Determination of microRNAs associated with adverse left ventricular remodeling after myocardial infarction.

Increasing evidence indicates that microRNA (miRNA) regulated mechanisms in myocardial healing and ventricular remodeling following acute myocardial infarction (AMI). We aim to comprehensively investigate changes of exosomal miRNA profile during the post-MI period and determine potential miRNAs associated to adverse left ventricular remodeling (ALVR). We prospectively evaluated ST-elevated MI patients with cardiac magnetic resonance imaging at the 2 weeks and 6 months after AMI (n = 10). ALVR was defined as an increase in LV end-diastolic and end-systolic volume > 13%. The blood samples were taken for miRNA measurements at the baseline, 2 and 6 weeks after AMI. In the miRNA profile assessment, 8 miRNAs were identified that were associated ALVR (miR-199a-5p, miR-23b-3p, miR-26b-5p, miR-301a-3p, miR-374a-5p, miR-423-5p, miR-483-5p and miR-652-3p). Three of them (miR-301a-3p, miR-374a-5p and miR-423-5p) differed significantly between patients with and without ALVR during follow-up period and the rest of them during the acute phase of AMI. The detection of these miRNAs, which have different role in various pathways, necessitate future mechanistic studies unravel the complex remodeling process after AMI.

Admission Monocyte/HDL Ratio Predicts Adverse Cardiac Remodeling After St-Elevation Myocardial Infarction.

Background: Inflammation plays a critical role in cardiac remodeling after myocardial infarction (MI). Monocyte to high-density lipoprotein-cholesterol (HDL-C) ratio (MHR) has emerged as a potential indicator of inflammation. Objectives: The study aimed to investigate the prognostic role of MHR at the time of hospital admission in late cardiac remodeling and subsequent 1-year mortality in an academic training and research hospital. Methods: This prospective multicenter study included 231 patients with acute ST-elevation MI. Left ventricular (LV) functions and volumes were assessed by cardiac magnetic resonance (CMR) imaging at 2 weeks and 6 months post-MI. The definition of adverse cardiac remodeling (AR) was based on the increase of LV end-diastolic volume by ≥ 12% at 6 months post-MI. All patients were followed for survival for 1 year after the second CMR imaging measurements. Results: At 6 months post-MI, 20 patients (23.8%) exhibited AR. The median MHR was higher in the AR group compared to the group without AR (2.2 vs. 1.5, p < 0.001). A positive correlation was found between MHR and infarct size in the groups with and without AR. High MHR was an independent predictor of AR (OR: 3.21, p = 0.002). The cut-off value of MHR in predicting AR was found to be >1.6 with 92.7% sensitivity and 70.1% specificity (AUC ± SE: 0.839 ± 0.03, p < 0.001). Mortality risk was 5.62-fold higher in the group with MHR of >1.6 (HR: 5.62, p < 0.001). Conclusions: These results indicate that admission MHR is a useful tool to predict patients with AR who are at risk of progression to heart failure and mortality after MI.

The evaluation of the metabolic and autonomic predictors of cardiovascular diseases in relation to prostatic hyperplasia symptoms.

OBJECTIVES: High prevalence of cardiovascular diseases is present in benign prostatic hyperplasia patients. Risk prediction models were developed for early identification of these cardiovascular risks. We aimed to evaluate cardiovascular metabolic and autonomic predictors in relation to lower urinary tract symptoms' severity evaluated by the IPSS score. METHODS: This study included 318 healthy individuals recently diagnosed with BPH. Laboratory tests including metabolic, hormonal and inflammatory markers were recorded. The cardiovascular risk indices like the atherogenic index of plasma and the triglyceride glucose index were calculated. The heart rate recovery after graded exercise was calculated. RESULTS: There was a significant positive correlation between the IPSS score and both the atherogenic and the triglyceride glucose indices (r = 0.388, p < 0.01 and r = 0.109, p = 0.032, respectively). IPSS score was also significantly negatively correlated with heart rate recovery specially at the 3rd minute after exercise (r = -0.547, p < 0.01). On the other hand, the IPSS score had a significant positive correlation with the inflammatory markers and a significant negative correlation with serum testosterone levels. CONCLUSIONS: Our study results suggest the presence of a combination of hormonal and inflammatory changes in BPH patients affecting the severity of LUTS which is correlated with metabolic and autonomic parameters that can predict an increased risk of CVD (Tab. 3, Ref. 47).

