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Background: The risk of syncope and sudden cardiac death due to ventricular arrhythmias increased in patients with aortic stenosis (AS). Recently, it was shown that Tp-e interval, Tp-e/QT, and Tp-e/QTc ratio can be novel indicators for prediction of ventricular arrhythmias and mortality. We aimed to investigate the association between AS and ventricular repolarization using Tp-e interval and Tp-e/QT ratio. Methods: Totally, 105 patients with AS and 60 control subjects were enrolled to this study. The severity of AS was defined by transthoracic echocardiographic examination. Tp-e interval, Tp-e/QT, and Tp-e/QTc ratios were measured from the 12-lead electrocardiogram. Results: Tp-e interval, Tp-e/QT, and Tp-e/QTc ratios were significantly increased in parallel to the severity of AS (P < 0.001, P = 0.001, and P = 0.001, respectively). Also, it was shown that Tp-e/QTc ratio had significant positive correlation with mean aortic gradient (r = 0.192, P = 0.049). In multivariate logistic regression analysis, Tp-e/QTc ratio and left ventricular mass were found to be independent predictors of severe AS (P = 0.03 and P = 0.04, respectively). Conclusions: Our study showed that Tp-e interval, Tp-e/QT, and Tp-e/QTc ratios were increased in patients with severe AS. Tp-e/QTc ratio and left ventricular mass were found as independent predictors of severe AS. Ann Noninvasive Electrocardiol 2015;00(0):1-7 aortic stenosis; Tp-e interval; Tp-e/QT ratio

AEMD and Vitamin D Deficiency Objectives Limited data are available regarding cardiac arrhythmias in vitamin D (VitD) deficiency. Therefore, we aimed to assess whether atrial electromechanical delay (AEMD) measured by tissue Doppler imaging (TDI), which is an indicator for atrial fibrillation (AF) development, is prolonged in patients with VitD deficiency as compared to the control group. The effect of vitD replacement on AEMD was also evaluated. Methods In this prospective study a total of 28 VitD-deficient and 56 age-, gender-, and BMI-matched VitD-sufficient healthy participants were enrolled. P-wave dispersion (PWd) was calculated on the 12-lead electrocardiogram. Both intra- and inter-AEMD were calculated by TDI. Measurements were performed at baseline in both groups and were repeated after 6-month replacement therapy in subjects with vitD deficiency. Results PWd and inter- and left intra-AEMD were significantly prolonged in patients with VitD deficiency compared to the control group (P 0.05) following replacement therapy. Conclusion PWd and left intra- and inter-AEMD are increased in patients with VitD deficiency. The serum 25(OH)D level was found as an independent predictor for AEMD in patients with VitD deficiency. Also a significant decrement was observed in inter-AEMD following vitD replacement therapy. Studies with longer follow-up are needed to investigate whether vitD-deficient patients with prolonged AEMD develop clinical arrhythmia and vitD replacement reduces the risk of atrial arrhythmias.

Objectives Vitamin D (VitD) deficiency affects the cardiovascular system via endocrine, paracrine, and autocrine pathways. Limited data are available regarding cardiac autonomic dysfunction in VitD deficiency. The aim of this study was to assess the cardiac autonomic functions by using heart rate recovery index (HRRI) and heart rate variability (HRV) in apparently healthy subjects with VitD deficiency. Methods A total of 24 VitD deficient and 50 age-, gender-, and body mass index–matched VitD sufficient healthy participants who admitted to outpatient clinics at a tertiary centre were enrolled. All study participants underwent Treadmill exercise test and 24-hour Holter recording to assess cardiac autonomic functions. HRRIs were calculated by subtracting first, second, and third minute heart rates during recovery period from maximal heart rate. Results Mean HRR1 (28.0 ± 8.3 vs 42.8 ± 6.4, P < 0.001), HRR2 (41.1 ± 11.2 vs 60.8 ± 10.4, P < 0.001), and HRR3 (44.9 ± 13.3 vs 65.9 ± 9.8, P < 0.001) were significantly higher in VitD sufficient group compared to VitD deficient group. HRV parameters as, SDNN (P = 0.040), SDANN (P < 0.001), RMSSD (P < 0.001), PNN50 (P < 0.001), and HF (P < 0.001) were significantly decreased in patients with VitD deficiency; but LF (P < 0.001) and LF/HF (P = 0.003) were significantly higher in VitD deficient group. Serum 25(OH)D level was positively correlated with HRRIs (P < 0.001), PNN50, RMSSD, SDANN, and HFnu; negatively correlated with LFnu and LF/HF (P < 0.05). Also, multivariate linear regression analysis showed that serum 25(OH)D level was significantly associated with HRRIs and HRV parameters (P < 0.001). Conclusion Our study results suggest that cardiac autonomic functions are impaired in patients with VitD deficiency despite the absence of overt cardiac involvement and symptoms. Further studies are needed to elucidate the prognostic significance and clinical implications of impaired autonomic functions in patients with VitD deficiency.

