Search

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.

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.

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.

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.

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

BackgroundMitral 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).MethodsFourty five (45) patients admitted with STEMI and at least mild IMR, revascularized by PCI were enrolled. According to presence of prior angina within 72 hours 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.ResultsAlthough 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).Conclusion 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 hours prior to STEMI, suggesting a relation with IPC.

espanolAntecedentes: el sincope vasovagal (VVS) es una condicion clinica comun que involucra antecedentes geneticos. El papel de los betabloqueantes en el tratamiento es controvertido. Objetivo: El objetivo de este estudio fue investigar el efecto del polimorfismo del gen beta-1 en la terapia con betabloqueantes en pacientes con VVS. Metodos: se incluyeron 123 pacientes que fueron diagnosticados de VVS despues de la prueba de la mesa basculante. Buscamos el polimorfismo Arg389Gly (rs1801253) en el gen del adrenoceptor beta-1. Resultados: En general, 64 pacientes (52%) tenian el genotipo Arg389Arg y 59 pacientes (48%) tenian el genotipo Arg389Gly. Los episodios sincopales de los pacientes con genotipo Arg389Arg fueron mas frecuentes en comparacion con los pacientes con genotipo Arg389Gly (episodios sincopales totales [TSE], 7,9 ± 3,7 frente a 6,4 ± 3,0; p = 0,012). La TSE en pacientes con genotipo Arg389Arg disminuyo significativamente despues de 18 meses de tratamiento con betabloqueantes (7,9 ± 3,7 frente a 3,0 ± 1,4, p Conclusiones: Los resultados de la terapia con betabloqueantes en pacientes con genotipo Arg389Arg sugieren que la fisiopatologia del VVS es una condicion multifactorial, con componentes geneticos, psicologicos y ambientales, por lo que la seleccion del tratamiento puede basarse en el polimorfismo de genes. (REV INVEST CLIN.2020; 72 (5): 300-7) EnglishBackground: 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 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)

Seda Tural Onur,1 Samim Emet,2 Sinem Nedime Sokucu,1 Imran Onur2 1Yedikule Chest Diseases and Thoracic Surgery Training and Research Hospital, Chest Disease, Zeytinburnu, Istanbul, Turkey; 2Department of Cardiology, Istanbul Faculty of Medicine, Istanbul University, Fatih, Istanbul, Turkey 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

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

WOS: 000216756300006 Aim: Arrhythmogenic right ventricular cardiomyopathy or dysplasia (ARVC/D) is characterized by the gradual replacement of the right ventricular myocardium with fibrous and adipose tissue and can cause ventricular tachyarrhythmia in young patients. Mean platelet volume (MPV) is reported to be an easily measurable marker reflecting platelet activation and plays an important role in the pathophysiology of cardiovascular disorders. In this study, we aimed to assess MPV in patients with ARVC/D. Methods: Twenty-nine patients (23 men, age: 38.0 +/- 13.1 years) with ARVC/D and forty-one healthy subjects (30 men, age: 39.3 +/- 11.8 years) were studied. Plasma MPV was measured in ARVC/D patients and control subjects. Results: The MPV was higher in patients with ARVC/D when compared with the control group (9.87 +/- 1.0 vs. 8.2 +/- 1.1 fl, p

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.

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 capacity2 (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.

