Evaluation of high altitude training camps with heart rate recovery and heart rate variability analysis: beneficial effect in elite swimmers.

BACKGROUND: The available evidence on the impact of altitude training on sports performance is inconclusive. Heart rate variability (HRV) and heart rate recovery (HRR) are among the most frequently used parameters in athletic performance analysis and monitoring. Our study aims to investigate the effect of high altitude training on HRR and HRV, which are reliable predictors of athletic performance. METHODS: Elite national swimmers were included in the study. Time domain and frequency domain analyzes were performed with the Polar Verity Sense device and Kubios HRV software. HRR were measured at one-minute intervals for the first 15 minutes after peak heart rate, and then recorded at the 20th, 25th and 30th minutes. RESULTS: A significant difference is observed from the beginning to the 11th minute. The P value at 1, 3, 5, 7 and 11 minutes is 0.001, 0.023, 0.032, 0.019 and 0.020, respectively. Similarly, a significant change was observed in delta HRR. Among the HRV parameters, RMSSD, SDNN, Poincaré SD1 and PNS are statistically significant. P values are 0.004, 0.018, 0.024 and 0.013 respectively. CONCLUSIONS: High altitude training program has a positive effect on HRV and CRV in elite swimmers. This condition is associated with increased cardiac parasympathetic activity. Time domain analyses have proven to be more beneficial for HRV. HRR and HRV are effective, reliable and inexpensive methods of performance monitoring of elite athletes.

The Relationship of Systolic Pulmonary Artery Pressure with Perioperative Mortality and Morbidity in Patients Undergoing Non-Cardiac Surgery: A Single-Center Experience.

OBJECTIVE: Pulmonary hypertension (PH) is associated with adverse perioperative events in patients undergoing non-cardiac surgery. In this study, we aimed to investigate the relationship between systolic pulmonary artery pressure (sPAP), evaluated by transthoracic echocardiography (TTE) before surgery, and perioperative mortality and morbidity in patients who underwent non-cardiac surgery in our center. METHODS: Of the 3425 retrospectively screened patients who underwent non-cardiac surgery, 3049 patients whose estimated sPAP values were previously determined by TTE were included in the study. Patients were classified into 3 groups according to their estimated sPAP levels. sPAP <35 mmHg formed group 1, 35-39 mmHg group 2, and ≥ 40 mmHg group 3. All demographic and perioperative data obtained from the database of our institute were compared in three groups. RESULTS: Of the 3049 patients enrolled in the study, 2406 (78.9%) were in group 1, 259 (8.5%) in group 2, and 384 (12.6%) in group 3. Thirty-day all-cause mortality was observed in 82 (2.7%) patients, cardiac mortality occurred in 9 patients (0.3%). In the group with sPAP ≥40 mmHg, cardiac mortality was 0.5% and all-cause mortality was 7.3%. Thirty-day all-cause mortality, acute pulmonary edema, and acute renal failure were significantly higher in group 3 than in the other groups. Cardiac mortality did not differ significantly between the groups. Age, sPAP value, and chronic obstructive pulmonary disease history were revealed as independent predictors of all-cause mortality in multivariate logistic regression analysis. CONCLUSION: In conclusion, increased sPAP is associated with adverse postoperative outcomes. The evaluation of sPAP with TTE before non-cardiac surgery in patients whose clinical features and examination findings suggest PH may contribute to preoperative risk assessment.

Evaluation of pulmonary arterial stiffness and comparison with right ventricular functions in patients with cirrhosis preparing for liver transplantation.

