Assessment of Tp-Te interval in patients with cardiac AL amyloidosis.

BACKGROUND: Prolonged Tp-Te interval is strongly associated with fatal ventricular arrhythmias and mortality. This association has been demonstrated in various diseases. However, the current literature does not give any information on Tp-Te interval in cardiac amyloid light-chain (AL) amyloidosis. METHODS: We retrospectively screened 116 cardiac AL amyloidosis patients and 35 patients were included in the study. Demographic, laboratory, 12-lead electrocardiographic (QTc, Tp-Te V1-V6) and transthoracic echocardiographic data of the patients were analysed and compared with 35 healthy controls. RESULTS: QTc and Tp-Te V2-V5 were significantly prolonged in the cardiac AL amyloidosis group (p < 0.05). Also, there was a positive and statistically significant correlation between the parameters of QTc and Tp-Te V3-V6, and also between the parameters of interventricular septum thickness at enddiastole and Tp-Te V2-V5. CONCLUSION: We present the first strong evidence of prolonged Tp-Te intervals in patients with cardiac AL amyloidosis. There may also be a relationship between prolonged Tp-Te interval and the development of arrhythmia in this patient group, as in some other groups. There is a need for prospective studies examining the relationship of prolonged Tp-Te interval with arrhythmias and its prognostic significance in cardiac AL amyloidosis.

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.

Prior angina reduces ischemic mitral regurgitation in patients with ST-Elevation myocardial infarction, role of ischemic preconditioning.

Mitral regurgitation may develop due to left ventricular (LV) remodeling within 3 months following acute myocardial infarction (AMI) and is called ischemic mitral regurgitation (IMR). Ischemic preconditioning (IPC) has been reported as the most important mechanism of the association between prior angina and the favorable outcome. The aim of this study was to investigate the effect of prior angina on the development and severity of IMR at 3rd month in patients with ST elevation MI (STEMI). Fourty five (45) patients admitted with STEMI and at least mild IMR, revascularized by PCI were enrolled. According to presence of prior angina within 72 h before STEMI, patients were then divided into two groups as angina (+) (n:26; 58%) and angina (-) (n:19; 42%). All patients underwent 2D transthoracic echocardiography at 1st, 3rd days and 3rd month. IMR was evaluated by proximal isovelocity surface area (PISA) method: PISA radius (PISA-r), effective regurgitant orifice area (EROA), regurgitant volume (Rvol). LV ejection fraction (EF %) was calculated by Simpson's method. High sensitive troponin T (hs-TnT), creatine phosphokinase myocardial band (CK-MB) and N-terminal pro-brain natriuretic peptid (NTpro-BNP) levels were compared between two groups. Although PISA-r, EROA and Rvol were similar in both groups at 1st and 3rd days, all were significantly decreased (p = 0.012, p = 0.007, p = 0.011, respectively) and EF was significantly increased (p< 0 .001) in angina (+) group at 3rd month. NTpro-BNP and hs-TnT levels at 1st day and 3rd month were similar, however CK-MB level at 3rd month was found to be significantly lower in the angina (+) group (p = 0.034). At the end of the 3rd month, it was observed that the severity of IMR evaluated by PISA method was decreased and EF increased significantly in patients who defined angina within 72 h prior to STEMI, suggesting a relation with IPC.

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.

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 tilt-table test. We searched for the polymorphism Arg389Gly (rs1801253) in the beta-1 adrenoceptor gene. Results: Overall, 64 patients (52%) had Arg389Arg genotype and 59 patients (48%) had Arg389Gly genotype. The syncopal episodes of patients 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. (REV INVEST CLIN. 2020;72(5):300-7)

A new electrocardiographic parameter associated with sudden cardiac death in pulmonary sarcoidosis.

