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Brugada syndrome (BrS) is a rare disorder characterized by coved or saddle-shaped ST-segment elevation in the right precordial leads on the electrocardiogram. Risk stratification in BrS remains challenging. A number of clinical, electrocardiographic, programmed ventricular stimulation and genetic risk factors have been identified as important predictors of future major arrhythmic events. There is a positive association between the number of risk factors and arrhythmic events. Hence, a multi-parametric approach would provide comprehensive risk assessment and more accurate risk stratification, assisting in therapeutic decisions making, including implantable cardioverter-defibrillator placement or identification of low-risk individuals. However, the extent to which each variable influences the risk and non-linear interactions between the different risk variables make risk stratification challenging. This paper aims to provide a focused review of the multi-parametric risk models for BrS risk stratification published in the literature. [Abstract copyright: Copyright © 2022 Elsevier Inc. All rights reserved.]

Introduction: Neutrophil-activating peptide 2 (NAP-2, CXCL7), a platelet-derived neutrophil chemoattractant, is involved in inflammation. We investigated associations between NAP-2 levels, neutrophil extracellular traps (NETs) formation, and fibrin clot properties in atrial fibrillation (AF). Materials and Methods: We recruited 237 consecutive patients with AF (mean age, 68±11 years; median CHA2DS2VASc score of 3 [2-4]) and 30 apparently healthy controls. Plasma NAP-2 concentrations were measured, along with plasma fibrin clot permeability (Ks) and clot lysis time (CLT), thrombin generation, citrullinated histone H3 (citH3), as a marker of NETs formation, and 3-nitrotyrosine reflecting oxidative stress. Results: NAP-2 levels were 89% higher in AF patients than in controls (626 [448-796] vs. 331 [226-430] ng/ml; p2DS2-VASc score, or the AF manifestation. Patients with NAP-2 in the top quartile (>796 ng/ml) were characterized by higher neutrophil count (+31.7%), fibrinogen (+20.8%), citH3 (+86%), and 3-nitrotyrosine (+111%) levels, along with 20.2% reduced Ks and 8.4% prolonged CLT as compared to the remaining subjects (all ps. Conclusions: Elevated NAP-2, associated with increased oxidative stress, has been identified as a novel modulator of prothrombotic plasma fibrin clot properties in patients with AF.

Background: Chronic kidney disease (CKD) is considered a risk factor for thromboembolic and bleeding events in patients with atrial fibrillation (AF). Aims: We sought to assess predictors of clinical outcomes among AF patients with advanced CKD. Methods: In a prospective cohort study, we enrolled 180 AF patients with stage 4 CKD, defined as estimated glomerular filtration rate of 15–29 ml/min/1.73 m2, on vitamin K antagonists (n = 90), and non-vitamin K antagonists oral anticoagulants (n = 90). We assessed biomarkers, including growth differentiation factor-15, cystatin C, and high-sensitivity cardiac troponin T, and prothrombotic state parameters, including plasma fibrin clot permeability (Ks). Results: The median age of the patients was 71.0 (64.0–75.0) years (men 65.0%). The median estimated glomerular filtration rate was 24.0 (21.0–25.0) ml/min/1.73 m2 while the median CHA2DS2-VASc score was 3.0 (2.0–4.0). Age (hazard ratio [HR], 1.11; 95% confidence interval [CI], 1.02–1.20) and decreased Ks (HR, 0.55; 95% CI, 0.34–0.90) were associated with thromboembolic events (n = 18; 4.7% per year). Previous bleeding (HR, 3.21; 95% CI, 1.22–8.45), growth differentiation factor-15 (HR, 1.48; 95% CI, 1.29–1.69), cystatin C (HR, 9.24; 95% CI, 2.15–39.67), and high-sensitivity cardiac troponin T (HR, 1.30; 95% CI, 1.14–1.48) were independent predictors of major or clinically relevant non-major bleeding (n = 27; 7.1% per year). After adjustment for age and comorbidities, only cystatin C (HR, 3.95; 95% CI, 1.08–14.37) predicted mortality (n = 25; 6.5% per year). Conclusions: Novel biomarkers might be useful in risk stratification of thromboembolic and bleeding events in AF patients with stage 4 CKD receiving oral anticoagulants.

Up to 20% of patients with chronic kidney disease have atrial fibrillation, and 40%-50% of atrial fibrillation patients suffer from chronic kidney disease. The 2 diseases share several risk factors and frequently coincide with each other. Both entities are associ ated with a prothrombotic state, which contributes to increased thromboembolic risk. Atrial fibrillation patients with chronic kidney disease have elevated risk of stroke, major bleeding, and mortality. Clinical risk scores, including CHA2DS2-VASc score, HAS-BLED score, or ORBIT score have a limited value in adverse clinical outcome risk stratification in patients with severe chronic kidney disease. However, the inclusion of renal function in the R(2)-CHA2DS2-VASc score does not improve significantly thromboembolic risk predic tion in atrial fibrillation. There is growing evidence suggesting that biomarkers, including N-terminal pro-B-type natriuretic peptide, high-sensitivity cardiac troponin, cystatin C, or growth differentiation factor-15, might be helpful in the assessment of thromboembolic, bleeding, and/or mortality risk in atrial fibrillation patients with chronic kidney disease. The first-choice anticoagulant therapy is based on direct oral anticoagulants in this subgroup. The highest risk of adverse events is observed in end-stage renal disease, and in Europe, in contrast to the USA, solely warfarin is recommended in such atrial fibrillation patients. Treatment of atrial fibrillation patients with chronic kidney disease should be closely moni tored with the selection of right anticoagulant agents at the appropriate dose. The current review paper summarizes available evidence and the challenges of the management of atrial fibrillation patients with chronic kidney disease with practical implications.

