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Prevalence, Characteristics, and Outcomes Associated With Early Vasculopathy in Patients With Chronic Lung Disease
Esteban Kosak Lopez1, Andrew Geller1, Raul Leguizamon1
1Department of Medicine Jefferson Einstein Philadelphia Hospital Philadelphia Pennsylvania USA.
Abstract:
Pulmonary hypertension associated with chronic lung disease (PH-CLD) meets precapillary PH criteria. Less is known CLD patients with "early vasculopathy," a phenotype characterized by elevated pulmonary vascular resistance (PVR) and normal mean pulmonary artery pressure (mPAP). In this study, we aimed to determine the prevalence, characteristics, and outcomes of the early vasculopathy phenotype among CLD patients. We performed a retrospective cohort analysis of adults with chronic obstructive pulmonary disease or obstructive sleep apnea undergoing right heart catheterization between 2018 and 2023. Patients were categorized into three cohorts: non-PH cohort (mPAP ≤ 20 mmHg, PVR ≤ 2 WU), early vasculopathy cohort (mPAP ≤ 20 mmHg, PVR > 2 WU), and precapillary PH cohort (mPAP > 20 mmHg, PVR > 2 WU). The primary endpoint was a 1-year composite of mortality and major adverse cardiovascular events. Of 243 patients with CLD, 7.4% (n = 18) had early vasculopathy, whereas 35.4% (n = 86) had non-PH, and 57.2% (n = 139) had precapillary PH. Among CLD patients with early vasculopathy, the median age was 67 years, 56% were males, and 67% were African Americans. Compared to other groups, the early vasculopathy cohort had the lowest right atrial pressure, pulmonary artery wedge pressure, and cardiac output. On multivariable analysis, the early vasculopathy group was at increased risk of 1-year composite outcome compared to the non-PH group (adjusted hazard ratio [aHR] = 2.37, [95% confidence interval [CI] 1.11-5.06]; p = 0.025). The association was attenuated after adjusting for left ventricular systolic dysfunction (aHR = 1.24, 95% CI [0.57-2.71]; p = 0.581). Early vasculopathy is an uncommon hemodynamic pattern potentially associated with adverse outcomes seemingly mediated by subclinical heart failure.
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