Investigating changes in ß-adrenergic gene expression (ADRB1 and ADRB2) in Takotsubo (stress) cardiomyopathy syndrome; a pilot study.

BACKGROUND: Takotsubo Cardiomyopathy (TC) is a rare disorder that is mostly caused by stress and is often misdiagnosed. We aimed to analyze Takotsubo Syndrome at the molecular level by using the Oxford Nanopore Minion Device and its protocol. METHODS AND RESULTS: Ten patients who were previously diagnosed with Takotsubo Syndrome (increased after decrease in ejection fraction and without critical stenosis in coronary arteries) and 10 healthy individuals in the control group were included in our project. The mean age was 53 ± 12.2 for the patient group and 52.4 ± 9.9 for the control group, and the left ventricular ejection fraction was 50.3 ± 11.5 for the patient group and 64.2 ± 2.8 for the control group (p < 0.05). Peripheral blood of patients and healthy individuals was taken and their DNA was obtained. By making long reads throughout the genome, the most studied regions responsible for ß-adrenergic signaling pathways; The gene expression level of cardiac ß-1 ADRB1 (rs1801253-ENST00000369295.4), G > C, (Gly389Arg) and cardiac ß-2 ADRB2 (rs1800888-ENSG00000169252), C > T, (Thr165Ile) adrenoceptors was investigated. As a result; no structural variation was detected leading to Takotsubo Cardiomyopathy. The results obtained from the bioinformatics analysis were also checked from the VarSome Tools and similar results were found. CONCLUSIONS: Many publications in TC susceptibility have that may lead to adrenergic pathway dysregulation, most studied adrenergic receptor genes in the similar literatures too. We searched for genetic variants in b1AR and b2AR genes in our study and however we could not find any variants in this study, we think larger numbers of cohort studies are needed.

Primary pulmonary arterial hypertension with preserved right ventricular function leads to lower extremity venous insufficiency.

Objectives Pulmonary hypertension with heart failure is related to venous insufficiency. However, there is no clear data whether pulmonary arterial hypertension with preserved right ventricular function cause venous insufficiency. In this study, we aim to investigate the relation between pulmonary arterial pressure with venous insufficiency in pulmonary arterial hypertension patients with preserved right ventricular function. Methods Between January 2012 and October 2014, 38 patients with a diagnosis of pulmonary arterial hypertension and 47 control group patients were included. Venous disability score and venous segmental disease score of both groups were calculated in order to measure venous insufficiency. The relationship between venous disability score and venous segmental disease scores and mean pulmonary arterial pressure and World Heart Organization functional capacity was examined. Results Total venous segmental disease score (5 ± 3.9 vs. 2 ± 1.8 p < 0.001), right venous segmental disease score (2.6 ± 2.2 vs. 1 ± 0.9 p < 0.001), left venous segmental disease score (2.4 ± 2.2 vs. 1 ± 0.9 p < 0.001), and venous disability scores (2.2 ±1 vs. 1.6 ± 0.7 p < 0.001) of patients with pulmonary arterial hypertension were higher than the control group. While the total venous segmental disease score was highly related to mean pulmonary arterial pressure (r = 0.829, p < 0.001), the venous disability score was only weakly related (r = 0.343, p = 0.037). Total venous segmental disease score (r = 0.606, p < 0.001) and venous disability scores (r = 0.601, p < 0.001) were moderately related with World Health Organization functional capacity intensity. Conclusions The degree of venous insufficiency increase in accordance with the mean pulmonary arterial pressure even in patients with preserved right ventricular function.

The effect of septoplasty on pulmonary artery pressure and right ventricular function in nasal septum deviation.

