Galectin-3 as a Novel Biomarker for Predicting Clinical Outcomes in Hospitalized COVID-19 Patients.

BACKGROUND: Galectin-3 has been shown to play a key pathophysiological role in pulmonary associated inflammatory response and lung fibrosis in COVID-19 and is a mediator for viral adhesion. However, there is limited data about its potential role in severity and prognosis of COVID-19. This study aimed to investigate the predictive role of serum galectin-3 concentrations in the severe clinical outcomes of hospitalized COVID-19 patients: the severity of pneumonia, in-hospital mortality, and the need for intensive care unit (ICU) admission. METHODS: This single-center study included 68 patients with laboratory- and radiologically-confirmed COVID-19 admitted to our emergency department. The study population was divided into patients with primary clinical out-comes (n = 32) and those without (n = 36). The need for ICU admission and/or in-hospital mortality were the primary clinical endpoints. The study group was also classified based on pneumonia severity: severe or mild/moderate. Blood samples were collected within 48 hours of admission to estimate serum galectin-3 concentrations. RESULTS: Multivariate regression analysis showed that lower concentrations of galectin-3 and arterial oxygen saturation (SpO2) were independently associated with the primary clinical outcomes (OR = 0.951, p = 0.035; OR = 0.862, p = 0.017, respectively); increased concentrations of galectin-3 were an independent predictor of severe pneumonia (OR = 1.087, p = 0.016). In the receiver operating characteristics curve analysis, serum galectin-3 concentrations at hospital admission predicted pneumonia severity with 52.1% sensitivity and 90% specificity with a cutoff of 38.76 ng/mL. CONCLUSIONS: Circulating galectin-3 at hospital admission could be a useful biomarker for identifying COVID-19 patients at high risk for severe pneumonia.

Circulating Levels of MicroRNAs in Hypertrophic Cardiomyopathy: The Relationship With Left Ventricular Hypertrophy, Left Atrial Dilatation and Ventricular Depolarisation-Repolarisation Parameters.

BACKGROUND: MicroRNAs are small, endogenous, non-coding RNAs that regulate the expression of many genes. It has recently been shown that circulating microRNAs may be biomarkers of hypertrophy and fibrosis in patients with hypertrophic cardiomyopathy (HCM). OBJECTIVE: To determine whether circulating levels of microRNAs involved in HCM are associated with electrocardiographic and echocardiographic parameters. METHODS: This study enrolled 20 patients with familial HCM and 20 blood donors. Peripheral serum levels of miR-29a-3p, miR-199a-5p and miR-451a were assessed by quantitative real-time polymerase chain reaction and compared with levels in the control group. Whether circulating levels of miRNAs in HCM patients correlated with electrocardiographic and echocardiographic parameters was also assessed. RESULTS: Median circulating levels of miR-29a and miR-451a were significantly higher in HCM than the control group. Median miR-199a levels did not differ between groups. However, circulating levels of miR-199a negatively correlated with corrected QT duration (Bazett formula). Median miR-29a levels positively correlated with QRS duration. In addition, circulating levels of miR-29a correlated with maximal wall thickness, left ventricular mass index and left atrial volume index. CONCLUSIONS: The data suggested that serum levels of miR-29a and miR-451a were significantly increased in HCM patients. As the circulating level of miR-29a correlated with QRS duration, left ventricular hypertrophy and left atrial dilatation, the serum miR-199a level negatively correlated with corrected QT duration. These miRNAs may be seen as potential biomarkers for further research in HCM pathophysiology.

The relationship between T-wave peak-to-end interval and hemodynamic parameters in patients with pulmonary arterial hypertension.

BACKGROUND: T-wave peak-to-end interval (TPEI) is a measure of repolarization dispersion on surface electrocardiogram (ECG). TPEI has been reported as a prognostic parameter with heart disorders. In this study, we aimed to evaluate the relationship between echocardiogram-derived right heart parameters, right heart catheterization (RHC) measurements, and TPEI in patients with precapillary pulmonary arterial hypertension (PAH). METHODS: Thirty-eight patients (29 females and 9 males, mean age of 54.9 ± 10.9 years) who had undergone RHC for a preliminary diagnosis of pulmonary hypertension (PH) were included in the study. We performed transthoracic echocardiography (TTE), and resting 12-lead ECG was recorded before RHC. TPEI was measured from leads of V1-V6, DII, DIII, and aVF, and these values are averaged to obtain the global TPEI. RESULTS: Duration of TPEI was significantly correlated with mean PAP, pulmonary vascular resistance (PVR), and cardiac index (CI). Longer TPEI was associated with higher N terminal probrain natriuretic peptide (NT pro-BNP) level, lower 6-min walk distance (6MWD), and lower tricuspid annular plane systolic excursion (TAPSE). CONCLUSION: Prolongation of TPEI could be a new predictor of adverse outcome in PAH and may provide additional prognostic information for patients with PAH.