OBJECTIVE: Pulmonary complications are common in patients with liver cirrhosis. Devolopment of pulmonary hypertension (PH) is associated with a poor prognosis in these patients. Pulmonary arterial stiffness (PAS) is considered an early sign of pulmonary vascular remodeling. The aim of this study is to investigate PAS and compare it with right ventricular (RV) functions in patients with cirrhosis who are scheduled for liver transplantation. METHODS: The study included 52 cirrhosis patients (mean age 51.01 ± 12.18 years, male gender 76.9%) who were prepared for liver transplantation and 59 age and sex matched (mean age 51.28 ± 13.63 years, male gender 62.7%) healthy individuals. Patients with left ventricular ejection fraction (LVEF) less than 55%, ischemic heart disease, more than mild valvular heart disease, chronic pulmonary disease, congenital heart disease, rheumatic disease, moderate to high echocardiographic PH probability, rhythm or conduction disorders on electrocardiography were excluded from the study. In addition to conventional echocardiographic parameters, PAS value, pulmonary vascular resistance (PVR) and RV ejection efficiency was calculated by the related formulas with transthoracic echocardiography (TTE). RESULTS: Demographic characteristics and cardiovascular risk factors of the groups were similar. PAS, PVR, and sPAP values were found to be significantly higher in the patient group (20.52 ± 6.52 and 13.73 ± 2.05; 1.43 ± 0.15 and 1.27 ± 0.14; 27.69 ± 3.91 and 23.37 ± 3.81 p < 0.001, respectively). RV FAC and RV Ee were significantly lower and RV MPI was significantly higher in the patient group (45.31 ± 3.85 and 49.66 ± 3.62, p < 0.001; 1.69 ± 0.35 and 1.85 ± 0.23, p = 0.005; 0.39 ± 0.07 and 0.33 ± 0.09, p = 0.001, respectively). PAS was significantly correlated with RV FAC and MPI (r = -0.423, p < 0.001; r = 0.301, p = 0.001, respectively). CONCLUSIONS: Increased PAS in cirrhosis patients may be associated with early pulmonary vascular involvement. Evaluation of RV functions is important to determine the prognosis in these patients. FAC, MPI, and RV Ee measurements instead of TAPSE or RV S' may be more useful in demonstrating subclinical dysfunction. The correlation of PAS with RV FAC and MPI may indicate that RV subclinical dysfunction is associated with early pulmonary vascular remodeling in patients with liver cirrhosis.

Evaluation of serum platelet-derived growth factor receptor-ß and brain-derived neurotrophic factor levels in microvascular angina.

OBJECTIVE: Microvascular angina (MVA) is a coronary microcirculation disease. Research on microcirculatory dysfunction has revealed several biomarkers involved in the etiopathogenesis of MVA. Platelet-derived growth factor receptor ß (PDGFR-ß) and brain-derived neurotrophic factor (BDNF) are 2 biomarkers associated with microcirculation, particularly pericytes function. The aim of this study was to investigate the role of PDGFR-ß and BDNF in MVA. METHODS: Ninety-one patients (median age, 56 y; age range, 40-79 y; 36 men) with MVA and 61 control group subjects (median age, 52 y; age range, 38-76 y; 29 men) were included in the study. Serum concentrations of PDGFR-ß and BDNF were measured with commercially available enzyme-linked immunosorbent assay kits. RESULTS: PDGFR-ß [2.82 ng/ml; interquartile range (IQR), 0.57-7.79 ng/ml vs. 2.27 ng/ml; IQR, 0.41-7.16 ng/ml; p<0.0005] and BDNF (2.41 ng/ml; IQR, 0.97-7.97 ng/ml vs. 1.92 ng/ml; IQR, 1.07-6.67 ng/ml; p=0.023) concentrations were significantly higher in patients with MVA compared with the controls. PDGFR-ß correlated positively with age (r=0.26, p=0.001), low-density lipoprotein (r=0.18; p=0.02), and BDNF (r=0.47; p<0.001), and BDNF showed a significant positive correlation with age (r=0.20; p=0.01). In binary logistic regression analysis, high-sensitivity C-reactive protein, uric acid, and PDGFR-ß values were found to be independent predictors of MVA. CONCLUSION: MVA is associated with higher PDGFR-ß and BDNF levels. This association may indicate an abnormality in microvascular function. Future studies are required to determine the role of these biomarkers in the pathogenesis of MVA.

Evaluation of Serum Urocortin 2 Levels in Patients with Hypertension.