Nasal septum deviation (NSD) can cause obstruction of the upper airway, which may lead to increased pulmonary artery pressure (PAP) and right ventricle dysfunction. The aim of the present study was to evaluate the effect of septoplasty on right ventricular function and mean PAP of patients with marked NSD. 25 patients with marked NSD (mean age = 31.8 ± 12.3 years) and 27 healthy volunteers (mean age = 34.5 ± 10.8 years) were enrolled. Echocardiography was performed for all subjects and right ventricular function and mean PAP were evaluated before and 3 months after septoplasty. Tricuspid annular plane systolic excursion (TAPSE) and tricuspid annulus early diastolic myocardial velocity (E') were significantly lower in patients with NSD than control subjects, while right ventricle myocardial performance index (RVMPI) and mean PAP were significantly higher (respectively, p = 0.006, 0.037, 0.049, 0.046). When preoperative and postoperative findings were compared, the mean PAP decreased whereas TAPSE increased significantly (respectively, p = 0.007, 0.03). The results of the present study demonstrated that mean PAP increased and right ventricular function worsened in patients with NSD. However, mean PAP decreased and right ventricular function tended to recover after septoplasty.

Autonomic modulation in hypertension without hypertrophy.

OBJECTIVES: Cardiac autonomic modulation and baroreflex sensitivity are altered in individuals with essential hypertension. Hypertension is considered as a strong and independent risk factor for supraventricular and ventricular arrhythmias. The aim of the present study was to evaluate cardiac autonomic control and the arrhythmogenic risk by using 24-h heart rate variability (HRV) and heart rate turbulence (HRT) analysis in essential hypertension without left ventricular hypertrophy (LVH). METHODS: Fifty-eight newly diagnosed untreated hypertensive patients without LVH (mean age 51 ± 12 years, 26 women) and 56 adult, healthy volunteers (mean age 49 ± 12 years, 24 women) were included in the study. Subjects with secondary causes of hypertension or autonomic dysfunction were excluded. The diagnosis of hypertension was based on ambulatory blood pressure monitoring results. Time-domain HRV parameters and HRT parameters were calculated from 24-hour Holter recordings. RESULTS: Values of SDNN and SDANN in the hypertension group were significantly lower than in the control group (P < 0.01 and P < 0.01, respectively). At least one of the turbulence onset (TO) and turbulence slope (TS) values were found abnormal in 10 of 32 hypertensive patients and in 5 of 24 control individuals (P = 0.38). There was no significant difference between HRT parameters, TO and TS (P = 0.67 and P = 0.12, respectively). CONCLUSIONS: Sympathetic tone begins to increase in hypertension before LVH develops. However, the impact of this increase on HRT is not clear. There is a need for further research to investigate the impact of hypertension and LVH on HRT.

The effect of zolmitriptan on cardiac autonomic modulation in patients with migraine: A double-blind, placebo-controlled, crossover study.

BACKGROUND: Triptans, which activate 5-hydroxytryptamine (5-HT)-1B/1D receptors in cerebral arteries, are very effective in aborting attacks of migraine. Although activation of 5-HT-1B/1D receptors diminishes the secretion of noradrenaline from cardiac sympathetic nerves, some studies report that they may cause chest discomfort, myocardial infarction and arrhythmias due to coronary vasospasm. The effect of zolmitriptan on cardiac autonomic modulation has not been evaluated in migraineurs. SUBJECTS AND METHODS: Ten patients with migraine (nine women, mean age 33 ± 4 years) were crossover randomized to 2.5 mg zolmitriptan or identical placebo at least 5 days apart. Both time domain parameters (the mean R-R interval, the standard deviation of RR interval [SDNN], and the root mean square of successive R-R interval differences) and frequency domain parameters (low frequency [LF], high frequency [HF], and LF/HF ratio) of heart rate variability (HRV) were obtained during supine position, controlled respiration and handgrip exercise before and 2 h after zolmitriptan or placebo administration. RESULTS: Baseline HRV parameters were similar for each occasion. Single dose zolmitriptan administration did not affect both time and frequency domain HRV parameters compared with the placebo. CONCLUSIONS: A single dose, 2.5 mg oral zolmitriptan administration did not change sympathetic and parasympathetic reactivity and sympathovagal balance in migraineurs.

