Implantation of cardiac electronic devices in active COVID-19 patients: Results from an international survey.

BACKGROUND: Cardiac implantable electronic device (CIED) implantation rates as well as the clinical and procedural characteristics and outcomes in patients with known active coronavirus disease 2019 (COVID-19) are unknown. OBJECTIVE: The purpose of this study was to gather information regarding CIED procedures during active COVID-19, performed with personal protective equipment, based on an international survey. METHODS: Fifty-three centers from 13 countries across 4 continents provided information on 166 patients with known active COVID-19 who underwent a CIED procedure. RESULTS: The CIED procedure rate in 133,655 hospitalized COVID-19 patients ranged from 0 to 16.2 per 1000 patients (P <.001). Most devices were implanted due to high-degree/complete atrioventricular block (112 [67.5%]) or sick sinus syndrome (31 [18.7%]). Of the 166 patients in the study survey, the 30-day complication rate was 13.9% and the 180-day mortality rate was 9.6%. One patient had a fatal outcome as a direct result of the procedure. Differences in patient and procedural characteristics and outcomes were found between Europe and North America. An older population (76.6 vs 66 years; P <.001) with a nonsignificant higher complication rate (16.5% vs 7.7%; P = .2) was observed in Europe vs North America, whereas higher rates of critically ill patients (33.3% vs 3.3%; P <.001) and mortality (26.9% vs 5%; P = .002) were observed in North America vs Europe. CONCLUSION: CIED procedure rates during known active COVID-19 disease varied greatly, from 0 to 16.2 per 1000 hospitalized COVID-19 patients worldwide. Patients with active COVID-19 infection who underwent CIED implantation had high complication and mortality rates. Operators should take these risks into consideration before proceeding with CIED implantation in active COVID-19 patients.

Commotio Cordis: Indeed?

We discuss an unusual case of a patient who initially presented with apparent commotio cordis but returned several months later with spontaneous wide complex tachycardia. This case highlights the importance of investigation of survivors of commotio cordis, especially if atypical, to determine if there is underlying cardiac disease. (Level of Difficulty: Beginner.).

Successful treatment of ventricular fibrillation storm triggered by short-long-short sequence; time to avoid managed ventricular pacing.

Sudden cardiac death (SCD) in hypertrophic cardiomyopathy (HCM) is caused by ventricular tachyarrhythmia that can be effectively treated by implantable cardioverter defibrillator (ICD) therapy. We report of a 28-year-old man with HCM and a dual chamber ICD, originally implanted for primary prevention of SCD, (programmed to AAI(R)-DDD(R); managed ventricular pacing (MVP) mode, Medtronic Inc. St Paul, MN USA). He presented with recurrent ICD shocks due to ventricular fibrillation (VF) despite antiarrhythmic therapy. Careful assessment of the stored electrograms demonstrated a repetitive pattern of VF initiation following short-long-short sequences. Initially, activation of ventricular rate stabilization (VRS) algorithm failed to prevent recurrent VF. Ultimately, deactivation of MVP and reprogramming the device to DDD mode with VRS on, resulted in arrhythmia suppression and avoidance of ICD shocks. Physicians should be aware that although VRS function is available in MVP mode, it does not function in the AAI mode during MVP; in order to effectively treat short-long-short sequence induced ventricular arrhythmia by device programming.

Ventricular fibrillation as the presenting manifestation of adrenocortical carcinoma.

We describe a case of a young adult in whom sudden cardiac death due to ventricular fibrillation was the presenting manifestation of an adrenocortical carcinoma. The arrhythmia was precipitated by severe hypokalemia induced by the aldosterone-secreting tumor. Sudden death has not been previously described as a manifestation of this adrenal neoplasm. Unexplained persistent hypokalemia after resuscitated sudden death (especially when combined with hypertension( should prompt investigation for an underlying secondary hypertension, particularly adrenal pathology. Adrenocortical carcinoma should be considered in the differential diagnosis of unexplained sudden death associated with unexplained hypokalemia.

Crosstalk between L-type calcium channels and ZnT-1, a new player in rate-dependent cardiac electrical remodeling.

Crosstalk between two membrane transport systems is an established mechanism underlying regulation. In this study, we investigated the interaction between ZnT-1, a putative plasma membrane zinc transporter, and L-type voltage-dependent calcium channels (LTCC). In the atrium of the myocardium decreased activity of the LTCC is a dominant feature of patients with atrial fibrillation. The trigger for this inhibition has been attributed to the rapid firing rates and consequent calcium overload in the atrial cardiomyocytes. However, the underlying mechanism of LTCC inhibition is still to be elucidated. Here, we showed that the expression of ZnT-1 inhibits the activity of L-type channels during electrical remodeling induced by rapid pacing. (i) Direct manipulations of ZnT-1 expression in cultured cardiomyocytes either by ZnT-1 overexpression or by ZnT-1 silencing with siRNA, decreased or enhanced, respectively, the barium influx through the LTCC. (ii) Co-expression of ZnT-1 with LTCC in Xenopus oocytes decreased whole cell barium current through LTCC. (iii) Rapid pacing of cultured cardiomyocytes (4 h, 100 ms cycle) increased ZnT-1 protein expression and inhibited the voltage-dependent divalent cation influx through the LTCC. Moreover, silencing ZnT-1 with siRNA prevented the rapid pacing induced inhibition of the LTCC (iv) Atrial pacing of anesthetized adult rats (4 h, 50 ms cycle) led to a significant increase in atrial ZnT-1 protein expression in parallel with the typical decrease of the refractory period in the atria. Taken together, these findings demonstrate that crosstalk between ZnT-1 and the L-type calcium channels may underlie atrial response to rapid pacing, suggesting that ZnT-1 is a significant participant in rate-dependent cardiac electrical remodeling.