Importance of Comprehensive Assessment in Brugada Syndrome. Reply to Kataoka, N.; Imamura, T. How to Diagnose and Risk Stratify Brugada Syndrome. Comment on "Matusik et al. Twelve-Lead ECG, Holter Monitoring Parameters, and Genetic Testing in Brugada Syndrome: Insights from Analysis of Multigenerational Family with a History of Sudden Cardiac Arrest during Physical Activity. J. Clin. Med. 2023, 12, 6581".

We would like to thank Dr. Imamura for their interest in our study and their valuable comments on diagnostics and risk stratification in Brugada syndrome (BrS) [...].

Twelve-Lead ECG, Holter Monitoring Parameters, and Genetic Testing in Brugada Syndrome: Insights from Analysis of Multigenerational Family with a History of Sudden Cardiac Arrest during Physical Activity.

Brugada syndrome (BrS) is an arrhythmogenic disorder increasing the risk of syncopal episodes and sudden cardiac death. BrS usually runs through families with reduced penetrance and variable expression. We analyzed the multigenerational family of a patient who died after sudden cardiac arrest with post-mortem diagnosis of BrS. We analyzed clinical history, comprehensive arrhythmic risk, genetic findings, and additional tests, including electrocardiogram (ECG), detailed 24-hour Holter ECG results, and standard echocardiography findings, and followed up the patients in the ambulatory clinic. We analyzed a pedigree of 33 members of four generations of the family (19 male and 14 female patients). In this family, we identified 7 patients with BrS (median Modified Shanghai Score and Sieira model: 4.5 (4-6) and 1 (0-4) points, respectively), including both parents of the deceased patient, and 8 relatives with negative sodium channel blocker drug challenge test. Genetic testing revealed a novel mutation in sodium voltage-gated channel alpha subunit 5 (SCN5A) c.941A>G, (p.Tyr314Cys) inherited from the father of the proband. Patients with BrS were characterized by longer P-wave duration (120 (102-155) vs. 92.5 (88-110) ms, p = 0.013) and longer PR intervals (211.3 ±26.3 vs. 161.6 ± 18.9 ms, p = 0.001), along with more frequent positive aVR sign, but did not differ in terms of QRS duration or T-wave characteristics in resting ECGs. BrS patients were characterized by lower mean, minimal, and maximal (for all p ≤ 0.01) heart rates obtained from Holter ECG monitoring, while there was no difference in arrhythmias among investigated patients. Moreover, visual diurnal variability of ST segment changes and fragmented QRS complexes were observed in patients with BrS in Holter ECG monitoring. There were no major arrhythmic events during median follow-up of 68.7 months of alive BrS patients. These results suggest ECG features which may be associated with a diagnosis of BrS and indicate a novel SCN5A variant in BrS patients. Twelve-lead Holter ECG monitoring, with modified precordial leads placement, may be useful in BrS diagnostics and risk stratification in personalized medicine.

Cardiac chambers perforation by pacemaker and cardioverter-defibrillator leads. Own experience in diagnosis, treatment and preventive methods.

Cardiac chamber perforation is an uncommon, but potentially dangerous, complication of implantation of a pacemaker (PM) or a cardioverter-defibrillator (ICD). Different clinical presentations are related to the time between implantation and perforation, localisation of the perforation and concomitant lesions in neighbouring organs. Diagnosis is based on concomitant analysis of the clinical picture, ECG tracings, PM or ICD function check-up with a programmer, and review of echocardiographic, X-ray and computed tomography pictures. We analysed seven cases of perforation. Perforating leads were removed in all cases and a new pacing system was implanted in five cases. Choice of operative technique (unscrewing and direct traction from device pocket, Cook system or surgical procedure with pericardial drainage) depended on the time elapsing between implantation and perforation, the presence of lesions of other organs, and the amount of fluid in the pericardial sac. Avoiding unsafe localisation of a pacing electrode in the apex and free wall of the right ventricle and in the free anterolateral wall of the right atrium, and avoiding leaving an extra length of pacing lead under tension and overscrewing of the lead helix seem to be the best ways of prevention.

