The Relationship between Frontal QRS-T Angle and Vitamin D Deficiency.

Background and Objectives: A deficiency in serum 25-hydroxyvitamin D levels is associated with a number of cardiovascular situations, such as high blood pressure, heart failure, atherosclerotic heart disease, and peripheral artery disease. The frontal QRS-T angle has recently been proposed as a marker of ventricular repolarization. A wider frontal QRS-T angle has been positively correlated with adverse cardiac events. The objective of our study was to examine the association between serum 25-hydroxyvitamin D level and the frontal QRS-T angle. Materials and Methods: A total of 173 consecutive patients aged 18-60 years undergoing routine cardiology check-up evaluation, and not receiving concurrent vitamin D treatment were included in the study. Patients were classified in three groups, depending on their vitamin D levels, and categorized as follows: Group 1-deficient (<20 ng/mL), Group 2-insufficient (20-29 ng/mL), or Group 3-optimal (≥30 ng/mL). The frontal QRS-T angle was determined using the automated reports generated by the electrocardiography machine. Results: The average age of participants was 45.8 (±12.2) years, and 55.5% of participants were female (p < 0.001). Individuals with low vitamin D concentrations exhibited a wider frontal QRS-T angle. It was determined that vitamin D level is an independent predictive factor for the frontal QRS-T angle. Conclusions: As the levels of 25-hydroxyvitamin D decrease, repolarization time assessed by frontal QRS-T angle is widened. Our findings indicate that lower concentrations of vitamin D may increase the susceptibility to ventricular arrhythmia.

Acute sleep deprivation: impairment of biventricular function assesed by speckle tracking echocardiography in healthy subjects.

OBJECTIVES: Sleep deprivation (SD) has been found to be associated with an increased incidence of adverse cardiovascular disease (CVD) events. The aim of this study was to investigate whether or not acute SD has a pathological effect on the geometry and the systolic and diastolic functions of the right and left heart chambers by standard transthoracic echocardiography (TTE) and speckle tracking echocardiography (STE) in healthy individuals with acute SD. METHODS: Nurses with no history of acute or chronic diseases underwent TTE and STE after working a night shift, a sleepless period of 24 h and 7 days of normal sleep after the night shift. Measurements of TTE and STE taken in the rested state were compared with those taken after 24 h of sleep deprivation. RESULTS: The study included 52 nurses (38 women, 73%). The mean age of the study population was 27.9 ± 7.4 years and mean BMI was 24.1 ± 4.8. Left atrial reservoir (51.5 ± 13.5 vs. 45.4 ± 10; p = 0.004), conduit (- 37.3 ± 11.3 vs. - 33.6 ± 7.9; p = 0.01), left ventricular global longitudinal strain (LVGLS, - 22.6 ± 2.4 vs. - 21.3 ± 2.4; p = 0.001), right ventricular global longitudinal strain (RVGLS, - 25.3 ± 3.7 vs. - 23.5 ± 3.9; p = 0.005) and right ventricular free wall longitudinal strain (RVFWSL, - 29.1 ± 4.2 vs. - 27 ± 4.5; p = 0.001) were impaired significantly after SD. CONCLUSION: This study is the first to investigate the negative effects of acute sleep deprivation on LV and RV strain in healthy adults using echocardiography. The findings showed that acute sleep deprivation leads to deterioration in function of both ventricles and left atrium. Speckle tracking echocardiography demonstrated subclinical diminished heart function.

Obstructive sleep apnea is associated with depressed myocardial mechanoenergetics.

PURPOSE: To evaluate the association between the myocardial mechanoenergetic efficiency index (MEEi) and the Apnea-Hypopnea Index (AHI) in the initial phase of obstructive sleep apnea (OSA) diagnosis. METHODS: In this cohort study, we included a total of 382 eligible participants without cardiovascular disease in a tertiary outpatient clinic between January 2013 and January 2015. We recorded demographic, clinical, polysomnographic and echocardiographic variables of the patients. In addition, myocardial mechanoenergetic efficiency (MEE) and MEEi were calculated by an echocardiography-derived validated measurement. RESULTS: The mean (±SD) age of the participants was 48.47 ± 12.13, and male/female ratio was 287/95. Comparing with non-OSA, MEEi was significantly lower in OSA patients at all stages (0.35 ± 0.08 vs. 0.42 ± 0.05; p < .001). MEEi was negatively correlated with hypertension (r = -0.518, p < .001), body mass index (r = -0.382, p < .001), AHI (r = -0.656, p < .001), total apne (r = -0.525, p < .001), hypopnea (r = -0.415, p < .001), systolic pulmonary pressure (r = -0.318, p < .001), relative wall thickness (RWT; r = -0.415, p < .001), and positive correlated with left ventricular ejection fraction (r = 0.586, p < .001). According to multiple linear regression analysis AHI (ß = -0.625, p < .001), total apnea (ß = -0.402, p = .001), hypopnea (ß = -0.395, p = .001), LV ejection fraction (ß = 0.478, p < .001) and RWT (ß = -0.279, p < .001) have an independent relationship with MEEi. CONCLUSIONS: MEEi was lower in OSA patients. A reduced MEEi may reflect a disturbance in energy use of the myocardium. Consequently, our results may provide insight into the mechanisms leading to structural cardiac diseases in OSA patients.