Could Aneurysm and Atherosclerosis-Associated MicroRNAs (miR 24-1-5p, miR 34a-5p, miR 126-5p, miR 143-5p, miR 145-5p) Also Be Associated with Coronary Artery Ectasia?

Background: Coronary artery ectasia (CAE), known for localized or diffuse excessive dilatation of the coronary artery, has an unknown etiology, but it has been reported that the underlying cause may be atherosclerosis and genetic changes that may affect the arterial lumen. MicroRNAs have been shown to have an effect in aneurysm diseases and are known to contribute to vascular development and atherosclerosis. The purpose of this study was to investigate whether they are also associated with CAE. Methods: This cross-sectional study consisted of 25 patients with CAE and 25 subjects with normal coronary arteries. Blood was collected and miRNA expression was detected using the Rotor-GeneQ real-time polymerase chain reaction cycler (Qiagen) to investigate expression levels of miR-24-1-5p, miR-34a-5p, miR-126-5p, miR-143-5p, and miR-145-5p. Results: Demographic variables of CAE (mean age 59.5 ± 1.7; 12 women) and controls (mean age 57.2 ± 2.1; 16 women) were similar. miR-126-5p (p = 0.014) and miR-145-5p (p = 0.003) levels were found to be <2-fold upregulated in CAE compared to controls; miR-143-5p also showed upregulation, but it was not significant (p = 0.078). Conversely, miR-24-1-5p (p = 0.032) levels were downregulated in CAE compared to controls. miR-34a-5p was also downregulated, but this was not considered significant (p = 0.185). Conclusions: According to our study findings, miR-126-5p, miR-145-5p, and miR-24-1-5p may be associated with CAE. These microRNAs could be of diagnostic and therapeutic significance for further studies of CAE involving abnormal angiogenesis and vascular disorders and potentially serve as useful biomarkers.

The Definition of Sarcomeric and Non-Sarcomeric Gene Mutations in Hypertrophic Cardiomyopathy Patients: A Multicenter Diagnostic Study Across Türkiye.

BACKGROUND: Hypertrophic cardiomyopathy is a common genetic heart disease and up to 40%-60% of patients have mutations in cardiac sarcomere protein genes. This genetic diagnosis study aimed to detect pathogenic or likely pathogenic sarcomeric and non-sarcomeric gene mutations and to confirm a final molecular diagnosis in patients diagnosed with hypertrophic cardiomyopathy. METHODS: A total of 392 patients with hypertrophic cardiomyopathy were included in this nationwide multicenter study conducted at 23 centers across Türkiye. All samples were analyzed with a 17-gene hypertrophic cardiomyopathy panel using next-generation sequencing technology. The gene panel includes ACTC1, DES, FLNC, GLA, LAMP2, MYBPC3, MYH7, MYL2, MYL3, PLN, PRKAG2, PTPN11, TNNC1, TNNI3, TNNT2, TPM1, and TTR genes. RESULTS: The next-generation sequencing panel identified positive genetic variants (variants of unknown significance, likely pathogenic or pathogenic) in 12 genes for 121 of 392 samples, including sarcomeric gene mutations in 30.4% (119/392) of samples tested, galactosidase alpha variants in 0.5% (2/392) of samples and TTR variant in 0.025% (1/392). The likely pathogenic or pathogenic variants identified in 69 (57.0%) of 121 positive samples yielded a confirmed molecular diagnosis. The diagnostic yield was 17.1% (15.8% for hypertrophic cardiomyopathy variants) for hypertrophic cardiomyopathy and hypertrophic cardiomyopathy phenocopies and 0.5% for Fabry disease. CONCLUSIONS: Our study showed that the distribution of genetic mutations, the prevalence of Fabry disease, and TTR amyloidosis in the Turkish population diagnosed with hypertrophic cardiomyopathy were similar to the other populations, but the percentage of sarcomeric gene mutations was slightly lower.

Prevalence of myocardial infarction polymorphisms in Afyonkarahisar, Western Turkey.

