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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 C, (Gly389Arg) and cardiac β-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. Supplementary Information The online version contains supplementary material available at 10.1007/s11033-021-06816-w.

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.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.A significant decrease in pulse wave velocity in the breast-fed group was detected compared to the non-breast-fed group (P0.05) 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.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.

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-firinogen -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 signifiantly 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 signifiant 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% confience 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 A, PAI-1 4G/5G, HPA1, MTHFR C677T, MTHFR A1298C, ACE I/D, APO B R3500Q ve APOE polimorfiminin kardiyovasküler hastalık Strip panel kullanılarak etkilerini değerlendirmeyi planladık. Hastalar iki gruba ayrıldı: PAD’lı 100 hasta (50 DM+, 50 DM-), PAD olmayan 60 kontrol hasta (30 DM+, 30 DM-). Bulgular: MTHFR A1298C ve PAI 4G/5G homozigot polimorfimi, PAD hastalarında kontrol grubuna göre anlamlı derecede yüksek bulundu (sırasıyla, p=0.035, p=0.004). Diğer genotipler ve polimorfim sıklıkları arasında anlamlı bir ilişki bulunamamıştır. Ayrıca DM varlığında PAI 4G/5G homozigot polimorfimi PAD oluşumunu etkili olduğu belirlendi (p=0.021). Regresyon analizinde PAD oluşumunda DM+ hastalarda PAI-1 4G/5G gen homozigot polimorfimi 17.1 kat daha riskli, (p=0.008) Gü- ven Aralığı (GA) %95 (2.113–138.660), MTHFR A1298C homozigos polimorfimi 316.6 kat daha riskli (p

Background The European Atherosclerosis Society Familial Hypercholesterolaemia Studies Collaboration (FHSC) global registry provides a platform for the global surveillance of familial hypercholesterolaemia through harmonisation and pooling of multinational data. In this study, we aimed to characterise the adult population with heterozygous familial hypercholesterolaemia and described how it is detected and managed globally. Methods Using FHSC global registry data, we did a cross-sectional assessment of adults (aged 18 years or older) with a clinical or genetic diagnosis of probable or definite heterozygous familial hypercholesterolaemia at the time they were entered into the registries. Data were assessed overall and by WHO regions, sex, and index versus non-index cases. Findings Of the 61 612 individuals in the registry, 42 167 adults (21 999 [53.6%] women) from 56 countries were included in the study. Of these, 31 798 (75.4%) were diagnosed with the Dutch Lipid Clinic Network criteria, and 35 490 (84.2%) were from the WHO region of Europe. Median age of participants at entry in the registry was 46.2 years (IQR 34.3-58.0); median age at diagnosis of familial hypercholesterolaemia was 44.4 years (32.5-56.5), with 40.2% of participants younger than 40 years when diagnosed. Prevalence of cardiovascular risk factors increased progressively with age and varied by WHO region. Prevalence of coronary disease was 17.4% (2.1% for stroke and 5.2% for peripheral artery disease), increasing with concentrations of untreated LDL cholesterol, and was about two times lower in women than in men. Among patients receiving lipid-lowering medications, 16 803 (81.1%) were receiving statins and 3691 (21.2%) were on combination therapy, with greater use of more potent lipid-lowering medication in men than in women. Median LDL cholesterol was 5.43 mmol/L (IQR 4.32-6.72) among patients not taking lipid-lowering medications and 4.23 mmol/L (3.20-5.66) among those taking them. Among patients taking lipid-lowering medications, 2.7% had LDL cholesterol lower than 1.8 mmol/L; the use of combination therapy, particularly with three drugs and with proprotein convertase subtilisin-kexin type 9 inhibitors, was associated with a higher proportion and greater odds of having LDL cholesterol lower than 1.8 mmol/L. Compared with index cases, patients who were non-index cases were younger, with lower LDL cholesterol and lower prevalence of cardiovascular risk factors and cardiovascular diseases (all p, Pfizer Independent Grant for Learning Change [16157823]; Amgen; Merck Sharp Dohme; Sanofi-Aventis; Daiichi Sankyo; Regeneron; National Institute for Health Research (NIHR) Imperial Biomedical Research Centre, UK; NIHR; Czech Ministry of Health [NU20-02-00261]; Canadian Institutes of Health Research; Austrian Heart Foundation; Tyrolean Regional Government; Gulf Heart Association, The EAS FHSC is an academic initiative that has received funding from a Pfizer Independent Grant for Learning & Change 2014 (16157823) and from investigator-initiated research grants to the European Atherosclerosis Society-Imperial College London from Amgen, Merck Sharp & Dohme, Sanofi-Aventis, Daiichi Sankyo, and Regeneron. KKR acknowledges support from the National Institute for Health Research (NIHR) Imperial Biomedical Research Centre, UK. KID acknowledges support from a PhD Studentship from NIHR under the Applied Health Research programme for Northwest London, UK (the views expressed in this publication are those of the authors and not necessarily those of the National Health Service, the NIHR, or the Department of Health). TF was supported by a grant from the Czech Ministry of Health (NU20-02-00261). JG receives support from the Canadian Institutes of Health Research. The Austrian Familial Hypercholesterolaemia registry has been supported by funds from the Austrian Heart Foundation and the Tyrolean Regional Government. The Gulf Familial Hypercholesterolaemia registry was done under the auspices of the Gulf Heart Association.