Left ventricular hypertrophy (LVH) is associated with adverse clinical outcomes and implicates clinical decision-making. The aim of our study was to assess the importance of different approaches in the screening for LVH. We included patients who underwent cardiac magnetic resonance (CMR) imaging and had available chest radiograph in medical documentation. Cardiothoracic ratio (CTR), transverse cardiac diameter (TCD), clinical and selected electrocardiographic (ECG)-LVH data, including the Peguero-Lo Presti criterion, were assessed. CMR–LVH was defined based on indexed left ventricular mass-to-body surface area. Receiver operating characteristics analyses showed that both the CTR and TCD (CTR: area under the curve: [AUC] = 0.857, p < 0.001; TCD: AUC = 0.788, p = 0.001) were predictors for CMR–LVH. However, analyses have shown that diagnoses made with TCD, but not CTR, were consistent with CMR–LVH. From the analyzed ECG–LVH criteria, the Peguero-Lo Presti criterion was the best predictor of LVH. The best sensitivity for screening for LVH was observed when the presence of heart failure, ≥40 years in age (each is assigned 1 point), increased TCD and positive Peguero-Lo Presti criterion (each is assigned 2 points) were combined (CAR2E2 score ≥ 3 points). CAR2E2 score may improve prediction of LVH compared to other approaches. Therefore, it may be useful in the screening for LVH in everyday clinical practice in patients with prevalent cardiovascular diseases.

Background: Late gadolinium enhancement (LGE) by cardiac magnetic resonance (CMR) may reveal myocardial fibrosis which is associated with adverse clinical outcomes in patients undergoing implantable cardioverter-defibrillator (ICD) placement. At the same time, transmural LGE in the posterolateral wall is related to nonresponse to conventional cardiac resynchronization therapy (CRT). Herein, the aim was to assess the presence and determinants of LGE in CMR in heart failure (HF) with reduced ejection fraction. Methods: Sixty-seven patients were included (17.9% female, aged 45 [29–60] years), who underwent LGE-CMR and had left ventricular ejection fraction (LVEF) as determined by echocardiography. Results: In HF patients with LVEF ≤ 35% (n = 29), ischemic and non-ischemic patterns of LGE were observed in 51.7% and 34.5% of patients, respectively. In controls (n = 38), these patterns were noted in 23.7% and 42.1% of patients, respectively. HF patients with LVEF ≤ 35% and transmural LGE in the posterolateral wall (31.0%) were characterized by older age, coronary artery disease (CAD) and previous myocardial infarction (MI) (61 ± 6 vs. 49 ± 16 years, p = 0.008, 100% vs. 40%, p = 0.003 and 78% vs. 25%, p = 0.014, respectively). In patients with LVEF ≤ 35%, LGE of any type, diagnosed in 86.2% of patients, was associated with CAD (68% vs. 0%, p = 0.02), while only trends were observed for its association with older age and previous MI (p = 0.08 and p = 0.12, respectively). Conclusions: Among HF patients with LVEF ≤ 35%, clinical factors including older age, CAD, and previous MI are associated with transmural LGE in the posterolateral wall, while CAD is associated with LGE. This data may have potential implications for planning ICD and CRT placement procedures.

Background: Discrepancies between increased left ventricular mass (LVM) and electrocardiographic (ECG) criteria for the diagnosis of left ventricular hypertrophy (LVH) are described in the literature. Aims: This study aimed to evaluate the usefulness of ECG criteria in the diagnosis of LVH, as determined by cardiac magnetic resonance (CMR) imaging, using various LVM indexing methods. Methods: We included 53 patients who underwent CMR imaging and had electrocardiograms of appropriate quality available in their medical records. The majority of the study patients had cardiovascular diseases. We defined CMR‑LVH as increased LVM, also assessed after LVM indexing to body surface area (LVM/BSA), height1.7, height2.7, or as the percentage of predicted LVM (%pLVM). To determine ECG‑LVH, 10 different ECG-LVH criteria were used. Results: The prevalence of CMR‑LVH ranged from 11% (for %pLVM) to 72% (for LVM/BSA). At the same time, for a single criterion, the prevalence of ECG‑LVH ranged between 1.9% (for R wave amplitude in lead V5 / V6 greater than 2.6 mV, Sokolow–Lyon product, and Gubner–Ungerleider criterion) and 45.3% (for Peguero–Lo Presti criterion), showing high sensitivity, from 55.3% (95% CI, 38.3–71.4) to 100% (95% CI, 54.1–100). The sensitivity of ECG‑LVH criteria when all criteria were applied together ranged from 57.9% (95% CI, 40.8–73.7) to 100% (95% CI, 63.1–100). The best performance regarding the endpoint of CMR‑LVH diagnosis after LVM indexing was achieved by the Peguero–Lo Presti and Cornell criteria (area under the curve, 0.621–0.876; P, 0.001–0.17). Conclusions: Thediagnosis of LVH strongly depends on ECG- and CMR‑based definitions. ThePeguero–Lo Presti criterion and the Cornell criteria, which are sex‑specific, may provide the highest level of diagnostic accuracy and should be considered when screening patients with cardiovascular diseases for LVH.

