Should We Change the Target of Therapy in Pulmonary Hypertension?
Panagiotis KaryofyllisEftychia DemeroutiPavlos HabibisStyliani ApostolopoulouEleftheria-Garyfallia TsetikaDimitrios TsiaprasPublished in: Life (Basel, Switzerland) (2023)
Despite the evolution of drug therapy in pulmonary arterial hypertension and the more aggressive treatment approach according to the guidelines, patients continue to have unacceptable mortality rates. Furthermore, specific drug therapy alone in chronic thromboembolic pulmonary hypertension also does not seem to have any beneficial impact on survival. As the function of the right ventricle (RV) determines the prognosis of patients with pulmonary hypertension, the treatment strategy should focus on modifying factors involved in RV dysfunction. Although some previous reports demonstrated that the survival of patients with pulmonary hypertension was associated with mPAP, nevertheless, mPAP is still not considered as a target of therapy. There are many examples of effective mPAP lowering with early and aggressive drug therapy in pulmonary arterial hypertension, or with interventions in chronic thromboembolic pulmonary hypertension. This effective mPAP reduction can lead to reverse RV remodeling, and thus, improvement in survival. In this article, the importance of mPAP lowering is stated, as well as why the change of our current strategy and considering mPAP reduction as the target of therapy could make pulmonary hypertension a chronic but not fatal disease.
Keyphrases
- pulmonary hypertension
- pulmonary arterial hypertension
- pulmonary artery
- mycobacterium tuberculosis
- newly diagnosed
- stem cells
- oxidative stress
- atrial fibrillation
- emergency department
- left ventricular
- cardiovascular disease
- risk factors
- mitral valve
- coronary artery
- ejection fraction
- clinical practice
- mesenchymal stem cells
- replacement therapy