| Summary: | Background: The aim of the study was to evaluate the relationship between MetS components and arterial stiffness in concert with left ventricular diastolic dysfunction (LVDD) in patients with high risk of cardiovascular disease.
Methods: A study was carried among 436 subjects (aged 53,8±6, 37,2% men) without overt atherosclerotic disease and systolic LV dysfunction. The average of observations was 4,4 years. According to the MetS components (pathologically increased waist circumference – W, increased triglyceride – T, increased fasting plasma glucose – G, low high-density lipoprotein level-H, arterial hypertension – B) patients were divided into the metabolic phenotypes. Arterial stiffness parameters (carotid to femoral pulse wave velocity (cfPW), aortic augmentation index (AIxHR75) were assessed by applanation tonometry. Cardioankle vascular index (CAVI) was calculated using the VaSera VS-1000. Impaired relaxation was described as E/A < 1,0 and E/e‘ mean < 13. Participants were considered as having pseudonorma/restrictive LVDD if the E/e‘mean ratio was≥13. In case of E/A > 1,0 and e‘ septal≥8cm/s and e‘ lateral≥10cm/s diastolic function was interpreted as normal.
Results: Most of study subjects had LVDD at the first visit (n = 358, n = 171 with relaxation abnormalities and n = 187 with pseudonormalisation). In presented cohort the most common metabolic phenotypes were: WTGHB (n = 70), WGB (n = 66), WTGB (n = 61), WTB (n = 46), WTHB (n = 30), WGHB (n = 27). During the observation period we found significant changes of LV diastolic function distribution between metabolic phenotypes (p < 0,001). All patients with WGHB phenotype at first visit had LVDD comparing with other groups. We found significant differences of arterial markers between first and follow up visits- in women (cfPWV 8,70 vs 8,94m/s, p < 0,001), in man (CAVI 8,05 vs 8,45, p < 0,001) and in whol cohort (AIxHR75 23,1 vs 24,1, p > 0,001).
Conclusion: Metabolic phenotype is closely associated with the development of LVDD. Some metabolic phenotypes promote early arterial aging.
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