scholarly journals Treatment of exercise pulmonary hypertension improves pulmonary vascular distensibility

2018 ◽  
Vol 8 (3) ◽  
pp. 204589401878738 ◽  
Author(s):  
William D. Wallace ◽  
Mehdi Nouraie ◽  
Stephen Y. Chan ◽  
Michael G. Risbano
Keyword(s):  
Pulmonary Hypertension ◽  
Vascular Disease ◽  
Arterial Compliance ◽  
Bicycle Ergometer ◽  
Peak Exercise ◽  
Pulmonary Vascular Disease ◽  
Heart Catheterization ◽  
Vasodilator Therapy ◽  
Pulmonary Vasodilators ◽  
Pulmonary Vasodilator

Exercise pulmonary hypertension (ePH) is an underappreciated form of exertional limitation. Despite normal resting pulmonary artery pressures, patients with ePH demonstrate early pulmonary vascular changes with reduced pulmonary arterial compliance (PAC) and vascular distensibility (α). Recent data suggest that targeted vasodilator therapy may improve hemodynamics in ePH, but it is not well-known whether such medications alter pulmonary vascular distensibility. Thus, we sought to evaluate if vasodilator therapy improved α a marker of early pulmonary vascular disease in ePH. Ten patients performed supine exercise right heart catheterization (exRHC) with bicycle ergometer to peak exercise. Patients diagnosed with ePH were treated with pulmonary vasodilators. A repeat symptom-limited exercise RHC was performed at least six months after therapy. Patients with ePH had evidence of early pulmonary vascular disease, as baseline PAC and α were reduced. After pulmonary vasodilator therapy, a number of peak exercise hemodynamics statistically improved, including a decrease of total pulmonary resistance and pulmonary vascular resistance, while cardiac output increased. Importantly, vasodilator therapy partially reversed the pathogenic decreases of α at the time of repeat exRHC. Pulmonary vascular distensibility, α, a marker of early pulmonary vascular disease, improves in ePH after therapy with pulmonary vasodilators.

scholarly journals Comprehensive Diagnostic Evaluation of Cardiovascular Physiology in Patients With Pulmonary Vascular Disease

2020 ◽  
Vol 13 (3) ◽  
Author(s):  
W. H. Wilson Tang ◽  
Jennifer D. Wilcox ◽  
Miriam S. Jacob ◽  
Erika B. Rosenzweig ◽  
Barry A. Borlaug ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Vascular Disease ◽  
Cardiopulmonary Exercise Test ◽  
Right Heart Catheterization ◽  
Repeated Measurements ◽  
Pulmonary Vascular Disease ◽  
Heart Catheterization ◽  
Right Heart ◽  
Unique Identifier ◽  
Hemodynamic Evaluation

Background: Invasive hemodynamic evaluation through right heart catheterization plays an essential role in the diagnosis, categorization, and risk stratification of patients with pulmonary hypertension. Methods: Subjects enrolled in the PVDOMICS (Redefining Pulmonary Hypertension through Pulmonary Vascular Disease Phenomics) program undergo an extensive invasive hemodynamic evaluation that includes repeated measurements at rest and during several provocative physiological challenges. It is a National Institutes of Health/National Heart, Lung, and Blood Institute initiative to reclassify pulmonary hypertension groups based on clustered phenotypic and phenomic characteristics. At a subset of centers, participants also undergo an invasive cardiopulmonary exercise test to assess changes in hemodynamics and gas exchange during exercise. Conclusions: When coupled with other physiological testing and blood -omic analyses involved in the PVDOMICS study, the comprehensive right heart catheterization protocol described here holds promise to clarify the diagnosis and clustering of pulmonary hypertension patients into cohorts beyond the traditional 5 World Symposium on Pulmonary Hypertension groups. This article will describe the methods applied for invasive hemodynamic characterization in the PVDOMICS program. Registration: URL: https://www.clinicaltrials.gov . Unique identifier: NCT02980887.

scholarly journals Pulmonary Hypertension in COPD: A Case Study and Review of the Literature

Medicina ◽  
2019 ◽  
Vol 55 (8) ◽  
pp. 432
Author(s):  
Steven J. Cassady ◽  
Robert M. Reed
Keyword(s):  
Pulmonary Hypertension ◽  
Clinical Symptoms ◽  
Severe Disease ◽  
Right Heart Catheterization ◽  
Chronic Obstructive ◽  
Heart Catheterization ◽  
Vasodilator Therapy ◽  
Obstructive Pulmonary Disease ◽  
Pulmonary Vasodilator

Pulmonary hypertension (PH) is a frequently encountered complication of chronic obstructive pulmonary disease (COPD) and is associated with worsened clinical symptoms and prognosis. The prevalence of PH-COPD is not concretely established as classification criteria vary historically, but the presence of severe disease out of proportion to underlying COPD is relatively rare. Right heart catheterization, the gold standard in diagnosis of PH, is infrequently performed in COPD, and the overlap in the clinical symptoms of PH and COPD presents diagnostic challenges. Proven treatments are limited. Trials exploring the use of vasodilator therapy in this patient group generally demonstrate improvements in hemodynamics accompanied by worsening gas exchange without clearly demonstrated improvements in clinically meaningful outcomes. In-depth workup of underlying pulmonary hypertension and use of pulmonary vasodilator medications may be appropriate on an individual basis. We present a case study and a review and discussion of the pertinent literature on this topic.