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. Amaç: Koroner arter ektazisi (KAE), koroner arterin lümeninin lokalize veya yaygın olarak dilatasyonu olup, sağlıklı komşu damar segment çapınına göre en az 1.5 kat dilate olması olarak tanımlanmıştır. KAE’nin etiyolojisi hala tam olarak bilinmemektedir, ancak en olası nedenin ateroskleroz olduğu gösterilmiştir. Bu çalışmada, KAE hastalarında koroner ateroskleroz gelişiminde etkili olduğu düşünülen ve trombofiliye yol açtığı gösterilmiş bazı gen polimorfizmlerini değerlendirmeyi amaçladık. Yöntemler: Çalışmamızda KAE (n=66) ve kontrol (normal koroner arter) (n=32) grubundaki 98 hastada trombofili genleri olarak bilinen Faktör V Leiden (G1691A), Faktör V H1299R, Protrombin G20210A, Faktör XIII V34L, B-Fibrinojen-455 G> A, PAI-1 4G/5G, MTHFR C677T ve MTHFR A1298C polimorfizmi değerlendirildi. Bulgular: Gruplar karşılaştırıldığında klinik özellikleri ve trombofilik genlerdeki polimorfizm sıklığı her iki grupta benzer olduğu görüldü. Ancak, gruplar arasında heterozigot ve/ veya homozigot polimorfizmi olup olmayanlar karşılaştırıldığında, KAE grubunda trombofilik gen polimorfizm olanlar anlamlı olarak daha fazla görüldü (p=0.023). Sonuç: Trombofilik gen polimorfizmi, KAE oluşumu ve klinik görünümü ile ilişkili olabilir.

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.

WOS: 000464336000007, PubMed ID: 30982817, 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

Pulmonary hypertension (PH) is one of the major complications of obstructive sleep apnea syndrome (OSAS). Pulmonary arterial stiffness (PAS) can be used in determination of PH. The aim of the present study was to evaluate the PAS and cardiac function of patients with OSAS and analyses the relationship between OSAS severity and PAS. Sixty newly diagnosed patients with OSAS (mean age 49.6 ± 11.7 years) and 30 healthy controls (mean age 46.4 ± 14 years) were enrolled. Right ventricle (RV) and left ventricle (LV) echocardiographic parameters and PAS values of study groups were compared. There were no significant differences in terms of LV ejection fraction, LV Tei-index and tricuspid annular plane systolic excursion. PAS, mean pulmonary arterial pressure (PAP) and RV Tei-index were significantly higher but tricuspid annulus early diastolic myocardial velocity was lower in patients with OSAS than control subjects (respectively p

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).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.Values of SDNN and SDANN in the hypertension group were significantly lower than in the control group (P0.01 and P0.01, 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).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.

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.

WOS: 000433285000010, PubMed ID: 28968197, Once-daily dosing of non-vitamin K antagonist oral anticoagulants (NOACs) may increase patient adherence to treatment but may also be associated with a higher risk of bleeding. In this study, we investigated the adherence to once-or twice-daily dosing of NOACs and the risk of bleeding in nonvalvular atrial fibrillation (NVAF) patients. This multicenter cross-sectional study, conducted between 1 September 2015 and 28 February 2016, included 2214 patients receiving NOACs for at least 3 months, due to NVAF. Patients receiving once-daily or twice-daily NOAC doses were 1: 1 propensity score matched for baseline demographic characteristics and the presence of other diseases. The medication adherence was assessed by the 8-item Morisky Medication Adherence Scale. Risk factors were investigated in relation to minor and major bleeding. The mean age of patients was 71 +/- 10 years, and 53% of the patients were women. The medication adherence was lower in patients receiving twice-daily NOAC doses compared to once-daily-dose group (47% versus 53%, p = 0.001), and there was no difference between the groups in terms of minor (15% versus 16%, p = 0.292) and major bleeding (3% versus 3%, p = 0.796). Independent risk factors for bleeding were non-adherence to medication (OR: 1.62, 95% CI: 1.23-2.14, p = 0.001), presence of 3 or more other diseases (OR: 10.3, 95% CI: 5.3-20.3, p < 0.001), and HAS-BLED (Hypertension, Abnormal renal and liver function, Stroke, Bleeding, Labile INR, Elderly, Drugs or alcohol) score (OR: 4.84, 95% CI: 4.04-5.8, p < 0.001). In summary, the once-daily dose of NOACs was associated with increased patient adherence to medication, while it was not associated with bleeding complications.

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 Conclusions The degree of venous insufficiency increase in accordance with the mean pulmonary arterial pressure even in patients with preserved right ventricular function.

Unilateral absence of a pulmonary artery a very rare congenital disorder. We here present a case of a 22-year-old female patient with agenesis of the right pulmonary artery accompanying patent ductus arteriosus and Eisenmenger syndrome, diagnosed by chest X-ray and multidetector computed tomography 5 days after giving birth.