INTRODUCTION: Urocortin 2 (UCN2), is an endogenous stress-related peptide belonging to the corticotropin-releasing factor (CRF) family, has a major role in the pathogenesis of congestive heart failure, ischemic heart disease, and hypertension. AIM: To investigate the role of UCN2 levels in patients with hypertension (HTN). METHODS: Serum UCN2 levels measured by ELISA were compared between patients with HTN (n = 86) and nonHTN (n = 53). RESULTS: Eighty-six patients with HTN [median age 66 (45-76); 38 men] and 53 patients with non-HTN [median age 62 (40-80); 39 men] were included into this study. Serum UCN2 (5.17 ng/ml; IQR, 1.26-11.68 ng/ml vs 0.79 ng/ml; IQR, 0.07-4.10 ng/ml, p < 0.0005) levels were found significantly elevated in patients with HTN compared to nonHTN control group. Concentrations of serum UCN2 were positively correlated with left ventricle mass index to body surface area (LV mass index to BSA, r = 0.20, p = 0.03), LV mass index to height2.7 (r = 0.28, p = 0.002) and body mass index (r = 0.24, p = 0.008). Additionally, logistic regression analysis was performed to UCN2, uric acid, creatinine, glomerular filtration rate, age, body mass index, coronary artery disease and diabetes mellitus which are the potential confounders of hypertension. According to logistic regression analysis serum UCN2 values were found out as an independent predictor of HTN. CONCLUSION: UCN2 levels, correlated with LV mass index were increased in HTN patients compared to nonHTN patients. These data provide evidence that there could be a relationship between high concentrations of UCN2 and HTN. UCN2 may appear as a promising choice of HTN treatment in the future.

The Effect of Urine pH and Urinary Uric Acid Levels on the Development of Contrast Nephropathy.

BACKGROUND: Hyperuricemia may cause acute kidney injury by activating inflammatory, pro-oxidative and vasoconstrictive pathways. In addition, radiocontrast causes an acute uricosuria, potentially leading to crystal formation. We therefore aimed to investigate the effect of urine acidity and urine uric acid level on the development of contrast-induced nephropathy (CIN) in patients undergoing elective coronary angiography. METHODS: We enrolled 175 patients who underwent elective coronary angiography. CIN was defined as a >25% increase in the serum creatinine levels relative to basal values 48-72 h after contrast use. Prior to coronary angiography and 48-72 h later, serum uric acid, urea, creatinine, bicarbonate levels, and spot uric acid to creatinine ratio (UACR) were measured. RESULTS: Of the 175 subjects included, 29 (16.6%) developed CIN. Those who developed CIN had a higher prevalence of diabetes, higher UACR (0.60 vs. 0.44, p = 0.014), higher contrast volume, and lower serum sodium level. With univariate analysis of a logistic regression model, the risk of CIN was found to be associated with diabetes (p = 0.0016, OR = 3.8 [95% CI: 1.7-8.7]), urine UACR (p = 0.0027, OR = 9.6 [95% CI: 2.2-42.2]), serum sodium (p = 0.0079, OR = 0.8 [95% CI: 0.77-0.96]), and contrast volume (p = 0.0385, OR = 1.8 [95% CI: 1.03-3.09]). In a multiple logistic regression model with stepwise method of selection, diabetes (p = 0.0120, OR = 3.2 [95% CI: 1.3-8.1]) and UACR (p = 0.0163, OR = 6.9 [95% CI: 1.4-33.4]) were the 2 risk factors finally identified. CONCLUSIONS: We have demonstrated that higher urine UACR is associated with the development of CIN in patients undergoing elective coronary angiography.

The quality of ECG data acquisition, and diagnostic performance of a novel adhesive patch for ambulatory cardiac rhythm monitoring in arrhythmia detection.