Amac: Bu calismada koroner arter baypas greft (KABG) ameliyatlarinin sonuclari, ameliyat sonrasi atriyal fibrilasyon, koroner damar yapisi ve koroner arter hastaliginin sekli ve genisligi ile iliskisi acisindan incelendi. Ca­lis­ma­pla­ni:­Ocak 2011 ve Mayis 2011 tarihleri arasinda klinigimizde ameliyat edilen ardisik 94 KABG hastasi (68 erkek, 26 kadin; ort. yas 61.4±10.9 yil; aralik 38-87 yil) bu prospektif gozlem calismasina alindi. Ameliyat sonrasi atriyal fibrilasyon gelisimini etkileyen faktorler icin lojistik regresyon analizi yapildi. Bagimsiz degiskenler olarak ameliyat sirasi parametreler (Gensini skoru, Rentrop skoru, revaskularize edilen damar sayisi, dominant koroner arter sistemi, dominant koroner arter sisteminin revaskularizasyonu, sol ana koroner arter hastaligi, basvuru zamani klinik tablosu, sol ventrikul disfonksiyonu ve sol atriyum capi) analiz edildi. Bul gu lar: Ameliyat sirasi 23 hastada (%24.5) atriyal fibrilasyon gelisti. Yirmi hasta amiodaron tedavisi ile normal sinus ritmine donduruldu. Uc hastada (%3.2) hastane mortalitesi oldu. Atriyal fibrilasyon gelisen ve gelismeyen hastalarda mortalite oranlari acisindan istatistiksel olarak anlamli bir fark yoktu. Sol ventrikul disfonksiyonu (p=0.034) ve sol ana koroner arter hastaligi (p=0.019) ameliyat sonrasi atriyal fibrilasyon gelisimi ile anlamli olarak iliskiliydi. Renal komplikasyon orani (p=0.030) ve sternal revizyon cerrahisi gerekliligi (p=0.003) acisindan iki grup arasinda anlamli bir farklilik yoktu. So­nuc:­Ameliyat sonrasi atriyal fibrilasyon kalp cerrahisinde sik karsilasilan bir komplikasyondur. Sol ventrikul disfonksiyonu, ameliyat sonrasi atriyal fibrilasyon gelisimi acisindan anlamli bir risk faktorudur. Koroner damar yapisi ve atriyal fibrilasyon gelisimi arasinda anlamli bir iliski olmasa da, sol ana koroner arter hastaligi ameliyat sonrasi atriyal fibrilasyon icin ciddi bir risk faktorudur. Anah tar soz cuk ler: Atriyal fibrilasyon; komplikasyon; koroner arter baypas greftleme; risk faktor. Background:­ This study aims to investigate the results of coronary artery bypass graft (CABG) surgeries in terms of the relation of postoperative atrial fibrillation, coronary vasculature, and the nature and extent of coronary artery disease. Methods: Between January 2011 and May 2011, 94 consecutive CABG patients (68 males, 26 females; mean age 61.4±10.9 years; range 38 to 87 years) who were operated in our clinic were enrolled in this prospective observational study. Logistic regression analysis was performed for the factors influencing the occurrence of postoperative atrial fibrillation. The perioperative parameters (Gensini score, Rentrop score, number of revascularized vessels, dominant coronary artery system, revascularization of the dominant coronary artery system, left main coronary artery disease, clinical status on admission, left ventricular dysfunction, and left atrium diameter) were analyzed as independent variables. Results:­Twenty-three patients (24.5%) developed perioperative atrial fibrillation. Twenty patients returned to normal sinus rhythm with amiodarone therapy. In-hospital mortality was observed in three patients (3.2%). There was no statistically significant difference in mortality rates among the patients with and without atrial fibrillation. Left ventricular dysfunction (p=0.034) and left main coronary artery disease (p=0.019) were found to be significantly associated with the occurrence of postoperative atrial fibrillation. The rate of renal complications (p=0.030) and the need for sternal revision surgery (p=0.003) were not significantly different between both groups. Conclusion:­ Postoperative atrial fibrillation is a frequently encountered complication of cardiac surgery. The left ventricular dysfunction is a significant risk factor for postoperative occurrence of atrial fibrillation. Although no significant association between coronary vasculature and atrial fibrillation, the left main coronary artery disease is a serious risk factor for postoperative atrial fibrillation.

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

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.