Objective: Cardiac autonomic dysfunction may develop in patients with polycystic ovary syndrome (PCOS). Heart rate variability (HRV) and heart rate turbulence (HRT) are used in assessing cardiac autonomic functions. The goal of this study was to compare the cardiac autonomic functions in patients with PCOS and healthy controls. To our knowledge, this is the first study evaluating cardiac autonomic functions in patients with PCOS with respect to both HRV and HRT. Methods: Twenty-three patients with PCOS (mean age 22.8±3.9 years) and 25 healthy female volunteers who were matched for age and body mass index (BMI) (mean age 23.5±6.2 years) were enrolled in this as case-control study. Twenty-four hour ambulatory electrocardiogram recordings of all participants were taken using Pathfinder software. The time domain parameters of HRV and HRT, including turbulence onset (TO) and turbulence slope, were calculated. Diagnosis of PCOS was made with physical and laboratory findings of hirsutism or biochemical hyperandrogenism and chronic anovulation. Diabetes mellitus, other hormon disorders or hormon therapy, pregnancy, atrial fibrilation, obesite, chronic diseases, disorders of the autonomic nervous system, a history of drug use affecting the autonomic nervous system were excluded. Results: There were no significant differences in HRV and HRT parameters between the two groups. Cardiovascular risk factors, such as BMI, blood pressure, fasting blood glucose, and lipid parameters, were also similar. Triangular index measure of HRV was negatively correlated with high density lipoprotein cholesterol levels (r=-0.47, p

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.

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.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.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, P0.001), 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).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.

© 2015 CLINICS.Objective: Fibromyalgia is characterized by diffuse musculoskeletal pain and discomfort. There are several reports regarding autonomic nervous system dysfunction in patients with fibromyalgia. Heart rate turbulence is expressed as ventriculophasic sinus arrhythmia and has been considered to reflect cardiac autonomic activity. Heart rate turbulence has been shown to be an independent and powerful predictor of sudden cardiac death in various cardiac abnormalities. The aim of this study is to determine whether heart rate turbulence is changed in female patients with fibromyalgia compared with healthy controls. Methods: Thirty-seven female patients (mean age, 40±11 years) with fibromyalgia, and 35 age- and sexmatched healthy female control subjects (mean age, 42±9 years) were included. Twenty-four hours of ambulatory electrocardiography recordings were collected for all subjects, and turbulence onset and turbulence slope values were automatically calculated. Results: The baseline clinical characteristics of the two groups were similar. There were no significant differences in turbulence onset and turbulence slope measures between patients and control subjects (turbulence onset: −1.648±1.568% vs. −1.582±1.436%, p = 0.853; turbulence slope: 12.933±5.693 ms/RR vs. 13.639±2.505 ms/RR, p = 0.508). Although body mass index was negatively correlated with turbulence slope (r= −0.258, p = 0.046), no significant correlation was found between body mass index and turbulence onset (r= 0.228, p = 0.054). Conclusion: To the best of our knowledge, this is the first study to evaluate heart rate turbulence in patients with fibromyalgia. It appears that heart rate turbulence parameters reflecting cardiac autonomic activity are not changed in female patients with fibromyalgia.

Because transthoracic echocardiography is an inexpensive, easy, and reproducible method, it is the most commonly used noninvasive diagnostic tool to determine pulmonary artery pressure (PAP). Tissue Doppler imaging (TDI) emerged as a new echocardiographic method that can be applied in various clinical conditions. In our study we aimed to evaluate the relationship between tricuspid lateral annulus TDI parameters and pulmonary artery systolic pressure (PASP) as estimated by continuous wave Doppler in patients with chronic obstructive pulmonary disease (COPD). A total of 51 (42 men, mean age: 62.3 +/- 8.2 years) patients with clinically stable COPD were included in the study. The tricuspid annular systolic myocardial velocity (Sm), velocity time integral of Sm (SmVTI), early (Em) and late (Am) peak diastolic myocardial velocities, and myocardial isovolumic relaxation time (IVRTm) were acquired as well as two-dimensional (2-D) and conventional Doppler data. When compared with values of patients without pulmonary hypertension (PHT), Sm, SmVTI, Em, and Em/Am values were found to be lower and IVRTm values higher in patients with PHT. When all the patients were analyzed, there was a significant negative correlation between PASP and Sm and SmVTI (r = -0.82, p0.001 and r = -0.84, p0.001, respectively). Sm velocityor = 12 cm/s had a sensitivity of 85% and a specificity of 93.3% for predicting PASP40 mmHg. SmVTIor = 2.5 cm had a sensitivity of 85.7% and a specificity of 90% for detecting PHT. In our study, there was significant negative correlation between tricuspid lateral annular Sm and SmVTI values and PASP in patients with stable COPD irrespective of the presence of PHT. Tricuspid annular Sm and SmVTI had very good level sensitivity and specificity for predicting PHT. In conclusion, it might be suggested that in cases where noninvasive PASP measurement is not possible, TDI can be used as an alternative and reliable method to assess PAP.