The aim of the study was to investigate relationship between polymorphisms in genes that are clinical and environmental features and the risk of myocardial infarction (MI) in Afyonkarahisar subjects living in Turkey. Prevalence of the several genes polymorphisms, ≤45 (42.04 ± 3.3) and ≥46 (57.19 ± 7.5) years were studied in individuals with MI and without MI (40.30 ± 9.01) individuals were studied. We tested 140 with MI individuals for factor V (FV) Leiden, FV H1299R, Prothrombin G20210A, factor XIII (FXIII) V34L, ß-fibrinogen b-455G/A, plasminogen activator inhibitor-1 (PAI-1)-675 4G/5G, human platelet antigens 1 (HPA-1) a/b, apolipoprotein B (ApoB) R3500Q, apolipoprotein E (ApoE), E2, E3, and E4, angiotensin-converting enzyme (ACE) D/I, 5,10 methylenetetrahydrofolate reductase (MTHFR) 677C/T, and MTHFR 1298A/C polymorphisms using a ViennaLab CVD strip assay. This study results were compared without MI control groups. According to the our results, prothrombin, factor XIII and MTHFRC677T deletions were the most frequent genetic variants in risk groups of hyperlipidemic patients (value of odds ratio sequentially [OR] = 4.5, p = 0.05, [OR] = 2.16, p = 0.04 and [OR] = 2.8, p = 0.09). MTHFRA1298C and PAI-1 deletions were most frequent genetic variants in risk groups for MI in patients with diabetes mellitus (value of odds ratio sequentially [OR] = 3.79, p = 0.06 and [OR] = 5 × 10(8), p = 0.000). ACE deletions were positively associated with family history of cardiovascular events (OR = 3.62, p = 0.03). We found a strong relationship between genetic variants and risk factors. Significant associations between genetic variants predicting cardiovascular events and common risk factors (hyperlipidemia, smoking, diabetes mellitus and family history) patients were found.

The effect of breastfeeding during infancy on arterial stiffness in young adults.

BACKGROUND: Breastfeeding has many benefits for health, also later in life. However, its effects on the cardiovascular system are still unclear. The aim of the present study was to evaluate the effect of exclusive breastfeeding as infants on arterial stiffness in young adults having no cardiovascular risk factors, using aortic pulse wave velocity, and brachial and aortic augmentation index. METHODS: Eighty-six subjects were included in the study from similar socioeconomic status. 46 subjects who had received exclusive breastfeeding for the first 4-6 months in infancy (26 women, mean age 26.7±4 years) (group 1) and 40 subjects who had received exclusive breastfeeding for less than 3 months or had never been breast-fed (22 women, mean age: 28±3.8 years) (group 2) were recruited. Parameters of arterial stiffness (aortic pulse wave velocity, brachial and aortic augmentation index) were investigated using an arteriograph (TensioMed, Budapest, Hungary), which works on an ossilometric basis. RESULTS: A significant decrease in pulse wave velocity in the breast-fed group was detected compared to the non-breast-fed group (P<0.05) but no significant difference was detected for aortic and brachial augmentation index. In addition there was a significant relationship between breastfeeding duration and aortic pulse wave velocity. CONCLUSIONS: Breast milk intake in infancy reduces the risk of cardiovascular disease in young adults, independent of other cardiovascular risk factors. It seems that there is a negative relationship between the duration of breastfeeding and the risk reduction.

The Relationships Between Chocolate Consumption and Endothelial Dysfunction in Patients with Heart Failure.

