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The American Journal of Managed Care August 2017
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Health Insurance and Racial Disparities in Pulmonary Hypertension Outcomes
Kishan S. Parikh, MD; Kathryn A. Stackhouse, MD; Stephen A. Hart, MD; Thomas M. Bashore, MD; and Richard A. Krasuski, MD
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Health Insurance and Racial Disparities in Pulmonary Hypertension Outcomes

Kishan S. Parikh, MD; Kathryn A. Stackhouse, MD; Stephen A. Hart, MD; Thomas M. Bashore, MD; and Richard A. Krasuski, MD
In a multicenter cohort of patients with newly diagnosed pulmonary hypertension, increased risk for mortality among African Americans was no longer observed after adjusting for insurance status.

Objectives: Pulmonary hypertension portends a poorer prognosis for blacks versus white populations, but the underlying reasons are poorly understood. We investigated associations of disease characteristics, insurance status, and race with clinical outcomes.

Study Design: Retrospective cohort study of patients presenting for initial pulmonary hypertension evaluation at 2 academic referral centers.

Methods: We recorded insurance status (Medicare, Medicaid, private, self-pay), echocardiographic, and hemodynamics data from 261 patients (79% whites, 17% blacks) with a new diagnosis of pulmonary hypertension. Subjects were followed for 2.3 years for survival. Adjustment for covariates was performed with Cox proportional hazards modeling.

Results: Compared with white patients, blacks were younger (50 ± 15 vs 53 ± 12 years; P = .04), with females representing a majority of patients in both groups (80% vs 66%; P = .08) and similar functional class distribution (class 2/3/4: 30%/52%/16% blacks vs 33%/48%/14% whites; P = .69). Blacks diagnosed with incident pulmonary hypertension were more frequently covered by Medicaid (12.5% vs 0.7%) and had less private insurance (50% vs 61%; P = .007) than whites. At presentation, blacks had more right ventricular dysfunction (P = .04), but similar mean pulmonary arterial pressure (46 vs 45 mm Hg, respectively; P = .66). After adjusting for age and functional class, blacks had greater mortality risk (hazard ratio [HR], 2.06; 95% confidence interval [CI], 1.18-3.44), which did not differ by race after additional adjustment for insurance status (HR, 1.74; 95% CI, 0.84-3.32; P =.13). 

Conclusions: In a large cohort of patients with incident pulmonary hypertension, black patients had poorer right-side heart function and survival rates than white patients. However, adjustment for insurance status in our cohort removed differences in survival by race.

Am J Manag Care. 2017;23(8):474-480
Takeaway Points

Black race was associated with a 2-fold mortality risk in patients with incident pulmonary hypertension after adjustment for age and functional class. However, this relationship was no longer observed after additional adjustment for insurance. 
  • A total of 261 consecutive patients with pulmonary hypertension were included in our cohort at time of first evaluation at 2 large tertiary referral centers (Duke University Medical Center and Cleveland Clinic). 
  • African American patients had more severe pulmonary vascular disease at presentation and greater than a 2-fold risk of death over study follow-up. 
  • Pulmonary hypertension is a fatal disease and access to medications is a public health issue due to high costs and racial disparities.
Pulmonary hypertension (defined as mean pulmonary artery pressure ≥25 mm Hg) encompasses a broad spectrum of diseases and patient populations. Prior efforts to characterize patients with pulmonary hypertension focused on the subset of those with “pure” pulmonary vascular disease, defined as pulmonary arterial hypertension (pulmonary capillary wedge pressure ≤15 mm Hg and pulmonary vascular resistance ≥3 Woods units). Given the dismal 5-year survival rate of 34% in the National Institutes of Health pulmonary arterial hypertension cohort 3 decades ago,1 therapeutic advances targeting functional capacity, disease progression, and mortality have led to the availability of endothelin receptor antagonists (ERAs),2-7 prostacyclins or their analogs,8-10 phosphodiesterase 5-inhibitors,11-13 and soluble guanylate cyclase stimulators.14,15 These advances in disease management have improved the care of patients with pulmonary arterial hypertension, but are expensive: the approximate annual costs are sildenafil, $12,761; bosentan, $55,890; ambrisentan, $56,736; iloprost, $92,146; epoprostenol (70 kg patient), $33,153; and treprostinil (70 kg patient), $97,615.16 Furthermore, 5-year survival, incorporating advances in modern therapies, remains low at 58% for patients with pulmonary arterial hypertension,17 and the development of pulmonary hypertension is among the most significant predictors of poor outcomes in patients with chronic heart failure and lung disease. 

