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Pulmonary Arterial Hypertension in Systemic Lupus Erythematosus: Prevalence and Predictors
Gregorio Miguel Pérez-Peñate1, Iñigo Rúa-Figueroa2, Gabriel Juliá-Serdá2
1From the Pneumology Service, Rheumatology Service, Cardiology Service, Anesthesiology Service, Hospital Universitario General de Gran Canaria "Doctor Negrín," Las Palmas de Gran Canaria; Cardiology Service, Hospital 12 de Octubre, Madrid, Spain.G.M. Pérez-Peñate, MD, Pneumology Service, Hospital Universitario General de Gran Canaria "Doctor Negrín"; I. Rúa-Figueroa, MD, Rheumatology Service, Hospital Universitario General de Gran Canaria "Doctor Negrín"; G. Juliá-Serdá, MD, Pneumology Service, Hospital Universitario General de Gran Canaria "Doctor Negrín"; F. León- Marrero, MD, Pneumology Service, Hospital Universitario General de Gran Canaria "Doctor Negrín"; A. García-Quintana, MD, Cardiology Service, Hospital Universitario General de Gran Canaria "Doctor Negrín"; J.R. Ortega-Trujillo, MD, Cardiology Service, Hospital Universitario General de Gran Canaria "Doctor Negrín"; C. Erausquin-Arruabarrena, MD, Rheumatology Service, Hospital Universitario General de Gran Canaria "Doctor Negrín"; C. Rodríguez-Lozano, MD, Rheumatology Service, Hospital Universitario General de Gran Canaria "Doctor Negrín"; P. Cabrera-Navarro, MD, Pneumology Service, Hospital Universitario General de Gran Canaria "Doctor Negrín"; N. Ojeda-Betancor, MD, Anesthesiology Service, Hospital Universitario General de Gran Canaria "Doctor Negrín"; M.Á. Gómez-Sánchez, MD, Cardiology Service, Hospital 12 de Octubre. gperpen@gobiernodecanarias.org.
Objective:
Pulmonary arterial hypertension (PAH) prevalence has been reported to be between 0.5% and 17% in systemic lupus erythematosus (SLE). This study assessed PAH prevalence and predictors in an SLE cohort.
Methods:
The Borg dyspnea scale, DLCO, N-terminal pro-brain natriuretic peptide (NT-proBNP), and Doppler echocardiographic (DE) were performed. An echocardiographic Doppler exercise test was conducted in selected patients. When DE systolic pulmonary arterial pressure was ≥ 45 mmHg or increased during exercise > 20 mmHg, a right heart catheterization was performed. Hemodynamic during exercise was measured if rest mean pulmonary arterial pressure was < 25 mmHg.
Results:
Of the 203 patients with SLE, 152 were included. The mean age was 44.9 ± 12.3 years, and 94% were women. Three patients had known PAH. The algorithm diagnosed 1 patient with chronic thromboembolic pulmonary hypertension and 5 with exercise-induced pulmonary artery pressure increase (4 with occult left diastolic dysfunction). These patients had significantly more dyspnea, higher NT-proBNP, and lower DLCO.
Conclusion:
These data confirm the low prevalence of PAH in SLE. In our cohort, occult left ventricular diastolic dysfunction was a frequent diagnosis of unexplained dyspnea. Dyspnea, DLCO, and NT-proBNP could be predictors of pulmonary hypertension in patients with SLE.
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