Ugur OZKERIM, Hasan KOCAAYAN, Sercan GUCENMEZ, Servet AKAR
Southern Clinics of Istanbul Eurasia - 2026;37(3):239-248
Objective: Evidence of subclinical myocardial and pericardial involvement has been described in patients with Familial Mediterranean Fever (FMF), even during clinically inactive periods. However, the potential impact of colchicine resistance on cardiac function has not been fully elucidated. The present study investigated myocardial performance in FMF patients with differing responses to colchicine therapy using speckle-tracking echocardiography. Methods: This study evaluated 74 patients diagnosed with FMF, including 57 colchicine-responsive and 17 colchicine-resistant individuals, together with 74 age- and sex-matched healthy controls. Participants with established cardiovascular risk factors were excluded. Colchicine resistance was defined by recurrent attacks occurring at least once every three months despite treatment with 2 mg/day or the maximum tolerated dose of colchicine, the requirement for biologic therapy, and/or the presence of amyloidosis, defined as proteinuria >=500 mg/day on at least two occasions or biopsy-confirmed disease. Demographic, clinical, and laboratory variables were collected using a standardized assessment form. All subjects underwent speckle-tracking echocardiographic evaluation performed by experienced cardiologists who were blinded to clinical information. Results: No significant differences were observed between colchicine-resistant and colchicine-responsive FMF patients with respect to age, sex distribution, or disease duration (p>0.05). Global longitudinal strain (GLS) values were significantly reduced in colchicine-responsive FMF patients compared with healthy controls (p<0.05). In contrast, GLS measurements did not differ significantly between colchicine-resistant and colchicine-responsive patient groups (p>0.05). Conclusions: Patients with FMF demonstrate subclinical myocardial dysfunction when compared with healthy individuals. However, resistance to colchicine therapy does not appear to be associated with additional impairment in myocardial strain parameters, suggesting that mechanisms independent of treatment response may contribute to cardiac involvement in FMF.