Essential hyperhidrosis is a well recognized dermatologic and neurologic disorder, characterized by excessive sweating of the eccrine sweat glands. It is also associated with cardiac autonomic dysfunction because sympathetic fibers to eccrine glands of palms of the hand arise from stellate and upper thoracic ganglia, which also innervate the heart. In this study, we investigated cardiac function in patients with essential hyperhidrosis by conventional and tissue Doppler imaging methods. Eighteen subjects with essential hyperhidrosis and eighteen control subjects were included in this study. Pulsed-wave Doppler parameters of the left and right ventricles, which represent diastolic filling abnormalities, were obtained by conventional Doppler and tissue Doppler imaging. Isovolumetric relaxation time, isovolumetric contraction time, ejection time and myocardial performance index were also calculated. Mitral inflow peak early (E(M)) and late (A(M)) velocities and E(M)/A(M) ratio, which represent diastolic filling of left ventricle, were significantly lower in hyperhidrotic subjects than in controls. Also, mitral lateral annulus early and late velocities and early/late velocity ratio, reflecting diastolic filling of left ventricle, were significantly lower in hyperhidrotic subjects than those of controls. However, there were no differences between hyperhidrotic subjects and control subjects with regard to the other echocardiographic indices of left and right ventricle diastolic functions. In conclusion, decreased mitral inflow suggests left ventricle diastolic dysfunction in patients with essential hyperhidrosis. This indicates that hyperactivity of sympathetic nervous system in patient with hyperhidrosis may alter cardiac function in long term.

Background Essential hyperhidrosis, a disorder of the eccrine sweat glands, is associated with sympathetic overactivity and the aim of the present study was to determine endothelium-dependent vasodilator function in patients with this condition. Methods and Results Using high-resolution ultrasound, the diameter of the brachial artery at rest and during reactive hyperemia (flow-mediated dilatation, %FMD endothelial-dependent stimulus to vasodilatation), as well as after sublingual administration of nitroglycerin (%NTG endothelium-independent vasodilatation) was measured in 18 subjects (mean age 27±5 years) with essential hyperhidrosis and 24 healthy control subjects (mean age 29±5 years). Baseline brachial artery diameter and FMD were comparable in both groups (BAD: 4.1±0.7 mm vs 4.3±0.5 mm (control), p=0.8; FMD: 5.6±1.9% vs 6.7±2.2%, p=0.1). The time-averaged flow velocity during peak reactive hyperemia was similar in the 2 groups (75±11 cm/s vs 72±10 cm/s, p=0.5), nor did NTG-induced dilatation in the patients with essential hyperhidrosis differ significantly from that in healthy control subjects (12.8±2.7% vs 14.0±3.6%, p=0.3). Conclusion These findings suggest that endothelium-dependent dilatation of large conduit arteries is preserved in essential hyperhidrosis and it seems to be a localized disorder of the eccrine sweat glands rather than a generalized disorder involving vascular endothelium. (Circ J 2005; 69: 707 - 710)

It is well known that hypertrophic tonsils and adenoids may cause upper-airway obstruction. The aim of this study is to determine the mean pulmonary arterial pressure (mPAP) in children with hypertrophic tonsils and adenoids and to clarify whether tonsillectomy and adenoidectomy (TA) has any effect on mean pulmonary arterial pressure of these children.Fifty-two randomly selected children (36 male, 16 female) aged between 4 and 11 (mean 7.7+/-2.5) a with a diagnosis of upper-airway obstruction resulting from hypertrophied tonsils and adenoids were included in our study. Thirty-three children were assigned as controls with similar age and sex distribution with the study groups. Mean pulmonary arterial pressure was measured by using Doppler echocardiography preoperatively and mean 5.4+/-2.9 months postoperatively in all subjects.When the mean pulmonary arterial pressure values of study and control group compared preoperatively, the mean pulmonary arterial pressure levels of the children in the study group were significantly higher than the mean pulmonary arterial pressure levels of the children in the control group (P.05) (study group mean PAP=23.13+/-7.68, control group mean PAP=16.11+/-7.24) (Levene's test, P.05). When the preoperative and postoperative results were compared, it was found that there was a statistically significant decrease in mean pulmonary arterial pressures in these 52 children (preoperative mean PAP=23.13+/-7.68, postoperative mean PAP=17.00+/-6.99) (paired sample t test, P.05). Twenty-seven of the 52 subjects in the study group were pulmonary hypertensive preoperatively. mPAPs of 18 of these children decreased to normal range yielding 9 subjects, and this was also found ststistically significant (McNemar test, P.001).This study showed that obstructive adenoid and tonsillar hypertrophy causes higher mPAP values in children and revealed that TA is an effective therapeutic measure in such patients.