The role of Beta-1 receptor gene polymorphism in Beta-Blocker therapy for vasovagal syncope.

BACKGROUND: Vasovagal syncope (VVS) is a common clinical condition involving genetic background. The role of beta-blockers in the treatment is controversial. OBJECTIVE: The aim of this study was to investigate the effect of beta-1 gene polymorphism on beta-blocker therapy in patients with VVS. METHODS: We included 123 patients who were diagnosed with VVS after the tilttable test. We searched for the polymorphism Arg389Gly (rs1801253) in the beta-1 adrenoceptor gene. RESULTS: Overall, 64 patients (52%) had Arg389Arg with Arg389Arg genotype were more frequent compared with patients having Arg389Gly genotype (total syncopal episodes [TSE], 7.9 ± 3.7 vs. 6.4 ± 3.0; p = 0.012). TSE in patients with Arg389Arg genotype decreased significantly after 18 months of beta-blocker treatment (7.9 ± 3.7 vs. 3.0 ± 1.4, p < 0.001). After 18 months of beta-blocker treatment, patients with Arg389Arg genotype had significantly fewer syncopal episodes than patients with Arg389Gly genotype (3.0 ± 1.4 vs. 6.8 ± 3.2, p < 0.001). CONCLUSIONS: Results of beta-blocker therapy in patients with Arg389Arg genotype suggest that VVS pathophysiology is a multifactorial condition, with genetic, psychological, and environmental components, and therefore, treatment selection can be based on gene polymorphism.

Predictive value of global and territorial longitudinal strain imaging in detecting significant coronary artery disease in patients with myocardial infarction without persistent ST-segment elevation.

INTRODUCTION: Two-dimensional (2D) speckle-tracking echocardiographic (STE) imaging is frequently performed in the assessment of cardiovascular diseases. We aim to investigate the role of the global and territorial longitudinal strain (GLS and TLS) values assessed via 2D STE imaging to detect significant coronary artery disease (CAD) in non-ST-segment elevation myocardial infarction (NSTEMI) patients without wall-motion abnormalities. METHODS: This study enrolled 150 patients with the diagnosis of NSTEMI. Patients who had typical chest pain with unstable angina characteristics within the last 24 hours were 18-80 years of age and had a typical rise and/or fall of cardiac biomarkers were included. Myocardial functions were assessed via myocardial deformation analyses of 2D STE images. RESULTS: The mean age of the CAD group was 52.91 ± 9.11, vs 50.31 ± 8.32 in the control group. In the CAD group, 56 patients were male (65%), whereas 21 were male (60%) in control group. GLS and TLS assessments demonstrated a statistically significant difference between CAD and control groups, with GLS values of -16.27 ± 1.91 and -18.74 ± 1.93 (P < 0.001), TLS-LAD values of -15.67 ± 1.83 and -18.54 ± 1.97 (P < 0.001), TLS-RCA values of -17.04 ± 1.81 and -19.20 ± 1.86 (P < 0.001), and TLS-Cx values of -17.40 ± 2.08 and -18.34 ± 2.18 (P = 0.028), respectively. Correlation analyses revealed that as high-sensitivity troponin (hsTnT) values increased, GLS decreased significantly, and further, an increase in severity of CAD resulted in decreased TLS-LAD, -CX and -RCA (TLS-LAD: P < 0.001, r = -0.743; TLS-CX: P < 0.001, r = -0.449; TLS-RCA: P < 0.001, r = -0.737). Multivariate analyses indicated that GLS and GRACE ACS risk scores are independent predictors of CAD in patients with NSTEMI (GLS: OR = 0.514, P < 0.001; GRACE score: OR = 0.938, P = 0.007). CONCLUSIONS: Global longitudinal strain (GLS) assessed with 2D STE is a promising, easy to perform and quick imaging method to predict CAD in patients with NSTEMI.

Endocan: a novel biomarker associated with well-developed coronary collateral circulation in patients with stable angina and chronic total occlusion.