BACKGROUND: Short and long ambulatory electrocardiographic monitoring with different systems is a widely used method to detect cardiac arrhythmias. In this study, we aimed to evaluate the effectiveness of a novel monitoring device on cardiac arrhythmia detection. METHODS: We used two different protocols to evaluate device performance. For the first one, 36 healthy subjects were enrolled. The standard 12­lead, 24-h Holter monitoring and the novel single lead electrocardiogram (ECG) Patch Monitor (EPM) device (BeyondCare®, Rooti Labs Ltd., Taipei, Taiwan) were simultaneously applied to all subjects for 24 h. The quality of ECG data acquisition of novel system was compared to that of standard Holter. The second phase included 73 patients that were referred from our outpatient arrhythmia clinic for evaluation of their symptoms relevant to the cardiac arrhythmias. Advanced algorithms, statistical methods (cross-correlation method, Pearson's correlation coefficient, Bland-Altman plots) were used to process and verify the acquired data. RESULTS: The overall average beat per minute correlation between BeyondCare® and standard 12­lead Holter was found 98% in 33 healthy subjects. The mean percentage of invalid measurements in BeyondCare® was 1.6% while the Holter's was 1.7%. In the second protocol of the study, prospective data from 67 patients who were referred for evaluation of their symptoms relevant to cardiac arrhythmias, showed that the mean BeyondCare® wear time was 4.7 ±â€¯0.5 days out of five total days per protocol. The mean analyzable wear time was 93.6%. The water-resistant design enabled 73.5% of the participants to take a shower. 7.3% of participants had minor skin irritations related to the electrodes. Among the patients with detected arrhythmia (40.2% of all patients), 29.6% had their first arrhythmia after the initial two days period. A clinically significant pause was detected in one patient, ventricular tachycardia was detected in four patients, and supraventricular tachycardia was detected in 15 patients. Paroxysmal atrial fibrillation was identified in seven patients. Three of them had their first episodes after the second day of monitoring. CONCLUSION: BeyondCare® Patch was well-tolerated and allowed prolonged time periods for continuous ECG monitoring, may result in an improvement in clinical accuracy and detection of arrhythmias by cloud-based artificial intelligence operating system.

Evaluation of serum sST2 and sCD40L values in patients with microvascular angina.

OBJECTIVES: Coronary microvascular dysfunction plays a major role in the pathogenesis of microvascular angina (MVA). Along with endothelial dysfunction, microvascular atherosclerosis and inflammation seem to contribute to the development of coronary microvascular dysfunction. Serum soluble ST2 (sST2) and serum soluble CD40 ligand (sCD40L) are two biomarkers associated with inflammation and atherosclerosis. The aim of this study was to investigate the role of these biomarkers in the pathogenesis of MVA and determine their possible association with coronary microvascular dysfunction. METHODS: A total of 152 patients were included in the study. Ninety-one patients with MVA {median age 56 years (40-79), of which 55 are women} and sixty-one controls {median age 52 (38-76), of which 29 are women} were included in the study. Serum concentration of sST2 and sCD40L were measured with a commercially available ELISA kit. RESULTS: Serum sST2 (median 13.6 ng/ml; interquartile range (IQR), 3.5-63.8 ng/ml vs median 10.6 ng/ml; IQR, 2.9-34.2 ng/ml, p < 0.0005) and sCD40L (median 5.3 ng/ml; IQR, 0.5-20.6 ng/ml vs median 2.2 ng/ml; IQR, 0.7-10.8 ng/ml, p < 0.0005) were significantly higher in patients with MVA compared to controls. Analysis of the associations between these biomarkers and potential contributors of MVA revealed that serum sST2 showed a positive correlation with LDL-cholesterol (r = 0.19, p = 0.016) and serum sCD40L concentrations correlated positively with hs-CRP (r = 0.22, p = 0.005). In logistic regression analysis, sCD40L and hs-CRP but not sST2 were found to be significantly associated with MVA. CONCLUSION: Higher serum concentrations of sST2 and sCD40L in MVA patients may be associated with inflammatory activation and coronary microvascular dysfunction. Larger studies are required for understanding their role in the pathogenesis of inflammatory and possibly fibrotic process in MVA patients.

Unilateral leg edema: Is it always vascular?

Unilateral lower extremity edema below the knee commonly results from deep venous thrombosis, venous insufficiency, or lymphedema. The patient history, a physical examination, and lower extremity venous duplex ultrasound often reveal the underlying etiology, which is frequently of vascular origin. Presently described is the case of a 23-year-old patient who underwent a diagnostic workup for unilateral leg swelling and was found to have a relatively uncommon cause of edema: lipedema. Lipedema is a disease characterized by subcutaneous adipose tissue deposition, and although diagnosed very rarely in general cardiology outpatient clinics, it has been demonstrated to be a cause of lower extremity edema in approximately one-fifth of cases in specialized clinics.