OBJECTIVE: Dietary recommendations, in addition to medications, have recently become important in the treatment of heart failure. Our study aimed to show the positive effects of both milk chocolate and dark chocolate on heart failure through endothelial functions. METHODS: Twenty patients with heart failure and reduced ejection fraction were included in the study. In this randomized, crossover study, some of the patients consumed milk chocolate and some consumed dark chocolate. We recorded the patients' 6-minute walking tests, flow- mediated dilatation values, plasma catechin, epicatechin, and N-terminal pro-brain natri- uretic peptide values before and after chocolate consumption. After 2 weeks, their chocolate consumption was changed. The same parameters were measured again. RESULTS: A significant decrease was observed in N-terminal pro-brain natriuretic peptide values after consumption of both milk chocolate (356 ± 54.2 and 310 ± 72.1 pg/mL; P = .007) and dark chocolate (341 ± 57 and 301 ± 60.1 pg/mL;P=.028). Flow-mediated dilation values increased after dark chocolate consumption (8.9 ± 3% and 14 ± 4.5%; P = .019). CONCLUSION: Chocolate consumption acutely decreases N-terminal pro-brain natriuretic pep- tide values in heart failure. Dark chocolate consumption also seems to improve endothelial functions by increasing flow-mediated dilation values.

Do mobile phones pose a potential risk to autonomic modulation of the heart?

BACKGROUND: It has long been speculated that mobile phones may interact with the cardiac devices and thereby cardiovascular system may be a potential target for the electromagnetic fields emitted by the mobile phones. Therefore, the present study was designed to test possible effects of radiofrequency waves emitted by digital mobile phones on cardiac autonomic modulation by short-time heart rate variability (HRV) analysis. METHODS AND RESULTS: A total of 20 healthy young subjects were included to the study. All participants were rested in supine position at least for 15 minutes on a comfortable bed, and then time and frequency domain HRV parameters were recorded at baseline in supine position for 5 minutes. After completion of baseline records, by using a mobile GSM (Global System for Mobile Communication) phone, HRV parameters were recorded at turned off mode, at turned on mode, and at calling mode over 5 minutes periods for each stage. CONCLUSION: Neither time nor frequency domain HRV parameters altered significantly during off mode compare to their baseline values. Also, neither time nor frequency domain HRV parameters altered significantly during turned on and calling mode compared to their baseline values. Short-time exposure to electromagnetic fields emitted by mobile phone does not affect cardiac autonomic modulation in healthy subjects.

Heart rate variability and heart rate turbulence in hypothyroidism before and after treatment.

BACKGROUND: Cardiac autonomic dysfunction may develop in patients with clinical or subclinical thyroid hormone deficiency. Heart rate variability (HRV) and heart rate turbulence (HRT) are used for evaluating changes in cardiac autonomic functions and also used to provide risk stratification in cardiac and noncardiac diseases. The aim of this study is to evaluate cardiac autonomic functions before and 6 months after thyroid replacement therapy in patients with thyroid hormone deficiency. METHODS: Forty hypothyroid patients (mean age 48 ± 13, four male) and 31 healthy controls (mean age 51 ± 12, three male) were included in the study. Twenty-four hour ambulatory electrocardiogram recordings were taken using Pathfinder Software Version V8.255 (Reynolds Medical). The time domain parameters of HRV analysis were performed using the Heart Rate Variability Software (version 4.2.0, Norav Medical Ltd, Israel). HRT parameters, Turbulence Onset (TO), and Turbulence Slope (TS) were calculated with HRT! View Version 0.60-0.1 software. RESULTS: HRV and HRT parameters were decreased in the patient group (SDNN; P < 0.001, SDANN; P < 0.009, RMSSD; P = 0.049, TO; P = 0.035, TS; P < 0.001). After 6 months of thyroid replacement therapy, there were no significant changes observed in either HRV or HRT. CONCLUSIONS: Hypothyroidism may cause cardiac autonomic dysfunction. Treating hypothyroidism with L-thyroxine therapy does not effectively restore cardiac autonomic function. HRV and HRT can be used as to help monitor cardiovascular-related risk in this population.

Acute effects of moxonidine on cardiac autonomic modulation.

