1.
Metabolic syndrome and its association with left ventricular dysfunction in patients with left bundle branch block.
Gharipour, M, Hashemi Jazi, M, Nilforoush, P, Batvandi, A, Mohammadi, R, Najafi, R
Acta bio-medica : Atenei Parmensis. 2015;(2):157-61
Abstract
BACKGROUND The present study and for the first time hypothesizes that the patients with left bundle branch block (LBBB) suffer considerably from metabolic syndrome (MetS) and this metabolic phenomenon can be associated with cardiac dysfunction status such as ventricular dilation and reduced left ventricular ejection fraction (LVEF) in these patients. METHODS A retrospective study was conducted on 220 consecutive patients with diagnosed LBBB. MetS status was diagnosed using the Adult Treatment Panel III of the National Cholesterol Education Program criteria. Systolic function state was assessed using two-dimensional echocardiography. RESULTS The overall prevalence of MetS among studied LBBB patients was 16.8%. Regarding left ventricular functional status in the two groups, the mean LVEF in the groups with and without MetS was 37.03 ± 9.09% and 43.43 ± 15.62% with a significant difference (p = 0.017). However, left ventricular dilation was similarly detected in both groups with and without MetS (21.6% versus 30.6%, p = 0.273). Multivariable linear regression model showed subjects with MetS had lower LVEF in the presence of confounders (Beta = 6.915, p = 0.039). CONCLUSION A notable number of LBBB patients suffered from MetS and this metabolic phenomenon is significantly associated with lowering left ventricular function in LBBB patients.
2.
Insulin resistance and subclinical abnormalities of global and regional left ventricular function in patients with aortic valve sclerosis.
Utsunomiya, H, Yamamoto, H, Kunita, E, Hidaka, T, Kihara, Y
Cardiovascular diabetology. 2014;:86
Abstract
BACKGROUND Insulin resistance, as a key mediator of metabolic syndrome, is thought to be associated with pathogenesis of calcific aortic valve disease and altered left ventricular (LV) function and structure. However, in patients with aortic valve sclerosis (AVS), the association between insulin resistance and subclinical impairment of LV function is not fully elucidated. METHODS We studied 57 patients (mean age 70 ± 8 years, 22 women) with asymptomatic AVS but normal LV ejection fraction in echocardiography. LV longitudinal and circumferential strain and strain rate was analyzed using two-dimensional speckle tracking echocardiography. Patients with uncontrolled hypertension and diabetes mellitus, chronic kidney disease, and concomitant coronary artery disease were excluded. They were divided into the insulin-resistant group (AVS+IR; N = 28) and no insulin-resistant group (AVS-IR; N = 29) according to the median value of homeostatic model assessment index. Computed tomography scans were also performed to measure the aortic valve calcium score and the visceral adipose tissue (VAT) area. In addition, age- and sex- adjusted 28 control subjects were recruited for the comparison. RESULTS There were no significant differences in LV ejection fraction or mass index among the groups. The AVS+IR group had a higher aortic valve calcium score (median 94 versus 21, P = 0.022) and a larger VAT area (113 ± 42 cm2 versus 77 ± 38 cm2, P = 0.001) than the AVS-IR group. Notably, LV global longitudinal strain, strain rate (SR), and early diastolic SR were significantly lower in the AVS+IR group than in the AVS-IR group and in control subjects (strain: -16.2 ± 1.6% versus -17.2 ± 1.2% and -18.9 ± 0.8%; SR: -1.18 ± 0.26 s(-1) versus -1.32 ± 0.21 s(-1) and -1.52 ± 0.08 s(-1); early diastolic SR: -1.09 ± 0.23 s(-1) versus -1.23 ± 0.18 s(-1) and -1.35 ± 0.12 s(-1); P < 0.05 for all comparison), whereas circumferential function were not significantly different. Multiple linear regression analyses revealed insulin resistance as an independent determinant of LV longitudinal strain (P = 0.017), SR (P = 0.047), and early diastolic SR (P = 0.049) regardless of LV mass index or VAT area. CONCLUSIONS Insulin resistance is a powerful independent predictor of subclinical LV dysfunction regardless of concomitant visceral obesity and LV hypertrophy. Thus, it may be a novel therapeutic target to prevent subsequent heart failure in patients with AVS.