Brugada syndrome (BrS) is a primary electrical disease predisposing to ventricular tachyarrhythmias and sudden cardiac death [...]

Background: Adequate contact between the catheter tip and tissue is important for optimal lesion formation and, in some procedures, it has been associated with improved effectiveness and safety. We evaluated the potential benefits of contact force-sensing (CFS) catheters during non-fluoroscopic radiofrequency catheter ablation (NF-RFCA) of idiopathic ventricular arrhythmias (VAs) originating from outflow tracts (OTs). Methods: A group of 102 patients who underwent NF-RFCA (CARTO, Biosense Webster Inc., Irvine, CA, USA) of VAs from OTs between 2014 to 2018 was retrospectively analyzed. Results: We included 52 (50.9%) patients in whom NF-RFCA was performed using CFS catheters and 50 (49.1%) who were ablated using standard catheters. Arrhythmias were localized in the right and left OT in 70 (68.6%) and 32 (31.4%) patients, respectively. The RFCA acute success rate was 96.1% (n = 98) and long-term success during a minimum 12-month follow-up (mean 51.3 ± 21.6 months) was 85.3% (n = 87), with no difference between CFS and standard catheters. There was no difference in complications rate between CFS (n = 1) and standard catheter (n = 2) ablations. Conclusions: There is no additional advantage of CFS catheters use over standard catheters during NF-RFCA of OT-VAs in terms of procedural effectiveness and safety.

Brugada syndrome (BrS) is a primary electrical disease associated with life-threatening arrhythmias. It is estimated to cause at least 20% of sudden cardiac deaths (SCDs) in patients with normal cardiac anatomy. In this review paper, we discuss recent advances in complex BrS pathogenesis, diagnostics, and current standard approaches to major arrhythmic events (MAEs) risk stratification. Additionally, we describe a protocol for umbrella reviews to systematically investigate clinical, electrocardiographic, electrophysiological study, programmed ventricular stimulation, and genetic factors associated with BrS, and the risk of MAEs. Our evaluation will include MAEs such as sustained ventricular tachycardia, ventricular fibrillation, appropriate implantable cardioverter–defibrillator therapy, sudden cardiac arrest, and SCDs from previous meta-analytical studies. The protocol was written following the Preferred Reporting Items for Systematic review and Meta-Analysis Protocols (PRISMA-P) guidelines. We plan to extensively search PubMed, Embase, and Scopus databases for meta-analyses concerning risk-stratification in BrS. Data will be synthesized integratively with transparency and accuracy. Heterogeneity patterns across studies will be reported. The Joanna Briggs Institute (JBI) methodology, A MeaSurement Tool to Assess systematic Reviews 2 (AMSTAR 2), and the Grading of Recommendations, Assessment, Development and Evaluation (GRADE) are planned to be applied for design and execution of our evidence-based research. To the best of our knowledge, these will be the first umbrella reviews to critically evaluate the current state of knowledge in BrS risk stratification for life-threatening ventricular arrhythmias, and will potentially contribute towards evidence-based guidance to enhance clinical decisions.

Continuous positive airway pressure (CPAP) treatment is considered effective in reducing ventricular arrhythmias (VAs) in patients with obstructive sleep apnea (OSA).We aimed to assess the influence of this treatment and to identify determinants of antiarrhythmic response.We included patients with OSA and VAs (corresponding to grades 2-5 in the Lown classification), who underwent CPAP treatment and controls, who refused CPAP therapy. Holter electrocardiographic monitoring was performed at baseline and after 3 months of follow‑up.The study consisted of 46 patients in the CPAP group and 30 controls. We observed a significant reduction in premature ventricular contractions (PVCs) and nonsustained ventricular tachycardia events (P = 0.007 and P = 0.03, respectively) in the CPAP group after 3 months, and no difference in controls. The effect of PVC reduction was significant in the patients with nocturnal dominance of PVCs (P = 0.002) and with desaturations equal to or below 80% (P = 0.001). PVC reduction rate (PVC at follow‑up / PVC at baseline) correlated inversely with night / day PVC ratio at baseline (R = -0.36; P = 0.02) and the lowest saturation (R = 0.32; P = 0.03) in the CPAP group. After adjustment for clinical data, night / day PVC ratio was an independent predictor of PVC reduction rate (unstandardized coefficient B = -0.19; 95% CI, -0.37 to -0.01; P0.05). Its value equal to or greater than 1.16 predicted good antiarrhythmic treatment response with sensitivity and specificity of 83% and 70%, respectively.CPAP treatment decreases VAs in OSA patients, especially those with severe desaturations and nocturnal domination of PVCs. Night / day PVC ratio might be a useful clinical parameter predicting reduction of PVCs in these patients.

Direct and indirect links between brain regions and cardiac function have been reported. We performed a systematic literature review to summarize current knowledge regarding the associations of heart rate variability (HRV) and brain region morphology, activity and connectivity involved in autonomic control at rest in healthy subjects. Both positive and negative correlations of cortical thickness and gray matter volumes of brain structures with HRV were observed. The strongest were found for a cluster located within the cingulate cortex. A decline in HRV, as well as cortical thickness with increasing age, especially in the orbitofrontal cortex were noted. When associations of region-specific brain activity with HRV were examined, HRV correlated most strongly with activity in the insula, cingulate cortex, frontal and prefrontal cortices, hippocampus, thalamus, striatum and amygdala. Furthermore, significant correlations, largely positive, between HRV and brain region connectivity (in the amygdala, cingulate cortex and prefrontal cortex) were observed. Notably, right-sided neural structures may be preferentially involved in heart rate and HRV control. However, the evidence for left hemispheric control of cardiac vagal function has also been reported. Our findings provide support for the premise that the brain and the heart are interconnected by both structural and functional networks and indicate complex multi-level interactions. Further studies of brain–heart associations promise to yield insights into their relationship to health and disease.

