T-wave inversion as a manifestation of COVID-19 infection: a case series.

PURPOSE: Cardiac involvement with COVID-19 infection has become evident by elevated troponin, cardiac arrhythmias, ST segment elevation, myocarditis, fulminant heart failure, and sudden cardiac death. We aimed to describe the association of COVID-19 and T-wave inversion (TWI) in a large case series. METHODS: We conducted an observational, retrospective study of confirmed COVID-19 cases with at least one electrocardiogram (ECG) in a large hospital in New York City (March 23, 2020-April 23, 2020). Patients with new TWI or pseudonormalization were further analyzed. Mortality and the need for invasive mechanical ventilation were the main outcomes. RESULTS: A total of 3225 patients were screened; 195 (6%) were selected for further analysis: 181 with TWI and 14 with T-wave pseudonormalization. Mean age was 66 ± 7 years; 51% were male. TWI were more commonly noted in the lateral (71%), followed by anterior (64%), inferior (57%), and septal (26%) leads. A total of 44 patients (23%) had elevated troponin. A total of 50 patients died (26%). Mortality rates of 35%, and 52% were observed in patients with diffuse TWI, and elevated troponin, respectively. Mortality rate of 80% was observed in patients with both elevated troponin and diffuse TWI. Additionally, 30% of the entire cohort and 58% of patients with elevated troponin required invasive mechanical ventilation. CONCLUSION: Our study demonstrates that new TWI is a relatively common finding in COVID-19 patients. Importantly, our findings suggest that new TWI or T-wave pseudonormalization, particularly with elevated troponin, was associated with higher rates of mechanical ventilation and in-hospital mortality.

Atrial fibrillation inducibility during cavotricuspid isthmus-dependent atrial flutter ablation as a predictor of clinical atrial fibrillation. A meta-analysis.

BACKGROUND: Atrial fibrillation (AF) and cavotricuspid isthmus (CTI)-dependent atrial flutter (AFL) are two separate entities that coexist in a significant percentage of patients. We sought to investigate whether AF inducibility during CTI AFL ablation predicted the occurrence of AF at follow-up after successful AFL ablation. METHODS: A systemic review of Medline, Cochrane, and Embase was done for all the clinical studies in which assessment of AF inducibility in patients undergoing ablation for CTI AFL was performed. Given the low heterogeneity (i.e., I 2 <25), we used a fixed effect model for our analysis. RESULTS: A total of 10 studies (4 prospective and 6 retrospective) with a total of 1299 patients (male, 73%; mean age 59 ± 11 years) fulfilled the inclusion criteria. During a mean follow-up period of 23 ± 7.6 months, 407 patients (31%) developed AF during AFL ablation. The overall incidence for new-onset AF during follow-up was 29% (47% in the group with inducible AF vs. 21% in the non-inducible group). The odds ratio (OR) for developing AF after AFL ablation in patients with AF inducibility for all studies combined was 3.72, 95% CI 2.83-4.89 [prospective studies (OR 5.52, 95% CI 3.23-9.41) vs. retrospective studies (OR 3.23, 95% CI 2.35-4.45)]. CONCLUSIONS: Although ablation for CTI AFL is highly effective, AF continues to be a long-term risk for individuals undergoing this procedure. AF induced by pacing protocols in patients undergoing CTI AFL predicts for future AF. Inducible AF is a clinically relevant finding that may help guide decisions for long-term anticoagulation after successful typical AFL ablation especially in patients with elevated CHADS-VASc scores (≥2) and in considering prophylactic PVI during CTI AFL ablation.

Atrial fibrillation inducibility during cavo-tricuspid isthmus dependent atrial flutter ablation for the prediction of clinical atrial fibrillation.

BACKGROUND: Atrial fibrillation (AF) and cavo-tricuspid isthmus (CTI) dependent atrial flutter (AFL) are two separate entities that coexist in a significant percentage of patients. METHODS: We sought to investigate whether AF inducibility during CTI AFL ablation predicted the occurrence of AF at follow up after AFL ablation. Univariate and multivariate analyses were performed. RESULTS: A total of 154 patients (male: 72%, age: 61±13) with AFL and without history of AF were included. All patients underwent successful CTI dependent AFL ablation demonstrated by bidirectional block. During ablation, AF was seen or induced in 28 (18%) patients. After a mean follow up of 34±24months a total of 50 patients (32%) were noted with clinically manifest AF. From the patients who had inducible AF during AFL ablation, 50% developed post-procedural AF. From those in whom AF could not be induced, only 29% were documented with AF after ablation. Univariate and multivariate analyses revealed that only age and AF inducibility during AFL ablation were predictors of AF. Univariate analysis (age p=0.038 and inducible AF p=0.032 with odds ratio of 1.030 [95% CI (1.002-1.059)] and 2.500 [95% CI (1.084-5.765)], respectively) and multivariate analyses (age p=0.011 and inducible AF p=0.016 with adjusted odds ratio of 1.043 [95% CI (1.010-1.077)] and 3.293 [95% CI (1.250-8.676)], respectively). CONCLUSION: AF inducibility in patients undergoing CTI AFL without history of AF is a strong predictor of AF occurrence in the future. Appropriate cardiology follow-up must be encouraged in this high-risk population as stroke prevention strategies can be appropriately introduced in a timely matter especially in patients with elevated CHA2DS2-VASc scores (≥2).

Drug-induced torsades de pointes in an underserved urban population. Methadone: is there therapeutic equipoise?

BACKGROUND: Although it has been well established that methadone use can result in prolonged QTc/torsades de pointes (TdP) and has been labeled as one of the main drugs that cause TdP, it is still prescribed indiscriminately, and several cases of methadone-associated TdP have been seen in our community. METHODS: Our objective was to determine the associated factors for prolonged QTc and the development of torsades de pointes (TdP) in our underserved patient population. We found 12,550 ECGs with prolonged QTc between 2002 and 2013. Medical records were reviewed in order to identify precipitating factors for prolonged QTc and to detect incidence of TdP. RESULTS: We identified 2735 patients with prolonged QTc who met the inclusion criteria. Of these, 89 (3%) experienced TdP. There was a greater prevalence of HIV infection in the TdP group (11.2 vs. 3.7%, p < 0.001). Furosemide, hydrochlorothiazide, selective serotonin reuptake inhibitors (SSRIs), amiodarone, ciprofloxacin, methadone, haloperidol, and azithromycin were the drugs most often associated with prolonged QTc (31, 8.2, 7.6, 7.1, 3.9, 3.4 and 3.3%, respectively). However, the agents most commonly associated with TdP were furosemide (39.3%), methadone (27%), SSRIs (19.1%), amiodarone (18%), and dofetilide (9%). The medications with statistical significance in the multivariate analysis for TdP development in descending order were as follows: ranolazine (odds ratios [OR] = 53.61, 95% confidence interval [CI] 5.4-524, p < 0.001), dofetilide (OR = 25, CI 6.47-103.16, p < 0.001), voriconazole (OR = 21.40, CI 3.24-124.25, p < 0.001), verapamil (OR = 10.98, CI 2.62-44.96, p < 0.001), sotalol (OR = 12.72, 1.95-82.81, p = 0.008), methadone (OR = 9.89, CI 4.05-24.15, p < 0.001), and SSRI (OR = 2.26, CI 1.10-5.96, p < 0.001). This multivariate analysis revealed that amiodarone and HIV infection were not implicated in TdP. CONCLUSION: Methadone was by far the leading medication implicated in the development of TdP and an independent predictor in both univariate and multivariate analyses despite the fact that it was not the most common QT-prolonging medication in our population.