INTRODUCTION: The interval from the peak to the end of the electrocardiographic T wave (Tp-Te) may correspond to malignant ventricular arrhythmias. In this study we aimed to assess Tp-Te variability and investigate the transmural dispersion of repolarisation in pulmonary sarcoidosis disease without proofed cardiac involvement. MATERIAL AND METHODS: This was a retrospective case-control study that included patients who had a pathologic and radiologic diagnosis of sarcoidosis. All data of the patients' demographic features and electrocardiographs were analysed. RESULTS: We enrolled 78 patients with sarcoidosis and 54 healthy volunteers as controls in our study. Men comprised 36% of the sarcoidosis group and 27% of controls. The mean age in the sarcoidosis and control group was 45.4 ±8.7 years (range: 23-58 years) and 44.6 ±11.9 years (range: 21-73 years), respectively. There was no significant difference between the groups for age or sex (p = 0.654, p = 0.246, respectively). There was a significant increase in Tp-Te results in all precordial leads in the sarcoidosis group compared with the control group (p < 0.05). CONCLUSIONS: Pulmonary sarcoidosis is suspected to have cardiac involvement; therefore, we need to develop new approaches. We present strong evidence that Tp-Te intervals were increased in patients with pulmonary sarcoidosis, which suggests that there may be a link between sarcoidosis and ventricular arrhythmias without proofed cardiac involvement.

Association between galectin-3 levels and isolated coronary artery ectasia.

BACKGROUND: Coronary artery ectasia (CAE) is a well-recognised disorder characterised by abnormal dilation of the coronary arteries. Underlying mechanisms associated with abnormal luminal dilation in CAE remain to be elucidated. However, histopathological features resemble those of coronary atherosclerosis. Galectin-3 (Gal-3) is a valuable biomarker for both progression and destabilisation of atherosclerotic lesions. To the best of our knowledge, there is no study in the literature examining serum Gal-3 levels in patients with isolated CAE. In the present study, therefore, we aimed to investigate the possible relationship between serum Gal-3 levels and isolated CAE. METHODS: Between March 2016 and March 2017 this prospective, case-controlled study included a total of 49 consecutive isolated CAE patients (31 males, 18 females) diagnosed with CAE by coronary angiography at the catheter laboratory of Medeniyet University, Goztepe Training and Research Hospital, and 43 individuals (19 males, 24 females) with normal coronary arteries. Physical examination, medical history, blood biochemistry and transthoracic echocardiography were performed in both groups. Serum concentrations of Gal-3 were measured using blood samples. RESULTS: Median Gal-3 levels were significantly higher in isolated CAE patients than in the controls [23.2 (23.9 ± 7.1) vs 16.8 ng/ml (17.8 ± 7.3); p < 0.001]. According to the Markis classification, the extent of CAE was not correlated with Gal-3 levels (p = 0.41). Multivariate regression analysis revealed that Gal-3 concentration was an independent predictor of isolated CAE. CONCLUSIONS: Our study results suggest that Gal-3 serum concentrations significantly increased in patients with isolated CAE, indicating that Gal-3 may be involved in the pathogenesis of isolated CAE.

[Can biomarkers help us to understand the pathogenesis of coronary slow flow? Endocan and omentin-I in slow coronary flow phenomenon]. / Biyobelirteçler koroner yavas akim patogenezini anlamamiza yardimci olabilir mi? Koroner yavas akim fenomeninde endokan ve omentin-I.

OBJECTIVE: The pathophysiology of the slow coronary flow (SCF) phenomenon is still unclear. The two most frequently cited mechanisms of SCF are endothelial dysfunction and subclinical diffuse atherosclerosis. The aim of this study was to investigate the relation of SCF to serum endocan levels which is associated with endothelial dysfunction and to serum omentin-I levels which is associated with atherosclerosis. METHODS: A total of 42 patients with SCF and 43 controls with normal coronary flow based on a coronary angiogram were enrolled. Serum endocan and omentin-I levels were measured and the presence of SCF was determined according to Thrombolysis in Myocardial Infarction frame count (TFC) calculations. RESULTS: The omentin-I level was significantly lower and the endocan level was significantly higher in patients with SCF than in the controls. Receiver operating characteristic curve analysis revealed that the sensitivity and specificity of endocan for SCF was 66% and 70%, respectively (area under the curve [AUC]: 0.760, 95% confidence interval [CI]: 0.65-0.86; p<0.001), and the comparable values for omentin were 66% and 61% (AUC: 0.630, 95% CI: 0.51-0.75; p=0.049). Multivariate logistic regression analysis revealed that a high endocan level (odds ratio [OR]: 6.8, 95% CI: 1.849-2.439, cutoff: 2.45 ng/mL; p=0.003) and a low omentin-I level (OR: 3.6, 95% CI: 1.057-12.893, cutoff: 4.63 ng/mL; p=0.041) were independently associated with the presence of SCF. In patients with SCF, the endocan level was positively correlated with the mean TFC, while the omentin-I level was negatively correlated (r=0.44; p<0.001 and r=-0.22; p=0.049, respectively). CONCLUSION: These results revealed that endocan and omentin-I might be useful biomarkers for predicting the presence and severity of SCF.