B2-agonists and anticholinergic drugs may alter cardiac autonomic modulation. The aim of this study was to investigate the effects of inhaled salbutamol and ipratropium bromide on heart rate variability (HRV).A randomized, double-blind, crossover design study was conducted on 13 healthy volunteers. Salbutamol, ipratropium or placebo was administered in three different testing sessions. Time domain parameters; mean R-R interval (mean-RR), the standard deviation of R-R interval (SDNN) and the root mean square of successive R-R interval differences (RMSSD) and power spectral analysis of HRV were assessed in the supine position and during handgrip exercise before and after taking each drug. In time domain analyses, ipratropium administration resulted in a reduced mean-RR, SDNN and RMSSD during handgrip exercise compared with baseline values (775 +/- 30 ms vs. 748 +/- 21 ms, P0.05; 57 +/- 5 ms vs. 50 +/- 5 ms, P0.05; 30 +/- 2 ms vs. 26 +/- 2 ms, P0.01, respectively). This effect was not detected with salbutamol or placebo administration. In frequency domain analyses, salbutamol but not ipratropium and placebo inhalation increased high frequency power/total power during handgrip exercise compared with baseline (0.09 +/- 0.02 vs. 0.12 +/- 0.02, P0.05).Ipratropium inhalation may alter autonomic control of the heart rate in therapeutic doses during mild sympathetic stimulation in healthy subjects, while salbutamol does not show these effects.

Long-term estrogen replacement therapy has favorable results on autonomic cardiovascular functions in postmenopausal women. Although acute estrogen administration has beneficial modulations on autonomic tone in animal studies, there are still controversies about the effects of acute estrogen on autonomic modulation to the heart in humans. The aim of this double-blind study was to investigate the acute effects of intranasal 17beta-estradiol administration on autonomic control of heart rate.Nineteen postmenopausal women with typical hormone profiles were crossover randomized to 300 micro g nasal 17beta-estradiol (Aerodiol, Servier, Chambray-les-Tours, France) or an identical placebo at least 5 days apart. Both time domain and frequency domain heart rate variability (HRV) parameters were obtained during controlled respiration (CR) and handgrip exercise (HGE), before and 45 min after 17beta-estradiol or placebo administration.Baseline HRV parameters were similar for each occasion. Time domain indices obtained after 17beta-estradiol administration were not significantly different from results obtained with the placebo. In frequency domain parameters, 17beta-estradiol administration resulted in a reduced low frequency to high frequency ratio (LF/HF ratio) when compared with the placebo during CR (0.72 +/- 0.09 vs 1.00 +/- 0.15, P0.05) but not during HGE (3.03 +/- 0.37 vs 2.86 +/- 0.30, P0.05).A single intranasal 17beta-estradiol administration acutely reduced sympathovagal balance to the heart during the course of parasympathetic maneuver in healthy postmenopausal women.

We present a case of a young boy in whom lacrimo-auriculo-dental-digital (LADD) syndrome with QT prolongation was detected. According to Bazett's formula, corrected QT was 504 ms. There were no published data about LADD syndrome with QT prolongation. This is the first case concerning LADD syndrome associated with QT prolongation. It is known that deafness and QT prolongation occur in potassium channel dysfunction. QT prolongation and deafness may be associated with potassium channel dysfunction in patients with LADD syndrome. As a result QT prolongation may be a new component of the LADD syndrome.

[No abstract available]

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, β-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.

We describe a 60-year-old woman with an anomalous right coronary artery originating from the tubular portion of the ascending aorta. The anomaly was diagnosed incidentally by transthoracic echocardiography. (J Am Soc Echocardiogr 2002;15:264-6.)

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.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.HRV and HRT parameters were decreased in the patient group (SDNN; P0.001, SDANN; P0.009, RMSSD; P = 0.049, TO; P = 0.035, TS; P0.001). After 6 months of thyroid replacement therapy, there were no significant changes observed in either HRV or HRT.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.

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.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.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.

Patients with end-stage renal disease (ESRD) are likely to have cardiac autonomic dysfunction, which is related with an increased risk of sudden death. The aim of this study is to detect cardiac autonomic dysfunction in patients with ESRD and to evaluate the possible acute effects of hemodialysis (HD) on cardiac autonomic functions measured by heart rate variability (HRV) and heart rate turbulence (HRT). Thirty-one (mean age 50 ± 13 years, 15 males) with ESRD on regular HD program and 31 healthy volunteers (mean age 51 ± 12 years, 15 males) were included in the study. Twenty-four-hour ambulatory electrocardiogram recordings were taken from the subjects before and after HD and from the control group. Heart rate variability and HRT parameters were calculated from these recordings. All of the HRV and HRT parameters were found to be significantly blunted in patients in comparison with healthy individuals. There were significant differences in HRV after HD, but similar differences were not observed in HRT parameters. Cardiac autonomic functions were significantly altered in patients with ESRD. Heart rate turbulence parameters seemed to be less affected from HD and may be more useful in the evaluation of cardiac autonomic functions in the ESRD population.