Is there a relationship between heart rate recovery and blood pressure in white coat hypertension?

Aim    Increasing evidence suggests that autonomic dysfunction may be involved in the etiology of white coat hypertension (WCH). The aim of this study was to evaluate cardiac autonomic function by using heart rate recovery (HRR) indices in patients with WCH classified according to their circadian rhythm type of blood pressure (BP).Material and methods    This cross-sectional study included 120 participants over the age of 18 yrs, including 50 patients diagnosed with WCH and 70 healthy controls with normal in- and out-of-office BP and without any known disease. Circadian rhythm types, i.e., dippers and non-dippers, were identified using ambulatory BP monitoring. The HRR indices were calculated by subtracting the 1st-minute (HRR1), 2nd-minute (HRR2), and 3rd-minute (HRR3) heart rates from the maximal heart rate recorded during stress testing.Results    The lesser decline in nighttime BP (6.4±2.14 and 13.3±2.2 mmHg, respectively; p<0.001) and the smaller mean HRR1 (25.5±3.0 and 30.3±3.1 beats / min, respectively; p<0.001) were evident in WCH non-dippers compared to WCH dippers. Linear regression analysis showed that HRR1 (ß±SE=0.43±0.11; p<0.001) and diastolic BP at maximum exercise (ß±SE=0.14±0.07; p=0.040) are independent risk factors for the blunted decline in nighttime BP.Conclusion    Delayed recovery of heart rate after an exercise stress test is associated with non-dipper type of circadian rhythm of BP. This was more pronounced in WCH patients, and these patients are at risk of autonomic dysfunction.

The relationship of benign prostatic hyperplasia's symptoms severity with the risk of developing atrial fibrillation.

Background: Attention is drawn to the increased incidence of atrial fibrillation (AF) in benign prostatic hyperplasia (BPH) patients recently. Early predicting of AF in these patients can help in decreasing its clinical consequences. The aim of our study is to determine the association between BPH symptoms and AF predictors atrial electromechanical delay (AEMD) and the P-wave dispersion (PWD). Methods: 218 healthy individuals recently diagnosed with BPH were assigned into three groups according to symptoms severity using the International prostate symptom score (IPSS) questionnaire. The first group with mild symptoms (IPSS score between 0 and 7, n = 78), the second group with moderate symptoms (IPSS score between 8 and 19, n = 86), and the third group with severe symptoms (IPSS score between 20 and 35, n = 54). PWD and AEMD calculations were performed for all participants. Results: There were statistically significant differences between the three groups in terms of AEMD and PWD (p < .01 and p < .01, respectively). In all three study groups, a significant positive correlation was observed between IPSS questionnaire scores and both AEMD and PWD (for AEMD r = .29, p = .013 and for PWD r = .27, p = .017). On the other hand, there were significant differences between the three groups in terms of the inflammatory markers C-reactive protein (CRP) and fibrinogen (p < .01 and p < .01, respectively) and in terms of serum testosterone levels (p < .01). Conclusions: We concluded that periodic evaluation of patients with BPH in terms of symptoms severity can be helpful not only from urological aspect, but also in the early prediction of possible serious cardiovascular morbidity and mortality.

The Role of Interferons in Cardiac Remodeling after Acute Myocardial Infarction.