Reduction of heart rate variability (HRV) parameters may be a risk factor and precede the occurrence of arrhythmias or the development of heart failure and complications in people with postinfarct left ventricular dysfunction and after coronary artery bypass grafting. Data on this issue in adults after a Fontan operation (FO) are scarce. This study assessed the association between HRV, exercise capacity, and multiorgan complications in adults after FO. Data were obtained from 30 FO patients (mean age 24 ± 5.4 years) and 30 healthy controls matched for age and sex. HRV was investigated in all patients by clinical examination, laboratory tests, echocardiography, a cardiopulmonary exercise test, and 24-h electrocardiogram. The HRV parameters were reduced in the FO group. Reduced HRV parameters were associated with patients’ age at the time of FO, time since surgery, impaired exercise capacity, chronotropic incompetence parameters, and multiorgan complications. Univariate analysis showed that saturated O2 at rest, percentage difference between adjacent NN intervals of &gt, 50 ms duration, and peak heart rate were associated with chronotropic index. Multivariable analysis revealed that all three variables were independent predictors of the chronotropic index. The results of this study suggest novel pathophysiological mechanisms that link HRV, physical performance, and organ damage in patients after FO.

Introduction Diabetes mellitus is an important and rapidly increasing problem in public health. It associates with endothelial dysfunction and increased endothelial permeability, which may lead to severe cardiovascular events. Objectives We aimed to evaluate the relationship between polymorphisms in the cytochrome b-245 alpha chain (CYBA) gene encoding p22phox, a key subunit of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, with endothelial function, atherosclerosis and systemic oxidative stress in type 2 diabetes mellitus (T2DM). Patients and methods Intima-media thickness (IMT), flow- and nitroglycerin-mediated dilatation (FMD and NMD) were measured in 182 patients with T2DM. Assessment of plasma levels of von Willebrand factor (vWF) and malondialdehyde (MDA) levels as well as genotyping of coding sequence C242T (rs4673) and promoter region A-930G (rs9932581) polymorphisms of CYBA were performed using standardized protocols. Results We observed a significant association of the impaired endothelial function, as measured by FMD, with the C allele of C242T, but not with the A-930G polymorphism. Functional relationship of the C242T polymorphism with endothelial dysfunction remained significant following a multivariable adjustment for major risk factors for atherosclerosis. Mean IMT, NMD, concentrations of MDA or vWF were not related to the specific genotypes of the investigated polymorphisms. Conclusions C242T, but not A-930G, polymorphism of CYBA significantly affects endothelial function in T2DM. Thus, it might be a useful marker of endothelial dysfunction in T2DM patients.

It is unclear whether chronic kidney disease (CKD) increases thromboembolism in atrial fibrillation (AF). We conducted a retrospective cross-sectional analysis of 502 non-anticoagulated AF patients (median age, 66 (60&ndash, 73) years, median CHA2DS2-VASc score, 3.0 (2.0&ndash, 4.0)) with an estimated glomerular filtration rate (eGFR) &ge, 15 mL/min/1.73 m2. Endogenous thrombin potential (ETP), clot permeability (Ks), and clot lysis time (CLT), among others, were determined. Patients with stage 4 CKD (n = 87, 17.3%) had higher ETP and prolonged CLT compared with those with stage 3 CKD. In patients with stages 3 to 4 CKD (n = 180, 35.9%) N-terminal pro-B-type natriuretic peptide predicted low Ks (the lowest quartile, odds ratio [OR] per 100 pg/mL: 1.03, 95% confidence interval [CI]: 1.01&ndash, 1.06) and prolonged CLT (the top quartile, OR per 100 pg/mL: 1.05, 95% CI: 1.02&ndash, 1.08), but not high ETP. In the whole cohort, after adjustment for CHA2DS2-VASc score, stage 4 CKD, but not stage 3 CKD, predicted high ETP (OR: 9.06, 95% CI: 4.44&minus, 18.46) and prolonged CLT (OR: 3.58, 95% CI: 1.76&ndash, 7.28), but not low Ks. compared to the reference eGFR category. This study is the first to demonstrate the prothrombotic and antifibrinolytic alterations in AF patients with stage 4 CKD, but not stage 3 CKD irrespective of clinical stroke risk factors.

Aims Inflammation is an important driver of hypertension. Periodontitis is a chronic inflammatory disease, which could provide a mechanism for pro-hypertensive immune activation, but evidence of a causal relationship in humans is scarce. We aimed to investigate the nature of the association between periodontitis and hypertension. Methods and results We performed a two-sample Mendelian randomization analysis in the ∼750 000 UK-Biobank/International Consortium of Blood Pressure-Genome-Wide Association Studies participants using single nucleotide polymorphisms (SNPs) in SIGLEC5, DEFA1A3, MTND1P5, and LOC107984137 loci GWAS-linked to periodontitis, to ascertain their effect on blood pressure (BP) estimates. This demonstrated a significant relationship between periodontitis-linked SNPs and BP phenotypes. We then performed a randomized intervention trial on the effects of treatment of periodontitis on BP. One hundred and one hypertensive patients with moderate/severe periodontitis were randomized to intensive periodontal treatment (IPT; sub- and supragingival scaling/chlorhexidine; n = 50) or control periodontal treatment (CPT; supragingival scaling; n = 51) with mean ambulatory 24-h (ABPM) systolic BP (SBP) as primary outcome. Intensive periodontal treatment improved periodontal status at 2 months, compared to CPT. This was accompanied by a substantial reduction in mean SBP in IPT compared to the CPT (mean difference of −11.1 mmHg; 95% CI 6.5–15.8; P Conclusion A causal relationship between periodontitis and BP was observed providing proof of concept for development of clinical trial in a large cohort of hypertensive patients. ClinicalTrials.gov: NCT02131922.

