Journal of Geriatric Cardiology (2019) 16: 478481 ©2019 JGC All rights reserved; www.jgc301.com http://www.jgc301.com; [email protected] | Journal of Geriatric CardiologyReview Open Access Approach to a patient with pulmonary hypertension Chakradhari Inampudi1, Anna R Hemnes2, Alexandros Briasoulis1,#1Division of Cardiovascular Diseases, University of Iowa Hospitals and Clinics, Iowa City, Iowa, USA 2Division of Allergy, Pulmonary and Critical Care Medicine, Vanderbilt University Medical Center, Nashville, Tennessee, USA Abstract Pulmonary hypertension is a common clinical condition that can complicate various cardiac and respiratory abnormalities. Interest in pulmonary hypertension has grown remarkably among the scientific community in the last decade. It is now clear based on the scientific advances have paved the way in understanding the effects of abnormal pulmonary hemodynamics development and its antecedent conse-quences on the right heart in reducing the quality of life and survival of the patient. J Geriatr Cardiol 2019; 16: 478481. doi:10.11909/j.issn.1671-5411.2019.06.007 Keywords: Pulmonary arterial hypertension 1 IntroductionPulmonary hypertension (PH) is a common clinical dis-order associated with varied heterogenous group of diseases, classified into five groups as per the World Symposium on Pulmonary Hypertension (WSPH).[1] It is defined by pul-monary artery mean pressure of ≥ 20 mmHg at rest as as-sessed by right heart catheterization (RHC).[2] A significant proportion of PH occurs in patients with left-sided heart disease and lung disease. In the recent years, an effort to identify and treat PH has gained significant attention as its development is linked to prognosis in various clinical situa-tions. Among the five groups, group one pulmonary arterial hypertension (PAH) characterized by significant advances with prolific development of impactful pharmacotherapeutic strategies that have been shown to significantly reduce the risk of clinical worsening but not mortality.[3] From diag-nostic strategies standpoint, the use of provocative maneu-vers like fluid challenge and exercise during RHC to elicit dynamic responses of the pulmonary artery wedge pressure (PAWP) to delineate the presence of left heart disease (LHD).[4,5] This has received attention in the recent years due to growing number of older people often with cardio-vascular risk factors being referred to the PH specialist cen-ters for PAH management and such therapy has been shown #Correspondence to: Alexandros Briasoulis, MD, PhD, Division of Car-diovascular Diseases, University of Iowa Hospitals and Clinics, Iowa City, Iowa, USA. E-mail: [email protected] Received: March 14, 2019 Revised: May 30, 2019 Accepted: June 24, 2019 Published online: June 28, 2019 to potentially cause harm in PH due to left heart disease (PH-LHD).[6] The following review was undertaken to pro-vide new insights in the pathophysiology and the emerging clinical perspective’s in the field of PH. 2Pathophysiology 2.1 Clinical classification PH encompasses a group of clinical entities that have categorized into five different groups based on the patient sub-groups with similar pathological findings, hemody-namic profiles and therapeutic management profiles. Such classification has enabled the scientific community to iden-tify the gaps in knowledge and limitations in support of therapeutic innovation.[1]2.2 PAH PAH, rare form of PH, characterized by pulmonary vas-cular remodeling mainly affecting the small pulmonary ar-teries ultimately leading to rise in pulmonary arterial pres-sure (PAP) and pulmonary vascular resistance (PVR), eventually culminating in progressive right heat failure and functional decline.[7] Since the initial WSPH proceedings, various scientific advances, have paved the way in identify-ing key cellular and molecular mechanisms that have been implicated in the pathobiology and are now being consid-ered as emerging therapeutic targets. In addition, genetic factors and immune dysfunction have also been identified to play a role in the pathology. It is important to recognize that the available treatments do not specifically target pulmonary vascular remodeling and the inflammatory pathways impli-