Influence of heart failure etiology on the effect of upgrading from right ventricular apical to biventricular or bifocal pacing in patients with permanent atrial fibrillation and advanced heart failure.

INTRODUCTION: Chronic heart failure (HF) results from various disease processes. There are no data on the effect of the etiology of HF on the improvement after pacemaker upgrade. OBJECTIVES The aim of the study was to assess changes in various parameters in patients with ischemic (IC) and nonischemic (NIC) cardiomyopathy after pacemaker upgrade in pacemaker-dependent patients with permanent atrial fibrillation, in the course of advanced HF during 12-month follow-up. PATIENTS AND METHODS: The study involved 34 patients who underwent an upgrade from right ventricular apical to biventricular or bifocal right ventricular pacing. In each patient, 12-lead electrocardiography, transthoracic echocardiography, 6-minute walking test, and the measurement of brain natriuretic peptide levels were performed. Ischemic etiology of HF was confirmed in 25 subjects. The subgroups of cardiomyopathy were compared in terms of the improvement in relative and absolute values of the parameters at 6 and 12 months. RESULTS: At baseline, the subgroups did not differ significantly in demographic data and the measured parameters. All patients completed the first period of follow­up showing clinical improvement after pacemaker upgrade. A significantly greater relative increase in the left ventricular ejection fraction was observed in the NIC subgroup at 6 months. The whole 12-month follow-up period was completed by a similar percentage of the IC and NIC patients (76% vs. 88.9%; P = 0.73). In the IC subgroup, a greater degree of mitral regurgitation was observed. CONCLUSIONS: Patients with IC or NIC who underwent an upgrade from right ventricular apical to biventricular or bifocal right ventricular pacing and completed a 12-month follow-up did not differ in clinical improvement. Significant differences were observed in echocardiographic parameters.

[AAI stimulation and nodal rhythm]. / Stymulacja AAI i rytm wezlowy.

We describe the case of a 77 year-old white woman treated by AAI pacing. Nodal rhythm with ventriculo-atrial conduction and retrograde P wave were observed in ECG Holter monitoring. The retrograde P wave was sensed by the pacemaker, which responded correctly.

[Echocardiographic examination in patients with corrected transposition of great arteries (L-TGA, ccTGA) with failure of systemic (anatomically) right ventricle treated with resynchronisation therapy]. / Badanie echokardiograficzne u pacjentów z wrodzona wada serca (L−TGA, ccTGA)leczonych terapia resynchronizujaca z powodu niewydolnosci systemowej anatomicznie prawej komory.

A congestive heart failure is common in population of adult patients with congenital heart disease, especially among patients with systemic right ventricle. According to literature 4-9% of patients with systemic right ventricle can be treated with resynchronisation therapy (CRT). Authors present results of echocardiographic examination in two patients with ccTGA treated by CRT because of failure of systemic right ventricle.

Percutaneous removal of endocardial implantable cardioverter-defibrillator lead displaced to the right pulmonary artery.

We describe a case of percutaneous removal of endocardial implantable cardioverter-defibrillator lead displaced to the right pulmonary artery. The procedure was performed from two accesses; from the lower one (femoral) and then, due to technical problems, from the upper one (subclavian). In the last stage the flattened Dotter's basket was introduced to the heart inside the Byrd dilator and then fastened to the described lead as the external 'splint'. This solution is an alternative to the recommended use of the internal metal leader with anchoring function in case of significant malformation of the internal lumen of the lead. The procedure we describe is an example of the sort of individual, original solution indispensable for the efficient and safe removal of untypically displaced leads.

[Necessity of endocardial lead removal in device upgrade in a patient with left subclavian vein occlusion - a case report]. / Koniecznosc usuniecia elektrody endokawitarnej przy rozbudowie ukladu stymulujacego serca u chorej z niedroznoscia zyly podobojczykowej lewej - opis przypadku.