Early morning blood pressure surge (MBPS) is a risk factor for cardiovascular events (CVEs), but the relationship with uric acid is not well understood. The authors aimed to determine the association between MBPS and increased uric acid and the effect of elevated MBPS and uric acid combination on CVEs. A total of 921 patients underwent 24-hour ambulatory blood pressure monitoring and were followed for a median of 40 months. During this period, 103 (11.2%) CVEs occurred. There was a significant relationship between increasing quartiles of serum uric acid level and increasing values of MBPS (P

Background Fragmented QRS complex (fQRS) is associated with worse outcomes in several cardiovascular conditions. However, alterations in fQRS in patients with ST elevation myocardial infarction (STEMI) who underwent primary percutaneous coronary intervention (PCI) and association of fQRS with myocardial blush grade (MBG) has not been investigated until now. In this study, we aimed to investigate the association of MBG after primary PCI with evolution of fQRS. Methods Our study consisted of 401 consecutive patients with STEMI who underwent primary PCI. Patients were categorized into two subgroups according to persistence or new-onset of fQRS (Group 1) and absence or resolution of fQRS (Group 2) at 48 hours after primary PCI. The evolution of fQRS on pre- and post-PCI ECG and their relation with myocardial reperfusion parameters were investigated. Results Patients in group 1 showed older age, higher rate of smoking, lower HDL-cholesterol, lower LVEF, higher angina-to-door time, higher TIMI frame count, and high rate of patients with MBG

Background Fragmented QRS complex (fQRS) is associated with cardiovascular outcomes in various patient populations. Although there were clinical studies investigating the association of fQRS with arrhythmic events in patients with systolic heart failure, the results were conflicting regarding the association of implantable cardioverter defibrillator (ICD) shocks and fQRS. In this study, we aimed to evaluate the association between the presence and extent of fQRS with appropriate ICD shocks and/or all-cause mortality. Methods A total of 215 patients (age: 58.2 ± 11.6 years, 72.5 % male) with the diagnosis of left ventricular systolic heart failure in whom ICD had been implanted for primary prophylaxis were enrolled. Standard ECG evaluation revealed fQRS complex in 123 patients (57.2 %). The phenomenon of fQRS was defined as deflections at the beginning of the QRS complex, on top of the R wave, or in the nadir of the S wave similar to the definition in CAD. Results At mean 23.5 ± 12.1 months follow-up, all-cause mortality was observed in 45 (20.9 %) patients and 111 (51.6 %) patients experienced appropriate ICD shocks. Median number of ECG leads with fQRS were higher in patients with appropriate ICD shocks (3 [2–6] vs 1 [0–2], P < 0.001, respectively). The presence of fQRS (HR: 6.64, 95 % CI: 3.54–12.4, P < 0.001) and the number of leads with fQRS (HR: 1.35, 95% CI: 1.22–1.67) were found as independent predictors of appropriate ICD shocks. Additionally, there was a negative correlation between left ventricular ejection fraction and the number of leads with fQRS (r = −0.434, P < 0.001). Rates of all-cause mortality did not differ between the fQRS(+) (29 [24 % ]) and fQRS(−) (16 [17 % ]) groups (P = 0.27). Conclusion Our findings suggest that the presence and extent of fQRS complex on standard 12-lead ECG predicts appropriate ICD shocks in patients with left ventricular systolic heart failure who underwent ICD implantation for primary prophylaxis.