OBJECTIVE: To determine the relationship of serial interferon (IFN) measurements and adverse cardiac remodeling (AR) after myocardial infarction (MI). STUDY DESIGN: Observational multi-centre study. PLACE AND DURATION OF STUDY: Departments of Cardiology of Diskapi Yildirim Beyazit Training and Research Hospital, Ataturk Training and Research Hospital, Numune Training and Research Hospital, and Dr. Nafiz Sincan Korez State Hospital, Turkey, from June 2015 to June 2020. METHODOLOGY: Forty-seven patients with acute MI were included. IFN levels were measured on the first day and at 14 days and 45 days post-MI. Reverse cardiac remodeling (RR) and AR were defined as the reduction of left ventricular end-diastolic volume by ≥12% and increases of ≥12% by cardiac magnetic resonance imaging at the 6-month follow-up. Statistical significance was accepted as p<0.05. RESULTS: Median IFN-α (50.1 vs. 34.8 pg/mL, p=0.035), IFN-ß (39.1 vs. 23.0 pg/mL, p=0.013), and IFN-γ (26.7 vs. 18.5 pg/mL, p=0.023) levels on the first day post-MI were higher in the AR group compared to the RR group. At 14 days post-MI, IFN levels had decreased in the AR group, while they had not changed in the RR group. At 45 days post-MI, IFN levels were similar between the AR and RR groups. High IFN-α level on the first-day post-MI was an independent predictor of AR (OR: 1.23, 95% CI: 1.06-1.43, p=0.008). CONCLUSION: High IFN levels in the acute phase post-MI are associated with AR. Among IFNs, IFN-α is an important predictor of AR. Stable IFN levels appear to be associated with cardiac healing. KEY WORDS: Cardiac remodeling, Interferons, Inflammation, Myocardial infarction.

Association of changes in the infarct and remote zone myocardial tissue with cardiac remodeling after myocardial infarction: a T1 and T2 mapping study.

Tissue structure in the infarct and remote zone myocardium post-acute myocardial infarction (MI) may offer prognostic information concerning left ventricular remodeling. We aimed to identify or establish a relationship between adverse remodeling (AR) and changes (Δ) in T1, T2 mapping and extracellular volume (ECV) in post MI periods. Fifty-four MI patients underwent 3 Tesla CMR performed 2 weeks (acute phase) and 6 months post-MI. We measured T1 mapping with MOLLI sequences and T2 mapping with TrueFISP sequences. Hematocrit was quantified in scanning time. ECV was performed post-gadolinium enhancement. AR was defined as an increase of ≥ 10% in left ventricular end-diastolic volume in 6 months. In the acute phase post-MI, high T2 relaxation times of the infarct and remote zone myocardium were associated with AR (OR 1.15, p = 0.023 and OR 1.54, p = 0.002, respectively). There was a decrease in T2 relaxation times of the remote zone myocardium at 6 months in patients with AR (42.0 ± 4.0 vs. 39.0 ± 3.5 ms, p < 0.001), while insignificant difference was found in patients without AR. Increased ΔECV (%) and decreased remote ΔT2 values were associated with AR (OR 1.04, p = 0.043 and OR 0.77, p = 0.007, respectively). The diagnostic performance analysis in predicting AR showed that acute-phase remote T2 was similar to that of remote ΔT2 (p = 0.875) but was superior to that of ΔECV (%) (ΔAUC: 0.19 ± 0.09, p = 0.038). In both acute phase and change of 6 months post-MI, the T2 relaxation times in remote myocardium are independently associated with AR, and this suggests higher inflammation in the remote myocardium in the AR group than the other group, even though no significant pathophysiological difference was observed in the healing of the infarct zone between both groups.

The Relationship between Extracellular Volume Compartments and Matrix Metalloproteinases-2 in Left Ventricular Remodeling after Myocardial Infarction. / A Relação entre Compartimentos de Volume Extracelular e Matriz Metaloproteinase 2 na Remodelação do Ventrículo Esquerdo após o Infarto do Miocárdio.