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.

Galectin-3: A Novel Biomarker Predicts Sudden Cardiac Death in Hypertrophic Cardiomyopathy.

BACKGROUND: Hypertrophic cardiomyopathy is a primary cardiac disease characterized by left ventricular hypertrophy, myocyte hypertrophy and irregularities and interstitial fibrosis in the absence of any cardiac or systemic diseases and may lead to sudden cardiac death (SCD). Galectin-3 is a ß-galactoside-binding lectin that has been associated with cardiac fibrosis and inflammation. In this study, we aimed to investigate the relationship between serum galectin-3 levels and the criteria for 5-year sudden death risk, recently defined in the European Society of Cardiology guidelines (2014), in patients with hypertrophic cardiomyopathy. MATERIALS AND METHODS: A total of 52 hypertrophic cardiomyopathy patients were enrolled in the study. Patients were questioned for sudden death risk predictors as outlined in the 2014 European Society of Cardiology guideline. A standardized clinical evaluation was carried out on the basis of previously described prognostic variables to calculate the 5-year risk of SCD. Blood samples were taken from all patients to measure serum galectin-3 levels. A statistical significance level of P < 0.05 was accepted in all tests. RESULTS: We found that there was a significant correlation between the estimated 5-year risk of SCD and serum levels of galectin-3. CONCLUSIONS: Galectin-3 may be an inexpensive and easily accessible parameter to predict arrhythmia risk. In addition, it can be used to determine antiarrhythmic prophylaxis as a predictor of an arrhythmia storm in implantable cardioverter defibrillator-implanted patients who are not available for magnetic resonance imaging.

T wave peak-to-end interval in COPD.

Introduction: The interval from the peak to the end of the electrocardiographic (ECG) T wave (Tp-Te) can estimate cardiovascular mortality and ventricular tachyarrhythmias. Objectives: In this study, we aimed to define a new ECG parameter in patients with COPD. Methods: This was a cross-sectional observational study that included COPD patients who were diagnosed previously and followed up in the outpatient clinic. All data of the patients' demographic features, history, spirometry, and electrocardiographs were analyzed. Results: We enrolled 134 patients with COPD and 40 healthy volunteers as controls in our study. Patients already known to be having COPD who were under follow-up for their COPD and diagnosed as having COPD according to the Global Initiative for Chronic Obstructive Lung Disease (GOLD) criteria were included. Men comprised 82.8% of the COPD group and 73.2% of controls. The mean age in the COPD and control group was 60.2±9.4 and 58.2±6.7 years, respectively. There was no significant difference between the groups for age or sex (p=0.207, p=0.267, respectively). There were 46 (34.3%) patients in group A, 23 (17.2%) patients in group B, 26 (19.4%) patients in group C, and 46 (29.1%) patients in group D as COPD group. There was a significant increase in Tp-Te results in all precordial leads in the COPD group compared with the control group (p<0.05). Precordial V4 lead has the most extensive area under the curve (0.831; sensitivity 76.5%, specificity 89.6%). Conclusion: We present strong evidence that Tp-Te intervals were increased in patients with COPD, which suggests that there may be an association between COPD and ventricular arrhythmias and cardiac morbidity.

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.

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.

Cardiac calcified amorphous tumors: CT and MRI findings.

PURPOSE: We aimed to evaluate computed tomography (CT) and magnetic resonance imaging (MRI) findings of cardiac calcified amorphous tumors (CATs). METHODS: CT and MRI findings of cardiac CATs in 12 patients were included. We retrospectively examined patient demographics, location, size, shape configuration, imaging features, calcification distribution of tumors, and accompanying medical problems. RESULTS: There was a female predominance (75%), with a mean age at presentation of 65 years. Patients were mostly asymptomatic on presentation (58.3%). The left ventricle of the heart was mostly involved (91%). CT findings of CATs were classified as partial calcification with a hypodense mass in four patients or a diffuse calcified form in eight. Calcification was predominant with large foci appearance as in partially calcified masses. On T1- and T2-weighted magnetic resonance images, CATs appeared hypointense and showed no contrast enhancement. CONCLUSION: The shape and configuration of cardiac CATs are variable with a narrow spectrum of CT and MRI findings, but large foci in a partially calcified mass or diffuse calcification of a mass on CT is very important in the diagnosis of cardiac CATs. Masses show a low signal intensity on T1- and T2-weighted images with no contrast enhancement on MRI.

