Hypermetabolism and lipid alterations postburn: A cardiovascular perspective

Authors

Mohammed AbuBaha, Department of Medicine, An-Najah National University, Nablus, State of Palestine, najah.edu.
Ameer Awashra, Department of Medicine, An-Najah National University, Nablus, State of Palestine, najah.edu.
Bara AbuBaha, Department of Medicine, An-Najah National University, Nablus, State of Palestine, najah.edu.
Anwar Zahran, Department of Medicine, An-Najah National University, Nablus, State of Palestine, najah.edu.
Mohammad Bdair, Department of Medicine, An-Najah National University, Nablus, State of Palestine, najah.edu.
Dana Sandouka, Department of Medicine, An-Najah National University, Nablus, State of Palestine, najah.edu.
Sarah Saife, Department of Medicine, An-Najah National University, Nablus, State of Palestine, najah.edu.
Bara Sawalmeh, Department of Medicine, An-Najah National University, Nablus, State of Palestine, najah.edu.
Amr Awad, Department of Medicine, An-Najah National University, Nablus, State of Palestine, najah.edu.
Abdalhakim Shubietah, Advocate Health - MidwestFollow

Recommended Citation

AbuBaha M, Awashra A, AbuBaha B, et al. Hypermetabolism and Lipid Alterations Postburn: A Cardiovascular Perspective. Cardiovasc Ther. 2026;2026:5983391. Published 2026 Feb 6. doi:10.1155/cdr/5983391

Affiliations

Advocate Illinois Masonic Medical Center

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.

Type

Article

PubMed ID

41660577