BMI-based assessments would systematically undervalue. Still the study is observational and whether reducing visceral adiposity through these (or any other) agents will improve outcomes in this population will need prospective investigation. Other limitations deserve acknowledgment are that the observational design precludes causal inference, adiposity and imaging were not acquired simultaneously, and the low absolute number of CV deaths may limit the precision of subgroup estimates. The healthy-volunteer bias inherent in UK Biobank cohorts also warrants caution before extrapolating to broader or higher-risk clinical populations. Nevertheless, the large sample size, long follow-up, and use of CMR-derived cardiac parameters represent considerable methodological strengths. 

A Simple Message for Clinical Practice 

In conclusion, this paper reinforces the take out the tape measure, message. WC and WHR are inexpensive, non-invasive, and readily obtainable in any clinical setting. The 2025 ESC consensus statement on obesity and cardiovascular disease already emphasizes the adverse role of visceral and ectopic fat depots in heart failure development (3); the present data extend this perspective to mortality risk in patients with established LV dysfunction.