RESUMEN
Regular expert follow-up, risk assessment, and early therapeutic intervention minimize worsening of pulmonary arterial hypertension (PAH). COVID-19 lockdown measures were challenging for chronic disease management. This retrospective, longitudinal analysis used US claims data (January 12, 2016 to September 11, 2021) for patients treated with PAH-specific medication to compare in-person outpatient and specialist visits, telemedicine visits, and PAH-related tests during 6-month assessment periods pre- and immediately post-COVID-19. Hospitalizations, costs, and outcomes were compared in patients with and without care disruptions (no in-person or telemedicine outpatient visits in immediate post-COVID-19 period). Patients in the immediate post-COVID-19 (N = 599) versus the pre-COVID-19 period (N = 598) had fewer in-person outpatient visits (mean 1.27 vs. 2.12) and in-person specialist visits (pulmonologist, 22.9% vs. 37.0% of patients; cardiologist, 27.5% vs. 33.8%); and more telemedicine visits (mean 0.45 vs. 0.02). In the immediate post-COVID-19 period, patients were less likely to have a PAH-related test versus the pre-COVID-19 period (incidence rate ratio: 0.700; 95% confidence interval: 0.615-0.797), including electrocardiograms (41.7% vs. 54.2%) and 6-minute walk distance tests (16.2% vs. 24.9%). In the immediate post-COVID-19 period, 48 patients had care disruptions and, in the following year, required more hospital days than those without care disruptions (N = 240) (median 10 vs. 5 days in total) and had higher overall hospitalization costs (median US$34,755 vs. US$20,090). Our findings support the need for minimizing care disruptions to potentially avoid incremental post-disruption healthcare utilization and costs among patients with serious chronic diseases such as PAH.
RESUMEN
Pulmonary hypertension (PH) represents a group of disorders characterized by elevated mean pulmonary artery (PA) pressure, progressive right ventricular failure, and often death. Some of the hallmarks of pulmonary hypertension include endothelial dysfunction, intimal and medial proliferation, vasoconstriction, inflammatory infiltration, and in situ thrombosis. The vascular remodeling seen in pulmonary hypertension has been previously linked to the hyperproliferation of PA smooth muscle cells. This excess proliferation of PA smooth muscle cells has recently been associated with changes in metabolism and mitochondrial biology, including changes in glycolysis, redox homeostasis, and mitochondrial quality control. In this review, we summarize the molecular mechanisms that have been reported to contribute to mitochondrial dysfunction, metabolic changes, and redox biology in PH.
RESUMEN
PURPOSE OF REVIEW: Pulmonary arterial hypertension (PAH) leads to progressive increases in pulmonary vascular resistance (PVR), right heart failure, and death if left untreated. This review will summarize and discuss recent updates in the classification and management of patients with PAH. RECENT FINDINGS: PAH requires careful hemodynamic assessment and is defined by a mean pulmonary artery pressure > 20 mmHg with normal left-sided filling pressures and a PVR ≥ 3 Wood units. Most patients with PAH require targeted pharmacotherapy based on multiparametric risk stratification. Significant improvements in clinical outcome have been realized through the approval of 14 unique pharmacotherapeutic options. The latest clinical recommendations provide the updated hemodynamic definition and clinical classification as well as evidence-based treatment recommendations. An important change is the focus on initial upfront combination therapy for most patients with PAH. Structured follow-up and escalation of treatment for those not achieving low-risk status is paramount.