Brief Review: Racial and Ethnic Disparities in Cardiovascular Care with a Focus on Congenital Heart Disease and Precision Medicine.

PURPOSE OF REVIEW: This is a brief review about racial and ethnic disparities in healthcare with focused attention to less frequently covered areas in the literature such as adult congenital heart disease, artificial intelligence, and precision medicine. Although diverse racial and ethnic populations such as Black and Hispanic groups are at an increased risk for CHD and have worse related outcomes, they are woefully underrepresented in large clinical trials. Additionally, although artificial intelligence and its application to precision medicine are touted as a means to individualize cardiovascular treatment and eliminate racial and ethnic bias, serious concerns exist about insufficient and inadequate available information from diverse racial and ethnic groups to facilitate accurate care. This review discusses relevant data to the aforementioned topics and the associated nuances. RECENT FINDINGS: Recent studies have shown that racial and ethnic minorities have increased morbidity and mortality related to congenital heart disease. Artificial intelligence, one of the chief methods used in precision medicine, can exacerbate racial and ethnic bias especially if inappropriate algorithms are utilized from populations that lack racial and ethnic diversity. Dedicated resources are needed to engage diverse populations to facilitate participation in clinical and population-based studies to eliminate racial and ethnic healthcare disparities in adult congenital disease and the utilization of artificial intelligence to improve health outcomes in all populations.

Race and Ethnicity Considerations in Patients With Coronary Artery Disease and Stroke: JACC Focus Seminar 3/9.

Notable racial and ethnic differences and disparities exist in coronary artery disease (CAD) and stroke epidemiology and outcomes despite substantial advances in these fields. Racial and ethnic minority subgroups remain underrepresented in population data and clinical trials contributing to incomplete understanding of these disparities. Differences in traditional cardiovascular risk factors such as hypertension and diabetes play a role; however, disparities in care provision and process, social determinants of health including socioeconomic position, neighborhood environment, sociocultural factors, and racial discrimination within and outside of the health care system also drive racial and ethnic CAD and stroke disparities. Improved culturally congruent and competent communication about risk factors and symptoms is also needed. Opportunities to achieve improved and equitable outcomes in CAD and stroke must be identified and pursued.

Increased Incidence of Chronic Kidney Injury in African Americans Following Cardiac Transplantation.

OBJECTIVES: This study examined whether African American race was associated with an elevated risk of chronic kidney disease (CKD) post-cardiac transplantation. BACKGROUND: CKD often occurs after cardiac transplantation and may require renal replacement therapy (RRT) or renal transplant. African American patients have a higher risk for kidney disease as well as worse post-cardiac transplant morbidity and mortality. It is unclear, however, if there is a propensity for African Americans to develop CKD after cardiac transplant. METHODS: The Institutional Review Board of Columbia University Medical Center approved the retrospective study of 151 adults (57 African American and 94 non-African American) who underwent single-organ heart transplant from 2013 to 2016. The primary outcome was a decrease in estimated glomerular filtration rate (eGFR), development of CKD, and end-stage renal disease (ESRD) requiring RRT after 2 years. RESULTS: African American patients had a significant decline in eGFR post-cardiac transplant compared to non-African American patients (- 34 ± 6 vs. - 20 ± 4 mL/min/1.73 m2, p < 0.0006). African American patients were more likely to develop CKD stage 2 or worse (eGFR < 90 mL/min/1.73 m2) than non-African American patients (81% vs. 59%, p < 0.0005). CONCLUSIONS: This is the first study to report that African American patients are at a significantly higher risk for eGFR decline and CKD at 2 years post-cardiac transplant. Future investigation into risk reduction is necessary for this patient population.

Heterogeneity of the action potential duration is required for sustained atrial fibrillation.

Atrial fibrillation (AF) is the most common cardiac arrhythmia and accounts for substantial morbidity and mortality. Recently, we created a mouse model with spontaneous and sustained AF caused by a mutation in the NaV1.5 channel (F1759A) that enhances persistent Na+ current, thereby enabling the investigation of molecular mechanisms that cause AF and the identification of novel treatment strategies. The mice have regional heterogeneity of action potential duration of the atria similar to observations in patients with AF. In these mice, we found that the initiation and persistence of the rotational reentrant AF arrhythmias, known as spiral waves or rotors, were dependent upon action potential duration heterogeneity. The centers of the rotors were localized to regions of greatest heterogeneity of the action potential duration. Pharmacologically attenuating the action potential duration heterogeneity reduced both spontaneous and pacing-induced AF. Computer-based simulations also demonstrated that the action potential duration heterogeneity is sufficient to generate rotors that manifest as AF. Taken together, these findings suggest that action potential duration heterogeneity in mice and humans is one mechanism by which AF is initiated and that reducing action potential duration heterogeneity can lessen the burden of AF.

