A Case of Bundle Branch Re-entrant Ventricular Tachycardia 1 Year After Transcatheter Aortic Valve Replacement.

Bundle branch re-entrant ventricular tachycardia (VT) (BBR-VT) is a unique type of ventricular tachycardia often seen in patients with advanced heart diseases. Rarely, it is found in patients with a structurally normal heart. We describe a case of BBR-VT in a patient with normal ventricular function, a year after transcatheter aortic valve replacement (TAVR) for aortic stenosis. A 73-year-old man with a past medical history of non-obstructive coronary artery disease and severe aortic stenosis status post-TAVR with a 23-mm Sapien valve (Edwards Lifesciences, Irvine, CA, USA) about 1 year prior presented with palpitations and syncope. The electrocardiogram (ECG) showed a wide complex tachycardia with a left bundle branch block (LBBB) pattern and atrioventricular dissociation. The tachycardia was incessant and paroxysmal during 24-h telemetry monitoring. An electrophysiology study showed a normal A-H interval of 90 ms and a prolonged H-V interval of 84 ms with evidence of a split His. A hemodynamically stable VT was induced with a cycle length of 453 ms, which was identical to the clinical VT. This was diagnosed to be BBR-VT given the typical ECG pattern of LBBB, the presence of His inscription before each ventricular signal, and the H-H interval variation-predicted V-V variation when there was a wobble in tachycardia cycle length. Injury of the His-Purkinje system post-TAVR can provide the substrate for the development of BBR-VT. Current published literature shows early occurrence post-TAVR, but our case suggests that the timing between the index procedure and arrhythmia occurrence can be variable.

Delayed cardiac repolarisation as a predictor of in-hospital mortality in patients with COVID-19.

OBJECTIVE: With the rapid influx of COVID-19 admissions during the first wave of the pandemic, there was an obvious need for an efficient and streamlined risk stratification tool to aid in triaging. To this date, no clinical prediction tool exists for patients presenting to the hospital with COVID-19 infection. METHODS: This is a retrospective cohort study of patients admitted in one of 13 Northwell Health Hospitals, located in the wider New York Metropolitan area between 1 March 2020 and 27 April 2020. Inclusion criteria were a positive SARS-CoV-2 nasal swab, a 12-lead ECG within 48 hours, and a complete basic metabolic panel within 96 hours of presentation. RESULTS: All-cause, in-hospital mortality was 27.1% among 7098 patients. Independent predictors of mortality included demographic characteristics (male gender, race and increased age), presenting vitals (oxygen saturation <92% and heart rate >120 bpm), metabolic panel values (serum lactate >2.0 mmol/L, sodium >145, mmol/L, blood urea nitrogen >40 mmol/L, aspartate aminotransferase >40 U/L, Creatinine >1.3 mg/dL and glycose >100 mg/L) and comorbidities (congestive heart failure, chronic obstructive pulmonary disease and coronary artery disease). In addition to those, our analysis showed that delayed cardiac repolarisation (QT corrected for heart rate (QTc) >500 ms) was independently associated with mortality (OR 1.41, 95% CI 1.05 to 1.90). Previously mentioned parameters were incorporated into a risk score that accurately predicted in-hospital mortality (AUC 0.78). CONCLUSION: In the largest cohort of COVID-19 patients with complete ECG data on presentation, we found that in addition to demographics, presenting vitals, clinical history and basic metabolic panel values, QTc >500 ms is an independent risk factor for in-hospital mortality.

New Precordial T Wave Inversions in Hospitalized Patients.

BACKGROUND: The incidence of precordial T changes has been described in athletes and in specific populations, while the etiology in a large patient population admitted to the hospital has not previously been reported. METHODS: All electrocardiograms (ECGs) read by the same physician with new (compared to prior ECGs) or presumed new (no prior ECGs) precordial T wave inversions of >1 mm (0.1 mV) in multiple precordial leads were retrospectively reviewed and various ECG, patient-related, and imaging parameters assessed. A total of 226 patients and their ECGs were initially selected for analysis. Of these, 35 were eliminated leaving 191 for the final analysis. RESULTS: Patients and their ECGs were divided into 5 groups based on diagnosis and incidence including Wellens syndrome, takotsubo, type 2 myocardial infarction, other (including multiple diagnoses), and unknown. Although subtle differences including number of T inversion leads, depth of T waves, QTc intervals, and other variables were present between some groups, diagnosis in individual cases required appropriate clinical, laboratory, or imaging studies. For example, although Wellens syndrome was identified in <20% of cases, a presenting history of chest discomfort with precordial T changes either on the admission or next-day ECG was highly sensitive and specific for this diagnosis. In some cases, type 2 myocardial infarction can also have a Wellens-like ECG phenotype without significant left anterior descending disease. CONCLUSIONS: Precordial T wave changes in hospitalized patients have various etiologies, and in individual cases, the changes on the ECG alone cannot easily distinguish the presumptive diagnosis and additional data are required.