Objective The purpose of this study is to describe morphologic features and delayed contrast-enhancement pattern of the noncompaction of the left ventricle in cardiac magnetic resonance (MR) imaging. Methods We retrospectively reviewed morphological cardiac MR imaging findings of ventricular noncompaction in 15 patients (eight men, seven women, and ages 6 months to 73 years old, mean 22 year). In 10 patients delayed contrast enhanced images were obtained after the morphological examination. Results In all patients, noncompaction was seen in the apical and midventricular-lateral segment. Basal-septal segment involvement was not determined in any patients. Noncompacted/compacted ratio was 2–4.5 (mean 3). In nine patients, right ventricular involvement was observed in addition to left ventricular noncompaction. Delayed contrast-enhancement was seen in eight out of 10 patients not only involved segments but also normal segments of the heart. Conclusion Cardiac MR imaging is a valuable imaging method in patients with suspected ventricular noncompaction by showing increased trabeculations, deep intertrabecular recesses and fibrosis. Fibrosis is a common finding in ventricular noncompaction.

Objectives: Increased homocysteine (HCY) levels are associated with an increased risk of cardiovascular disease. Plasma HCY is increased in chronic heart failure (CHF) patients, and previous studies suggest that hyperhomocysteinemia causes adverse cardiac remodeling and affects pump function. We aimed to evaluate the HCY levels in patients with diastolic heart failure with preserved left ventricular ejection fraction (LVEF). Methods: We prospectively studied 68 patients (39 females and 29 males) who were hospitalized for symptomatic heart failure, as well as 40 age- and sex-matched healthy subjects who comprised the control group. CHF was diagnosed in all cases based on Framingham diagnostic criteria. CHF with preserved LVEF was defined as cases with CHF with an LVEF of 50% or more. Patients with regional left ventricular wall motion abnormalities, atrial fibrillation, and renal failure were excluded. Results: The mean age was 65.5 ± 9.6 years in the heart failure group and 65.2 ± 9.7 years in the control group. The mean LVEF was 59.8 ± 5.3 in the heart failure group and 61.4 ± 5.2 in the control group. The mean total fasting HCY concentrations were significantly higher in patients with heart failure (16.9 ± 5.27 µmol/l vs. 10.15 ± 3.49 µmol/l, respectively; p < 0.001). Multiple regression analysis indicated that NT-proBNP, hs-CRP, E/A ratio, and HbA1C were independently associated with hyperhomocysteinemia. Conclusions: Our results suggest that hyperhomocysteinemia is prevalent in heart failure with preserved ejection fraction. Larger scale studies are needed to clarify its pathogenic mechanisms and effects on the natural history of heart failure.

Aspirin resistance may increase the risk of major adverse cardiac events (MACE) more than threefold in patients with stable coronary artery disease (CAD). This study aimed to determine the prevalence of aspirin resistance in patients with stable CAD, the role of aspirin resistance on outcome in the follow-up, and the effect of clopidogrel therapy in MACE prevention in aspirin-resistant individuals. We detected the prevalence of aspirin resistance in 234 patients with stable CAD. Platelet function was determined by PFA-100 with collagen and/or epinephrine and collagen and/or ADP cartridges. The mean follow-up time was 20.6 +/- 6.9 months. The primary endpoints of the study were occurrence of myocardial infarction, unstable angina, stroke and cardiac death. Of patients, 22.2% (n = 52) were aspirin resistant by PFA-100. During follow-up, MACE occurred in eight patients (15.4%) with aspirin resistance and in 20 patients (11.0%) with aspirin-sensitive platelet aggregation (P = 0.269). MACE increased in aspirin-resistant patients after termination of clopidogrel therapy. Eleven patients experienced MACE after cessation of clopidogrel therapy (P < 0.001). The MACE risk in patients with stable CAD having detected aspirin resistance was similar compared with patients having aspirin-sensitive platelet aggregation by PFA-100. The MACE prevalence increased during follow-up, however, just after cessation of clopidogrel therapy.