Angiogenesis and arteriogenesis have a crucial role in the formation of coronary collateral vessels. It has been shown that endocan and vascular cell adhesion molecule-1 (VCAM-1) are potential angiogenetic factors. We investigated the relationship between serum endocan levels and grade of coronary collaterals, and also the correlation of endocan levels with serum VCAM-1 levels. Patients with stable angina and at least one total coronary occlusion at invasive coronary angiography were included in our study. Collateral degree was graded according to Rentrop and Cohen's classification. Patients who had grade 0 or 1 collateral vessels were included in the poorly-developed collateral group, and those with grade 2 or 3 coronary collateral vessels were included in the well-developed collateral group. Serum endocan and VCAM-1 levels were significantly higher in the well-developed collateral group (436.6 ± 213.3 ng/mL vs. 216.1 ± 78.5 ng/mL, p < .001; 11.02 ± 6.58 ng/mL vs. 6.78 ± 1.14 ng/mL, p < .001, respectively). In a logistic regression analysis, only serum endocan level remained as an independent predictor for good collateral development. In the ROC curve analysis, 282 ng/mL endocan level had an a 82 % sensitivity and 86 % specificity for prediction of the well-developed collateral group. Higher endocan level was related to better coronary collateral development. In the event that these results are confirmed in further studies, endocan may be considered as an anti-ischemic treatment strategy in order to improve collateral development.

Galectin-3 correlates with arrhythmogenic right ventricular cardiomyopathy and predicts the risk of ventricular -arrhythmias in patients with implantable defibrillators.

Background Arrhythmogenic right ventricular dysplasia (ARVD) is a heritable disorder characterized by fibro-fatty replacement of right ventricular myocytes, increased risk of ventricular arrhythmias, and sudden cardiac death. Galectin-3 (GAL3) is known to play an important role in a number of fibrotic conditions, including cardiac fibrosis. Many studies have focused on the association between GAL3 levels and cardiac fibrosis in heart failure. However, the role of GAL3 in the pathogenesis of ARVD and ventricular arrhythmias has not yet been evaluated thoroughly. The aim of this study was to explore GAL3 levels in patients with ARVD and its association with ventricular arrhythmias. Methods Twenty-nine patients with ARVD and 24 controls were included. All patients with ARVD had an implantable cardiac defibrillator (ICD) for primary or secondary prevention. Ventricular arrhythmia history was obtained from a chart review and ICD data interrogation. Galectin-3 levels were measured using an enzyme-linked immunosorbent assay. Results Patients with ARVD had higher plasma GAL3 levels (16.9 ± 2.6 ng/mL vs 11.3 ± 1.8 ng/mL, P < 0.001) than the control group. Ten patients had sustained or non-sustained ventricular arrhythmias during follow-up. In the multivariable analysis, left ventricular disease involvement (HR: 1.05; 95% CI: [1.01-1.12]; P = 0.03); functional capacity >2 (HR: 1.21; 95% CI: [1.13-1.31]; P < 0.005); and GAL3 levels (HR: 1.05; 95% CI: [1.00-1.11]; P = 0.01) independently predicted VT/VF. Conclusion We demonstrated that serum GAL3 was significantly elevated in patients with ARVD. Also, serum GAL 3 levels could be regarded as a candidate biomarker in the diagnosis of ARVD which needs to be tested in larger prospective studies. In addition, GAL3 levels were higher in patients with VT/VF as compared with those without VT/VF.

Usefulness of T(peak) -T(end) interval to distinguish arrhythmogenic right ventricular cardiomyopathy from idiopathic right ventricular outflow tract tachycardia.

BACKGROUND: The two predominant etiologies of right ventricular tachycardia (VT) are arrhythmogenic right ventricular cardiomyopathy (ARVC) and idiopathic VT arising from the right ventricular outflow tract (RVOT). Discrimination between these two entities is critical, as their prognoses and therapeutic options differ. The Tpeak -Tend (Tpe) interval reflects the transmural repolarization dispersion and its prolongation is associated with high mortality. METHODS: We compared the sinus rhythm electrocardiogram (ECG) of 43 patients (24 male, 43 ± 16 years) with VT originating from right ventricle. Five patients under antiarrhythmic drug therapy were excluded. Tpe interval was measured in each precordial leads and compared among patients with ARVC and RVOT-VT. RESULTS: Twenty-five patients (16 male, 42 ± 16 years) met the Task Force criteria for the diagnosis of ARVC, and 13 patients (seven male, 45 ± 14 years) had idiopathic RVOT tachycardia. Patients with ARVC had significantly prolonged Tpe intervals in all precordial leads compared to patients with idiopathic RVOT VT (137.1 ± 32.6 ms vs 93.8 ± 16.9 ms; P < 0.001 in V1, 133.2 ± 35.5 ms vs 104.7 ± 16.9 ms; P = 0.01 in V2, 125.7 ± 31.5 ms vs 99.1 ± 19.6 ms; P = 0.09 in V3, 121.9 ± 26.5 ms vs 92.3 ± 19.7 ms; P = 0.001 in V4, 123.1 ± 26.5 ms vs 99.5 ± 20:1 ms; P = 0.04 in V5 and 126.9 ± 32.2 ms vs 89 ± 11.3 ms; P < 0.001 in V6, respectively). For the diagnosis of ARVC, Tpe cut-off value of 97 ms in V1 had 84% sensitivity and 62% specificity (area under curve = 0.880). CONCLUSION: In patients with VT of RV origin, the prolonged Tpe interval in sinus rhythm electrocardiogram supports the diagnosis of ARVC.