Cardiovascular implantable electronic devices (CIED) encompass permanent cardiac pacemakers (PM) and implantable cardioverterdefibrillators (ICD). CIED play an important role in treatment of cardiac arrhythmias, including significant bradyarrhythmias and tachyarrhythmias. The conventional right ventricular endocardial leads as well as right ventricular pacing may increase valvular defects (especially dysfunction of tricuspid and mitral valve), cause adverse cardiac remodelling and lead to a decrease in left ventricular ejection fraction. These changes may be due to mechanical damage to the leaflets or other structures of the tricuspid apparatus, such as the annulus, papillary muscles or chordae tendineae. In addition, the endocardial lead passing through the tricuspid valve may adhere to it and exacerbate the inflammatory processes and fibrosis of its leaflets. On the other hand, right ventricular pacing leads to electromechanical dyssynchrony of the cardiac muscle. New forms of CIED therapy such as leadless pacemakers, His bundle pacing, synchronized left ventricular pacing or biventricular pacing may reduce some adverse changes induced by the right ventricular pacing with the use of conventional cardiac pacemakers. Similarly, subcutaneous cardioverter-defibrillators, despite limitations, may prevent some complications associated with traditional implantable cardioverterdefibrillator lead.

BACKGROUND Atrial septal defect (ASD) and patent foramen ovale (PFO) are specific types of atrial septal communications (ASC). OBJECTIVES We aimed to assess quality of life (QoL) in patients before and after percutaneous closure of ASC and determine the factors influencing QoL in this group of patients. MATERIAL AND METHODS We performed a clinical assessment and conducted an SF-36 questionnaire, electrocardiography and echocardiography studies in patients before and 6 months after percutaneous ASC closure. RESULTS Patients with ASD (n = 56) had a lower SF-36 total score than those with PFO (n = 73), before and after percutaneous ASC occlusion (both p < 0.001). After the procedure, the improvement of SF-36 total score in patients with ASD or atrial fibrillation was greater (p < 0.001 and p = 0.005, respectively). We observed correlations between improvement of QoL and baseline supraventricular extrasystolic beats (rs = 0.28; p = 0.002), but not ventricular extrasystolic beats (rs = 0.03; p = 0.76). Quality of life improvement was predicted in patients with ASD by higher baseline tricuspid annular plane systolic excursion (TAPSE) and right ventricular longitudinal dimension R2 = 0.38; p < 0.001. However, in patients with PFO, this was predicted by TAPSE, lack of arterial hypertension and usage of angiotensin-converting enzyme inhibitors, R2 = 0.30; p < 0.001. CONCLUSIONS Patients with ASD have lower QoL than those with PFO before and after percutaneous ASC occlusion. Six months after the procedure, the improvement of QoL in patients with ASD was higher than in those with PFO. The change in QoL self-assessed by patients after the procedure was associated with episodes of arrhythmia and was predicted with echocardiographic and clinical parameters.

OBJECTIVE To analyze and compare the effectiveness and safety of transvenous lead extraction (TLE) with mechanical systems of pacing leads older than 20 years (group A) versus younger leads (group B). METHODS We performed TLE of 591 pacing leads in 377 patients. Fifty (8.5%) leads in 43 (11.4%) patients were implanted for equal to or more than 20 years. The mean dwell time of all extracted leads was 8.9 years (range, 0.1-36.0). Infection related to cardiovascular implantable electronic device was an indication for TLE in 18.3% of patients. RESULTS Complete lead removal and complete procedural success rates were similar between both groups (94.7% in group A vs 97.1% in group B, P = 0.445, and 90.7% in group A vs 95.8% in group B, P = 0.329, respectively). Incomplete lead removal in group A was observed only in leads older than 20 years. Removal of leads in group A was associated with significantly longer fluoroscopy time compared with group B (4.6 vs 1.9 minutes, P

Background It is unclear whether a prothrombotic state occurs in atrial fibrillation (AF) with low stroke risk. Methods We studied 118 patients with AF with the Congestive Heart Failure, Hypertension, Age (≥ 75 years), Diabetes, Stroke/Transient Ischemic Attack/Systemic Embolism, Vascular Disease, Age (65-74 years), Sex (Female) (CHA2DS2-VASc) score of 1 in men or 2 in women vs 52 patients with AF with the CHA2DS2-VASc score of 0 in men or 1 in women. Plasma clot permeability (Ks), a measure of fibrin clot density, and clot lysis time (CLT), endogenous thrombin potential (ETP), von Willebrand factor antigen, and plasminogen activator inhibitor-1 were evaluated in nonanticoagulated subjects. Results Patients with the CHA2DS2-VASc score of 1 (beyond sex), compared with those with 0, had lower Ks, prolonged CLT, increased ETP, von Willebrand factor antigen, and plasminogen activator inhibitor-1 (all P Conclusions A prothrombotic state (increased thrombin generation, denser fibrin clots, impaired fibrinolysis, and endothelial injury) characterizes patients with AF with 1 additional clinical stroke risk factor (beyond sex), with age 65-74 years being particularly associated with prothrombotic indices.