PH Grand Rounds: Confronting the Challenge of Sarcoidosis-Associated Pulmonary Hypertension

2015 ◽  
Vol 14 (3) ◽  
pp. 166-169
Author(s):  
Deborah J. Levine ◽  
Kishan S. Parikh ◽  
Terry Fortin ◽  
Sudarshan Rajagopal
Keyword(s):  
Pulmonary Hypertension ◽  
Right Heart Catheterization ◽  
World Health ◽  
Heart Catheterization ◽  
Vasodilator Therapy ◽  
Pulmonary Vasodilator ◽  
High Clinical Suspicion ◽  
Routine Monitoring ◽  
Group 5 ◽  
Health Organization

Pulmonary hypertension (PH) associated with sarcoidosis (World Health Organization Group 5) carries a poor prognosis and likely occurs through multiple mechanisms. Routine monitoring and a high clinical suspicion must be maintained to establish early diagnosis. Imaging and other ancillary tests may suggest PH in these patients, but as with all PH groups, right heart catheterization is needed for confirmation and for differentiating contributors to PH. Although there appears to be a role for treatment in select patients with significant concomitant pulmonary arterial hypertension (PAH), pulmonary vasodilator therapy can also risk worsening hypoxia secondary to ventilation/perfusion mismatch. The medical management of patients with sarcoidosis-associated pulmonary hypertension (SAPH) will be better informed with further study in large, randomized trials. At this time, there are no US Food and Drug Administration-approved therapies, including PAH medications, for patients with SAPH.

scholarly journals Pulmonary Vascular Disease in the Single-Ventricle Patient: Is it Really Pulmonary Hypertension and if So, How and When Should We Treat it?

2019 ◽  
Vol 18 (1) ◽  
pp. 14-18
Author(s):  
Stephanie S. Handler ◽  
Jeffrey A. Feinstein
Keyword(s):  
Pulmonary Blood Flow ◽  
Single Ventricle ◽  
Fontan Circulation ◽  
Pulmonary Vascular Disease ◽  
Vasodilator Therapy ◽  
Pulmonary Vasodilators ◽  
Pulmonary Vasodilator ◽  
Late Morbidity ◽  
Fontan Patients

Despite significant improvements in the surgical and postoperative care for patients with single-ventricle physiology culminating in the Fontan circulation, significant late morbidity and mortality remains. In the setting of passive (ie, non-“pump” driven) pulmonary blood flow, pulmonary vascular resistance (PVR) plays a key role in determining cardiac output, and even slight elevations in PVR may result in significant morbidity. There is now great interest to treat Fontan patients with pulmonary vasodilators in an attempt to “optimize” PVR (and by extension, quality of life) and/or improve an elevated PVR. This review discusses the hemodynamic implications of the Fontan circulation, the evidence for use of pulmonary vasodilator therapy, and possible target physiologic mechanisms.

Pulmonary Vascular Disease in Secundum Atrial Septal Defect with Pulmonary Hypertension

CHEST Journal ◽  
1986 ◽  
Vol 89 (5) ◽  
pp. 694-698 ◽  
Author(s):  
Shigeo Yamaki ◽  
Togo Horiuchi ◽  
Makoto Miura ◽  
Yasuyuki Suzuki ◽  
Eiji Ishizawa ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Atrial Septal Defect ◽  
Vascular Disease ◽  
Septal Defect ◽  
Pulmonary Vascular Disease ◽  
Secundum Atrial Septal Defect

Newborn rat response to single vs. combined cGMP-dependent pulmonary vasodilators

2014 ◽  
Vol 306 (2) ◽  
pp. L207-L215 ◽  
Author(s):  
Masahiro Enomoto ◽  
Amish Jain ◽  
Jingyi Pan ◽  
Yulia Shifrin ◽  
Todd Van Vliet ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Synergistic Effect ◽  
Soluble Guanylate Cyclase ◽  
Pulmonary Arteries ◽  
Small Heat Shock Protein ◽  
No Donor ◽  
Clinical Exposure ◽  
Pulmonary Vasodilators ◽  
Pulmonary Vasodilator

Inhaled nitric oxide (NO) and other cGMP- or cAMP-dependent pulmonary vasodilators are often used in combination for the treatment of the persistent pulmonary hypertension of the newborn syndrome. There is in vitro evidence to indicate that NO downregulate the pulmonary vascular response to cGMP-dependent agonists raising concern as to whether a synergistic effect is observed when employing a combined strategy in newborns. Hypothesizing that a synergistic effect is absent, we evaluated newborn and juvenile rat pulmonary arteries to determine the individual and combined vasodilatory effect of cGMP- and cAMP-dependent agonists. In precontracted near-resistance pulmonary arteries, the addition of sildenafil reduced vasorelaxation response to NO donor S-nitroso- N-acetyl penicillamine (SNAP). A similar decrease in SNAP-induced vasodilation was observed in arteries pretreated with BAY 41–2272 (10−9 M), a soluble guanylate cyclase stimulator cGMP, and its downstream protein kinase activator. cGMP also reduced the vasorelaxant response to the cAMP-dependent forskolin. Inhibition of endogenous vascular NO generation enhanced SNAP-induced relaxation. The present data suggest that the mechanism involved in the cGMP desensitization to other relaxant agonists involves downregulation of the small heat shock protein HSP20 and is evident in rat pulmonary and systemic vascular smooth muscle cells. In newborn rats with chronic hypoxia-induced pulmonary hypertension, the combination of sildenafil and inhaled NO resulted in a lesser reduction in pulmonary vascular resistance compared with their individual effect. These data suggest that clinical exposure to one cGMP-dependent pulmonary vasodilator may affect the response to other cGMP- or cAMP-mediated agonists.

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