Evaluation of human immunodeficiency virus infection-related left ventricular systolic dysfunction by tissue Doppler strain echocardiography.

OBJECTIVE: Cardiovascular involvement causes significant morbidity and mortality among patients with human immunodeficiency virus (HIV) infection. Since the introduction of highly active antiretroviral treatment (HAART), subtle changes in left ventricular (LV) function, which may be clinically silent, have become more pronounced in HIV patients. Echocardiographic strain imaging (SI) may detect subclinical myocardial dysfunction at an earlier stage compared with conventional echocardiography. The aim of this study was to evaluate tissue Doppler-derived LV strain and strain rate (SR) along with conventional measures of LV function in asymptomatic, stable adult HIV patients on HAART. METHODS: Twenty-one patients with HIV infection (mean age: 37.8 ± 11.9 years, 11 males) who had no cardiovascular complaints and 27 healthy volunteers (mean age: 40.9 ± 5.8 years, 14 males) were enrolled. Traditional parameters including LV ejection fraction (EF) were measured along with tissue velocity imaging (TVI) and tissue Doppler SI parameters using transthoracic echocardiography. RESULTS: The mean duration of HIV infection was 30.8 ± 25.1 (3-120) months. The mean LVEF in HIV group was within normal limits but lower than controls (64.5% ± 10.2% vs. 72.2% ± 6.4%, P = 0.003). There were no differences in other major traditional measures, as well as TVI parameters between groups. LV systolic strain and SR parameters were impaired indicating subtle LV systolic dysfunction in HIV group. No difference in diastolic function was observed between groups. CONCLUSION: Left ventricular systolic strain parameters may be utilized to demonstrate subtle LV systolic dysfunction in asymptomatic HIV patients.

Ventricular arrhythmias in mitral valve prolapse syndrome and their relationship with electrocardiographic repolarization parameters.

OBJECTIVE: The aim of present study is to compare ventricular and supraventricular arrhythmia incidences in subjects with and without mitral valve prolapse (MVP) syndrome and to examine if an association exists between ventricular arrhythmias and repolarization parameters in patients with MVP syndrome. METHODS: This cross-sectional study involved 41 subjects with MVP Syndrome and 41 subjects with palpitation but without MVP (control group). All subjects were subjected to lead-electrocardiogram, transthoracic echocardiography, and 24-h Holter monitoring to identify repolarization abnormalities, structural abnormalities, and supraventricular and ventricular arrhythmias. The QRS width, QTC interval, and Tpeak-Tend intervals were measured for each participant. RESULTS: The number of subjects who had premature ventricular contractions (PVCs), couplets, and non-sustained ventricular tachycardia (NSVTs) was significantly higher in the MVP group compared to the control group. Left ventricular end-systolic diameter (LVESD) and left ventricular end-diastolic diameter (LVEDD) and left atrial diameter were also significantly higher in the MVP group than the control group. QRS width and Tpeak-Tend interval were also significantly higher in subjects with MVP than the controls. Correlation analysis showed a positive correlation between the severity of mitral regurgitation (MR) and the number of PVCs and couplets, while there was a significant correlation between left atrium (LA) diameter and the number of the PVCs and NSVTs. CONCLUSION: Subjects with MVP experience ventricular arrhythmias more often including PVCs, couplets, and NSVTs compared to subjects without MVP. LVESD, LVEDD, LA diameter, QRS width, and Tpeak-Tend interval were increased in MVP subjects than those without MVP. There is an association between the severity of the MR and the frequency of the PVCs, couplets, or NSVTs.

Intracardiac masses: Single center experience within 12 years: I-MASS Study.