Surface unipolar electrogram characteristics to predict site of origin of outflow tract arrhythmias using noninvasive mapping.

BACKGROUND: Noninvasive electroanatomic mapping (NIEAM) demonstrate patterns of depolarization that are useful in identifying the chamber of origin (COO) in outflow tract ventricular arrhythmias (OTVA). However, its use in predicting exact site of origin (SOO) has not yet been validated. METHODS: NIEAMs (CardioInsight, Medtronic) from 40 patients (age 62.5 ± 2.6) undergoing ablation for OTVA were reviewed for diagnostic accuracy in predicting the SOO. Earliest arrhythmia breakout and directionality of earliest instantaneous unipolar electrograms (uEGMs) on NIEAMs were evaluated subjectively by two observers for quality and amplitude. Sites with most negative earliest uEGMs on right and left ventricular outflow tracts, as well as epicardial surface were manually identified. Using NIEAM-based activation timing of the lateral mitral annulus and basal septum COO was identified for each OTVA. Predictions of SOO using NIEAMs was compared with true SOO from invasive study. NIEAMs SOO predictions were compared with subjective 12 lead electrocardiogram (ECG) review by two observers. RESULTS: Review of arrhythmia breakout and signal directionality had poor diagnostic value in predicting SOO in OTVA (50.6% and 49.4%, 56.6% and 43.4%, respectively) and underperformed compared with ECG interpretation (59.1% and 80.5%). After excluding uEGMs with poor characteristics, the uEGM with most negative amplitude at the COO was predictive of the true SOO with 96.4% sensitivity and specificity. CONCLUSION: We propose a stepwise approach when interpreting NIEAMs for OTVA where patterns of activation are evaluated first to determine the COO, followed by identification of the site with most negative amplitude instantaneous uEGM to determine SOO.

Unusual presentation of left ventricular rupture.

We describe a case of 49-year-old man who presented with chest pain and was diagnosed with non-ST elevation myocardial infarction. Transthoracic echocardiogram (TTE) showed severe global hypokinesis of left ventricle with ejection fraction of 25%-30%. Left heart catheterisation showed severe right coronary stenosis and focal 60%-70% distal left anterior descending artery stenosis. Cardiac MRI (CMR) was done for evaluation of viability which showed a large pseudoaneurysm which was missed on TTE and left ventriculogram. Our case demonstrates the increasing importance of cardiac MRI in the diagnosis of left ventricular pseudoaneurysm. In our case left ventricular pseudoaneurysm was missed on TTE and left ventriculogram. It was diagnosed on CMR which was ordered for evaluation of myocardium viability.

In-Hospital Outcomes of Percutaneous Coronary Intervention in America's Safety Net: Insights From the NCDR Cath-PCI Registry.

OBJECTIVES: This study compared risk-adjusted percutaneous coronary intervention (PCI) outcomes of safety-net hospitals (SNHs) and non-SNHs. BACKGROUND: Although risk adjustment is used to compare hospitals, SNHs treat a disproportionate share of uninsured and underinsured patients, who may have unmeasured risk factors, limited health care access, and poorer outcomes than patients treated at non-SNHs. METHODS: Using the National Cardiovascular Data Registry CathPCI Registry from 2009 to 2015, we analyzed 3,746,961 patients who underwent PCI at 282 SNHs (hospitals where ≥10% of PCI patients were uninsured) and 1,134 non-SNHs. The relationship between SNH status and risk-adjusted outcomes was assessed. RESULTS: SNHs were more likely to be lower volume, rural hospitals located in the southern states. Patients treated at SNHs were younger (63 vs. 65 years), more often nonwhite (17% vs. 12%), smokers (33% vs. 26%), and more likely to be admitted through the emergency department (48% vs. 38%) and to have an ST-segment elevation myocardial infarction (20% vs. 14%) than non-SNHs (all p < 0.001). Patients undergoing PCI at SNHs had higher risk-adjusted in-hospital mortality (odds ratio: 1.23; 95% confidence interval: 1.17 to 1.32; p < 0.001), although the absolute risk difference between groups was small (0.4%). Risk-adjusted bleeding (odds ratio: 1.05; 95% confidence interval: 1.00 to 1.12; p = 0.062) and acute kidney injury rates (odds ratio: 1.01; 95% confidence interval: 0.96 to 1.07; p = 0.51) were similar. CONCLUSIONS: Despite treating a higher proportion of uninsured patients with more acute presentations, risk-adjusted PCI-related in-hospital mortality of SNHs is only marginally higher (4 additional deaths per 1,000 PCI cases) than non-SNHs, whereas risk-adjusted bleeding and acute kidney injury rates are comparable.