BACKGROUND: Matrix metalloproteinases (MMPs) can affect myocardial extracellular volume (ECV) and its compartments, and this can provide more detailed information about the mechanism of adverse left ventricular (LV) remodeling (AR) after acute myocardial infarction (MI). OBJECTIVES: To investigate the role of changes (Δ) in ECV compartments (matrix volume (MVi) and cell volume (CVi)) in the development of AR after MI, and their relationship with MMP-2 expressions. METHODS: Ninety-two first MI patients who underwent 3 Tesla cardiovascular magnetic resonance imaging performed 2 weeks (baseline) and 6 months post-MI. We measured T1 mapping with MOLLI sequences. ECV was performed post-gadolinium enhancement. ECV and LV mass were used to calculate MVi and CVi. AR was defined as an increase of ≥ 12% in LV end-diastolic volume in 6 months. MMPs were measured using a bead-based multiplex immunoassay system at first day (baseline) and 2 weeks post-MI. P <0.05 was accepted as statistically significant. RESULTS: Mean ECV and mean MVi baseline levels were higher in AR group compared to without AR group (42.9±6.4 vs 39.3±8.2%, p= 0.037; 65.2±13.7 vs 56.7±14.7 mL/m2, p=0.010; respectively). CVi levels was similar between groups. A positive correlation was found between baseline levels of MMP-2 and baseline levels of ECV (r=0.535, p<0.001) and MVi (r=0.549, p<0.001). Increased ΔMVi levels was independently predictor of AR (OR=1.03, p=0.010). ΔMVi had superior diagnostic performance compared to ΔECV in predicting AR (ΔAUC: 0.215±0.07, p<0.001). CONCLUSION: High MVi levels are associated with AR, and ΔMVi was independently predictor of AR. This may be associated with MMP-2 release due to increased inflammatory response.

FUNDAMENTO: As matrizes metaloproteinases (MMPs) podem afetar o volume extracelular (VEC) e seus compartimentos, e isso pode oferecer informações mais detalhadas sobre o mecanismo de remodelação adversa (RA) do ventrículo esquerdo (VE) após o infarto agudo do miocárdio (IM). OBJETIVOS: Investigar o papel que as alterações (Δ) nos compartimentos de VEC (volume matriz (MVi) e volume celular (CVi)) desempenham no desenvolvimento de RA após o IM, e sua relação com as expressões de MMP-2. MÉTODOS: Um total de noventa e dois pacientes com primeiro IM passaram por exames de imagens por ressonância magnética cardiovascular 3 Tesla realizados 2 semanas (linha de base) e 6 meses após o IM. Medimos o mapeamento T1 com sequências MOLLI. O VEC foi obtido após o realce pelo gadolínio. O VEC e a massa do VE foram usados para calcular o MVi e o CVi. A RA foi definida como um aumento de ≥ 12% no volume diastólico final do VE em 6 meses. As MMPs foram medidas usando-se um sistema de imunoensaio multiplex em grânulos no primeiro dia (linha de base) e 2 semanas após o IM. Um P valor <0,05 foi aceito como estatisticamente significativo. RESULTADOS: Os níveis de linha de base de MVi média e VEC médio foram mais altos no grupo com RA em comparação com o grupo sem RA (42,9±6,4 vs. 39,3±8,2 %, p= 0,037; 65,2±13,7 vs. 56,7±14,7 mL/m2, p=0,010; respectivamente). Os níveis de CVi eram semelhantes entre os grupos. Foi encontrada uma correlação positiva entre os níveis de linha de base de MMP-2 e os níveis de linha de base de VEC (r=0,535, p<0,001) e MVi (r=0,549, p<0,001). O aumento dos níveis de ΔMVi foi um preditor independente da RA (RC=1,03, p=0,010). O ΔMVi teve um desempenho diagnóstico superior quando comparado ao ΔVEC na previsão do (ΔAUC: 0,215±0,07, p<0,001). CONCLUSÃO: Níveis altos de MVi estão associados à RA, e o ΔMVi foi um preditor independente de RA. Isso pode estar associado à liberação de MMP-2 devido ao aumento da resposta inflamatória.

Higher levels of TWEAK and matrix metalloproteinase-3 during the acute phase of myocardial infarction are associated with adverse left ventricular remodeling.