Acute effects of salt on blood pressure are mediated by serum osmolality.

It is classically thought that it is the amount of salt that is critical for driving acute blood pressure responses. However, recent studies suggest that blood pressure responses, at least acutely, may relate to changes in serum osmolality. Here, we test the hypothesis that acute blood pressure responses to salt can be altered by concomitant water loading. Ten healthy patients free of any disease and medication underwent 4 interventions each a week apart in which they took 300 mL of lentil soup with no salt (visit 1), lentil soup with 3 g salt (visit 2), or lentil soup with 3 g salt and 500 mL water (visit 3) or 750 mL water (visit 4). At each visit, hourly blood measurements and blood pressure measurements (baseline, 1st, 2nd, 3rd, and 4th hour) were performed and plasma osmolarity, sodium and copeptin levels were measured. Patients receiving the 3 g salt showed a 6 mOsm/L change in osmolality with a 2.5 mmol/L change in plasma sodium and 10 mm Hg rise in systolic blood pressure at 2 hours. When the same patients drank salty soup with water, the changes in plasma osmolarity, plasma sodium, and blood pressure were prevented. The ability to raise blood pressure acutely with salt appears dependent on changes in plasma osmolality rather than the amount of salt. Our findings suggest that concurrent intake of water must be considered when evaluating the role of salt in blood pressure.

The impact of exercise on physical function, cardiovascular outcomes and quality of life in chronic kidney disease patients: a systematic review.

The prevalence of chronic kidney disease (CKD) and end-stage renal disease (ESRD) is increasing steadily. CKD does not only relate to morbidity and mortality but also has impact on quality of life, depression and malnutrition. Such patients often have significantly decreased physical activity. Recent evidence suggests that low physical activity is associated with morbidity, mortality, muscle atrophy, quality of life impairment, cardiovascular outcomes and depression. Based on this, it is now recommended to regularly improve the physical activity of these patients. Furthermore, studies have shown the beneficial effects of various exercise programs with respect to outcomes such as low physical activity muscle atrophy, quality of life, cardiovascular outcomes and depression. Despite these encouraging findings, the subject is still under debate, with various aspects still unknown. In this review, we tried to critically summarize the existing studies, to explore mechanisms and describe future perspectives regarding physical activity in CKD/ESRD patients.

Iron in kidney and heart failure: from theory to practice.

There is evidence that serum iron levels, regardless of the presence of anemia, directly impact outcomes in congestive heart failure (CHF) including quality of life, hospitalization rate and overall survival. Despite modern medical treatments, the prognosis of CHF remains grim. Ironically, simple iron replenishment may serve as a powerful tool in the armamentarium. This review will start from fundamental concepts of iron in oxygen delivery and analyze evidence-based outcomes in CHF iron-directed therapeutic trials. Imaging rationale that dovetails with this pathophysiology will also be detailed in a clinician-directed fashion.

Cardiovascular Effects of Continuous Positive Airway Pressure Treatment in Patients With Obstructive Sleep Apnea: A Meta-Analysis.

Continuous positive airway pressure (CPAP) is the first-line treatment of obstructive sleep apnea (OSA). Obstructive sleep apnea is a predictor of cardiovascular (CV) events. In this meta-analysis, we evaluated the effect of CPAP on left ventricular ejection fraction (LVEF), CV events, CV mortality, and all-cause mortality in patients with OSA. Nine articles (n = 9610 patients) were analyzed. Four different meta-analyses were performed: evaluation of LVEF, assessment of all-cause mortality, CV mortality, and CV events. Continuous positive airway pressure treatment was associated with a significant increase in LVEF (mean difference: 2.1%, 95% confidence interval [CI]: 0.8%-3.4%). There was a nonsignificant reduction in all-cause mortality (hazard ratio [HR]: 0.92, 95% CI: 0.73-1.15) but a significant reduction of 66% in the risk of CV mortality associated with the CPAP treatment (HR: 0.34, 95% CI: 0.17-0.68, P = .002). There was a nonsignificant reduction in the risk of CV events in the CPAP-treated patients (HR: 0.84, 95% CI: 0.60-1.18, P = .31). Our meta-analyses showed that CPAP treatment improves LVEF and could have a beneficial effect on CV mortality.