Although the MR imaging features of cardiac masses and their differential diagnosis are well defined in the literature, we present a report of two lately observed myxoma cases, which were not seen on non-contrasted sequences, but were well visualized after contrast administration. From this point of view, we think that it would be adequate to call these tumors as “ghost tumors”. To the best of our knowledge, this is the very first report of MR imaging findings of mobile pediculated intracardiac masses, and it is our belief that mobile intracardiac masses do not cause a phase difference and therefore cannot be observed on non-contrasted sequences. Furthermore, we would like to stress that contrast administration is required in order to differentiate “ghost tumors” from completely resolved intracardiac thrombus.

Although it is well known that chronic effect of smoking on cardiovascular system, relation between coronary vascular reactivity and ventricular functions after acute smoking has not been well understood. The purpose of this study was to assess the relation between coronary flow velocity reserve and ventricular diastolic functions measured by tissue Doppler imaging after acute smoking. We found that coronary flow velocity and diastolic functions of right ventricle were decreased. Also, there was a correlation between coronary flow velocity reserve and diastolic ratio of the ventricle. Acute smoking may affect diastolic functions of the ventricles, especially right ventricle via changes of coronary flow.

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.

OBJECTIVE Standard echocardiographic methods reflect chamber dynamics and do not provide a direct measure of myocardial fiber shortening. Therefore we evaluated longitudinal left ventricular myocardial function by tissue Doppler echocardiography; strain (S), strain rate (SR), tissue Doppler velocity (TDV) in newly diagnosed mild to moderate hypertensive patients. METHODS Our cross-sectional and observational study population consisted of 57 patients and 48 normotensive control subjects. Patients with obesity, diabetes mellitus, regional wall motion abnormality, secondary hypertension and a history or clinical evidence of cardiovascular disease, arrhythmias or conduction abnormalities were excluded from the study. Ejection fraction, endocardial fractional shortening (eFS), meridional end-systolic stress (mESS), stress-adjusted eFS (observed /predicted eFS) were measured by M-mode echocardiography. Relationship between the left ventricular mass index and mESS was assessed by Pearson's linear regression model. RESULTS Hypertensive patients had significantly decreased longitudinal myocardial function compared to control subjects determined by septal (-1.25+/-0.30 vs. -1.02+/-0.33, p

Longitudinal myocardial function (LMF) may be impaired while systolic function is still normal. We investigated relationship between LMF and hypertensive organ damage in newly diagnosed stage I hypertensive patients. A total of 57 patient with never treated stage I hypertension and 48 matched healthy control subject were enrolled in the study. Conventional 2-D, Doppler and tissue wave Doppler imaging (TDI) echocardiography were used. LMF was evaluated by the septal and lateral strain (S) and strain rate (SR) measurements. Hypertensive complications were evaluated by the urine microalbumin levels and retinal examination. A multivariate regression analysis was perfomed to assess the relation between the variables. Ejection fraction, mid-wall fractional shortenning, systolic movement rates (TDs) in TDI were similar both in hypertensive and control groups. In patients with left ventricular hypertrophy, septal TDs (7.29 +/- 1.28 vs. 8.06 +/- 1.19 cm, P = 0.03), lateral TDs (8.46 +/- 1.83 vs. 9.87 +/- 2.42 cm, P = 0.01) and lateral S (-13.02 +/- 7.83 vs. -18.86 +/- 8.60%, P = 0.01) values were significantly lower. Septal S (-13.67 +/- 3.52 vs. -19.09 +/- 5.96%, P0.01) and SR (-0.83 +/- 0.29 vs. -1.22 +/- 0.28 1/S, P0.01) were significantly decreased in hypertensive patients with microalbuminuria. Septal S value was also significantly decreased in patients with retinopathy (-14.76 +/- 5.55 vs. -20.20 +/- 5.44%, P = 0.01). Multivariate analysis showed that only septal and lateral S values were independent factors for the retinopathy and left ventricular hypertrophy, respectively. In hypertensive patients, LMF established by the measurement of S and SR, might be impaired and also related with end organ damage while global circumferential function is preserved.