WOS: 000287018600003, PubMed: 21131254, Objective: Rheumatoid arthritis (RA) is a chronic systemic disease. The risk of cardiovascular morbidity and mortality is high in patients with RA. Heart rate turbulence (HRT) expresses ventriculophasic sinus arrhythmia and has been considered to reflect cardiac autonomic activity. It has been shown that HRT is an independent and powerful predictor of mortality. The aim of this study is to determine if HRT changes in patients with RA in comparison with the healthy controls. Methods: The study was performed as a cross-sectional study. Twenty-six patients with RA (mean age 56+/-10 year, 18 women) and 26 healthy controls (mean age 55+/-9 years, 18 women) were enrolled in this study. All participants underwent 24 hours Holter electrocardiogram monitoring. HRT measurements, turbulence onset (TO) and turbulence slope (TS), were calculated in patients and healthy controls that have at least one ventricular premature complex (VPC) in their Holter recordings. TO is a measure of the early sinus acceleration and TS is the measure of the rate of sinus deceleration that follows the sinus acceleration after a VPC. Mann-Whitney U test was used for comparison of continuous variables and the Chi-square test for comparison of categorical variables. Results: There were no statistically significant differences in TO and TS between the RA and control groups (TO: -2.2+/-3.1% vs -2.8+/-2.5%, p=0.25; TS: 11.5+/-9.7 ms/RR vs 15.5+/-10.9 ms/RR, p=0.10). Conclusion: HRT parameters, which determine the autonomic dysfunction, did not seem to be altered in patients with RA. (Anadolu Kardiyol Derg 2011 1: 11-5)

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. (PACE 2010; 929–933)

Acute effects of smoking on left and right ventricular function is determined by conventional and tissue Doppler imaging methods in this study. Pulsed-wave Doppler indices of the left and right ventricle diastolic function, including mitral and tricuspid inflow peak early and late velocity and their ratio were obtained from 20 healthy subjects by conventional Doppler and tissue Doppler imaging. Echocardiographic indices of left and right ventricles, including isovolumetric relaxation time, deceleration time, isovolumetric contraction time, ejection time, and myocardial performance index of right ventricle were measured before and 30 minutes after smoking a cigarette. Mitral and tricuspid inflow parameters and right ventricular myocardial performance index significantly altered after smoking a cigarette. Among the tissue Doppler imaging parameters, mitral and tricuspid lateral annulus diastolic, but not systolic, velocities altered after smoking a cigarette. Acute cigarette smoking alters left and right ventricular diastolic functions in healthy nonsmokers.

Acute cigarette smoking enhances adrenergic activity and thus may be associated with hemodynamic changes in the cardiovascular system. In this study, the acute effect of cigarette smoking on heart rate variability (HRV) was studied. Fifteen subjects were included in the study. Time domain (the mean R-R interval, the standard deviation of R-R interval, and the root mean square of successive R-R interval differences) and frequency domain (high-frequency, low-frequency ratio, and low-frequency/high-frequency ratio) parameters of HRV were obtained from all participants for each 5-minute segment: 5 minutes before and 5, 10, 15, 20, 25, and 30 minutes after smoking a cigarette. The mean R-R interval, the standard deviation of R-R interval, and the root mean square of successive R-R interval differences significantly decreased within the first 5-minute period compared with baseline, and then the standard deviation of R-R interval increased within the 20- to 30-minute period. The low-frequency high-frequency ratio significantly decreased within the first 5 minutes after smoking and then remained unchanged throughout the study period. Similarly, low-frequency and high-frequency power increased within the first 5 minutes compared with baseline. Acute cigarette smoking alters HRV parameters, particularly within the first 5 to 10 minutes after smoking.

Acute effects of smoking on left ventricular function have been studied previously. However, effects on right ventricular function have not yet been investigated. In this study, we attempted to investigate, through a combination of conventional and tissue Doppler imaging (TDI), the acute effects of smoking on both left and right ventricular function in chronic smokers. Thirty chronic smokers (with smoking habits ofor =1 pack/day for 74 +/- 1.3 years) underwent a complete transthoracic echocardiographic examination (2-dimensional, pulsed-wave Doppler transmitral and transtricuspid recordings, and TDI recordings of mitral and tricuspid annular velocities) by 3.5-MHz sector transducer. Pulsed-wave Doppler indices of left and right ventricular diastolic function-such as mitral and tricuspid inflows, peak early (E) and late (A) velocities, and E/A ratios-were obtained by conventional Doppler and TDI. Echocardiographic indices of the left and right ventricles--including isovolumetric relaxation time, isovolumetric contraction time, ejection time, and myocardial performance index of right ventricle-were also measured before and 30 minutes after each subject smoked a cigarette. Both mitral and tricuspid inflow measurements changed significantly after smoking a cigarette. Among the TDI measurements, mitral lateral annulus and tricuspid lateral annulus (diastolic, but not systolic) velocities changed after smoking a cigarette. Also, the right ventricular myocardial performance index increased immediately after smoking a cigarette. We found that acute cigarette smoking impaired both left and right ventricular diastolic function in chronic smokers.

Background: The aim of this study was to evaluate normal subjects with isolated left bundle branch block (LBBB) using tissue Doppler imaging (TDI) for the presence of intraventricular asynchrony. Methods and Results: For this purpose, 23 subjects with isolated LBBB were compared with age-matched asymptomatic healthy subjects without LBBB with respect to global ejection fraction (EF) and isovolumic contraction time (ICTm) in separate left ventricular segments. TDI evaluation revealed prolongation of the ICTm in all of the segments in the LBBB group. Moreover, the ICTm differed significantly in each segment in the LBBB group. The ICTm in the lateral segments were shown to be longer compared to the anteroseptal segments. Conclusion: Our results indicate the presence of intraventricular asynchrony in isolated LBBB. This fact may play a role in the decreased global EF and increased cardiac mortality in patients with isolated LBBB.