Objective: The aim of this cross-sectional, retrospective, descriptive study was to review and classify cardiac masses systematically and to determine their frequencies. Methods: The medical records of 64,862 consecutive patients were investigated within 12 years. Every patient with a cardiac mass imaged by transthoracic echocardiography (TTE) and confirmed with an advanced imaging modality such as transesophageal echocardiography (TEE), computed tomography (CT) and/or cardiac magnetic resonance imaging (CMR) was included. Acute coronary syndromes triggering thrombus formation, vegetations, intracardiac device and catheter related thrombi were excluded. Results: Data demonstrated 127 (0.195%) intracardiac masses consisting of 33 (0.050%) primary benign, 3 (0.004%) primary malignant, 20 (0.030%) secondary tumors, 3 (0.004%) hydatid cysts and 68 (0.104%) thrombi respectively. The majority of primary cardiac tumors were benign (91.67%), predominantly myxomas (78.79%), and the less malignant (8.33%). Secondary cardiac tumors were common than the primary malignant tumors (20:3), with male dominancy (55%), lymphoma and lung cancers were the most frequent. Intracardiac thrombi was the majority of the cardiac masses, thrombi accompanying malignancies were in the first range (n = 17, 25%), followed by autoimmune diseases (n = 13, 19.12%) and ischemic heart disease with low ejection fraction (n = 12, 17.65%). Conclusions: This retrospective analysis identified 127 patients with cardiac masses. The majority of benign tumors were myxoma, the most common tumors that metastasized to the heart were lymphoma and lung cancers, and the thrombi associated with malignancies and autoimmune diseases were the most frequent.

Association between Multiplate-measured aspirin resistance and vitamin D deficiency in stable coronary artery disease.

Introduction: Insufficient inhibition of platelets in patients with atherosclerosis despite antiplatelet therapy leads to important clinical consequences. The present study evaluated the role of vitamin D (VD) deficiency in aspirin resistance (AR) in patients with stable coronary artery disease (CAD) treated with aspirin. Material and methods: This study included 70 patients with stable CAD who had been using 100 mg aspirin for at least seven days. Serum 25-hydroxyvitamin D [25-(OH)D] concentration was measured and patients with 25-(OH)D level < 20 ng/dl were defined as the VD deficient group. A Multiplate Platelet Function Analyzer (Multiplate) device was used to evaluate AR. Patients were defined as aspirin-sensitive (AS) when their AUC was ≤ 30 U, and aspirin resistant (AR) when their AUC was > 30 U. Results: AUC was > 30 U in 15 (21%) patients and these patients were considered AR. The mean 25-(OH)D level was 18.7 ±12.2 ng/ml in all patients. Forty-five (64%) patients were VD deficient. The rate of AR was higher in the VD deficient group than the sufficient group (29% vs. 8%, p = 0.041). The mean AUC was higher in the VD deficient group than the sufficient group (30.2 ±29.1 vs. 15.3 ±13.1 U; p = 0.018). In ROC analysis 25-(OH)D level < 19.25 ng/dl predicted AR with 86.7% sensitivity, 61.8% specificity (AUC = 0.696, 95% CI: 0.551-0.840, p = 0.021). Conclusions: In the current study, an association was found between VD deficiency and AR in patients with stable CAD. VD supplementation may reduce platelet aggregation and overcome AR.

Impairment of right ventricular longitudinal strain associated with severity of pneumonia in patients recovered from COVID-19.

