Search

Catheter ablation of ventricular arrhythmias has evolved considerably since it was first described more than 3 decades ago. Advancements in understanding the underlying substrate, utilizing pre-procedural imaging, and evolving ablation techniques have improved the outcomes of catheter ablation. Ensuring safety and efficacy during catheter ablation requires adequate planning, including analysis of the 12 lead ECG and appropriate pre-procedural imaging. Defining the underlying arrhythmogenic substrate and disease eitology allow for the developed of tailored ablation strategies, especially for patients with non-ischemic cardiomyopathies. During ablation, the type of anesthesia can affect VT induction, the quality of the electro-anatomic map, and the stability of the catheter during ablation. For high risk patients, appropriate selection of hemodynamic support can increase the success of VT ablation. For patients in whom VT is hemodynamically unstable or difficult to induce, substrate modification strategies can aid in safe and successful ablation. Recently, there has been an several advancements in substrate mapping strategies that can be used to identify and differentiate local late potentials. The incorporation of high-definition mapping and contact-sense technologies have both had incremental benefits on the success of ablation procedures. It is crucial to harness newer technology and ablation strategies with the highest level of peri-procedural safety to achieve optimal long-term outcomes in patients undergoing VT ablation.

A 17-year-old boy was admitted for management of ventricular fibrillation (VF) with intermittent Brugada pattern on ECG. On evaluation, cardiac MRI revealed myocardial scar and mediastinal lymphadenopathy. 18-Fluorodeoxyglucose positron emission tomography scan showed inflammation in the heart, lungs, and lymph nodes. He was diagnosed as a case of cardiac sarcoidosis (CS) and treated with steroids. However, there was a reactivation of cardiac inflammation and the development of a second VF storm. Following catheter ablation, the patient's arrhythmia improved. This report highlights the inflammation due to CS mimicking channelopathic features.

There has been an increased use of cardiac pacemaker device utilization in cardiac patients with a corresponding increase of device-related infections in these patients. The common cause of postpacemaker implantation infection is either Gram-positive or Gram-negative bacteria. Infection of pacemaker implantation site due to nontuberculous mycobacteria is rare. Globally, thirty-two cases of pacemaker device infections caused by nontuberculous mycobacteria were reported. It is important to carry out not only species identification of mycobacteria but also drug susceptibility testing to start precise treatment to those patients, who are infected with atypical mycobacteria. We report a patient with pacemaker pocket infection due to Mycobacterium chelonae.

Summary of the Consensus Statement: This statement has been prepared keeping Indian heart failure patients in mind. Optimal management of CHF improves quality of life, reduces hospitalization rates and prolongs survival for people with this condition. Echocardiography is the single most useful test in the evaluation of heart failure, and is necessary to confirm the diagnosis. Plasma B-natriuretic peptide (BNP) measurements may be useful in excluding CHF but not mandatory in India. Educate people with CHF about lifestyle changes (e.g., increase physical activity levels, reduce salt intake and manage weight). Educate people with CHF about CHF symptoms and how to manage fluid load. Avoid prescribing drugs that exacerbate CHF. Prescribe angiotensin-converting enzyme inhibitors (ACEI) at effective doses for people with all grades of systolic heart failure, and titrate to the highest recommended dose tolerated. Angiotensin II receptor antagonists (ARA) may be used as alternatives in people who cannot tolerate ACEIs. Mineralocorticoid receptor antagonists (MRAs) should also be used. For people with stabilised systolic heart failure, prescribe beta-blockers that have been shown to improve outcome in heart failure (e.g., bisoprolol, carvedilol, extended release metoprolol or nebivolol). Titrate to the highest recommended dose tolerated. Prescribe diuretics, digoxin and nitrates for people already using ACEIs and beta-blockers to manage symptoms as indicated. For people who have systolic heart failure (New York Heart Association (NYHA) Class II-IV) despite appropriate doses of ACEIs and diuretics, consider prescribing spironolactone. Eplerenone can be considered in certain setting especially post myocardial infarction though it is more expensive. Consider direct sinus node inhibition with ivabradine for people with CHF who have impaired systolic function, have had a recent heart failure hospitalisation and are in sinus rhythm with a heart rate >70 bpm despite beta blockers or where beta blockers are contraindicated Check for, and treat, iron deficiency in people with CHF to improve their symptoms, exercise tolerance and quality of life Consider assessing people with CHF for biventricular pacemakers and implantable defibrillators. Patients with end stage heart failure have an option for heart transplant and ventricular assist devices which is now available in select centers.

Focal left atrial tachycardia (FLAT) although a common cause of supraventricular tachycardia(SVT) among children, the one's arising from left atrial appendage (LAA) present a unique challenge for successful ablation because of anatomical location. We present two children with FLAT arising from the epicardial LAA, successfully mapped and ablated through percutaneuous epicardial approach.