Atrial rhythm disturbances, particularly atrial fibrillation (AF), are frequently encountered in trained athletes. P wave dispersion (PWD) is a recent electrocardiographic (ECG) marker that reflects velocity of atrial impulse propagation. However, it remains unknown whether the P wave duration and PWD are different between athletes and sedentary controls. In this study we therefore determined the P wave duration and PWD, markers for conduction abnormalities, in trained athletes and controls. Fifty athletes and sex and age-matched 40 healthy sedentary controls were included in the study. All of the athletes were the members of a local athletic college and they were regularly maintaining their sportive activities; the duration of athletic competition was 7.7 +/- 3.3 years and the average athletic time was 10.1 +/- 1.6 hours/week. The 12-lead surface ECG was obtained from each subject in the supine position. The P wave duration was measured, and the difference between the maximum and minimum P wave duration was defined as the PWD. Distribution of sex, age, body mass index, blood pressure was similar in athletic groups and controls. Heart rate was significantly lower in the athletes than in the controls (66 +/- 7 vs 73 +/- 9 beats/min, p < 0.05). Maximum and minimum P wave durations were not statistically different in athletic group and controls (115 +/- 6 vs 114 +/- 4 ms and 74 +/- 8 vs 74 +/- 7 ms, respectively). In addition, PWD did not differ significantly in both groups (41 +/- 6 vs 40 +/- 7 ms, respectively). Thus, athlete's heart is not associated with prolonged P wave duration and increased PWD, indicating that P wave duration or PWD could not be used as a predictor for AF developed in trained athletes.

Cigarette smoking has been shown to temporarily alter cerebral flow velocity and vasomotor reactivity, so the aim of this study was to assess the acute effects of smoking a single cigarette on the common carotid artery (CCA) hemodynamics in healthy nonsmokers.Using a 7.0 MHz linear transducer of a computed sonography system, the CCA hemodynamics, including the diameter of the left and right CCA, peak systolic velocity, maximum end-diastolic velocity, time-averaged maximum velocity pulsatility index, resistivity index, flow volume, diameter and area of the CCAs, were measured in 16 healthy nonsmokers before and immediately after smoking a cigarette. Compared with the baseline, heart rate and blood pressure significantly increased, the diameter, flow volume and area of each CCA were unchanged, and the pulsatility index and resistivity index were significantly altered after smoking. In addition, the peak systolic velocity, maximum end-diastolic velocity and time-averaged maximum velocity were significantly altered after smoking.Cigarette smoking significantly altered the CCA hemodynamics in nonsmokers, probably as a consequence of enhanced adrenergic activity.

This study evaluated systemic and ocular acute safety and intraocular pressure (IOP)-lowering efficacy of travoprost 0.004% and bimatoprost 0.03%, compared to brimonidine 0.2% and betaxolol 0.25% in healthy subjects.Nineteen (19) young men, ages between 24 and 42, were enrolled in a single-center, institutional randomized, double-masked, crossover clinical trial. Baseline IOP, heart rate, blood pressure, and respiratory rate were recorded at hour 0. At minute 30, heart rate, blood pressure, respiratory rate, and spirometry were measured. At hour 1, color Doppler imaging of retrobulbar vessels was performed. At hour 2, heart rate, blood pressure, and respiratory rate were measured; spirometry and a 15-minute treadmill test were performed. The same protocol was applied after one drop of a study medication was instilled into each eye on four subsequent visits at 5-day intervals.Travoprost and bimatoprost did not cause significant reductions in systolic blood pressure during exercise and recovery. The mean respiratory rate and forced expiratory volume in 1 second were not significantly altered by any study medication. Travoprost reduced the resistive index and increased blood velocities in the ophthalmic artery and its branches. Bimatoprost caused a significant increase in end diastolic velocity of the ophthalmic artery. At hour 6, all medications reduced IOP significantly (p0.05). The most frequent ocular side effect of travoprost and bimatoprost was conjunctival hyperemia.Travoprost and bimatoprost were found to be systemically safe and caused an increase in blood-flow velocities of the retrobulbar vessels after a single-dose application. Their ocular hypotensive effect was comparable to that of brimonidine and greater than that of betaxolol in healthy subjects.

WOS: 000223781500007, PubMed: 15282063, Introduction and objectives. Rilmenidine is an antihypertensive drug whose anti hypertensive effect occurs via a sympatholytic action on the central nervous system. However, the effects of rilmenidine on autonomic cardiovascular function are not clear. The aim of this study was to evaluate the acute effect of rilmenidine on autonomic cardiac function by measuring heart rate variability. Subjects and method. A total of 20 healthy men (mean age, 26 3 years) were included in the study; 1 mg of rilmenidine or placebo was given to participants on different days in a double-blind crossover randomized study protocol. After drug administration, time domain and frequency domain parameters of heart rate variability were determined before and after 2 h with the patient in supine decubitus and during the handgrip exercise with 5-min electrocardiographic recordings. Results. Rilmenidine caused an increase in mean RR values after administration when compared to pre-drug administration recordings with the patient in supine decubitus (929 ms vs 860 ms, P