Myocardial injury caused by COVID-19 was reported in hospitalized patients previously. But the information about cardiac consequences of COVID-19 after recovery is limited. The aim of the study was comprehensive echocardiography assessment of right ventricular (RV) in patients recovered from COVID-19. This is a prospective, single-center study. After recovery from COVID-19, echocardiography was performed in consecutive 79 patients that attended follow-up visits from July 15 to November 30, 2020. According to the recovery at home vs hospital, patients were divided into two groups: home recovery (n = 43) and hospital recovery (n = 36). Comparisons were made with age, sex and risk factor-matched control group (n = 41). In addition to conventional echocardiography parameters, RV global longitudinal strain (RV-GLS) and RV free wall strain (RV-FWS) were determined using 2D speckle-tracking echocardiography (2D STE). Of the 79 patients recovered from COVID-19, 43 (55%) recovered at home, while 36 (45%) required hospitalization. The median follow-up duration was 133  ±  35 (87-184) days. In patients recovered from hospital, RV-GLS and RV-FWS were impaired compared to control group (RV-GLS: -17.3  ±  6.8 vs. -20.4  ±  4.9, respectively [p = 0.042]; RV-FWS: -19.0  ±  8.2 vs. -23.4  ±  6.2, respectively [p = 0.022]). In subgroup analysis, RV-FWS was impaired in patients severe pneumonia (n = 11) compared to mild-moderate pneumonia (n = 28), without pneumonia (n = 40) and control groups (-15.8  ±  7.6 vs. -21.6  ±  7.6 vs. -20.8  ±  7.7 vs. -23.4  ±  6.2, respectively, [p = 0.001 for each]) and RV-GLS was impaired compared to control group (-15.2  ±  6.9 vs. -20.4  ±  4; respectively, [p = 0.013]). A significant correlation was detected between serum CRP level at hospital admission and both RV-GLS and RV-FWS (r = 0.285, p = 0.006; r = 0.294, p = 0.004, respectively). Age (OR 0.948, p = 0.010), male gender (OR 0.289, p = 0.009), pneumonia on CT (OR 0.019, p = 0.004), and need of steroid in treatment (OR 17.424, p = 0.038) were identifed as independent predictors of impaired RV-FWS (> -18) via multivariate analysis. We demonstrated subclinic dysfunction of RV by 2D-STE in hospitalized patients in relation to the severity of pneumonia after recovery from COVID-19. 2D-STE supplies additional information above standard measures of RV in this cohort and can be used in the follow-up of these patients.

Role of global longitudinal strain in discriminating variant forms of left ventricular hypertrophy and predicting mortality.

OBJECTIVE: In this study, we aimed to compare the functional adaptations of the left ventricle in variant forms of left ventricular hypertrophy (LVH) and to evaluate the use of two-dimensional speckle tracking echocardiography (2D-STE) in differential diagnosis and prognosis. METHODS: This was a prospective cohort study of 68 patients with LVH, including 20 patients with non-obstructive hypertrophic cardiomyopathy (HCM), 23 competitive top-level athletes free of cardiovascular disease, and 25 patients with hypertensive heart disease (HHD). All the subjects underwent 2D transthoracic echocardiography (TTE) and 2D-STE. The primary endpoint was all-cause mortality. Global longitudinal strain (GLS) below -12.5% was defined as severely reduced strain, -12.5% to -17.9% as mildly reduced strain, and above -18% as normal strain. RESULTS: The mean LV-GLS value was higher in athletes than in patients with HCM and HHD with the lowest value being in the HCM group (HCM: -11.4±2.2%; HHD: -13.6±2.6%; and athletes: -15.5±2.1%; p<0.001 among groups). LV-GLS below -12.5% distinguished HCM from others with 65% sensitivity and 77% specificity [area under curve (AUC)=0.808, 95% confidence interval (CI): 0.699-0.917, p<0.001]. The median follow-up duration was 6.4±1.1 years. Overall, 11 patients (16%) died. Seven of these were in the HHD group, and four were in the HCM group. The mean GLS value in patients who died was -11.8±1.5%. LV-GLS was significantly associated with mortality after adjusting age and sex via multiple analysis (RR=0.723, 95% CI: 0.537-0.974, p=0.033). Patients with GLS below -12.5% had a higher risk of all-cause mortality compared with that of patients with GLS above -12.5% according to Kaplan-Meier survival analysis for 7 years (29% vs. 9%; p=0.032). The LV-GLS value predicts mortality with 64% sensitivity and 70% specificity with a cut-off value of -12.5 (AUC=0.740, 95% CI: 0.617-0.863, p=0.012). CONCLUSION: The 2D-STE provides important information about the longitudinal systolic function of the myocardium. It may enable differentiation variable forms of LVH and predict prognosis.

Influences of genetic variants in interleukin-15 gene and serum interleukin-15 levels on coronary heart disease.

Interleukin-15 (IL-15) is a potent proinflammatory cytokine that is now considered a key component of atherosclerosis. Proinflammatory gene polymorphisms lead to variations in the production and level of the proteins. In light of these findings, we hypothesized that variations in the gene coding for IL-15 influence the risk of coronary heart disease (CHD) by modulating the IL-15 levels. To test this hypothesis, we examined 5 single nucleotide polymorphisms (SNPs) in IL-15 gene and IL-15 levels in 102 patients with acute coronary syndrome (ACS), 102 patients with chronic ischemic stable CHD and 162 healthy control subjects. This study is the first report showing the influences of IL-15 gene variants and IL-15 levels on CHD. The five single nucleotide polymorphisms (SNPs) within the IL-15 gene, G367A, C267T, A14035T, C13687A, and A10504G were carried out by polymerase chain reaction/restriction fragment length polymorphism (PCR/RFLP). Serum IL-15 levels were significantly higher in both acute and chronic patients than in controls. Genetic variants of IL-15 gene and IL-15 levels were associated with CHD. In conclusion, our study supports the hypothesis that genetic variation in IL-15 gene and IL-15 levels influence the risk of CHD. Further studies are needed to confirm our hypothesis.