Objectives The association of QRS duration (QRSd) with ventricular dyssynchrony is well-known in systolic heart failure (HF). However, there are no data regarding the relationship between QRSd and atrial dyssynchrony in patients with HF. We aimed to investigate the association of QRSd with intra-atrial and inter-atrial dyssynchrony in patients with systolic HF by using color tissue Doppler imaging (TDI). Methods The study consisted of 70 systolic HF patients and 35 healthy controls. According to QRSd, HF patients were categorized into 2 subgroups as narrow QRS (n = 35) and wide QRS (n = 35) groups. Time intervals between the onset of P-wave and the onset of A-wave on color TDI from the right atrium (P-RA), inter-atrial septum (P-IAS) and left atrium (P-LA) were measured. Atrial dyssynchrony was defined as differences between P-RA and P-IAS (RA dyssynchrony), between P-LA and P-IAS (LA dyssynchrony) and between P-RA and P-LA (inter-atrial dyssynchrony). Results In patients with either HF groups, we observed significant impairment in intra-atrial and inter-atrial synchronicity compared with the controls (P

Objectives Left ventricular (LV) synchronous contraction is impaired in patients with hypertension (HT). The deleterious effects of HT on cardiovascular system are more evident in patients with nondipper HT than dippers. In this study, we aimed to investigate the effect of nondipping HT on LV systolic synchronicity compared with dippers and controls. Methods One hundred patients with newly diagnosed essential HT and 50 normotensive subjects were enrolled in this study. The hypertensive patients were assigned 2 groups comprising 55 dippers and 45 nondippers. Each subject underwent a comprehensive transthoracic echocardiographic examination. The evaluation of systolic dyssynchrony was performed by tissue synchronization imaging, and the time to regional peak systolic tissue velocity (Ts) in LV was measured on the basis of 12 segmental models. The standard deviation (SD) of the 12 LV segments (Ts-SD-12) and maximal difference in Ts between any two of the 12 LV segments (Ts-12) were calculated. Results Compared with the control group, the synchronicity indexes were significantly prolonged in the hypertensive patients. Furthermore, Ts-SD-12 and Ts-12 values were found to be significantly impaired in patients with nondipper HT, compared with dippers: Ts-SD-12 (38.1 ± 18.7 vs. 31.8 ± 15.4, P ≤ 0.001); Ts-12 (123.0 ± 50.6 vs. 98.4 ± 42.3, P ≤ 0.001). Stepwise multivariate logistic regression analysis revealed a significant negative association between LV dyssynchrony indices and percentage decline in BP level from day to night. Conclusion Synchronous systolic contraction of LV is found to be significantly impaired in patients with nondipping circadian pattern of HT compared with dippers and the controls.

Uric acid (UA) is independently associated with the emergence of hypertension. Nocturnal nondipping pattern of hypertension is associated with a greater risk of cardiovascular, renal, and cerebrovascular complications than dippers. The aim of the present study was to evaluate the relationship between the circadian blood pressure rhythm and UA level in patients with newly diagnosed essential hypertension. The study included 112 essential hypertensive patients and 50 healthy controls. The hypertensive patients were divided into two groups according to the results of 24-hour ambulatory blood pressure monitoring, including 60 dippers (35 men, 25 women; mean age, 52.6±15.8 years) and 52 nondippers (29 men, 23 women; mean age, 55.9±13.2 years). Nondippers had significantly higher serum UA levels than the dippers and controls (5.8±0.8, 5.1±0.9 and 4.2±0.9 mg/dL, respectively; P