Abstract
Pulmonary hypertension (PH) is a progressive disorder characterized by a chronic in-crease in pulmonary arterial pressure, frequently resulting in right-sided heart failure and potentially death. Co-existing medical conditions are important factors in PH, since they not only result in the genesis of the disorder, but may also contribute to its progression. Various studies have assessed the impact of thyroid disorders and other endocrine conditions (namely estrogen exposure, obesity, and diabetes mellitus) on the progression of PH. The complex interactions that hormones may have with the cardiovascular system and pulmonary vascular bed can create several pathogenetic routes that could explain the effects of endocrine disorders on PH development and evolution. The aim of this review is to summarize current knowledge on the role of concomitant thyroid disorders, obesity, diabetes mellitus, and estrogen exposure as potential modifiers for PH, and especially for pulmonary arterial hypertension, and to discuss possible pathogenetic routes linking them with PH. This information could be valuable for practicing clinicians so as to better evaluate and/or treat concomitant endocrine conditions in the PH population.
Highlights
Pulmonary hypertension (PH) is a progressive disorder characterized by a chronic increase in pulmonary arterial pressure, frequently resulting in right-sided heart failure and potentially death [1]
According to the latest European Society of Cardiology/European Respiratory Society (ESC/ERS) guidelines published in 2016 [1], PH has been traditionally defined as a mean pulmonary arterial pressure ≥25 mm Hg at rest measured by right-heart catheterization (RHC)
In the Sixth World Symposium on PH in 2018, it was suggested that PH should be diagnosed when mean pulmonary arterial pressure is greater than 20 mm Hg measured by RHC at rest [2]
Summary
Pulmonary hypertension (PH) is a progressive disorder characterized by a chronic increase in pulmonary arterial pressure, frequently resulting in right-sided heart failure and potentially death [1]. PAH is a distinct PH group whose pathobiology arises mainly from the pulmonary vascular bed; it is defined, as per the ESC/ERS guidelines, by an elevated mPAP (≥25 mm Hg) and pulmonary vascular resistance-PVR (>3 Wood Units), combined with a pulmonary arterial wedge pressure ≤15 mm Hg, at rest by means of RHC [1].; of note that mPAP >20 mm Hg and PVR ≥3 Wood Units are the proposed changes in the Sixth World Symposium [2]. The aim of the present review is to summarize current knowledge on the role of thyroid diseases, obesity, diabetes mellitus, and estrogen exposure as potential modifiers for PH, with a special focus on PAH, and to discuss the possible pathogenetic routes linking these endocrine conditions with PH. Evidence in the literature suggests that the cardiac and vascular alterations caused by thyroid hormone abnormalities could have as an end-target the pulmonary vascular bed inducing a hypertensive condition [10]
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