INTRODUCTION Rare cardiovascular diseases and disorders (RCDDs) constitute an important clinical problem, and their proper classification is crucial for expanding knowledge in the field of RCDDs. OBJECTIVES The aim of this paper is to provide an updated classification of rare arrhythmogenic and conduction disorders, and rare arrhythmias (RACDRAs). METHODS We performed a search for RACDRAs using the Orphanet inventory of rare diseases, which includes diseases with a prevalence of no more than 5 per 10 000 in the general population. We supplemented this with a search of PubMed and Scopus databases according to a wider definition proposed by the European Parliament and the Council of the European Union. RESULTS RACDRAs are categorized into 2 groups, primary electrical disorders of the heart and arrhythmias in specific clinical settings. The first group is further divided into subgroups of major clinical presentation: disorders predisposing to supraventricular tachyarrhythmias, ventricular tachyarrhythmias, bradyarrhythmias, and others. The second group includes iatrogenic arrhythmias or heart rhythm disturbances related to medical treatment, arrhythmias associated with metabolic disorders, and others. We provide a classification of RACDRAs and supplement them with respective RCDDs codes. CONCLUSION The clinical classification of RACDRAs may form a basis to facilitate research and progress in clinical practice, both in diagnostic and therapeutic approaches.

It is unclear whether a prothrombotic state occurs in atrial fibrillation (AF) with low stroke risk.We studied 118 patients with AF with the Congestive Heart Failure, Hypertension, Age (≥ 75 years), Diabetes, Stroke/Transient Ischemic Attack/Systemic Embolism, Vascular Disease, Age (65-74 years), Sex (Female) (CHAPatients with the CHAA prothrombotic state (increased thrombin generation, denser fibrin clots, impaired fibrinolysis, and endothelial injury) characterizes patients with AF with 1 additional clinical stroke risk factor (beyond sex), with age 65-74 years being particularly associated with prothrombotic indices.

Background: Atrial septal communications (ASCs) include atrial septal defects (ASDs) and patent foramen ovale (PFO). Aim: The purpose of this study was to assess P-wave dispersion (PWD) and the prevalence of arrhythmia in patients before and after ASC closure. Methods: We analysed the clinical history and performed 12-lead electrocardiograms, echocardiograms, and 24-h Holter electrocardiograms in patients with ASC, before and six months after ASC closure. Results: We included patients with ASD (n = 56) and PFO (n = 73). PWD before percutaneous ASC closure was predicted by right ventricular outflow tract (RVOT) proximal diameter, left atrial area, ASD, smoking, and paroxysmal dyspnoea, R2 = 0.67; p < 0.001. RVOT proximal diameter was an independent predictor of PWD, both in patients with ASD and PFO. Six months after successful closure of ASC, a reduction in PWD was observed in the whole group of patients as well as in patients with ASD and PFO considered separately. A decrease in PWD was associated with reduction of maximum P-wave duration. At the same time, in the whole group, we noticed a reduction in the number of supraventricular and ventricular extrasystolic beats and fewer atrial fibrillation (AF) episodes, p < 0.04 for all variables. Postprocedural AF episodes in patients with ASD were predicted by PWD of 80 ms. Conclusions: Percutaneous closure of ASC is associated with a reduction of PWD and fewer arrhythmia episodes six months after the procedure. PWD predicts AF episodes after ASD closure.

Purpose Chronic inflammatory disorders of the oral cavity, such as periodontitis, were recently linked to systemic immune activation. Since fungal oral infections have not yet been studied in this respect, the aim of our study is to determine whether the local inflammation caused by oral fungal infection of the palatal tissue (denture stomatitis—DS) is associated with the systemic inflammatory response. This question is becoming essential as the population ages. Materials and Methods Peripheral blood of DS patients (n = 20) and control patients (n = 24) was assessed with flow cytometry to determine lymphocyte and monocyte profiles. Intracellular cytometric analysis was carried out to establish cytokine production by T cells. DS was diagnosed based on clinical symptoms of DS such as swelling and redness of oral mucosa, confirmed by microbiological swabs for fungal colonization with Candida species. The control group was recruited from denture users without clinical and microbiological signs of oral infections. Results Percentages of peripheral lymphocytes, T cells, monocytes, and their subpopulations were similar in both studied groups. The exception was median percentages of CD25+ T cell subsets, which were significantly lower in DS patients than in control subjects. This reduction was observed in both CD4 T cell subset (16.7% and 28.1%; p = 0.0006) and CD8 T cell subset (4.6% and 7.0%; p = 0.007) Conclusions While DS and associated local fungal infection do not overtly affect activation of monocytes or lymphocytes, the number of CD 25+ T cells is significantly lower in the DS patients, possibly indicating limited potential for the infection clearance in denture-using aging patients.