INTRODUCTION: It is known that the levels of tumor necrosis factor-like weak inducer of apoptosis (TWEAK/TNFSF12) increase after myocardial infarction (MI) and that it interacts with sCD163. It has also been argued that TWEAK can induce matrix metalloproteinases (MMPs) in macrophages. AIM: To investigate the roles of TWEAK, sCD163, and MMPs in left ventricular (LV) adverse remodeling (AR) in the early post-MI period. MATERIAL AND METHODS: Forty-six patients with ST-elevation myocardial infarction (STEMI) who underwent primary percutaneous coronary intervention were enrolled in the study. Post-MI LV functions and volumes were assessed by cardiac magnetic resonance imaging at 2 weeks and 6 months. Cytokines and MMPs were measured using a bead-based multiplex immunoassay system at 1 day (baseline) and 2 weeks post-MI. AR was defined as an increase in LV end-diastolic volume of ≥ 10% at the 6-month follow up. RESULTS: The TWEAK, MMP-2, and MMP-3 baseline levels were higher in the patients with AR than those without AR. At 2 weeks post-MI, these expression levels were similar in patients with and without AR, but sCD163 expression was increased in patients without AR. The TWEAK and MMP levels were positively correlated in the early period post-MI. At first day post-MI, higher levels of TWEAK and MMP-3 were predictors of AR (OR = 1.03, p = 0.006; OR = 1.08, p = 0.015; respectively). CONCLUSIONS: TWEAK can induce MMPs in the early period post-MI, and these higher levels contribute to development of AR. Increased sCD163 levels at 2 weeks post-MI seem to be associated with the healing process through neutralizing the excessive inflammatory effects of TWEAK.

Assessment of epicardial adipose tissue thickness and total calcium score in sarcoidosis patients.

OBJECTIVE: Increased thickness of epicardial adipose tissue (EAT) and the total coronary artery calcium score (TCACS) are independent predictors of atherosclerosis. The aim of this study was to investigate whether EAT thickness, measured using thoracic computed tomography, and TCACS were greater in patients with sarcoidosis. METHODS: This was a retrospective study. The details of participants who presented at the cardiology and pulmonology outpatient clinics between January 2011 and December 2018 with dyspnea, chest pain, or palpitations from the hospital data system were reviewed. Patients with transthoracic echocardiography and thorax computed tomography (CT) (CT) records were identified, and those who were diagnosed with sarcoidosis, had no other health problems, and did not take any medication were included in the study. RESULTS: A total of 45 controls and 78 sarcoidosis patients were enrolled. The mean age of the controls was 46.15±13.1 years, while it was 46.26±12.37 years in the sarcoidosis group, which represented no significant difference between the groups (p>0.05). When the groups were compared in terms of a fasting blood test, erythrocyte sedimentation rate (ESR), TCACS, EAT thickness, levels of C-reactive protein (CRP), total cholesterol, low-density lipoprotein (LDL), and triglycerides, it was observed that CRP and EAT thickness were higher in the sarcoidosis group. CONCLUSION: The results of this study indicated that the thickness of EAT calculated using thorax CT was greater in sarcoidosis patients; however, the TCACS was similar in both groups. In addition, there was a positive correlation between EAT thickness and the level of total cholesterol, LDL, triglycerides, CRP, and the sedimentation rate. These findings suggest that atherosclerosis may start earlier in those with sarcoidosis than in the healthy population.

A Relação entre Compartimentos de Volume Extracelular e Matriz Metaloproteinase 2 na Remodelação do Ventrículo Esquerdo após o Infarto do Miocárdio / The Relationship between Extracellular Volume Compartments and Matrix Metalloproteinases-2 in Left Ventricular Remodeling after Myocardial Infarction