Leadless pacemaker implantation: A feasible and reasonable option in transcatheter heart valve replacement patients.

BACKGROUND: Leadless pacemakers (LPMs) have been shown to have lower postoperative complications than traditional permanent pacemakers but there have been no studies on the outcomes of LPMs in patients with transcatheter heart valve replacements (THVRs). This study determined outcomes of LPMs compared to transvenous single-chamber pacemakers (SCPs) post-THVR. METHODS: This is a retrospective single-center study including 10 patients who received LPMs post-THVR between February 2017 and August 2018 and a comparison group of 23 patients who received SCP post-THVR between July 2008 and August 2018. LPM or SCP was implanted at the discretion of electrophysiologists for atrial fibrillation with slow ventricular response or sinus node dysfunction with need for single-chamber pacing only. RESULTS: LPMs were associated with decreased tricuspid regurgitation (P = 0.04) and decreased blood loss during implantation (7.5 ± 2.5 cc for LPMs vs 16.8 ± 3.2 cc for SCPs, P = 0.03). Five LPM patients had devices positioned in the right ventricular septum as seen on transthoracic echocardiogram. Frequency of ventricular pacing was similar between LPM and SCP groups. In the LPM group, one case was complicated by a pseudoaneurysm and one death was due to noncardiac causes. There was one pneumothorax and one pocket infection in the SCP group. CONCLUSIONS: In this small retrospective study, LPMs were feasible post-THVR and found to perform as well as SCPs, had less intraprocedural blood loss, and were associated with less tricuspid regurgitation. Further, larger studies are required to follow longer-term outcomes and complications.

Conduction Abnormalities Associated with Tricuspid Annuloplasty in Cardiac Transplantation.

Prophylactic DeVega tricuspid annuloplasty (DVA) of the donor heart has been reported to improve tricuspid regurgitation (TR), renal dysfunction, and mortality in cardiac transplant recipients. This is the first study to investigate the electrical, as well as, hemodynamic effects of DVA during orthotopic heart transplantation (OHT). Electrocardiographic, echocardiographic, and hemodynamic data of 76 patients with DVA and 104 patients without DVA who underwent OHT between 2013 and 2017 at Columbia University Medical Center (New York, NY) were studied. Patients with DVA were older (56.5 ± 1.2 vs. 52.4 ± 1.0 years of age; p = 0.017) and predominantly men (78% vs. 68%; p = 0.02). There were no significant differences in right ventricular function and TR. Patients with DVA had increased incidence of right bundle branch block compared with without DVA (37% ± 5.9% vs. 9% ± 2.9%; p < 0.001). Three patients with DVA developed complete heart block (CHB), whereas no patients without DVA developed CHB (p = 0.04). Four patients with DVA received a pacemaker (PPM), whereas only one patient in the without DVA group received a PPM. Complete heart block was significantly increased in patients who received prophylactic DVA. Possible risk of conduction abnormalities should be considered with performance of DVA annuloplasty in cardiac transplant recipients.

Aberrant sodium influx causes cardiomyopathy and atrial fibrillation in mice.

Increased sodium influx via incomplete inactivation of the major cardiac sodium channel Na(V)1.5 is correlated with an increased incidence of atrial fibrillation (AF) in humans. Here, we sought to determine whether increased sodium entry is sufficient to cause the structural and electrophysiological perturbations that are required to initiate and sustain AF. We used mice expressing a human Na(V)1.5 variant with a mutation in the anesthetic-binding site (F1759A-Na(V)1.5) and demonstrated that incomplete Na+ channel inactivation is sufficient to drive structural alterations, including atrial and ventricular enlargement, myofibril disarray, fibrosis and mitochondrial injury, and electrophysiological dysfunctions that together lead to spontaneous and prolonged episodes of AF in these mice. Using this model, we determined that the increase in a persistent sodium current causes heterogeneously prolonged action potential duration and rotors, as well as wave and wavelets in the atria, and thereby mimics mechanistic theories that have been proposed for AF in humans. Acute inhibition of the sodium-calcium exchanger, which targets the downstream effects of enhanced sodium entry, markedly reduced the burden of AF and ventricular arrhythmias in this model, suggesting a potential therapeutic approach for AF. Together, our results indicate that these mice will be important for assessing the cellular mechanisms and potential effectiveness of antiarrhythmic therapies.