Scientific publications
Emmanuel E. Egom* (Corresponding author)
Other affiliations: California Wellness Foundation · Institut de Recherches Médicales et d’Etudes des Plantes Médicinales · Institut du Savoir Montfort
Mfopa Adamou
Ibrahima Djoulde
Njimona Ibrahim
Mountchissi Célestin
Lum Abienwi Ambe
Medou Mba Fabrice
Moustapha
René Kamgang
Pulmonary Circulation
HIV-associated pulmonary arterial hypertension (HIV-PAH) remains one of the most consequential cardiopulmonary complications in people living with HIV (PLWH), persisting despite expanded antiretroviral therapy (ART) coverage. Although contemporary hemodynamic criteria define pulmonary hypertension (PH) as mean pulmonary arterial pressure (mPAP) > 20 mmHg and pulmonary arterial hypertension (PAH) as pre-capillary physiology confirmed by right heart catheterization (mPAP > 20 mmHg, pulmonary arterial wedge pressure ≤ 15 mmHg, pulmonary vascular resistance > 2 Wood units), global epidemiologic certainty remains uneven. In high-income settings, prospective screening paradigms incorporating catheter confirmation estimate HIV-PAH prevalence at approximately 0.5%, exemplified by the multicenter French study reporting 0.46%. In contrast, in sub-Saharan Africa-home to more than 26 million PLWH-the population prevalence of catheter-confirmed HIV-PAH remains undefined, with echocardiography-based studies in symptomatic cohorts reporting substantially higher rates of elevated pulmonary pressures. Mechanistically, HIV-PAH is best conceptualized as a multi-hit pulmonary vasculopathy driven by viral proteins (Tat, Nef, gp120), chronic immune activation, endothelial dysfunction, oxidative stress, dysregulated endothelin signaling, and growth-factor pathways, with amplification by endemic co-factors and host susceptibility. Clinically, HIV-PAH is a "clinically nonspecific phenotype", frequently obscured by tuberculosis-related lung disease, anemia, left heart disease, and other causes of dyspnea in resource-limited settings. Early recognition is critical because prognosis depends on preservation of right ventricular function. A practical, resource-appropriate strategy is required: heightened clinical suspicion, echocardiography-anchored detection, systematic exclusion of alternative PH etiologies, rational biomarker use, and referral pathways to right heart catheterization where feasible. ART optimization is necessary but insufficient; PAH-targeted therapies can improve functional and hemodynamic outcomes, though HIV-specific randomized evidence remains limited. Implementation science and mechanism-informed research in endemic regions are urgently needed to close the diagnostic and therapeutic gap.