Tachycardia detection and therapy algorithms in Implantable Cardioverter-Defibrillators (ICD) reduce, but do not eliminate inappropriate ICD shocks. Awareness of the pros and cons of a particular algorithm helps to predict its utility in specific situations. We report a case where PR logic™, an algorithm commonly used in currently implanted ICDs to differentiate supraventricular tachycardia (SVT) from ventricular tachycardia resulted in inappropriate detection and shock for an SVT, and discuss several solutions to the problem.

Background: Autosomal recessive Long QT syndrome is characterized by prolonged QTc along with congenital bilateral deafness depends on mutations in K+ channel genes. A family of a Long QT syndrome proband from India has been identified with novel indel variations. Methods: The molecular study of the proband revealed 4 novel indel variations in KCNQ1. In-silico analysis revealed the intronic variations has led to a change in the secondary structure of mRNA and splice site variations. The exonic variations leads to frameshift mutations. DNA analysis of the available family members revealed a carrier status. Results and Conclusion: It is thus predicted that the variations may lead to a change in the position of the splicing enhancer/inhibitor in KCNQ1 leading to the formation of a truncated S2–S3 fragment of KCNQ1 transmembrane protein in cardiac cells as well as epithelial cells of inner ear leading to deafness and aberrant repolarization causing prolonged QTc.

Background: Assessment of ventricular dyssynchrony in patients with heart failure is used for selecting candidates for cardiac resynchronization therapy (CRT). The patterns of regional distribution of dyssynchrony in a population with LBBB with and without heart failure have not been well delineated. This aspect forms the object of the study.Methods: Tissue Doppler Imaging (TDI) data of consecutive patients with heart failure and LBBB (Group A) was compared with those with LBBB and normal LV function (Group B). All patients had standard 2D-echocardigraphic examination and TDI. Tissue velocity curves obtained by placing sample volumes in opposing basal and mid segments of septal, lateral, inferior, anterior and posterior walls were analyzed. Inter ventricular dyssynchrony (IVD) was assessed by the difference between aortic and pulmonary pre ejection intervals. LV dyssynchrony (LVD) was assessed by the difference in times to peak velocity. A delay of ≥ 40 msec was considered significant for presence of IVD and LVD.Results: There were 103 patients in Group A and 25 in Group B. The mean QRS duration and PR intervals respectively were 146 ± 25 vs. 152±20 msec and 182± 47 vs. 165±36 msec. (p=NS) LVEF in the 2 groups were (32 ± 6 % vs. 61± 11%; p< 0.01). Prevalence of dyssynchrony in the HF group compared to Group B was 72% vs. 16%, (P

Objective: Among the inherited cardiomyopathies, Arrhythmogenic right ventricular dysplasia/cardiomyopathy is unique with a peculiar pathology of fibro-fatty replacement. Studies have been carried out all over the world and several groups have reported clinical heterogeneity in manifestation of ARVD/C related symptoms. Present study is an attempt to identify the clinical profile of ARVD/C patients from Asian Indian origin.Methods: 31 patients in the span of three years were diagnosed with ARVD/C. Diagnosis was based on proposed task force criteria.Results: The mean age at diagnosis was 32.9 ± 16.4 years with slight tilt in male to female ratio (1.46). About 80% cases had palpitations, syncope in 45.16% and dyspnea in 22.5%, whereas 16% of patients were asymptomatic. About 50% of patients revealed a family history of confirmed ARVD/C or sudden death of a family member without any known cause. ECG showed T-wave inversion in about 60% cases, prolongation of QRS was observed in 20% cases. RV dilatation was observed in 80% of patients and 66.7% showed systolic dysfunction. RV free wall motion abnormalities were found in 33% patients. Most of the early onset cases with less than 30 years of age showed family history indicative of ARVD/C. Familial study in three patients indicated early onset of condition in younger generations in two families. Conclusion: ARVD/C in India shows relatively early age at onset when compared with other Asian populations with more than half of patients showing the disease below the age of 30 years. History in most of the early onset cases revealed family history indicating strong genetic influence.

Hypertrophic Cardiomyopathy (HCM) is an autosomal dominant disorder of the myocardium which is hypertrophied resulting in arrhythmias and heart failure leading to sudden cardiac death (SCD). Several sarcomeric proteins and modifier genes have been implicated in this disease. Troponin I, being a part of the Troponin complex (troponin I, troponin C, troponin T), is an important gene for sarcomeric function. Four mutations (1 novel) were identified in Indian HCM cases, namely, Pro82Ser, Arg98Gln, Arg141Gln and Arg162Gln in Troponin I protein, which are in functionally significant domains. In order to analyse the effect of the mutations on protein stability and protein-protein interactions within the Troponin complex, an in silico study was carried out. The freely available X-ray crystal structure (PDB ID: 1JIE) was used as the template to model the protein followed by loop generation and development of troponin complex for both the troponin I wild type and four mutants (NCBI ID: PRJNA194382). The structural study was carried out to determine the effect of mutation on the structural stability and protein-protein interactions between three subunits in the complex. These mutations, especially the arginine to glutamine substitutions were found to result in local perturbations within the troponin complex by creating/removing inter/intra molecular hydrogen bonds with troponin T and troponin C. This has led to a decrease in the protein stability and loss of important interactions between the three subunits. It could have a significant impact on the disease progression when coupled with allelic heterogeneity which was observed in the cases carrying these mutations. However, this can be further confirmed by functional studies on protein levels in the identified cases.

Abstract Background Troponin I (TNNI3) is the inhibitory subunit of the thin filament regulatory complex Troponin, which confers calcium-sensitivity to striated muscle actomyosin ATPase activity. Mutations (2-7%) in this gene had been reported in hypertrophic cardiomyopathy patients (HCM). However, the frequencies of mutations and associated clinical presentation have not been established in cardiomyopathy patients of Indian origin, hence we have undertaken this study. Methods We have sequenced all the exons, including the exon-intron boundaries of TNNI3 gene in 101 hypertrophic cardiomyopathy patients (HCM), along with 160 healthy controls, inhabited in the same geographical region of southern India. Results Our study revealed a total of 16 mutations. Interestingly, we have observed Arginine to Glutamine (R to Q) mutation at 3 positions 98, 141 and 162, exclusively in HCM patients with family history of sudden cardiac death. The novel R98Q was observed in a severe hypertrophic obstructive cardiomyopathy patient (HOCM). The R141Q mutation was observed in two familial cases of severe asymmetric septal hypertrophy (ASH++). The R162Q mutation was observed in a ASH++ patient with mean septal thickness of 29 mm, and have also consists of allelic heterogeneity by means of having one more synonymous (E179E) mutation at g.4797: G → A: in the same exon 7, which replaces a very frequent codon (GAG: 85%) with a rare codon (GAA: 14%). Screening for R162Q mutation in all the available family members revealed its presence in 9 individuals, including 7 with allelic heterogeneity (R162Q and E179E) of which 4 were severely affected. We also found 2 novel SNPs, (g.2653; G → A and g.4003 C → T) exclusively in HCM, and in silico analysis of these SNPs have predicted to cause defect in recognition/binding sites for proteins responsible for proper splicing. Conclusion Our study has provided valuable information regarding the prevalence of TNNI3 mutations in Indian HCM patients and its risk assessment, these will help in genetic counseling and to adopt appropriate treatment strategies.

Introduction: Rheumatic heart disease with persistent atrial fibrillation (RHD‐AF) is associated with increased morbidity. However, there is no standardized approach for the maintenance of sinus rhythm (SR) in them. We aimed to determine the utility of a stepwise approach to achieve SR in RHD‐AF. Methods: Consecutive patients with RHD‐AF from July 2021 to August 2023 formed the study cohort. The stepwise approach included pharmacological rhythm control and/or electrical cardioversion (Central illustration). In patients with recurrence, additional options included AF ablation or pace and ablate strategy with conduction system pacing or biventricular pacing. Clinical improvement, NT‐proBNP, 6‐Minute Walk Test (6MWT), heart failure (HF) hospitalizations, and thromboembolic complications were documented during follow‐up. Results: Eighty‐three patients with RHD‐AF (mean age 56.13 ± 9.51 years, women 72.28%) were included. Utilizing this approach, 43 (51.81%) achieved and maintained SR during the study period of 11.04 ± 7.14 months. These patients had improved functional class, lower NT‐proBNP, better distance covered for 6MWT, and reduced HF hospitalizations. The duration of AF was shorter in patients who achieved SR, compared to those who remained in AF (3.15 ± 1.29 vs 6.93 ± 5.23, p = 0.041). Thirty‐five percent (29) maintained SR after a single cardioversion over the study period. Only one underwent AF ablation. Of the 24 who underwent pace and ablate strategy, atrial lead was implanted in 22 (hybrid approach), and 50% of these achieved and maintained SR. Among these 24, none had HF hospitalizations, but patients who maintained SR had further improvement in clinical and functional parameters. Conclusions: RHD‐AF patients who could achieve SR with a stepwise approach, had better clinical outcomes and lower HF hospitalizations. [ABSTRACT FROM AUTHOR]