BACKGROUND: Moxonidine, an imidazoline I1 receptor agonist, is a centrally acting antihypertensive agent having sympatholytic effect. However, there are only limited data regarding the effects of this drug on autonomic cardiac functions. METHODS AND RESULTS: In this study we investigated the acute effects of moxonidine on cardiac autonomic modulation by heart rate variability (HRV) analysis. The effects of oral 0.4-mg moxonidine were studied on 11 healthy male volunteers in a randomized, double-blind, placebo controlled, and crossover study. After 15 minutes rest, time and frequency domain parameters of HRV were calculated from 5-minute continue electrocardiography recordings in supine position, during controlled respiration (15 breath/min) and during handgrip exercise before and 1 hour after taking placebo or moxonidine. Baseline parameters before taking placebo and moxonidine were similar (P > 0.05). Moxonidine, but not placebo, caused an increase in heart failure (HF) (119 +/- 21 vs 156 +/- 23, P = 0.029) and HFnu (39 +/- 4 vs 47 +/- 4, P = 0.033) and decrease in LFnu (61 +/- 4 vs 53 +/- 4, P = 0.033) and LF/HF ratio (1.96 +/- 0.36 vs 1.12 +/- 0.35, P = 0.010) in supine position compared with baseline parameters. However, there was no difference in other time or frequency domain parameters during controlled breathing and handgrip exercise either with moxonidine or placebo administration (P > 0.05). Single dose of moxonidine administration increases cardiovagal tone but parasympathetic and sympathetic autonomic maneuvers attenuated its short term effects on HRV in healthy male subjects.

Evaluation of the CT imaging findings in the diagnosis of pulmonary hypertension due to chronic thromboembolism.

PURPOSE: Chronic thromboembolic pulmonary hypertension (CTEPH) is the only pulmonary hypertension that can be treated surgically. Multidedector computerized tomography angiography (MDCTA) is considered as an important tool. In this study, the important CT findings of CTEPH and the vascular MDCTA findings of CTEPH were classified as central, peripheral, central and peripheral. The aim of this study was to investigate the relationship between these groups with parenchymal and hemodynamic findings. MATERIALS AND METHODS: MDCTA examinations of 26 patients who had been diagnosed with CTEPH were retrospectively reviewed. Vascular, cardiac and parenchymal findings were examined in MDCTA. Patients were divided into three groups as peripheral, central and peripheral and central chronic thromboembolism. The relationship between these groups with demographic, vascular, parenchymal and hemodynamic findings was investigated. RESULTS: The most common vascular finding was the wall filling defects attached to the lobar and/or segmental arterial walls, while the parenchymal finding was the fibrotic shrinkage. There were no statistically significant differences between the three groups compared to parenchymal findings which are mosaic pattern, brochiectasis, fibrotic changes and atelectasis, pulmonary artery diameter, right atrial diameter and RV/LV ratio. Age and sex were not different in patients between the three groups. CONCLUSION: The results of the this study confirm the important role of MDCTA in the evaluation of vascular, cardiac and parenchymal findings in the patients with CTEPH and identifying patients that would most benefit from surgical treatment by visualization of the segmental and subsegmental branches of the pulmonary arteries.

Analysis of thrombophilic gene mutations in coronary artery ectasia.

OBJECTIVE: Coronary artery ectasia (CAE) is defined as localized or diffuse dilatation in the coronary artery lumen of at least 1.5 times the diameter of adjacent healthy reference segments. The etiology of CAE is still unknown, but the most likely cause is atherosclerosis. The aim of this study was to evaluate several gene polymorphisms that are thought to have an effect on the development of coronary atherosclerosis and have been shown to cause thrombophilia in CAE patients. METHODS: The factor V Leiden (G1691A), factor V H1299R, prothrombin G20210A, factor XIII V34L, beta-fibrinogen-455 G>A, plasminogen activator inhibitor (PAI)-1 4G/5G, and methylenetetrahydrofolate reductase (MTHFR) C677T, and MTHFR A1298C polymorphisms were evaluated in 66 patients with CAE and 32 individuals with normal coronary arteries. RESULTS: Comparison of the CAE and control groups revealed that the clinical features and the frequency of polymorphism in the thrombophilic genes were similar in both groups. However, when heterozygous and/or homozygous polymorphism was compared between groups, it was found that there was a significantly higher finding of thrombophilic gene polymorphism in the CAE group (p=0.023). CONCLUSION: Thrombophilic gene polymorphism may be associated with the formation and clinical presentation of CAE.

