Appropriate and Inappropriate ICD Shocks in Patients with LVADS: Prevalence, Associated Factors, and Etiologies.

BACKGROUND: Implantable cardioverter-defibrillator (ICD) shocks are a common complication following Left Ventricular Assist Device (LVAD) implantation; however, there is limited data on their frequency and causes. OBJECTIVE: To define the incidence, programming, patient characteristics, and factors associated with appropriate and inappropriate ICD shocks in persons with LVADs. METHODS: We performed a retrospective review at Duke University Hospital of all LVAD recipients implanted between January 1, 2013 to June 30, 2019 with a pre-existing ICD. ICD shocks were adjudicated by the treating physician and a 2nd reviewer for the purpose of this study. RESULTS: Among 421 patients with an ICD in situ undergoing LVAD implant, 147 (33.9%) patients had at least one shock following LVAD implantation. Among 134 patients with complete device history, there were a total of 330 shock episodes: 255 (77.3%) appropriate and 75 (22.7%) inappropriate. Etiologies for inappropriate shocks included SVT (n=66, 20.0%), physiologic oversensing (n=1, 0.3%), and non-physiologic oversensing (n=8, 2.4%) including LVAD electromagnetic interference (n=1, 0.3%). ICD programming with shorter detection delay (p < 0.001) and absence of anti-tachycardia pacing programming (p = 0.001) in high-rate zones was seen more commonly in inappropriate shock than appropriate shock. CONCLUSIONS: The rate of inappropriate shocks in LVAD recipients is very high and is most often due to supraventricular arrhythmias. LVAD electromagnetic interference is a rare cause of ICD shock. Implementation of current consensus AHA recommendations for LVAD programming with long detection delays and high rate cutoffs may help avoid inappropriate ICD shocks.

Cardiovascular Burden of the V142I Transthyretin Variant.

Importance: Individual cohort studies concur that the amyloidogenic V142I variant of the transthyretin (TTR) gene, present in 3% to 4% of US Black individuals, increases heart failure (HF) and mortality risk. Precisely defining carrier risk across relevant clinical outcomes and estimating population burden of disease are important given established and emerging targeted treatments. Objectives: To better define the natural history of disease in carriers across mid to late life, assess variant modifiers, and estimate cardiovascular burden to the US population. Design, Setting, and Participants: A total of 23 338 self-reported Black participants initially free from HF were included in 4 large observational studies across the US (mean [SD], 15.5 [8.2] years of follow-up). Data analysis was performed between May 2023 and February 2024. Exposure: V142I carrier status (n = 754, 3.2%). Main Outcomes and Measures: Hospitalizations for HF (including subtypes of reduced and preserved ejection fraction) and all-cause mortality. Outcomes were analyzed by generating 10-year hazard ratios for each age between 50 and 90 years. Using actuarial methods, mean survival by carrier status was estimated and applied to the 2022 US population using US Census data. Results: Among the 23 338 participants, the mean (SD) age at baseline was 62 (9) years and 76.7% were women. Ten-year carrier risk increased for HF hospitalization by age 63 years, predominantly driven by HF with reduced ejection fraction, and 10-year all-cause mortality risk increased by age 72 years. Only age (but not sex or other select variables) modified risk with the variant, with estimated reductions in longevity ranging from 1.9 years (95% CI, 0.6-3.1) at age 50 to 2.8 years (95% CI, 2.0-3.6) at age 81. Based on these data, 435 851 estimated US Black carriers between ages 50 and 95 years are projected to cumulatively lose 957 505 years of life (95% CI, 534 475-1 380 535) due to the variant. Conclusions and Relevance: Among self-reported Black individuals, male and female V142I carriers faced similar and substantial risk for HF hospitalization, predominantly with reduced ejection fraction, and death, with steep age-dependent penetrance. Delineating the individual contributions of, and complex interplay among, the V142I variant, ancestry, the social construct of race, and biological or social determinants of health to cardiovascular disease merits further investigation.