Association of Psychosocial Risk Factors With Quality of Life and Readmissions 1 Year After LVAD Implantation.

BACKGROUND: Among patients with advanced heart failure (HF), treatment with a left ventricular assist device (LVAD) improves health-related quality of life (HRQOL). We investigated the association between psychosocial risk factors, HRQOL and outcomes after LVAD implantation. METHODS: A retrospective cohort (n = 9832) of adults aged ≥ 19 years who received durable LVADs between 2008 and 2017 was identified by using the Interagency Registry for Mechanically Assisted Circulatory Support (INTERMACS). Patients were considered to have psychosocial risk factors if ≥ 1 of the following were present: (1) substance abuse; (2) limited social support; (3) limited cognitive understanding; (4) repeated nonadherence; and (5) major psychiatric disease. Multivariable logistic and linear regression models were used to evaluate the association between psychosocial risk factors and change in Kansas City Cardiomyopathy Questionnaire (KCCQ)-12 scores from baseline to 1 year, persistently poor HRQOL (KCCQ-12 score < 45 at baseline and 1 year), and 1-year rehospitalization. RESULTS: Among the final analytic cohort, 2024 (20.6%) patients had ≥ 1 psychosocial risk factors. Psychosocial risk factors were associated with a smaller improvement in KCCQ-12 scores from baseline to 1 year (mean ± SD, 29.1 ± 25.9 vs 32.6 ± 26.1; P = 0.015) for a difference of -3.51 (95% confidence interval [CI]: -5.88 to -1.13). Psychosocial risk factors were associated with persistently poor HRQOL (adjusted odds ratio [aOR] 1.35, 95% confidence interval [CI] 1.04-1.74), and 1-year all-cause readmission (adjusted hazard ratio [aHR] 1.11, 95% CI 1.05-1.18). Limited social support, major psychiatric disorder and repeated nonadherence were associated with persistently poor HRQOL, while major psychiatric disorder was associated with 1-year rehospitalization. CONCLUSION: The presence of psychosocial risk factors is associated with lower KCCQ-12 scores and higher risk for readmission at 1 year after LVAD implantation. These associations are statistically significant, but further research is needed to determine whether these differences are clinically meaningful.

Gender and Race Differences in HeartMate3 Left Ventricular Assist Device as a Bridge to Transplantation.

BACKGROUND: Gender and racial disparities exist after left ventricular assist device (LVAD) implantation. Compared with older devices, the HeartMate 3 (HM3) (Abbott Cardiovascular) has demonstrated improved survival. Whether HM3 differentially improves outcomes by gender or race and ethnic groups is unknown. OBJECTIVES: The purpose of this study is to examine differences by gender and race in the use of HM3 among patients listed for heart transplantation (HT) and associated waitlist and post-transplant outcomes. METHODS: The authors examined all patients (20% women, 33% Black) who received LVADs as bridge to transplantation (BTT) between January 2018 and June 2020, in the OPTN (Organ Procurement and Transplantation Network) database. Trends in use of HM3 were evaluated by gender and race. Competing events of death/delisting and transplantation were evaluated using subdistribution hazard models. Post-transplant outcomes were evaluated using multivariate logistic regression adjusted for demographic, clinical, and donor characteristics. RESULTS: Of 11,524 patients listed for HT during the study period, 955 (8.3%) had HM3 implanted as BTT. Use of HM3 increased for all patients, with no difference in use by gender (P = 0.4) or by race (P = 0.2). Competing risk analysis did not demonstrate differences in transplantation or death/delisting in men compared with women (HT: adjusted HR [aHR]: 0.92 [95% CI: 0.70-1.21]; death/delisting: aHR: 0.91 [95% CI: 0.59-1.42]), although Black patients were transplanted fewer times than White patients (HT: aHR: 0.72 [95% CI: 0.57-0.91], death/delisting: aHR: 1.36 [95% CI: 0.98-1.89]). One-year post-transplant survival was comparable by gender (aHR: 0.52 [95% CI: 0.21-1.70]) and race (aHR: 0.76 [95% CI: 0.34-1.70]), with no differences in rates of stroke, acute rejection, or graft failure. CONCLUSIONS: Use of HM3 among patients listed for HT has increased over time and by gender and race. Black patients with HM3 were less likely to be transplanted compared with White patients, but there were no differences in post-transplant outcomes between these groups or between men and women.

Focal myocardial infarction induces global remodeling of cardiac sympathetic innervation: neural remodeling in a spatial context.

Myocardial infarction (MI) induces neural and electrical remodeling at scar border zones. The impact of focal MI on global functional neural remodeling is not well understood. Sympathetic stimulation was performed in swine with anteroapical infarcts (MI; n = 9) and control swine (n = 9). A 56-electrode sock was placed over both ventricles to record electrograms at baseline and during left, right, and bilateral stellate ganglion stimulation. Activation recovery intervals (ARIs) were measured from electrograms. Global and regional ARI shortening, dispersion of repolarization, and activation propagation were assessed before and during sympathetic stimulation. At baseline, mean ARI was shorter in MI hearts than control hearts (365 ± 8 vs. 436 ± 9 ms, P < 0.0001), dispersion of repolarization was greater in MI versus control hearts (734 ± 123 vs. 362 ± 32 ms(2), P = 0.02), and the infarcted region in MI hearts showed longer ARIs than noninfarcted regions (406 ± 14 vs. 365 ± 8 ms, P = 0.027). In control animals, percent ARI shortening was greater on anterior than posterior walls during right stellate ganglion stimulation (P = 0.0001), whereas left stellate ganglion stimulation showed the reverse (P = 0.0003). In infarcted animals, this pattern was completely lost. In 50% of the animals studied, sympathetic stimulation, compared with baseline, significantly altered the direction of activation propagation emanating from the intramyocardial scar during pacing. In conclusion, focal distal anterior MI alters regional and global pattern of sympathetic innervation, resulting in shorter ARIs in infarcted hearts, greater repolarization dispersion, and altered activation propagation. These conditions may underlie the mechanisms by which arrhythmias are initiated when sympathetic tone is enhanced.