Dopamine2 (D2)-like receptor antagonists are widely used for the treatment of gastroparesis and vomiting. Metoclopramide (MCP), a peripheral and central D2-like receptor antagonist, stimulates the sympathetic nervous system and may alter autonomic modulation, but the net effect of MCP to the heart is not known. The aim of our study was to investigate the effects of MCP on cardiac autonomic modulation, using power spectral analysis of heart rate variability. We evaluated the effect of MCP on cardiac autonomic modulation during prolonged supine and standing positions in 9 healthy men. We intravenously administered 10 mg MCP and placebo in a double blind and crossover manner to all participants during continuous electrocardiography recording. Placebo or MCP was administered after 15 minutes in supine position (REST phase), where participants remained for an additional 50 minutes (PSUP phase) and then stood up for 10 minutes (STA phase). Five-minute intervals were selected for power spectral analysis, and average values were calculated for low frequency (LF), normalized unit of LF (LFnu), high frequency (HF), normalized unit of HF (HFnu) components of the power spectrum, and for LF/HF ratio.Heart rate alterations were statistically significant during placebo administration (Friedman's p < 0.0001). These changes were related to the decrease in PSUP phase and increase in STA phase in post hoc analyses. There was a trend toward lower LFnu in PSUP phase (Friedman's p = 0.050), but LF/HF ratio changes did not reach a statistically significant level during placebo administration. MCP administration prevented the decrease in heart rate and LFnu component was seen with placebo in PSUP phase. Heart rate alterations also reached a significant level during MCP administration (Friedman's p = 0.002), and post hoc analyses showed that these changes were mainly related to the increase in STA phase. In contrast to placebo, MCP administration resulted in significant alterations in LFnu and LF/HF ratio (Friedman's p = 0.004 and p = 0.003, respectively). Two-way ANOVA model for LF/HF ratio changes showed that MCP induced a significant upward shift in LF/HF ratio than placebo during each phase of the study (F = 5.570; p = 0.031). We concluded that the net effect of MCP on sympathovagal balance is an increased sympathetic drive to the heart. MCP prevented the decrease in sympathetic drive to the heart during prolonged supine position and augmented sympathetic drive to the heart during mild sympathetic stimulation such as induced by standing up.

Background: Sildenafil is an effective and widely used therapeutic agent for erectile dysfunction. Deaths have been reported due to sildenafil use and most of them are attributed to concurrent use of nitrates. However, the effects of sildenafil on QT intervals, QT dispersion, and the possible risk of ventricular arrhythmia have not been studied before. Our aim in this study was to evaluate the effect of sildenafil citrate on QT intervals and QT dispersion. Methods: Thirty-six patients with erectile dysfunction were included in this study. Twenty-one patients had coronary artery disease whereas 12 of them also had accompanying diabetes mellitus. Standard 12-lead electrocardiograms (ECG) were recorded three times: before, and at the first and fourth hours of 50 mg sildenafil citrate ingestion. All QT parameters were corrected for heart rate. Results: Mean age of the patients was 54 ± 12 years. The mean heart rate did not differ significantly between the three ECG examinations. The corrected and uncorrected maximum and minimum QT intervals were not significantly different between the three ECG examinations. The QT dispersion and corrected QT dispersion before and 1 hour and 4 hours after sildenafil ingestion were 31 ± 9 ms, 36 ± 10 ms; 32 ± 11 ms, 37 ± 14 ms; 27 ± 8 ms, 32 ± 9 ms, respectively (P > 0.05). Conclusions: Sildenafil does not prolong QT intervals or increase QT dispersion in patients with erectile dysfunction. Our results suggest that the risk of ventricular arrhythmia does not increase with ingestion of 50 mg sildenafil.

Cardiac involvement in rheumatoid arthritis (RA) has been reported previously. However, evaluation of ventricular function in this disease by the use of recently proposed Doppler echocardiographic methods has not been reported before. Thus, the aim of this study was to evaluate ventricular function by measurement of myocardial performance index (MPI) and transmitral flow propagation velocity (TFPV). Thirty-two patients with long-standing RA and 32 control subjects (mean ages 52 +/- 11 and 50 +/- 10 years, respectively) participated in this study. Systolic function was assessed by subjective evaluation of wall motion for both ventricles and by fractional shortening for the left ventricle (LV). LV diastolic function was evaluated by standard pulsed-wave Doppler echocardiography, MPI and TFPV. Right ventricular (RV) function was evaluated by MPI. No subject had signs or symptoms of clinically overt heart failure. Systolic function was normal in all subjects. Among the echocardiographic indices of LV diastolic function the peak E velocity, E velocity/A velocity ratio, isovolumetric relaxation time, MPI and TFPV in the RA group were significantly different from those of the controls ( P0.05). However, we did not observe a significant difference in RV echocardiographic indices between the two groups. Our results show that there is LV diastolic dysfunction in patients with long-standing RA. The lack of a history of cardiotoxic antirheumatic drug use among our patients suggests that this abnormality is due to RA itself.