# Hypermetabolism and Lipid Alterations Postburn: A Cardiovascular Perspective

## TL;DR

Severe burns cause long-term metabolic and cardiovascular issues, including lipid changes and heart stress, requiring better long-term care strategies.

## Contribution

This review introduces a new perspective on postburn care by emphasizing the need for proactive cardiometabolic monitoring and multidisciplinary approaches.

## Key findings

- Burn survivors show atherogenic dyslipidemia and increased cardiovascular risk years after injury.
- Metabolic changes include elevated small-dense LDL, reduced HDL-C, and persistent hypertriglyceridemia.
- Imaging and metabolomics reveal lasting endothelial injury and cardiac dysfunction in young survivors.

## Abstract

Severe thermal burns involving ≥ 20% of total body surface area (TBSA) initiate a distinct, prolonged physiological cascade extending well beyond the acute phase. This dysregulated response features chronic hypermetabolism, lipid remodeling, and sustained cardiovascular stress. While survival has improved with advances in acute care, the long‐term cardiometabolic effects, particularly the link between lipid abnormalities and cardiovascular risk, remain underexplored. This review highlights the complex pathophysiology of burn‐induced hypermetabolism, including elevated resting energy expenditure, catecholamine‐driven lipolysis, mitochondrial uncoupling, and maladaptive adipose browning. Even in metabolically healthy individuals, these mechanisms promote atherogenic dyslipidemia, characterized by hepatic steatosis, elevated small‐dense LDL, reduced HDL‐C, and persistent hypertriglyceridemia. Emerging lipidomic and clinical data correlate these changes with increased Framingham risk scores, systemic inflammation, and TBSA extent. Simultaneously, cardiovascular vulnerability increases due to myocardial remodeling, autonomic dysfunction, and vascular impairment, particularly in young survivors with prolonged metabolic responses. Imaging and metabolomics reveal endothelial injury, subclinical cardiac dysfunction, and elevated arrhythmogenic risk persisting years after healing. We evaluate current interventions, β‐blockers, omega‐3 fatty acids, statins, anti‐inflammatory agents, and structured rehabilitation, within a multimodal framework. Additionally, we identify critical gaps, including the need for precision metabolic modulation, omics‐based monitoring, and tailored cardiovascular risk algorithms. Recognizing severe burns as systemic illnesses with delayed but measurable cardiovascular consequences requires a paradigm shift in long‐term care. This review advocates for proactive, multidisciplinary cardiometabolic surveillance as an essential component of postburn recovery. This review follows the TITAN 2025 guideline for transparency in research and reporting.1