Alhough there is a similar prevalence of pulmonary hypertension in black (6.6%) and white populations (6.8%),18,19 Black individuals have been shown to have a worse prognosis.20-23 Furthermore, age-standardized death rates for pulmonary arterial hypertension patients from 2 separate epidemiological studies, from 1980 to 1984 and 2000 to 2002, have diverged between whites (increasing from 5.0%-5.3%) and blacks (increasing from 4.8%-7.3%),21 with little insight into why these racial disparities currently exist. However, the Registry to Evaluate Early and Long-term Pulmonary Arterial Hypertension Disease Management (REVEAL) registry of patients with pulmonary arterial hypertension in the United States reported no difference in time-to-recognition of disease from symptom onset by race.24 We sought to investigate the association of race with survival in a population of patients referred to 2 large tertiary care centers for invasive evaluation of pulmonary hypertension. Additionally, given that cost may be a barrier to pulmonary arterial hypertension medications, associated equipment for intravenous/inhaled administration, and specialized care, we investigated the role of insurance status on mortality.

Consecutive patients who were evaluated at 2 pulmonary hypertension referral centers for initial hemodynamic assessment between 1998 and 2009, and found to have mean pulmonary artery pressure of at least 25 mm Hg, were prospectively entered in a database. Each patient underwent a diagnostic work-up, including echocardiography and cardiac catheterization with vasodilator testing, if indicated. Only patients with known insurance type were included in our study. The study was approved by the institutional review boards at Duke University Medical Center and the Cleveland Clinic Foundation. 

Right heart catheterization was performed by the same experienced cardiologist (RAK) in the cardiac catheterization laboratories at the 2 medical centers, using a single end-hole, balloon flotation catheter (either Bard Pulmonary Wedge Catheter [Medtronic; Minneapolis, Minnesota] or Balloon Wedge Pressure Catheter [Arrow International, Inc; Cleveland, Ohio]). Contrast injections during left heart catheterization, if performed, followed all hemodynamic measurements. Standard hemodynamic measurements from right heart catheterization were obtained, including mean right atrial pressure, right ventricular, systolic and diastolic pressures, pulmonary artery systolic, diastolic and mean pressures, and mean pulmonary capillary wedge pressure. Mean arterial blood pressure, cardiac index, pulmonary vascular resistance, systemic vascular resistance, and response to vasodilator challenge were also recorded in the database when indicated.

All echocardiograms were performed within 30 days of cardiac catheterization using a phase-arrayed scanner with a 4- or 8-MHz transducer, depending on body habitus and image quality. Standard 2-dimensional images were obtained in the parasternal long- and short-axis views, apical 2- and 4-chamber views, and subcostal view, and Doppler gradients were obtained to estimate valvular gradients. Assessment of right ventricular size was reported as a grade from 0 to 3, where 0 = normal, 1 = mildly enlarged, 2 = moderately enlarged, and 3 = severely enlarged. Right ventricular function was graded on a 4-point scale for systolic dysfunction, where 0 = no dysfunction, 1 = mild dysfunction, 2 = moderate dysfunction, and 3 = severe dysfunction. The degree of tricuspid regurgitation was determined using color-flow Doppler and assigned a grade from 0 to 4+, depending on the extent of color flow relative to the right atrial area. Estimated right ventricular pressures were obtained by applying continuous wave Doppler to the tricuspid regurgitation jet to the Bernoulli equation and added to the estimated right atrial pressure. If tricuspid regurgitation velocity could not be adequately visualized by color Doppler, saline microbubbles were injected to improve image quality. Saline microbubble injection was also used to assess for intracardiac shunting if flow across the interatrial septum was noted by color Doppler on subcostal imaging. Assessments were made by experienced imaging cardiologists at both academic medical centers.