Evaluation of Resting Cardiac Power Output as a Prognostic Factor in Patients with Advanced Heart Failure.

If the heart is represented by a hydraulic pump, cardiac power represents the hydraulic function of the heart. Cardiac pump function is frequently determined through left ventricular ejection fraction using imaging. This study aims to validate resting cardiac power output (CPO) as a predictive biomarker in patients with advanced heart failure (HF). One hundred and seventy-two patients with HF severe enough to warrant cardiac transplantation were retrospectively reviewed at a single tertiary care institution between September 2010 and July 2013. Patients were initially evaluated with simultaneous right-sided and left-sided cardiac catheter-based hemodynamic measurements, followed by longitudinal follow-up (median of 52 months) for adverse events (cardiac mortality, cardiac transplantation, or ventricular assist device placement). Median resting CPO was 0.54 W (long rank chi-square = 33.6; p < 0.0001). Decreased resting CPO (<0.54 W) predicted increased risk for adverse outcomes. Fifty cardiac deaths, 10 cardiac transplants, and 12 ventricular assist device placements were documented. The prognostic relevance of resting CPO remained significant after adjustment for age, gender, left ventricular ejection fraction, mean arterial pressure, pulmonary vascular resistance, right atrial pressure, and estimated glomerular filtration rate (HR, 3.53; 95% confidence interval, 1.66 to 6.77; p = 0.0007). In conclusion, lower resting CPO supplies independent prediction of adverse outcomes. Thus, it could be effectively used for risk stratification in patients with advanced HF.

Serum Uric Acid and Risk for Acute Kidney Injury Following Contrast.

Contrast-induced acute kidney injury (CI-AKI) is a common cause of hospital-acquired acute kidney injury (AKI). We evaluated the evidence that uric acid (UA) plays a pathogenic role in CI-AKI. Ten studies were eligible for inclusion for meta-analysis. Hyperuricemia predicted risk for cases with AKI in prospective cohort studies. Higher levels of serum UA (SUA), as defined by the authors, were associated with a 2-fold increased risk to develop AKI (pooled odds ratio 2.03; 95% confidence interval [CI] 1.48-2.78). Significant heterogeneity was found in cohort studies ( P = .001, I2 = 85.7%). In 2 clinical trials, lowering of SUA with saline hydration was significantly associated with reduced risk for AKI compared with saline hydration alone or saline hydration with N-acetyl cysteine. An analysis of 2 randomized controlled trials found that allopurinol with saline hydration had a significant protective effect on renal function (assessed by serum creatinine values) compared with hydration alone (mean difference: -0.52 mg/dL; 95% CI: -0.81 to -0.22). Hyperuricemia independently predicts CI-AKI. Two clinical trials suggest lowering SUA may prevent CI-AKI. The mechanism by which UA induces CI-AKI is likely related to acute uricosuria.

Gut hormones and gut microbiota: implications for kidney function and hypertension.

Increased blood pressure (BP) and chronic kidney disease are two leading risk factors for cardiovascular disease. Increased sodium intake is one of the most important risk factors for development of hypertension. Recent data have shown that gut influences kidney function and BP by variety of mechanisms. Various hormones and peptides secreted from gut such as gastrin, glucocorticoids, Glucagon-like peptide-1 impact on kidney function and BP especially influencing sodium absorption from gut. These findings stimulate scientist to find new therapeutic options such as tenapanor for treatment of hypertension by blocking sodium absorption from gut. The gastrointestinal tract is also occupied by a huge community of microbes (microbiome) that under normal condition has a symbiotic relationship with the host. Alterations in the structure and function of the gut microbiota have been shown to play a key role in the pathogenesis and complications of numerous diseases including hypertension. Based on these data, in this review, we provide a summary of the available data on the role of gut and gut microbiota in regulation of BP and kidney function.

Sclerostin, cardiovascular disease and mortality: a systematic review and meta-analysis.