Clinical manifestation of Brugada syndrome (BrS) mainly results from polymorphic ventricular arrhythmias and includes sudden cardiac arrest (SCA). The Brugada sign, besides being present in true BrS, may result from different causes. Moreover, electrocardiogram findings in some clinical situations may resemble the BrS electrocardiographic pattern. Thus, differential diagnosis is crucial in the proper management of patients suspected of having BrS. Lifestyle modifications and close follow-up with or without pharmacologic treatment and/or implantable cardioverter-defibrillator placement constitute the most common approach to managing BrS patients. However, the role of ablation in BrS treatment is increasing. Due to diagnostic and therapeutic difficulties, the management of BrS is often challenging. This review provides new concepts and algorithms in the diagnostics and treatment of patients suspected of having BrS. JRCD 2017; 3 (5): 151–160

Patients with atrial fibrillation (AF) are at increased risk of stroke and systemic thromboembolism and prevention of such episodes is ensured by choosing appropriate anticoagulation. In paroxysmal drug‐refractory AF, catheter ablation is the recommended choice of treatment. The decision on whether to stop administration of oral anticoagulant before catheter ablation procedures is often unclear. We present the case of a 67‐year‐old hypertensive woman with a 5‐year history of symptomatic, drug‐refractory paroxysmal AF, who was admitted for pulmonary vein isolation (PVI) and was anticoagulated with dabigatran. After successful transseptal puncture, an intravenous injection of 10 000 units of heparin was administered. Radiofrequency ablation was initiated at the left pulmonary trunk. After the second application of radiofrequency ablation, a drop in arterial blood pressure to 70/50 mmHg was observed. Urgent echocardiography revealed the presence of fluid within the epicardial surface of the left ventricular apex up to 19 mm, behind the right ventricle and right atrium up to 11 mm. Subsequently, all catheters were removed from the left atrium, and 50 mg of protamine sulfate, dopamine, and intravenous fluids were immediately administered. Idarucizumab was urgently delivered to the catheterisation laboratory and was available during patient hospitalisation in the intensive care unit. However, prior to patient discharge, echocardiography revealed only a trace amount of fluid in the pericardium and the use of idarucizumab was not indicated. Interruption of anticoagulation treatment with dabigatran before ablation is not required. Idarucizumab increases the safety of PVI in patients treated with dabigatran. JRCD 2018; 3 (8): 281–283

Complete atrioventricular block (AVB) is rare during pregnancy. Congenital atrioventricular block is the most common type of heart block in this group of patients. About one‑third of female patients with complete AVB remain asymptomatic until adulthood and may be first diagnosed during pregnancy. We present a case of a 31‑year‑old pregnant woman with complete AVB who was in her final stage of pregnancy. After reviewing the various advantages and disadvantages of feasible approaches with the patient, we decided to use fluoroscopy‑guided temporary backup pacemaker implantation. Estimated radiation skin dose was small and safe. The patient agreed to this treatment plan. Four days prior to scheduled cesarean delivery (39 weeks of gestation), during a one‑day stay in the hospital, the patient underwent single‑chamber temporary pacemaker implantation (using transvenous active fixation lead and external re‑sterilized pacemaker). The abdominal and pelvic regions were covered with a lead shield. The caesarean delivery was uneventful and the baby was healthy with an Apgar score of 10. JRCD 2017; 3 (6): 205–209.

INTRODUCTION We evaluated the influences of selected factors on electrical lead failure (ELF) occurrence in patients referred for transvenous lead extraction (TLE) procedures. METHODS AND RESULTS The study cohort consisted of 432 patients referred for TLE procedures due to various indications (42 - lead-dependent infective endocarditis, 47 - pocket infection, 343 - noninfectious indications) with a total of 804 endocardial leads. In the analyzed group, there were 192 patients with ELF, denoted as group ELF(+) (200 malfunctioning endocardial leads). The percentage of women was higher in the ELF(+) group than in the ELF(-) group (42.7% vs 30.0%; P = 0.006). The ELF(+) patients had more endocardial leads implanted via subclavian vein puncture (80.0% vs 72.4%; P = 0.032), had more indwelling leads in the cardiovascular system (1.94 vs 1.8; P = 0.03), were older (68.9 vs 66.0 years old; P = 0.028), and had better left ventricular ejection fractions than the ELF(-) patients (48.0% vs 40.7%; P

We present 24-hour electrocardiography recording with observed DDD pacemaker pacing inhibition. Discussed Holter monitoring fi ndings are puzzling and may result from pacemaker sensing malfunction. However, its aetiology may be diverse. The detailed explanation of underlying mechanisms is provided and literature is reviewed.

Background Dense fibrin clot formation and hypofibrinolysis have been reported in atrial fibrillation (AF). It is unclear which factors affect fibrin clot properties in AF. Methods and results We investigated plasma fibrin clot permeability (K s ), clot lysis time (CLT), endogenous thrombin potential (ETP) as well as other coagulation and fibrinolysis parameters along with N-terminal pro-B-type natriuretic peptide (NT-proBNP) in 160 AF patients (median age, 70.5years). Previous stroke ( n =15; 9.4%) was associated with decreased K s ( P =0.04) and longer CLT ( P =0.005), together with higher antiplasmin ( P =0.03) and lower tissue-type plasminogen activator ( P =0.01). Lower K s ( P =0.04) and tendency towards longer CLT ( P =0.10) were observed in patients with a left atrium diameter>40mm. Patients with a CHA 2 DS 2 -VASc score of 3 or more (82.5%) were characterized by higher thrombin-activatable fibrinolysis inhibitor antigen ( P =0.009). K s was inversely correlated with log NT-proBNP ( r =−0.34, P r =−0.24, P =0.002) and C-reactive protein ( r =−0.18, P =0.02), while CLT was positively correlated with log NT-proBNP ( R =0.61, P r =0.37, P r =0.59, P s (the lowest quartile,≤6×10 −9 cm 2 ), while NT-proBNP (OR: 1.21; 95% CI: 1.12–1.31) and PAI-1 (OR: 1.30; 95% CI: 1.12–1.51) both predicted prolonged CLT (the top quartile,≥109min). Conclusion In AF patients prothrombotic fibrin clot properties assessed ex vivo are determined by PAI-1 and NT-proBNP and this phenotype is associated with prior ischemic stroke.

