RESUMEN

Pulmonary arterial hypertension (PAH) is a severe condition characterized by increased pulmonary vascular resistance and right ventricular failure. This review examines the intersection of PAH and pregnancy, highlighting the significant physiological, hemodynamic, and hormonal changes that exacerbate PAH during gestation. Pregnancy is contraindicated in PAH patients due to high maternal and fetal morbidity and mortality rates. However, some patients choose to continue their pregnancies, necessitating a comprehensive understanding of the implications and management strategies. Effective management of PAH in pregnant patients involves individualized treatment plans. Prepartum management focuses on optimizing therapy and monitoring hemodynamic status. Prostacyclin analogs and phosphodiesterase inhibitors are commonly used, though their safety profiles require further investigation. Intrapartum management prioritizes preventing right ventricular failure, utilizing therapies such as intravenous epoprostenol, inhaled iloprost, and inhaled nitric oxide. Managing PAH in pregnancy requires careful planning, continuous monitoring, and tailored therapeutic strategies to navigate the complex interplay of physiological changes and mitigate risks. Future research should focus on elucidating the pathophysiology of PAH during pregnancy and developing safer, more effective treatments to improve maternal and fetal outcomes.

RESUMEN

INTRODUCTION: There are currently limited effective treatments available to improve lusitropy in patients suffering from heart failure with preserved ejection fraction. The role of PDE9A in diastolic dysfunction has been well-studied over recent years, with a special focus on its association with myocardial hypertrophy. Recent insights into PDE9A inhibition have brought to light the potential for reversal of cardiac remodeling, with multiple studies showing promising results in preclinical data. AREAS COVERED: This expert opinion provides an overview of the role of PDE9A in diastolic heart dysfunction along with the efficacy of PDE9A inhibitors in laboratory models of heart failure with preserved ejection fraction. EXPERT OPINION: The available data on PDE9A inhibition in preclinical studies suggest that there is potential for reversal of diastolic dysfunction and myocardial hypertrophy, however, conflicting data suggests that further studies are required before progressing to clinical trials.

Asunto(s)

3',5'-AMP Cíclico Fosfodiesterasas , Insuficiencia Cardíaca , Inhibidores de Fosfodiesterasa , Humanos , Animales , Insuficiencia Cardíaca/tratamiento farmacológico , Insuficiencia Cardíaca/fisiopatología , Inhibidores de Fosfodiesterasa/farmacología , 3',5'-AMP Cíclico Fosfodiesterasas/antagonistas & inhibidores , Cardiomegalia/tratamiento farmacológico , Cardiomegalia/fisiopatología , Remodelación Ventricular/efectos de los fármacos , Volumen Sistólico/efectos de los fármacos

RESUMEN

The dynamic between pulmonary hypertension (PH) and COVID-19 has been under investigation since 2020, early in the pandemic. Although the pathophysiology of PH has been well-studied, new discoveries regarding the multisystemic effects of COVID-19 are still being uncovered. The cardiopulmonary effects of COVID-19 have led investigators to inquire about the interplay between these 2 conditions. Several factors are suggested to contribute to an increased risk of developing PH after infection with SARS-CoV-2. This includes cytokine storm, acute respiratory distress syndrome, and fibrotic changes seen in post-COVID-19 lung disease. Additionally, it has been proposed that certain medications used to treat PH may be applied to patients suffering from the cardiopulmonary complications of COVID-19. This review will focus on the interplay between COVID-19 and PH, with a special focus on the risk of developing PH after SARS-CoV-2 infection and the outcomes of patients with preexisting PH who are diagnosed with COVID-19. The potential benefits of utilizing off-label PH medications for COVID-19 patients will also be discussed.