Cardiovascular and Inflammatory Insights in Familial Mediterranean Fever

Familial Mediterranean fever (FMF) is a hereditary autoinflammatory disorder characterised by recurrent serosal inflammation and marked elevations in acute-phase reactants. Beyond episodic fever and serositis, there is growing recognition of persistent low-grade inflammation even between attacks. This subclinical inflammatory milieu promotes endothelial dysfunction, platelet activation and perturbations in lipid metabolism, factors known to drive atherogenesis. Consequently, patients with FMF manifest early signs of vascular injury, including increased carotid intima–media thickness, augmented epicardial adipose tissue and electrocardiographic repolarisation abnormalities. While colchicine remains the cornerstone of therapy, evidence suggests that residual inflammation may persist despite optimal dosing, raising concerns about long-term cardiovascular risk. Better characterisation of surrogate markers—ranging from soluble endothelial biomarkers to structural and functional imaging—has begun to inform strategies for early detection and risk stratification. The interplay between innate immune pathways and metabolic regulation in FMF not only sheds light on disease-specific complications but also offers a clinical model for inflammation-induced atherogenesis more broadly.

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Cardiovascular and Inflammatory Insights in Familial Mediterranean Fever publication trend

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Technical terms

Endothelial dysfunction: Impaired ability of the vascular endothelium to regulate vasodilation and maintain antithrombotic balance.

Asymmetric dimethylarginine (ADMA): An endogenous inhibitor of nitric oxide synthase linked to reduced nitric oxide availability and vascular stiffness.

Epicardial adipose tissue: Visceral fat depot located between the myocardium and visceral pericardium, associated with local inflammatory signalling.

QT dispersion: The difference between the longest and shortest QT intervals on a surface electrocardiogram, reflecting heterogeneity of ventricular repolarisation.

Colchicine: An anti-microtubule agent that suppresses neutrophil activity and cytokine release, used to prevent attacks in FMF.

Serum endocan: A soluble dermatan sulfate proteoglycan secreted by activated endothelial cells, serving as a biomarker of endothelial inflammation.

References

1. Cardiovascular and Metabolic Risk Factors in Inherited Autoinflammation. The Journal of Clinical Endocrinology & Metabolism (2014).
2. Familial Mediterranean Fever as an Emerging Clinical Model of Atherogenesis Associated with Low-Grade Inflammation. The Open Cardiovascular Medicine Journal (2010).
3. Serum endocan, asymmetric dimethylarginine and lipid profile in children with familial Mediterranean fever. Pediatric Research (2024).
4. Association of familial Mediterranean fever and epicardial adipose tissue: A systematic review and meta‐analysis. Health Science Reports (2022).
5. Relation Between Familial Mediterranean Fever and QT Markers (QTc, QTd, and QTcd): A Systematic Review and Meta-Analysis. Cureus (2022).