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Abstract

The relationship between obesity and cardiovascular outcomes has long intrigued clinicians and researchers. The study by Kumar et al. [1], “Impact of General and Central Obesity on In-Hospital Outcomes in STE-ACS Patients Undergoing Primary PCI,” provides timely insights into this complex association by evaluating both general obesity, measured by BMI, and central obesity, assessed via waist circumference, in a substantial cohort of 1,099 patients.
Traditionally, BMI has been the dominant metric for assessing obesity in cardiovascular risk stratification. While BMI offers a quick anthropometric index, it fails to capture the nuances of fat distribution, particularly the detrimental metabolic and vascular effects of visceral adiposity. Kumar et al. categorized patients into four phenotypes—neither obese nor centrally obese, obese only, centrally obese only, and both obese and centrally obese. This approach allowed a more granular understanding of how fat location influences acute coronary outcomes.
A counterintuitive finding emerged: patients without either obesity or central obesity (G1) exhibited the highest incidence of in-hospital heart failure (10.8%), whereas those with central obesity—with or without general obesity—had markedly lower rates (~4.4–4.5%). Mortality differences were not statistically significant, though the highest mortality rate (3.5%) occurred in patients with both general and central obesity. These results resonate with the well-debated “obesity paradox” in acute coronary syndromes (ACS), where excess body mass, despite long-term risks, may confer short-term survival benefits.
The “obesity paradox” has been reported across registries and meta-analyses in ACS and heart failure populations, where higher BMI correlates with reduced short-term mortality and complications post-PCI [2–4]. Possible mechanisms include greater metabolic reserve, attenuated catabolic stress, and higher circulating levels of protective adipokines. By contrast, central obesity is strongly associated with insulin resistance, dyslipidemia, and inflammation, and has been linked to adverse long-term outcomes [5,6].
The observation that central obesity did not worsen in-hospital outcomes, but was instead associated with fewer cases of heart failure, raises important questions. Could acute-phase metabolic and hemodynamic reserves overshadow the chronic harmful effects of visceral fat? Or might these findings reflect unmeasured confounders, such as myocardial preconditioning, procedural differences, or medication adherence?
The marked sex disparity is noteworthy—central obesity was more prevalent among women, while men predominated in the non-obese groups. This aligns with known postmenopausal hormonal shifts that promote visceral fat accumulation in women [7]. Given growing evidence that women with central obesity exhibit distinct metabolic and vascular responses, the intersection of sex and fat distribution warrants further targeted research.
Several practice-relevant messages arise as:

Waist circumference should complement BMI in ACS risk assessment, as BMI alone may underestimate risk in individuals with “normal-weight obesity.”
Clinicians must distinguish between acute and chronic risks. While obesity may attenuate certain in-hospital complications, its long-term cardiovascular burden remains substantial.
Incorporating sex-specific risk stratification could refine prognostic accuracy and personalize post-PCI prevention strategies.

This study is limited by its single-center design, short-term focus, and exclusion of patients with chronic kidney disease. Additionally, inflammatory biomarkers, body composition imaging, and cardiorespiratory fitness were not assessed—factors that may mediate the observed associations. Future multicenter, prospective studies incorporating BMI, waist circumference, waist-to-height ratio, and advanced imaging (e.g., CT-based visceral fat quantification) are needed to clarify the acute versus chronic prognostic roles of adiposity phenotypes in STE-ACS. Mechanistic research exploring adipokines, inflammation, and endothelial function could further unravel the paradox.
Kumar et al.’s study underlines that in cardiovascular medicine, “where” fat is stored matters as much as “how much” fat is present. Their findings challenge the reliance on BMI alone, highlight central obesity’s nuanced role in acute ACS outcomes, and emphasize sex-specific differences that could inform individualized care. In the era of precision cardiology, such refined risk stratification holds promise for improving both short- and long-term outcomes in ACS patients.
References

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