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Aim: CRT has been shown to be very beneficial for patients with reduced LVEF, symptomatic HF and increased QRS width. But many patients do not benefit from CRT. Maximum deflection index (MDI) is a quantitive measure of the rapidity of depolarization of the myocardium. In previous studies, high MDI was found to indicate epicardial origin of ventricular tachycardia. We aimed to detect the relationship between echocardiographic intraventricular dyssynchrony and MDI.Methods: We included 144 patients with HF, QRS≥120ms, LBBB, NYHA II-IV, LVEF<35% and scheduled for CRT (90 male, 54 female; mean age 65.3±9.9years). Septal-lateral >60ms delay for the beginning of systolic velocity in TDI and septum-posterior >130ms delay in M-mode were accepted as intraventricular dyssynchrony. The MDI was calculated by dividing the time from onset of the QRS complex to the earliest point of maximum deflection in V5-V6 by the QRS duration.Results: Septal-lateral delay was associated with MDI and QRS width in bivariate analysis. In logistic regression analysis, MDI (beta=0,264, p=0.001) and QRS width (beta=0,177, p=0.028) were found to be independent parameters for predicting significant septal-lateral delay. MDI was also associated with significant septum-posterior delay in bivariate correlations and ROC curve (p<0.05 for all). In bivariate analysis MDI was associated with intraventricular dyssynchrony in both non-strict LBBB (r=0.261, p=0.010) and strict LBBB (r=0.305, p=0.035) groups.Conclusion: MDI is closely associated with all echocardiographic intraventricular dyssynchrony parameters. We suggest that MDI may be used as a marker to detect patients with increased intraventricular dyssynchrony. It may be useful to integrate MDI to CRT patient selection procedure in order to minimize nonresponders. [ABSTRACT FROM AUTHOR]

Background: Vitamin D regulates the renin-angiotensin system, suppresses proliferation of vascular smooth muscle and improves endothelial cell dependent vasodilatation. These mechanisms may play a role on pathogenesis of arterial and left ventricular stiffness. Objectives: We aimed to investigate the association between serum 25-hydroxyvitamin D with arterial and left ventricular stiffness in healthy subjects. Methods: We studied 125 healthy subjects without known cardiovascular risk factors or overt heart disease (mean age: 60.2±11.9 years). Serum 25-hydroxyvitamin D was measured using a direct competitive chemiluminescent immunoassay. The subjects were divided into two groups according to the serum vitamin D level; vitamin D sufficient (≥20ng/ml, n=56) and vitamin D deficient (<20ng/ml, n=69). Indexes of LV stiffness such as E/A and E/E' were measured. Pulse wave velocity (PWV), which reflects arterial stiffness, was calculated using the single-point method via the Mobil-O-Graph® ARC solver algorithm. Results: Systolic blood pressure, level of serum calcium, PWV and E/E' values were higher and E/A values were lower in vitamin D deficient group compared with vitamin D sufficient group. Multiple linear regression analysis showed that vitamin D level was independently associated with E/E' (β=-0.364, p<0.001), serum calcium (r=-0.136, p=0.014), PWV (β=-0.203, p=0.003), E/A (β=0.209, p=0.001) and systolic blood pressure (β=-0.293, p<0.001). Conclusion: 25-Hydroxyvitamin D levels are associated with increased ventricular and arterial stiffness as well as systolic blood pressure in healthy subjects. [ABSTRACT FROM AUTHOR]

Statins have many favorable pleiotropic effects beyond their lipid-lowering properties. The aim of this study was to evaluate the impact of long-term statin pretreatment on the level of systemic inflammation and myocardial perfusion in patients with acute myocardial infarctions. This was a retrospective study of 1,617 patients with acute ST-segment elevation myocardial infarctions who underwent primary percutaneous coronary intervention <12 hours after the onset of symptoms. Angiographic no-reflow was defined as postprocedural Thrombolysis In Myocardial Infarction (TIMI) flow grade ≤2. Long-term statin pretreatment was significantly less common in the no-reflow group (6.2% vs 21%, p <0.001). The serum lipid profiles of the groups were similar (p >0.05 for all parameters). Baseline C-reactive protein levels (10 ± 8.2 vs 15 ± 14 mg/L, p <0.001) and the frequency of angiographic no-reflow (3.9% vs 14%, p <0.001) were significantly lower, and myocardial blush grade 3 was more common (50% vs 40%, p = 0.006) in the statin pretreatment group (n = 306). Moreover, the frequency of complete ST-segment resolution (>70%) (70% vs 59%, p <0.001) and the left ventricular ejection fraction were higher (49 ± 7.5% vs 46 ± 8.3%, p <0.001) and peak creatine kinase-MB was lower (186 ± 134 vs 241 ± 187 IU/L, p <0.001) in the statin-treated group. In conclusion, long-term statin pretreatment is associated with lower C-reactive protein levels on admission and better myocardial perfusion after primary percutaneous coronary intervention, leading to lower enzymatic infarct area and a more preserved left ventricular ejection fraction. This is a group effect independent of lipid-lowering properties. [ABSTRACT FROM AUTHOR]