BACKGROUND AND AIM: Chronic kidney disease mineral and bone disorder (CKD-MBD) is associated with increased morbidity and mortality. Several cross-sectional studies investigated the association of serum sclerostin levels with mortality and vascular calcification. We aimed to investigate the effect of sclerostin on cardiovascular events (CVE), all-cause/cardiovascular mortality and vascular calcification in patients with CKD through systematic review and meta-analysis. The primary outcome was the association between sclerostin level and development of fatal and nonfatal CVE and all-cause mortality. MATERIALS AND METHODS: A literature search was performed using electronic databases Medline Ovid/Medline, PubMed/Medline, EMBASE and ISI Web of Science. Extracted hazard ratios from the included study protocols were pooled separately using the random-effects model (DerSimonian Laird). The equivalent z test was performed for each pooled HR, and if p < 0.05 it was considered statistically significant. RESULTS: In our final analysis, we included nine observational prospective studies involving 1788 patients (minimum 91 and maximum 673 patients). For the all-cause mortality, three studies with 503 patients showed that sclerostin levels were not significantly associated with all-cause mortality risk (HR = 1.01, 95 % CI 0.99-1.03, p = 0.16; heterogeneity χ 2 = 12.24, I 2 = 84 %, p = 0.002). For cardiovascular mortality, two studies with 412 patients showed that sclerostin levels were not significantly associated with cardiovascular mortality risk (HR = 1.03, 95 % CI 0.99-1.07, p = 0.17; heterogeneity χ 2 = 10.74, I 2 = 91 %, p = 0.001). CONCLUSION: Although the studies are mostly small in size, heterogeneous and have conflicting results, we have demonstrated that serum sclerostin levels were not associated with all-cause and cardiovascular mortality.

Hypertension as an autoimmune and inflammatory disease.

Hypertension that is considered idiopathic is called essential hypertension and accordingly has no clear culprit for its cause. However, basic research and clinical studies in recent years have expanded our understanding of the mechanisms underlying the development of essential hypertension. Of these, increased oxidative stress, both in the kidney and arterial wall, closely coupled with inflammatory infiltration now appear to have a prominent role. Discovery of regulatory and interleukin-17-producing T cells has enabled us to better understand the mechanism by which inflammation and autoimmunity, or autoinflammation, lead to the development of hypertension. Despite achieving considerable progress, the intricate interactions between oxidative stress, the immune system and the development of hypertension remain to be fully elucidated. In this review, we summarize recent developments in the pathophysiology of hypertension with a focus on the oxidant stress-autoimmunity-inflammation interaction.

Flow in the left anterior descending coronary artery in patients with migraine headache.

Migraine is a common neurovascular disorder characterized by attacks of severe headache, autonomic and neurologic symptoms. Migraine can affect many systems in the body, yet its effects on cardiovascular system are unclear. We hypothesized that migraine and coronary microvascular angina may be manifestations of a common systemic microvascular dysfunction and clinically associated. Forty patients with migraine and 35 healthy volunteers were included into the study. Using transthoracic Doppler echocardiography, coronary flow was visualized in the middle or distal part of the left anterior descending artery. Coronary diastolic peak flow velocities were measured with pulse wave Doppler at baseline and after dipyridamole infusion (0.56 mg/kg/4 min). Coronary flow reserve of <2 was considered normal. In addition, thorough 2-dimensional and Doppler echocardiographic examinations were also performed. Fifty-two women and 23 men were included. Coronary flow reserve was significantly lesser in the migraine group than in the control group (1.99 ± 0.3 vs 2.90 ± 0.5, p <0.05). In addition, mitral annular velocities were lower and the ratio of early mitral inflow velocity to early mitral annular velocity (E/E' lateral and E/E' septal) was higher in migraineurs than in the control group (p <0.05 for all), indicating diastolic function abnormalities in the migraine group. In conclusion, these findings suggest that there is an association between coronary microvascular dysfunction and migraine independently of the metabolic state of the patients. A common pathophysiologic pathway of impaired endothelial vasodilatation, vasomotor dysfunction, and increased systemic inflammatory factors may play a role in these 2 clinical conditions and could be the underlying cause of subclinical systolic and diastolic left ventricular dysfunction in migraineurs.