Pulmonary hypertension work-up for all patients also included chest radiography, (chest computed tomography if chest radiography was abnormal), ventilation-perfusion scanning, full pulmonary function testing, electrocardiography, and echocardiography, in addition to catheterization. Test results, demographics, and medical histories were obtained from medical records and entered in the database. Insurance status at the time of the assessment was recorded as either Medicare, Medicaid, private, or self-pay, and confirmed by appointment schedulers at the time of the initial appointment. Race was self-reported at the time of catheterization. Long-term survival was assessed using electronic health records and confirmed using the Social Security Death Index. Variables of interest included the following: idiopathic pulmonary arterial hypertension (no attributable etiology of pulmonary hypertension), New York Heart Association (NYHA) class (functional class 1: no symptoms and class 4: severe symptoms), systemic hypertension and atrial fibrillation (by medical history), serum sodium and creatinine (venous laboratory values drawn at time of heart catheterization), and arterial oxygen saturation (obtained by femoral arterial blood sample at time of heart catheterization).

Only white and black patients were included in our study; patients who self-identified as other races were excluded. Descriptive statistics were presented as mean ± standard deviation (SD) for continuous variables and as a percentage for discrete variables. Comparison of categorical variables was performed using the χ2 test or Fisher’s exact test, where appropriate. Comparisons of continuous variables between groups were performed using 2-sided t tests and 1-way analysis of variance. Statistical significance was assumed with P <.05. Survival analyses were performed using the Kaplan-Meier and Cox proportional hazards regression methods. Two proportional hazards models were utilized to investigate the effect of demographics, hemodynamics, echocardiographic measurements, and insurance status. Each model was constructed in a forward step-wise manner, investigating the effect of each covariate and potential interactions individually. Potential covariates included in the adjustment models were variables with baseline differences having P <.20, including known predictors of death in the pulmonary hypertension population (including right atrial pressure, pulmonary artery pressure, pulmonary vascular resistance, right ventricular function, cardiac index, functional status), and race. Based on the size of the cohort, the maximum number of covariates included in each model was predetermined to be 5 to limit overfitting. Differences in the survival functions were assessed for significance using the Wilcoxon test. All analyses were performed using JMP version 12.0 software (SAS Institute; Cary, North Carolina).

A total of 250 patients (82% white, 18% black) were included in the study. An additional 11 patients self-identified as Asian/Pacific Islander, Hispanic, or Native American were excluded from the analysis. The median follow-up period was 2.3 years (whites: 2.0; interquartile range [IQR], 1.1-2.0 years; blacks: 1.7 years; IQR, 0.9-1.7; P = .02). Overall, black patients were younger, more likely to have diabetes, and coverage with Medicaid versus private insurance compared with white patients (Table 1). Etiology of pulmonary vascular disease was idiopathic pulmonary arterial hypertension in 42% of whites, but only 29% in blacks. Functional class distribution was similar for both races.

Comparison of pulmonary hypertension characteristics was also performed using invasive hemodynamics and echocardiography at presentation. Black individuals had higher right atrial pressure, decreased right ventricular function, and more severe tricuspid regurgitation than whites. Other markers of pulmonary hypertension severity, including pulmonary vascular resistance, cardiac index, and right ventricular size, did not differ by race (Table 2).

No drug prescribing differences were seen between black and white patients. During follow-up, 55% of patients received at least 1 pulmonary arterial hypertension-specific therapy (ERA, prostanoid or phosphodiesterase 5-inhibitor) and 16% received combination pulmonary hypertension-specific therapy. The most commonly utilized pharmacologic agents in descending order of frequency included sildenafil (used in 29.6% of patients), bosentan (16.8%), epoprostenol (15.8%), treprostinil (6.8%), and iloprost (2.8%). None of these agents were associated with improved survival by univariate analysis.

Differences in baseline characteristics between patients who survived and those who died were examined (Table 3). Older age, worse functional class, diabetes, serum sodium and creatinine values, and insurance status were associated with death by completion of the study follow-up period. Analysis by race revealed that 20 of 45 (44%) black patients and 67 of 205 (33%) white patients had died at the end of the 2.3-year follow-up period (Figure). With adjustment for baseline differences in age and NYHA functional class, blacks had increased risk for death (hazard ratio, 2.06; 95% confidence interval [CI], 1.18-3.44; P = .012) (Table 4). However, when insurance status was added to the model, blacks and whites had no statistically significant difference in survival rates (P = .13).

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