Endothelial dysfunction in hemodialysis patients with failed renal transplants.

BACKGROUND: Endothelial dysfunction (ED) is a common precursor and denominator of cardiovascular events including development of atherosclerosis. In this cross-sectional study, we aimed to investigate ED, measured by coronary flow reserve (CFR) in hemodialysis (nHD) patients who were never transplanted and patients with failed renal transplants restarting hemodialysis (fTx-HD). METHODS: Forty nHD (24 males, mean age 39 ± 9 yr) and 43 fTx-HD patients (27 males, mean age 36 ± 9 yr) were included in the study. Clinical and biochemical parameters, including high-sensitive C-reactive protein (hs-CRP) levels were determined. Also, CFR measurements were used to evaluate ED. RESULTS: There were no significant differences regarding age, gender, smoking status, systolic and diastolic blood pressure levels, mean duration of HD treatment as well as Kt/V((urea)) values between the two groups. Time spent on dialysis in the nHD group and dialysis duration following failure of renal allograft in the fTx-HD group were similar. Serum creatinine, hemoglobin, hematocrit, calcium and phosphorus levels were similar between the two groups as well. When compared to nHD group, serum total cholesterol (139 ± 3 vs. 154 ± 3 mg/dL, p = 0.045), serum albumin (3.8 ± 0.3 g/dL vs. 4.1 ± 0.2 g/dL, p < 0.0001) and CFR (1.60 ± 0.2 vs. 1.75 ± 0.3, p = 0.028) levels were significantly lower, while serum hs-CRP levels (11 ± 15 mg/L vs. 3 ± 4 mg/L, p = 0.001) were significantly higher in the fTx-HD group. Serum hs-CRP negatively correlated (r = -0254, p = 0.021), while serum albumin positively correlated (r = 0402, p = 0.001) with CFR values. CONCLUSION: ED is more prominent in fTx-HD than the nHD patients. Inflammation, caused by failed renal allograft can be responsible for this abnormality.

Improvement of coronary flow velocity reserve with telmisartan in patients with autosomal-dominant polycystic kidney disease.

OBJECTIVES: Endothelial dysfunction (ED) has been reported in patients with autosomal-dominant polycystic kidney disease (ADPKD). Coronary flow velocity reserve (CFVR) is a noninvasive test showing endothelial function of epicardial coronary arteries and coronary microcirculatory function. The aim of this study was to investigate the effect of the angiotensin receptor blocker, telmisartan, on CFVR in patients with ADPKD. METHODS: Thirteen patients with ADPKD and well-preserved renal function and 22 healthy controls were included in the study. CFVR was measured at baseline and after dipyridamole infusion by echocardiography. CFVR was calculated as the ratio of hyperemic to baseline average peak diastolic velocities. After the baseline evaluation of CFVR, patients started telmisartan at a dose of 80 mg/day and were followed for 12 months. CFVR was remeasured after 6 and 12 months of therapy. RESULTS: Patients with ADPKD had significantly lower CFVR compared to healthy subjects. CFVR increased significantly after 6 months and 12 months of telmisartan therapy (P = 0.001) in patients with ADPKD. CONCLUSION: One year of telmisartan therapy significantly improved CFVR in patients with ADPKD. This finding suggests that the stimulation of the renin-angiotensin-aldosterone system contributes to the ED in these patients.

The Role of Aortic Stiffness Parameters in Evaluating Myocardial Ischemia.