The effects of genetic polymorphisms and diabetes mellitus on the development of peripheral artery disease.

OBJECTIVE: Peripheral artery disease (PAD) is a condition caused by the narrowing of limb arteries due to atherosclerosis. In recent years, polymorphisms in a number of genes have been shown to contribute to the risk of PAD development. However, whether the contribution of these inheritable factors is independent of traditional cardiovascular risk factors remains unclear. This study was an investigation of the effects of diabetes mellitus (DM) and genetic background, examined singly and together, on the pathogenesis of PAD. METHODS: The effects of the factor V Leiden (G1691A), factor V H1299R, prothrombin G20210A, factor XIII V34L, B-fibrinogen -455 G>A, PAI-1 4G/5G, HPA1, MTHFR C677T, MTHFR A1298C, ACE I/D, APO B R3500Q, and APOE polymorphisms were evaluated using a cardiovascular disease strip assay (CVD StripAssay). Two groups were created: 100 patients with PAD (50 with DM, 50 without DM) and 60 controls without PAD (30 with DM, 30 without DM). RESULTS: There was a significantly greater presence of the MTHFR A1298C and PAI 4G/5G homozygous polymorphisms in the PAD patients compared with the control group (p=0.035, p=0.004, respectively). There were no significant associations between the other genotypes and polymorphism frequencies. In the presence of DM, the PAI-1 4G/5G homozygous polymorphism was linked to the formation of PAD (p=0.021). Regression analysis indicated that the PAI-1 4G/5G gene homozygous polymorphism demonstrated a 17.1 times greater risk for DM with PAD [95% confidence interval (CI): 2.113-138.660; p=0.008] and the MTHFR A1298C homozygous polymorphism demonstrated a 316.6 times greater risk (95% CI: 10.763-9315.342; p<0.001) for the possibility of DM with PAD. CONCLUSION: The MTHFR A1298C and PAI 4G/5G homozygous polymorphisms may be associated with the development of PAD. The presence of the PAI 4G/5G homozygous polymorphism with DM was a powerful predictor for the development of PAD.

[Snapshot evaluation of heart failure in Turkey: Baseline characteristics of SELFIE-TR]. / Türkiye'de kalp yetersizliginin anlik görüntüsü: SELFIE-TR bazal karakteristik özellikleri.

OBJECTIVE: Heart failure (HF) is an important health issue of the 21st century and the prevalence in Turkey has been reported as 2.9%. A national profile, frequency data, characteristics of different phenotypes, and risk factors have not yet been well established. The Snapshot Evaluation of Heart Failure Patients in Turkey (SELFIE-TR) was an analysis of a representative sample of HF patients from Turkey. METHODS: A total of 23 centers with at least 2 cardiologists from the 12 NUTS-1 regions of Turkey were invited to participate in the research. The contributing centers shared the data of a consecutive enrollment of HF patients, as confirmed by an investigator, on a pre-selected day of each week for the month of October or November of 2015. RESULTS: The mean age of the entire cohort was 63.3+-13.3 years (male/female ratio: 751/303, 71.3%/28.7%). There were 712 acute HF patients and 342 chronic HF patients. The total number of HF patients with reduced ejection fraction (HFrEF), heart failure with mid-range ejection fraction, and heart failure with preserved ejection fraction was 801 (75%), 176 (16.7%), and 77 (7.3%), respectively. The patients with chronic HF were younger than those with acute HF (61.1+-13.3 years vs 67.9+-12.1 years; p<0.001). Among the whole cohort, hypertension was observed in 46%, diabetes mellitus was present in 27.5%, chronic obstructive pulmonary disease was present in 12.8%, and previous myocardial infarction was noted in 45.2%. In patients with HFrEF, the use of an angiotensin-converting enzyme inhibitor or angiotensin receptor blocker, a beta blocker, or a mineralocorticoid receptor antagonist was noted in 74.7%, 89.7%, and 60.9%, respectively. CONCLUSION: The SELFIE-TR findings provide important insight, since it is the first study to make a snapshot of HF patients in our country. These data may help to create standardized prevention and treatment strategies.