We describe a method of regaining venous access to the heart in a patient with permanent atrial stimulation, in whom the pacing system upgrade to the atrio-ventricular one was necessary. However, left subclavian vein occlusion was found. We used an existing lead as a conduit. During such treatment the lead was removed. After a recanalisation the therapeutic aim was achieved - there were two new leads implanted.

[Pacemaker implantation in a patient with cor triatriatum sinister - preoperative evaluation]. / Wszczepienie stymulatora serca u chorego z rozpoznaniem serca trójprzedsionkowego lewostronnego - ocena przedoperacyjna w echokardiografii przezprzelykowej.

A case of 72 year old-male with cor triatriatum sinister, permanent atrial fibrillation and symptomatic bradycardia is presented. Patient was scheduled for pacemaker implantation. A preoperative evaluation with transesophageal echocardiography revealed a nonrestrictive membrane in left atrium, normal right superior vena cava and absence of persistent left superior vena cava and other cardiac anomalies. A right ventricular pacemaker lead was implanted through left subclavian approach. Preoperative evaluation shortened a radiation exposure and procedure time.

[The impact of nitrates and mono-therapy and nitrates combined with angiotensin converting enzyme inhibitors on left ventricular remodeling and exercise capacity in patients after acute myocardial infarction]. / Porównanie wplywu nitratów w monoterapii oraz w skojarzeniu z inhibitorem konwertazy angiotensyny na remodelowanie lewej komory oraz wydolnosc wysilkowa u pacjentów po zawale serca.

The objective of this paper was to evaluate potential beneficial effects of combined treatment with slow-release nitrates and angiotensin converting enzyme inhibitors (ACE) on left ventricular remodeling and exercise capacity in patients after acute myocardial infarction. In this study, 141 patients (aged 34 to 74, mean 56.6 years) with sufficient circulation received combined treatment with 24 hour nitroglycerin infusion followed by oral nitrates (isosorbide mononitrate 50 mg OD) from day 2 day 42 after myocardial infarction and ACE inhibitor (captopril 25 mg BID or enalapril 5 mg BID versus placebo) from day 10 to day 42. On days 10 and 42, echocardiographic examination was carried out and recorded on an optical disc. Simultaneously, on the same days, the treadmill exercise test (modified Bruce protocol) was performed. In the echocardiographic study the left ventricular endodiastolic and endosystolic volumes (biplane Simpson formula), ejection fraction, left ventricular wall motion score and left ventricular mass index were analyzed. Treadmill test criteria, used in the study, included exercise duration time and workload (METS). For each patient the data obtained examination II and I were measured and the differences in their values were classified. The obtained results were analyzed with one-way and three-way ANOVA test. A Kruskal-Wallis test was also used in one variable analysis. Results were analyzed after repartition of patients into groups according type of treatment (angiotensin converting ing enzyme inhibitor or placebo), infarct location (anterior or inferior wall) and enzyme level (CPK < 2000 IU/L or CPK > 2000 IU/L). A p value < 0.1 was considered statistically significant. In a single factor analysis ANOVA proved that the patients treated with nitrates and captopril showed greater improvement in exercise capacity (in METS) than patients treated with enalapril or placebo (+1.26 captopril, +0.2 enalapril and +0.29 placebo, p = 0.043). In addition, a decrease in left ventricular mass index was evident only in patients treated with angiotensin converting enzyme inhibitor (placebo +7.37 gm/m2, captopril -12.17 gm/m2, enalapril -10.14 gm/m2, p = 0.0032). The triple factor analysis ANOVA test revealed that the change in endodiastolic left ventricular volume depends on combination of three factors: infarct location, type of treatment and level of cardiac enzymes (p = 0.009). A decrease in left ventricular endodiastolic volume between day 42 and 10 was observed only in patients with inferior wall infarct and CPK level < 2000 IU/L, irrespective of treatment type and in patients with inferior wall infarct and CPK level > 2000 IU/L treated with angiotensin enzyme inhibitor. We noticed also that heart failure, considered as contraindication to randomization, was in addition the most frequent (up to day 10) cause for study termination and initiation of treatment with angiotensin enzyme inhibitor.