Investigation of the arterial stiffness and associated factors in patients with familial Mediterranean fever

Objective: Because of the ongoing and recurring inflammatory state in familial Mediterranean fever (FMF), patients may experience a high risk of cardiovascular events. Our aim was to investigate the arterial stiffness and associated factors in patients with FMF. Methods: Sixty-nine consecutive FMF patients (including 11 females) and 35 controls (including 5 females) were enrolled in the study. The demographical, clinical, and laboratory data and genetic mutations of the patients were recorded. In the study, FMF patients according to the Tel-Hashomer criteria were included, whereas patients with other known inflammatory rheumatologic disease, atherosclerotic cardiovascular disease, hypertension, diabetes, those under the age of 18 years, or those refusing to participate in the study were excluded. Arterial stiffness measurements were performed using the TensioMed device (TensoMed Ltd, Budapest, Hungary). Results: The patient and control groups were similar in terms of the mean ages, BMIs, gender, systolic blood pressures, and smoking. FMF patients had a higher pulse wave velocity (PWV) (7.73±1.3 and 7.18±1.1 m/s; p=0.03) and lower brachial and aortic augmentation indexes (–64.6±14.6% and –54.6±25.9%, p=0.041 and 4.9±7.4% and 14.0±11.5%, p=0.025, respectively) compared with the controls. Thirty-one (45%) patients were in the “during-attack” state and had higher PWV (8.17±1.6 and 7.38±0.9 m/s; p=0.027) compared with the asymptomatic patients. PWV was correlated to serum CRP, WBC, ESR, fibrinogen, and neutrophil/lymphocyte ratios (r=0.666, 0.429, 0.441, 0.388, and 0.460, respectively). The genetic mutation and predominant attack type had no effect on arterial stiffness. Conclusion: FMF patients have increased arterial stiffness during attacks compared with asymptomatic patients and controls. The impaired arterial stiffness is correlated to the severity of the inflammatory state rather than to the attack type or genetic mutations. (Anatol J Cardiol 2017; 17: 132-8) Keywords: