Riata lead failure manifests as electrical storm with lead parameters showing unique postural variations: a case report.

BACKGROUND: Riata implantable cardioverter-defibrillator (ICD) leads are prone to a unique type of mechanical lead failure causing conductor externalization (CE) which may be complicated by a delayed-onset electrical lead failure (ELF). CASE SUMMARY: A 60-year-old male with symptomatic, severe ischaemic cardiomyopathy, and atrial fibrillation following a prior anterior wall myocardial infarction received a dual-chamber ICD with 7F-RiataST ventricular lead as a primary prevention strategy against sudden cardiac death in 2008. In 2017, a pulse generator replacement was performed for elective replacement indicator status. At that time, CE was noted in the ventricular lead but the electrical lead parameters were normal, hence lead replacement was decided against and the patient was closely followed up thereafter. Four years later, the patient presented with multiple ICD shocks within 48 h. Implantable cardioverter-defibrillator interrogation showed noise on the ventricular electrogram (EGM) channel that was detected as ventricular fibrillation (VF) episodes, triggering inappropriate ICD therapy (five ICD detected VF events within 24 h triggering three antitachycardia pacing therapies and one shock). Lead impedance and R-wave amplitude were within normal range in supine position but dramatically worsened in sitting posture. A new ventricular lead was implanted and the old lead abandoned. The patient has not experienced any device therapy in the follow-up period. DISCUSSION: An electrically inert CE of Riata ICD leads needs close follow-up because an ELF may occur even after several years. A careful analysis of EGMs including postural changes in lead parameters can aid in detection and better characterization of underlying electrical dysfunction following CE.

Prevalence and predictors of left atrial appendage inactivity in patients of rheumatic mitral stenosis in sinus rhythm: An observational study.

BACKGROUND: Systemic thromboembolism is a known complication of rheumatic mitral stenosis (RMS) in sinus rhythm (SR). Left atrial appendage (LAA), the commonest site of thrombus formation is usually hypocontractile (inactive) in such patients. We aimed to study the prevalence of LAA inactivity (LAAI) in severe RMS and assess its independent predictors. METHODS: The study population consisted of 100 patients of severe RMS in SR. Transthoracic and transesophageal echocardiography were done to assess LAA contractile function. Patients with LAA-peak emptying velocity < 25 cm/seconds were defined as having LAAI. RESULTS: The mean age of study subjects was 31.66±8.69 years and 56% were females. 73% patients had LAAI (Group A), while remaining 27% had normal LAA function (Group B). Mitral-valve area (MVA) and lateral annulus systolic velocity (Sa-wave) were significantly lower while mitral valve mean gradient (MVMG) and serum fibrinogen were significantly higher (all p-values < 0.001) in group A patients. On multivariate binary logistic regression analysis, MVMG (p < 0.001), Sa-wave (p = 0.02), and serum fibrinogen (p = 0.005) were independent predictors of LAAI. Optimal cut-off values of MVMG, Sa-wave and serum fibrinogen for predicting LAAI were 11.5 mm Hg, 6.8 cm/seconds and 300 mg/dl, respectively. Sixty-Seven (90.55%) patients in group A compared to 13(48.1%) in group B had LA/LAA smoke. LAAI was the only independent predictor of left atrium (LA)/LAA smoke with or without associated thrombus. CONCLUSION: There is high prevalence of LAAI in patients of severe MS in SR. MVMG, Sa-wave, and serum fibrinogen levels are independent predictors of LAAI. LAAI is an independent predictor of LA/LAA smoke with or without associated thrombus.

COVID-19 induced ventricular tachycardia storm unmasking a clinically silent cardiomyopathy: a case report.

BACKGROUND: Coronavirus disease (COVID-19) is a systemic illness characterized by raging impact of cytokine storm on multiple organs. This may trigger malignant ventricular arrhythmias and unmask a clinically silent cardiomyopathy. CASE SUMMARY: A 57-year-old gentleman, known case of hyperthyroidism and diabetes, was referred to our emergency department with history of two ventricular tachycardia (VT) episodes requiring direct current cardioversion in last 3 h followed by another episode in our emergency department that was cardioverted. There was no past history of cardiac illness. His 12-lead electrocardiogram (during sinus rhythm) along with screening echocardiography suggested Arrhythmogenic right ventricular cardiomyopathy (ARVC). He was coincidentally found to be COVID-19 positive by reverse transcription-polymerase chain reaction (RT-PCR) as part of our routine screening. However, he had no fever or respiratory complaints. We noted raised systemic inflammatory markers and cardiac troponin T which progressively increased over the next 4 weeks paralleled by an increase in ventricular premature contraction burden and thereafter started decreasing and returned to baseline by 6th week when the patient became COVID-19 negative by RT-PCR. Subsequently, a single-chamber automated implantable cardioverter-defibrillator implantation was done following which there was a transient increase in these biomarkers that subsided spontaneously. The patient is asymptomatic during 6 weeks of follow-up. DISCUSSION: COVID-19-associated cytokine surge triggering VT storm and unmasking a clinically silent ARVC has not yet been reported. The case highlights a life-threatening presentation of COVID-19 and indicates a probable link between inflammation and arrhythmogenicity.