In the United States, donor lungs are allocated to transplant candidates on the basis of lung allocation scores (LAS). However, additional factors beyond the LAS can impact who is transplanted, including listing and donor-organ acceptance practices. These factors can result in differential selection, undermining the objectivity of lung allocation. Yet their impact on the lung transplant pathway has been underexplored. We sought to systematically examine sources of differential selection in lung transplantation via qualitative methods. We conducted semistructured qualitative interviews with lung transplant surgeons and pulmonologists in the United States between June 2019 and June 2020 to understand clinician perspectives on differential selection in lung transplantation and the LAS. A total of 51 respondents (30 surgeons and 21 pulmonologists) identified many sources of differential selection arising throughout the pathway from referral to transplantation. We synthesized these sources into a conceptual model with five themes: ) transplant center's degree of risk tolerance and accountability; ) successfulness and fairness of the LAS; ) donor-organ availability and regional competition; ) patient health versus program health; and ) access to care versus responsible stewardship of organs. Our conceptual model demonstrates how differential selection can arise throughout lung transplantation and facilitates the further study of such selection. As new organ allocation models are developed, differential selection should be considered carefully to ensure that these models are more equitable.

<p><strong>OBJECTIVES: </strong>The increased relative risk of heart failure (HF) from systemic lupus erythematosus (SLE) is greatest at younger ages, but the etiology remains unclear. We identified risk factors for HF in children and adults with SLE and evaluated associations between SLE manifestations and HF.</p>

<p><strong>METHODS: </strong>Incident SLE cases without preceding HF were identified using Clinformatics DataMart® (OptumInsight, Eden Prairie, MN) US claims data (2000-2015), and categorized by age of SLE onset (children 5-17, young adults 18-24, adults 25-44 years old). The primary outcome was the first HF ICD-9-CM diagnosis code (428.x), categorized as early-onset (&lt; 6 months) or delayed-onset. Multivariable logistic regression was used to identify factors associated with early or delayed-onset HF. Cox proportional hazards regression was used to identify time-dependent associations between the onset of SLE manifestations and incident HF.</p>

<p><strong>RESULTS: </strong>There were 523 (2.3%) HF cases among 1,466 children, 2,163 young adults and 19,349 adults age 25-44 with SLE. HF in children and young adults was early-onset in 50% and 60% of cases, respectively, compared to 35% of cases in adults 25-44 years old. There was a temporal association between incident myopericarditis and valvular disease diagnoses and early-onset HF, whereas nephritis and hypertension were more strongly associated with delayed-onset HF. Black race remained independently associated with a 1.5-fold increased HF risk at any time.</p>

<p><strong>CONCLUSION: </strong>Hypertension remains an important traditional CV risk factor across all ages and should be managed aggressively even in younger patients with SLE. Cardiac dysfunction due to acute cardiac manifestations of SLE may contribute to the very high relative incidence of early HF diagnoses among younger SLE patients. Therefore, future prospective studies will need to address heterogeneity in the types and severity of heart failure in order to determine etiology and which patients should be monitored.</p>

<p><strong>OBJECTIVE: </strong>The authors sought to determine whether use of methylphenidate in adults is associated with elevated rates of serious cardiovascular events compared with rates in nonusers.</p>

<p><strong>METHOD: </strong>This was a cohort study of new users of methylphenidate based on administrative data from a five-state Medicaid database and a 14-state commercial insurance database. All new methylphenidate users with at least 180 days of prior enrollment were identified. Users were matched on data source, state, sex, and age to as many as four comparison subjects who did not use methylphenidate, amphetamines, or atomoxetine. A total of 43,999 new methylphenidate users were identified and matched to 175,955 nonusers. Events of primary interest were 1) sudden death or ventricular arrhythmia, 2) stroke, 3) myocardial infarction, and 4) a composite endpoint of stroke or myocardial infarction.</p>

<p><strong>RESULTS: </strong>The age-standardized incidence rate per 1,000 person-years of sudden death or ventricular arrhythmia was 2.17 (95% CI=1.63-2.83) in methylphenidate users and 0.98 (95% CI=0.89-1.08) in nonusers, for an adjusted hazard ratio of 1.84 (95% CI=1.33-2.55). Dosage was inversely associated with risk. Adjusted hazard ratios for stroke, myocardial infarction, and the composite endpoint of stroke or myocardial infarction did not differ statistically from 1.</p>

<p><strong>CONCLUSIONS: </strong>Although initiation of methylphenidate was associated with a 1.8-fold increase in risk of sudden death or ventricular arrhythmia, the lack of a dose-response relationship suggests that this association may not be a causal one.</p>

<p><strong>MAIN OBJECTIVE: </strong>To compare the incidence rates of serious cardiovascular events in adult initiators of amphetamines or atomoxetine to rates in non-users.</p>

<p><strong>METHODS: </strong>This was a retrospective cohort study of new amphetamines (n=38,586) or atomoxetine (n=20,995) users. Each medication user was matched to up to four non-users on age, gender, data source, and state (n=238,183). The following events were primary outcomes of interest 1) sudden death or ventricular arrhythmia, 2) stroke, 3) myocardial infarction, 4) a composite endpoint of stroke or myocardial infarction. Cox proportional hazard regression was used to calculate propensity-adjusted hazard ratios for amphetamines versus matched non-users and atomoxetine versus matched non-users, with intracluster dependence within matched sets accounted for using a robust sandwich estimator.</p>

<p><strong>RESULTS: </strong>The propensity-score adjusted hazard ratio for amphetamines use versus non-use was 1.18 (95% CI: 0.55-2.54) for sudden death/ventricular arrhythmia, 0.80 (95% CI: 0.44-1.47) for stroke, 0.75 (95% CI: 0.42-1.35) for myocardial infarction, and 0.78 (95% CI: 0.51-1.19) for stroke/myocardial infarction. The propensity-score adjusted hazard ratio for atomoxetine use versus non-use was 0.41 (95% CI: 0.10-1.75) for sudden death/ventricular arrhythmia, 1.30 (95% CI: 0.52-3.29) for stroke, 0.56 (95% CI: 0.16-2.00) for myocardial infarction, and 0.92 (95% CI: 0.44-1.92) for stroke/myocardial infarction.</p>

<p><strong>CONCLUSIONS: </strong>Initiation of amphetamines or atomoxetine was not associated with an elevated risk of serious cardiovascular events. However, some of the confidence intervals do not exclude modest elevated risks, e.g. for sudden death/ventricular arrhythmia.</p>