The utility of cardiac MRI in diagnosis of infective endocarditis: preliminary results.

PURPOSE: We aimed to evaluate the utility of cardiac magnetic resonance imaging (MRI) for the diagnosis of infective endocarditis (IE). METHODS: Sixteen patients with a preliminary diagnosis of IE (10 women and six men; age range, 4-66 years) were referred for cardiac MRI. MRI sequences were as follows: echo-planar cine true fast imaging with steady-state precession (true-FISP), dark-blood fast spin echo T1-weighted imaging, T2-weighted imaging, dark-blood half-Fourier single shot turbo spin echo (HASTE), and early contrast-enhanced first-pass fast low-angle shot (FLASH). Delayed contrast-enhanced images were obtained using three-dimensional inversion recovery FLASH after 15±5 min. The MRI features were evaluated, including valvular pathologies on cine MRI and contrast enhancement on the walls of the cardiac chambers, major thoracic vasculature, and paravalvular tissue, attributable to endothelial extension of inflammation on contrast-enhanced images. RESULTS: Fourteen valvular vegetations were detected in eleven patients on cardiac MRI. It was not possible to depict valvular vegetations in five patients. Vegetations were detected on the aortic valve (n=7), mitral valve (n=3), tricuspid and pulmonary valves (n=1). Delayed contrast enhancement attributable to extension of inflammation was observed on the aortic wall and aortic root (n=11), paravalvular tissue (n=4), mitral valve (n=2), walls of the cardiac chambers (n=6), interventricular septum (n=3), and wall of the pulmonary artery and superior mesenteric artery (n=1). CONCLUSION: Valvular vegetation features of IE can be detected by MRI. Moreover, in the absence of vegetations, detection of delayed enhancement representing endothelial inflammation of the cardiovascular structures can contribute to the diagnosis and treatment planning of IE.

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.

Serum omentin 1 level is associated with coronary artery disease and its severity in postmenopausal women.

We evaluated whether serum omentin levels are associated with coronary artery disease (CAD) and its severity among postmenopausal women. We enrolled 193 consecutive postmenopausal women who had undergone coronary angiography for suspected stable CAD. The study population was divided into 2 groups based on the results of coronary angiography (CAD group, n=110 and control group, n=83). Omentin 1 levels were measured and disease severity was assessed using the SYNTAX score (SS) in the CAD group. Those patients with angiographic CAD had significantly decreased omentin 1 levels, compared to those without CAD (247.5+127.4 vs 506+246 ng/mL, P<.001). After adjusting for cardiovascular risk factors, a decreased omentin 1 level was found to be an independent predictor of both angiographic CAD and a high SS. Our data indicate that a decreased omentin 1 level is associated with CAD and its severity among postmenopausal women.

Effect of cigarette smoking on platelet aggregation.

BACKGROUND: Cigarette smoking may increase platelet aggregation and cause atherothrombotic cardiovascular events. We aimed to investigate the impact of cigarette smoking on platelet function in patients with ischemic coronary heart disease (CHD). METHODS: Twenty patients with ischemic stable CHD under aspirin therapy (300 mg/d), who continue to smoking despite all warnings, and 20 nonsmokers with CHD are enrolled in the study. Platelet function is studied at the morning, before and 15 minutes after the first cigarette, by the Platelet Function Analyzer (PFA)-100, with collagen and epinephrine and collagen and adenosine diphosphate cartridges. Post aspirin platelet hyperactivity is defined as having a closure time (CT) shorter than 186 seconds despite regular aspirin intake. Serial CT measurements are analyzed by paired samples t test. RESULTS: Persistent platelet activity was present in 4 smoker (20%) and 3 nonsmoker (15%) patients at the beginning. Platelet activity measured by the PFA-100 is been increased significantly after cigarette smoking (P = .004). Shorter CTs were determined after smoking in all patients with and without baseline persistent platelet activity, and 4 more participants became aspirin nonresponder (P = .004). No significant differences in demographic, hematological, and biochemical parameters were determined between aspirin responders and nonresponders. CONCLUSIONS: We determined that cigarette smoking may increase platelet aggregation in patients with ischemic CHD in an aspirin nonresponsive manner. Our results emphasize the importance of quitting cigarette smoking in patients with CHD.