Arterial stiffness and dipper/nondipper blood pressure status in women with preeclampsia.

INTRODUCTION: The aim of this study was to investigate the clinical relevance of dipper status in women with preeclampsia by comparing arterial stiffness index (SI) values, and dipper and nondipper status. METHODS: A total of 60 pregnant women in their third trimester were enrolled in the study. SI values were measured using a digital photoplethysmographic method (Pulse Trace System, Micro Medical Ltd., Gillingham, Kent, UK). Twenty-four-hour ambulatory blood pressure was measured by a SpaceLabs 90217 oscillometric device (SpaceLabs Inc., Redmond, WA, USA). Systolic blood pressure (SBP), diastolic blood pressure (DBP), mean arterial pressure (MAP), and pulse pressure (PP) were recorded. Those preeclamptic women whose mean nighttime blood pressure measurements were at least 10% lower compared with mean daytime measurements were classified as dipper status, and those with a decrease of less than 10% were classified as nondipper status. RESULTS: Seventeen women were preeclamptic with a dipper status, 13 women had nondipper status preeclampsia, and 30 women were normotensive. SI values were significantly higher in preeclamptic women compared with normotensive women (8.8+/-1.2 m/s vs. 5.9+/-0.8 m/s, P<0.001), but SI values of preeclamptic women with dipper status and preeclamptic women with nondipper status did not differ significantly from each other (P=0.485). CONCLUSION: There was no significant difference in SI values between the dipper and nondipper preeclamptic groups. These results indicate that dipper and nondipper measurements may not be suitable for clinical follow-up of preeclamptic women.

The Genetic Determination of the Differentiation Between Ischemic Dilated Cardiomyopathy and Idiopathic Dilated Cardiomyopathy.

AIMS: Most dilated cardiomyopathies are either an ischemic dilated cardiomyopathy (IsDC) or an idiopathic dilated cardiomyopathy (IdDC). The treatments for both IsDC and IdDC are of a similar nature (upwards of 90%). Coronary revascularization, however, is only feasible for IsDC. The purpose of this study was to determine if microRNAs (miRNAs) could be used as biomarkers to distinguish between IsDC and IdDC. MATERIALS AND METHODS: Patients were divided into two groups: IsDC and IdDC, with 25 patients in each group, and 10 healthy persons serving as a control group. In our study, the following miRNA expressions were detected using the Rotor Gene Q real-time polymerase chain reaction cycler (Qiagen) for all IsDC and IdDC subjects: let-7b-5p, let-7c-5p, miR-1-3p, miR-15b-5p, miR-17-5p, miR-19a-3p, miR-19b-3p, miR-20a-5p, miR-20b-5p, miR-23a-3p, miR-24-3p, miR-27a-3p, miR-28-5p, miR-30e-5p, miR-99b-5p, miR-100-5p, miR-101-3p, miR-103a-3p, miR-106a-5p, miR-125b-5p, miR-126-3p, miR-126-5p, miR-140-5p, miR-191-5p, miR-195-5p, miR-199a-3p, miR-214-3p, miR-222-3p, miR-342-3p, and miR-378a-3p. RESULTS: We found that miR-24-3p, miR-28-5p, miR-100-5p, miR-103-3p, miR-125b5p, miR-214-3p, let-7b-5p, and let-7c-5p were each overexpressed by more than twofold in both the IsDC and IdDC groups when compared to the controls. We also found that miR-15b-5p and miR-106a-5p may be used to distinguish between patients with IsDC and IdDC. CONCLUSIONS: Our study has demonstrated that miR-15b-5p and miR-106a-5p expression levels could potentially serve as useful biomarkers for distinguishing between IsDC and IdDC.