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.

Epicardial Fat Tissue Thickness and Omentin in Patients with Atrial Fibrillation

Abstract Background: Although electrical and structural remodeling has been recognized to be important in the pathophysiology of atrial fibrillation, the mechanisms underlying remodeling process are unknown. There has been increasing interest in the involvement of inflammatory molecules and adipokines released from the epicardial fat tissue in the pathophysiology of atrial fibrillation. Objectives: In our study, we aimed to investigate the relationship of atrial fibrillation with increased epicardial adipose tissue, inflammatory molecules released from this tissue and omentin. Methods: Thirty-six patients who were followed up with a diagnosis of permanent AF at the cardiology outpatient clinic 33 individuals without atrial fibrillation (controls) were included in the study. Epicardial adipose tissue thickness of patients was measured by echocardiography. Serum omentin, IL 6, IL 1 beta, TNF alpha and CRP levels were measured. Man-Whitney U test was performed for comparisons and significance was established at 5% (p<0.05). Results: Epicardial adipose tissue thickness was significantly greater in the patient group (6mm [4-5.5]) than controls (4mm [3-5.5]) (p <0.001). No significant difference was found in the concentrations of omentin or inflammatory molecules between the groups. Conclusion: No relationship was found between atrial fibrillation and serum levels or omentin or inflammatory markers. A relationship between epicardial adipose tissue thickness measured by echocardiography and atrial fibrillation was determined.

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.

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.

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.

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.

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.

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.

[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.

What have we learned from Turkish familial hypercholesterolemia registries (A-HIT1 and A-HIT2)?

BACKGROUND AND AIMS: Familial hypercholesterolemia (FH) is a common genetic disease of high-level cholesterol leading to premature atherosclerosis. One of the key aspects to overcome FH burden is the generation of large-scale reliable data in terms of registries. This manuscript underlines the important results of nation-wide Turkish FH registries (A-HIT1 and A-HIT2). METHODS: A-HIT1 is a survey of homozygous FH patients undergoing low density lipoprotein (LDL) apheresis (LA). A-HIT2 is a registry of adult FH patients (homozygous and heterozygous) admitted to outpatient clinics. Both registries used clinical diagnosis of FH. RESULTS: A-HIT1 evaluated 88 patients (27 ±â€¯11 years, 41 women) in 19 centers. All patients were receiving regular LA. There was a 7.37 ±â€¯7.1-year delay between diagnosis and initiation of LA. LDL-cholesterol levels reached the target only in 5 cases. Mean frequency of apheresis sessions was 19 ±â€¯13 days. None of the centers had a standardized approach for LA. Mean frequency of apheresis sessions was every 19 ±â€¯13 (7-90) days. Only 2 centers were aware of the target LDL levels. A-HIT2 enrolled 1071 FH patients (53 ±â€¯8 years, 606 women) from 31 outpatients clinics specialized in cardiology (27), internal medicine (1), and endocrinology (3); 96.4% were heterozygous. 459 patients were on statin treatment. LDL targets were attained in 23 patients (2.1% of the whole population, 5% receiving statin) on treatment. However, 66% of statin-receiving patients were on intense doses of statins. Awareness of FH was 9.5% in the whole patient population. CONCLUSIONS: The first nationwide FH registries revealed that FH is still undertreated even in specialized centers in Turkey. Additional effective treatment regiments are urgently needed.

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.

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.

Safety of once- or twice-daily dosing of non-vitamin K antagonist oral anticoagulants (NOACs) in patients with nonvalvular atrial fibrillation: A NOAC-TR study.

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.

Is CHA2DS2-VASc Score Different in Patients with Non-valvular Atrial Fibrillation Suffering from Cerebral and Non-cerebral Thromboembolism?CHA2DS2-VASc Score in Thromboembolism.