Multiple myeloma (MM) is associated with amyloidosis in approximately 15% of the patients. The most frequent presenting signs of such an association are nephrotic syndrome, cardiomyopathy and peripheral neuropathy. Amyloid arthropathy is not a frequent feature. We report a patient with immunoglobulin D (IgD) lambda type MM with presenting symptoms related to mucocutaneous amyloidosis and also amyloid arthropathy. He had no clinical and laboratory involvement due to nephrotic syndrome or cardiomyopathy. IgD myeloma is a rare form of MM and therefore much of the information about the disease is derived from case reports describing patients with associated symptoms. Our case also shows an unusual organ distribution of amyloid.

Aspirin resistance could be defined as thrombotic and embolic cardiovascular events despite regular aspirin therapy. The study aimed to determine the profile and prevalence of aspirin resistance in coronary artery disease patients. We evaluated the prevalence of aspirin resistance in a cohort of 505 patients with the diagnosis of coronary artery disease taking 80-300 mg regular aspirin daily. Platelet functions were analyzed by the Platelet Function Analyzer (PFA)-100 with collagen and epinephrine cartridges and collagen and ADP cartridges. A closure time of 186 s or less with the collagen and epinephrine cartridge was defined as aspirin resistance. Of the patients, 118 (23.4%) were aspirin resistant by the PFA-100. Aspirin-resistant patients were more likely to be older than aspirin-sensitive patients (P = 0.024). No statistically significant differences between the aspirin-resistant and aspirin-sensitive individuals were present in gender, major risk factors of coronary artery disease, number and localization of involved coronary vessels, serum lipid levels, and blood counts. According to the high prevalence of coronary heart disease, many people are affected by aspirin resistance, which may play a role in adverse cardiovascular events. Monitoring of platelet function in patients with coronary heart disease may support the optimization of antiplatelet therapy with additional and/or alternative agents.

Summary Objective Relationship between adult growth hormone deficiency (AGHD) and increased cardiovascular disease risk is very well known in hypopituitary patients treated with conventional hormone replacement therapy other than growth hormone (GH) administration. Endothelial dysfunction, an early and reversible event in pathogenesis of atherosclerosis, is associated with increased vascular smooth muscle tone, arterial stiffening and intima-media thickness (IMT). Coronary flow reserve (CFR) measurement by transthoracic Doppler echocardiography (TTDE) reflects coronary microvascular and endothelial functions, as a cheaper and an easy screening test. We have used TTDE to evaluate endothelial function and coronary microvascular function in AGHD. Design Cross-sectional observational study. Patients A total of 10 GH-deficient adults on conventional replacement therapy other than GH (4 males, 6 females; mean age 37 ± 11 years) and 15 healthy subjects (7 males, 8 females; mean age 41 ± 11 years) were studied. Patients and controls were all nonsmokers, normotensive and nondiabetic. Measurements IGF-1, free T4, lipid profile, insulin, glucose, insulin resistance (IR), anthropometrical and physical parameters were recorded. CFR recordings and IMT measurements were performed using the Vivid 7 echocardiography device. Results IMT were significantly higher in patients than controls (0·70 + 0·19 mm and 0·53 + 0·13 mm, respectively; P = 0·02). CFR was significantly lower in patients than in controls (1·96 ± 0·35 and 2·62 ± 0·45, respectively; P

The diagnosis of subclinical hypothyroidism and detection of its effects on cardiovascular system is important. Also, the patients with subclinical hypothyroidism even at the very early stage are at increased risk for developing atherosclerosis. We evaluated coronary microvascular circulation and endothelial dysfunction of epicardial coronary arteries by the measurement of coronary flow velocity reserve via a non invasive technique, transthoracic Doppler echocardiography in subclinical hypothyroidism. Coronary flow reserve in patients with subclinical hypothyroidism such as in overt hypothyroidism was lower than that of euthyroid subject. As a conclusion, endothelial and microvascular dysfunction, which are early harbingers of atherosclerosis, are shown in overt and subclinical hypothyroidism.