Abstract
Objective: Nonalcoholic fatty liver disease (NAFLD) is the main cause of chronic liver disease and is associated with an increased risk of cardiovascular death. Fatty liver index (FLI) is a validated marker of NAFLD and can be used as a screening measure of hepatic steatosis. The purpose of the study was to compare the progression of hypertension-mediated organ damage (HMOD) in hypertensive patients with and without NAFLD. Design and method: Hypertensive patients (n = 60) without a history of cardiovascular disease participated in the study (mean age, 52 years; males, 55%; baseline clinic BP, 145/92 mmHg) and were followed for one year. In the baseline visit, FLI was calculated, and patients were divided into two groups by FLI below 60 or 60 or above (i.e., high-risk of NAFLD). All patients underwent clinic and 24-hour ambulatory BP measurements, echocardiographic examination, nailfold capillaroscopy, pulse wave velocity, and urinary albumin excretion assessment (albumin to creatinine ratio, [ACR]). Left ventricular mass index (LVMI) was also calculated using the Devereux formula. Results: In baseline visit, patients with FLI > or = 60 (n = 32) compared to the control group had higher values of ACR (26.5±57mg/g vs. 9.6±6.3 mg/g, p = 0.02) and lower values of capillary densities (75±18cap/mm2 vs. 86±12cap/mm2, p = 0.002), whereas there was no relative difference in PWV and LVMI. At the end of follow-up, patients with FLI > or = 60 had higher values of ACR (12.6±11.9 mg/g vs. 6.8±5.3 mg/g p = 0.025), PWV (9.9±2m/sec vs. 8.8±1.3 m/sec, p = 0.02), LVMI (81.4±13.2 g/m2 vs. 72.5±13.2 g/m2, p = 0.02) but lower number of capillaries (65.1±8.8 cap/mm2 vs. 79.6±7.5 cap/mm2, p<0.001). Linear regression analysis revealed that FLI > or = 60 was an independent determinant of follow-up ACR, PWV, LVMI, and the number of capillaries. Conclusions: Increased FLI may adversely modify the progression of HMOD in hypertension.
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