BACKGROUND: Thromboembolic complication is directly related to CHA2DS2-VASc score in patients with non-valvular atrial fibrillation (NVAF). In this study we compared the CHA2DS2-VASc score and in-hospital mortality between NVAF patients with non-cerebral thromboembolism and those with stroke. METHODS: We retrospectively reviewed medical records of 213 patients with NVAF who experienced stroke and 115 patients with NVAF who experienced non-cerebral thromboembolism between 2010 and 2015. In all patients, CHA2DS2-VASc score before the event was calculated. RESULTS: The mean CHA2DS2-VASc score was similar in patients with stroke (4.52±1.66) and those with non-cerebral thromboembolism (4.29±2.02) (p=0.196). In-hospital mortality rate was similar between the groups (19% vs. 17%, p=0.756). The rates of coronary artery disease (52% vs. 38%, p=0.014), prior transient ischemic attack (16% vs. 5%, p=0.001), and prior non-cerebral thromboembolism (18% vs. 3%, p<0.001) were higher in patients with non-cerebral thromboembolism. Warfarin (55% vs. 14% p<0.001) and antiplatelet use (56% vs. 40%, p=0.004) was more common in the non-cerebral embolism group, while non-vitamin K antagonist oral anticoagulant (NOAC) use was more common in the stroke group (15% vs. 7% p=0.026). CONCLUSION: The patients with stroke had similar CHA2DS2-VASc score and in-hospital mortality compared to patients with non-cerebral thromboembolism.

The effect of sleep apnea severity on cardiac autonomic activity during night time in obstructive sleep apnea patients / O efeito da gravidade da apneia do sono sobre atividade cardíaca autonômica durante o período noturno em pacientes com apneia obstrutiva do sono

ABSTRACT CONTEXT AND OBJECTIVE: Impaired autonomic cardiac function is an important consequence of obstructive sleep apnea (OSA). This impairment is mainly due to intermittent hypoxia episodes following apneas. However, the impact of apnea severity on autonomic cardiac function remains unclear. The aim of this study was to evaluate the relationship between the severity of sleep apnea and heart rate turbulence (HRT) and heart rate variability (HRV) in OSA. DESIGN AND SETTING: Observational cross-sectional study conducted in the Departments of Cardiology and Pulmonary Diseases, Afyon Kocatepe University, Turkey. METHODS: 106 patients with OSA and 27 healthy volunteers were enrolled. Based on apnea hypopnea index (AHI) values, obstructive sleep apnea severity was classified as follows: mild OSA (AHI ≥ 5 and < 15), moderate OSA (AHI ≥ 15 and ≤ 30) and severe OSA (AHI > 30). HRV and HRT parameters were assessed via 24-hour digital Holter electrocardiogram recordings for all subjects. RESULTS: HRV and HRT results were significantly lower among OSA patients than among control subjects (P < 0.05). However, there were no significant differences in HRT and HRV between the three patient subgroups. Correlations did emerge between AHI and the NN-interval parameter RMSSD and between oxygen desaturation and turbulence slope (respectively: r = -0.22, P = 0.037; and r = -0.28, P = 0.025). CONCLUSION: HRT and HRV results deteriorate in OSA. Correlations between apnea severity and these parameters seem to be present.

RESUMO CONTEXTO E OBJETIVO: Função autonômica cardíaca prejudicada é consequência importante da apneia obstrutiva do sono (AOS). Este prejuízo deve-se principalmente a episódios de hipóxia intermitente após apneias. No entanto, o impacto da gravidade da apneia na função cardíaca autonômica permanece obscuro. O objetivo deste estudo foi avaliar a relação entre gravidade da apneia do sono com turbulência da frequência cardíaca (TFC) e variabilidade da frequência cardíaca (VFC) em pacientes com AOS. DESENHO E LOCAL: Estudo observacional transversal conduzido nos Departamentos de Cardiologia e Doenças Pulmonares, Afyon Kocatepe University, Turkey. MÉTODOS: 106 pacientes com AOS e 27 voluntários saudáveis foram recrutados. Com base nos valores do índice de apneia-hypopneia (IAH), a gravidade da apneia obstrutiva do sono foi classificada assim: AOS leve (IAH ≥ 5 e < 15), AOS moderada (IAH ≥ 15 e ≤ 30) e AOS grave (IAH > 30). Parâmetros da VFC e TFC foram avaliados por meio de gravações de eletrocardiograma digital Holter de 24 horas para todos os sujeitos. RESULTADOS: Os resultados da VFC e TFC foram significativamente menores nos pacientes com OSA, em comparação com indivíduos controle (P < 0,05). No entanto, não houve diferenças significativas em VFC e TFC, entre os três subgrupos de pacientes. Correlações surgiram entre IAH e o parâmetro do intervalo-NN, RMSSD, e entre dessaturação de oxigênio e declive da turbulência (respectivamente; r = -0,22, P = 0,037; e r = -0,28, P = 0,025). CONCLUSÃO: Os resultados da VFC e TFC deterioram em AOS. Parece haver relação entre a gravidade da apneia e tais parâmetros.