Resumo Fundamento: As matrizes metaloproteinases (MMPs) podem afetar o volume extracelular (VEC) e seus compartimentos, e isso pode oferecer informações mais detalhadas sobre o mecanismo de remodelação adversa (RA) do ventrículo esquerdo (VE) após o infarto agudo do miocárdio (IM). Objetivos: Investigar o papel que as alterações (Δ) nos compartimentos de VEC (volume matriz (MVi) e volume celular (CVi)) desempenham no desenvolvimento de RA após o IM, e sua relação com as expressões de MMP-2. Métodos: Um total de noventa e dois pacientes com primeiro IM passaram por exames de imagens por ressonância magnética cardiovascular 3 Tesla realizados 2 semanas (linha de base) e 6 meses após o IM. Medimos o mapeamento T1 com sequências MOLLI. O VEC foi obtido após o realce pelo gadolínio. O VEC e a massa do VE foram usados para calcular o MVi e o CVi. A RA foi definida como um aumento de ≥ 12% no volume diastólico final do VE em 6 meses. As MMPs foram medidas usando-se um sistema de imunoensaio multiplex em grânulos no primeiro dia (linha de base) e 2 semanas após o IM. Um P valor <0,05 foi aceito como estatisticamente significativo. Resultados: Os níveis de linha de base de MVi média e VEC médio foram mais altos no grupo com RA em comparação com o grupo sem RA (42,9±6,4 vs. 39,3±8,2 %, p= 0,037; 65,2±13,7 vs. 56,7±14,7 mL/m2, p=0,010; respectivamente). Os níveis de CVi eram semelhantes entre os grupos. Foi encontrada uma correlação positiva entre os níveis de linha de base de MMP-2 e os níveis de linha de base de VEC (r=0,535, p<0,001) e MVi (r=0,549, p<0,001). O aumento dos níveis de ΔMVi foi um preditor independente da RA (RC=1,03, p=0,010). O ΔMVi teve um desempenho diagnóstico superior quando comparado ao ΔVEC na previsão do (ΔAUC: 0,215±0,07, p<0,001). Conclusão: Níveis altos de MVi estão associados à RA, e o ΔMVi foi um preditor independente de RA. Isso pode estar associado à liberação de MMP-2 devido ao aumento da resposta inflamatória.

Abstract Background: Matrix metalloproteinases (MMPs) can affect myocardial extracellular volume (ECV) and its compartments, and this can provide more detailed information about the mechanism of adverse left ventricular (LV) remodeling (AR) after acute myocardial infarction (MI). Objectives: To investigate the role of changes (Δ) in ECV compartments (matrix volume (MVi) and cell volume (CVi)) in the development of AR after MI, and their relationship with MMP-2 expressions. Methods: Ninety-two first MI patients who underwent 3 Tesla cardiovascular magnetic resonance imaging performed 2 weeks (baseline) and 6 months post-MI. We measured T1 mapping with MOLLI sequences. ECV was performed post-gadolinium enhancement. ECV and LV mass were used to calculate MVi and CVi. AR was defined as an increase of ≥ 12% in LV end-diastolic volume in 6 months. MMPs were measured using a bead-based multiplex immunoassay system at first day (baseline) and 2 weeks post-MI. P <0.05 was accepted as statistically significant. Results: Mean ECV and mean MVi baseline levels were higher in AR group compared to without AR group (42.9±6.4 vs 39.3±8.2%, p= 0.037; 65.2±13.7 vs 56.7±14.7 mL/m2, p=0.010; respectively). CVi levels was similar between groups. A positive correlation was found between baseline levels of MMP-2 and baseline levels of ECV (r=0.535, p<0.001) and MVi (r=0.549, p<0.001). Increased ΔMVi levels was independently predictor of AR (OR=1.03, p=0.010). ΔMVi had superior diagnostic performance compared to ΔECV in predicting AR (ΔAUC: 0.215±0.07, p<0.001). Conclusion: High MVi levels are associated with AR, and ΔMVi was independently predictor of AR. This may be associated with MMP-2 release due to increased inflammatory response.

The effects of Ramadan fasting on heart rate variability in healthy individuals: a prospective study.