The 24-hr electrocardiogram (ECG) interpretation in patients with double-chamber pacemakers may be challenging. The difficulty increases if not well-known pacemaker algorithm and device malfunction coexist. We show atrial synchronization pace (ASP) in a patient with ventricular lead damage. We provide detailed description of electrocardiogram and intracardiac electrogram. ASP may confuse 24-hr ECG monitoring interpretation, especially in patients with ventricular lead dysfunction.

Brugada syndrome (BrS) is a cardiac channelopathy associated with ventricular arrhythmias and sudden cardiac death. Diagnosis of BrS is based on type 1 BrS electrocardiogram (ECG) pattern (coved pattern) presence, observed spontaneously or after provocation test. The worldwide prevalence of BrS ECG patterns is estimated to reach 0.4% and strongly depends on the population studied. BrS results from various genetic mutations of sodium, calcium and potassium channels and/or associated proteins affecting ion currents. SCN5A mutations are the most prevalent in BrS. Pathogenesis of BrS is explained by the depolarization theory, the repolarization theory and the neural crest theory, which seem to be complimentary, at least partially. This review summarizes current diagnostic criteria of BrS and epidemiology of BrS ECG patterns. We also discuss the recent understanding of BrS pathophysiology and the role of genetic testing in BrS. JRCD 2017; 3 (3): 73–80.

Oxidative stress is a molecular dysregulation in reactive oxygen species (ROS) metabolism, which plays a key role in the pathogenesis of atherosclerosis, vascular inflammation and endothelial dysfunction. It is characterized by a loss of nitric oxide (NO) bioavailability. Large clinical trials such as HOPE and HPS have not shown a clinical benefit of antioxidant vitamin C or vitamin E treatment, putting into question the role of oxidative stress in cardiovascular disease. A change in the understanding of the molecular nature of oxidative stress has been driven by the results of these trials. Oxidative stress is no longer perceived as a simple imbalance between the production and scavenging of ROS, but as a dysfunction of enzymes involved in ROS production. NADPH oxidases are at the center of these events, underlying the dysfunction of other oxidases including eNOS uncoupling, xanthine oxidase and mitochondrial dysfunction. Thus NADPH oxidases are important therapeutic targets. Indeed, HMG-CoA reductase inhibitors (statins) as well as drugs interfering with the renin-angiotensin-aldosterone system inhibit NADPH oxidase activation and expression. Angiotensin-converting enzyme (ACE) inhibitors, AT1 receptor antagonists (sartans) and aliskiren, as well as spironolactone or eplerenone, have been discussed. Molecular aspects of NADPH oxidase regulation must be considered, while thinking about novel pharmacological targeting of this family of enzymes consisting of several homologs Nox1, Nox2, Nox3, Nox4 and Nox5 in humans. In order to properly design trials of antioxidant therapies, we must develop reliable techniques for the assessment of local and systemic oxidative stress. Classical antioxidants could be combined with novel oxidase inhibitors. In this review, we discuss NADPH oxidase inhibitors such as VAS2870, VAS3947, GK-136901, S17834 or plumbagin. Therefore, our efforts must focus on generating small molecular weight inhibitors of NADPH oxidases, allowing the selective inhibition of dysfunctional NADPH oxidase homologs. This appears to be the most reasonable approach, potentially much more efficient than non-selective scavenging of all ROS by the administration of antioxidants.

We have read the paper by Javaheri et al. [(1)][1] with great interest. We agree with the investigators that treatment of sleep apnea (SA) may be extremely beneficial to many groups of patients with cardiovascular disease (CVD) [(1)][1]. We would like to point out that early diagnosis of SA may

Atrial fibrillation (AF) is leading cardiac arrhythmia with important clinical implications. Its diagnosis is usually made on the basis on 12-lead ECG or 24-hour Holter monitoring. More and more clinical evidence supports diagnostic use of cardiac event recorders and cardiovascular implantable electronic devices (CIED). Treatment options in patients with atrial fibrillation are extensive and are based on chosen rhythm and/or rate control strategy. The use and selected contraindications to AF related pharmacotherapy, including anticoagulants are shown. Nonpharmacological treatments, comorbidities and risk factors control remain mainstay in the treatment of patients with AF. Electrical cardioversion consists important choice in rhythm control strategy. Much progress has been made in the field of catheter ablation and cardiac surgery methods. Left atrial appendage occlusion/closure may be beneficial in patients with AF. CIED are used with clinical benefits in both, rhythm and rate control. Pacemakers, implantable cardioverter-defibrillators and cardiac resynchronization therapy devices with different pacing modes have guaranteed place in the treatment of patients with AF. On the other hand, the concepts of permanent leadless cardiac pacing, atrial dyssynchrony syndrome treatment and His-bundle or para-Hisian pacing have been proposed. This review summarizes and discusses current and novel treatment options in patients with atrial fibrillation.