BACKGROUND: Arterial stiffness is a process resulting in deterioration of hemodynamic function of the aorta, a decrease in its compliance and elasticity, caused by the proportional change of components of the extracellular matrix. Although many researches have been done to determine the etiologies of myocardial ischemia in the absence of obstructive coronary artery disease, none of them has investigated the relation between the parameters of aortic stiffness and the myocardial ischemia documented by the exercise stress test. The present cross-sectional study aimed to investigate the difference of aortic stiffness parameters between the groups separated by exercise stress test result as positive and negative ischemic findings in the absence of obstructive coronary artery disease. METHODS: The present study included 79 patients who were admitted to Istanbul Faculty of Medicine, Department of Cardiology with complaint of chest pain. Forty patients (21 women and 19 men) have ischemic findings on the exercise electrocardiography (ECG) test and 39 patients (20 women and 19 men) have normal exercise ECG results. The patients who have positive exercise ECG findings underwent coronary angiography and all the patients had non-obstructive coronary artery disease. Demographic features (age, sex and comorbidities) were statistically similar between the groups. Aortic stiffness measurements (pulse wave velocity, pulse pressure, aortic augmented pressure, augmentation index, systolic pressure-time index, diastolic pressure-time index and subendocardial viability ratio) were done with tonometric methods. RESULTS: There was no significant difference between the two groups in terms of the aortic stiffness parameters. Systolic blood pressure (P = 0.33), diastolic blood pressure (P = 0.24), pulse pressure (P = 0.60), systolic pressure-time index (P = 0.10), diastolic pressure-time index (P = 0.91), subendocardial viability ratio (P = 0.19), aortic augmented pressure (P = 0.87), augmentation index (P = 0.58) and pulse wave velocity (P = 0.56) were detected between the two groups. Biochemical parameters were found similar between the two groups. Only low-density lipoprotein levels were slightly higher in patients with negative exercise stress test result (139 vs. 123 mg/dL, P = 0.02). CONCLUSION: There is no finding supporting that the aortic stiffness identifies the patients with non-obstructive coronary artery disease but with signs of myocardial ischemia and further investigation of other causes of myocardial ischemia is required.

Effect of bariatric surgery on flow-mediated dilation and carotid intima-media thickness in patients with morbid obesity: 1-year follow-up study.

OBJECTIVE: Obesity is associated with increased cardiovascular (CV) mortality and morbidity. Bariatric surgery (BS) is currently an established therapeutic approach for severely obese patients. Carotid intima-media thickness (CIMT) and brachial artery flow-mediated dilation (FMD) provide important prognostic information beyond traditional CV risk factors. This study aimed to examine the effect of bariatric surgery-induced weight loss on CIMT and brachial artery FMD in morbidly obese patients. METHODS: A total of 23 morbidly obese patients (40.4±5.6 years, 13 females) were examined before and after BS for 1 year with 3-month periods. CIMT, FMD, body composition, and metabolic parameters were determined. RESULTS: All the patients exhibited significant weight loss following BS (p<0.001). Carotid intima-media thickness reduction was not significant from baseline to 6 months (p=0.069), but at 9 months (p=0.004), it became significant. Similarly, the difference between the preoperative and 6-month FMD assessments was not significant (p=0.057), but at 9 months (p<0.001), it became significant. CONCLUSION: Our study reveals that weight loss following BS causes improvements in CV risk factors, which is evident after 9 months of surgery.

Silent myocardial dysfunction in vitamin D deficiency.

INTRODUCTION: Vitamin D (VD) deficiency is a common disease that occurs in all stages of life. A growing number of studies call attention to the relationship between VD deficiency and cardiovascular disease. The aim of this study was to investigate the effect of VD on subclinical left ventricular (LV) function in diabetic and non-diabetic patients with no significant coronary artery disease. MATERIAL AND METHODS: We recruited 140 patients (80 diabetics and 60 non-diabetics) with symptoms of stable ischemic heart disease who underwent coronary angiography and who had no significant coronary artery disease in our clinic. The 25(OH)D3 levels were measured and patients who had 25-(OH)D3 levels below 20 ng/dl were defined as the VD deficient group. In addition to conventional echocardiographic parameters, tissue Doppler echocardiography was used for LV diastolic functions and 2D speckle tracking strain echocardiography (2D STE) for evaluating the longitudinal deformation indices of the LV myocardium. RESULTS: In all groups, LV global longitudinal strain (GLS) was significantly impaired in patients with VD deficiency (p < 0.001) compared to patients without VD deficiency. LV global longitudinal strain rate (GLSR) was significantly impaired in patients with VD deficiency (p = 0.003). The GLS was negatively associated with 25-(OH)D3 in the VD deficiency group (r = -0.52623, p < 0.001). Conversely, GLS was positively associated with 25-(OH)D3 levels in the normal VD group (r = 0.28, p = 0.048). CONCLUSIONS: VD deficiency is associated with impaired myocardial GLS. The present study demonstrated that VD deficiency may be the cause of subclinical myocardial dysfunction in patients with or without diabetes mellitus and no history of significant coronary artery disease.