OBJECTIVE: Ramadan fasting is one of the five fundamental rituals of Islam. Heart rate variability (HRV) is an independent predictor of increased mortality of patients with myocardial infarction and congestive heart failure. Although many patients in this region fast once a year, the effects of fasting on the HRV, which has a prognostic significance for patients with myocardial infarction and congestive heart failure, are not known. Therefore, the study on the effects of one month fast of HRV in healthy volunteers seems to be reasonable to address. METHODS: Our study is a prospective cohort study that includes a total of 40 healthy volunteers with sinus rhythm between 19 and 40 years of age (16 female and 24 male). HRV was determined twice by ambulatory 24-hour Holter recordings at fasting in the middle of Ramadan and first week after Ramadan month. Mean values of continuous variables were compared by using the Student t-test or Mann-Whitney U test. Paired t-test or Wilcoxon test were used for comparison of variables between groups. RESULTS: When two groups compared, statistically significant differences were found in terms of RR (p=0.049), SDNNI (p=0.010), rMSSD (p=0.009), pNN50 (p=0.015), T power (p=0.009), LF (p=0.008), Lfnu (p=0.002), HF (p=0.022) and Hfnu (p=0.013) values. CONCLUSION: In our study, HRV parameters were found to be increased in Ramadan month, so we think that Ramadan fasting enhances the activity of the parasympathetic system.

Assessment of atrial conduction time in patients with Behçet's disease.

OBJECTIVE: Behçet's disease is characterized by increased inflammatory activity, and there there might be an increased risk of atrial arrhythmia in patients with this disease. Our study is aimed to evaluate a novel method of measuring atrial electromechanical features expressed as interatrial and intraatrial electromechanical delay by tissue Doppler echocardiography in patients with Behçet's disease. METHODS: We evaluated 57 patients (mean age: 36.3±12.1 years) with Behçet's disease and 34 sex and age matched healthy volunteers (mean age: 38.4±8.6 years) as control group. P-wave dispersion (PWD) was calculated from the 12-lead surface ECG, interatrial and intraatrial electromechanical delay were measured by tissue Doppler imaging and conventional echocardiography. RESULTS: Interatrial electromechanical delay and intraatrial electromechanical delay were prolonged in patients with active Behçet's disease compared with the patients with inactive disease and the controls (p<0.0001, p<0.0001, p=0.013 and p=0.001, respectively). Erythrocyte sedimentation rate and high-sensitivity C-reactive protein values of of patients with active Behçet's were significantly higher than those with inactive Behçet's disease and the controls (p<0.0001 and p<0.0001, respectively). High-sensitivity C-reactive protein and erythrocyte sedimentation rate were correlated with interatrial electromechanical delay in patients with Behçet's disease (r=0.44, p=0.001 and r=0.64, p<0.0001, respectively). CONCLUSIONS: The prolongation of atrial electromechanical conduction might be related with changes in structure and electrophysiological properties of the atrial myocardium or the conduction system in patients with active Behçet's disease.

Endothelial nitric oxide synthase levels and their response to exercise in patients with slow coronary flow.

BACKGROUND: Endothelial dysfunction plays a key role in the aetiopathogenesis of slow coronary flow (SCF) even if there is no obstructive epicardial lesion. Reduced plasma levels of endothelial nitric oxide synthase (eNOS) are an important indicator of endothelial dysfunction. We aimed to determine plasma levels of eNOS and their relationship with exercise in patients with SCF. METHODS: Twenty-two patients with SCF in at least one coronary artery and 17 healthy individuals were included in this study. The TIMI frame count method was used to determine SCF. Plasma levels of eNOS before and after effort were determined in the patient and control groups. RESULTS: Basal eNOS levels in the patient group were lower than in the control group (p = 0.040), and plasma eNOS levels after exercise decreased more significantly in the patient group compared to the control group (p = 0.002). Median decreases of eNOS in response to exercise were higher in the SCF group than in the control group (p < 0.001), and the decrease observed in the control group was not statistically significant (p = 0.35). There were significantly negative correlations between TIMI frame count and plasma levels of eNOS at baseline and after exercise (r = -0.51, p = 0.015, r = -0.58, p = 0.005, respectively). Moreover, there was also a positive correlation between the rate-pressure product and plasma levels of eNOS after exercise in patients with SCF (r = 0.494, p = 0.019). CONCLUSION: Our findings indicate an important pathophysiological relationship between the severity of SCF in which endothelial dysfunction plays a role in its pathogenesis and the level of circulating plasma levels of eNOS.