Pulmonary Vascular Disease and Bronchopulmonary Dysplasia: Evaluation and Treatment of Pulmonary Hypertension

NeoReviews ◽  
2011 ◽  
Vol 12 (11) ◽  
pp. e645-e651 ◽  
Author(s):  
Steven H. Abman
Keyword(s):  
Pulmonary Hypertension ◽  
Vascular Disease ◽  
Bronchopulmonary Dysplasia ◽  
Pulmonary Vascular Disease

scholarly journals Digital Subtraction Pulmonary Angiography in Children with Pulmonary Hypertension due to Bronchopulmonary Dysplasia

2019 ◽  
Vol 7 (2) ◽  
pp. 26 ◽  
Author(s):  
Bibhuti Das ◽  
Michelle-Marie Jadotte ◽  
Jaime Mills ◽  
Kak-Chen Chan
Keyword(s):  
Pulmonary Hypertension ◽  
Vascular Disease ◽  
Bronchopulmonary Dysplasia ◽  
Preliminary Data ◽  
Pulmonary Arteries ◽  
Pulmonary Angiography ◽  
Pulmonary Vascular Disease ◽  
Digital Subtraction ◽  
Extreme Prematurity

Bronchopulmonary dysplasia (BPD) is the most common respiratory sequelae of prematurity and histopathologically features fewer, dysmorphic, pulmonary arteries. We present our experience with the digital subtraction pulmonary angiography (DSPA) findings of a segmental vascular filling abnormality in three children who were born at extreme prematurity and have pulmonary hypertension due to severe BPD. Our preliminary data suggest that DSPA may be useful in evaluating the severity of pulmonary vascular disease in children with BPD.

scholarly journals Pulmonary Vascular Disease in Bronchopulmonary Dysplasia

2016 ◽  
Vol 15 (2) ◽  
pp. 92-99 ◽  
Author(s):  
Steven H. Abman ◽  
Alicia Grenolds ◽  
Peter Mourani
Keyword(s):  
Pulmonary Hypertension ◽  
Vascular Disease ◽  
Bronchopulmonary Dysplasia ◽  
Premature Birth ◽  
Clinical Course ◽  
Diagnostic Evaluation ◽  
Pulmonary Vascular Disease ◽  
Premature Newborns ◽  
The Impact

Pulmonary vascular disease and pulmonary hypertension (PH) contributes significantly to the pathogenesis, pathophysiology, and clinical course of infants with bronchopulmonary dysplasia (BPD). This article briefly reviews the impact of premature birth on the developing lung circulation, mechanisms that contribute to the development of PH in premature newborns, and the diagnostic evaluation and management of severe PH in infants with BPD.

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

scholarly journals Lower DLco% identifies exercise pulmonary hypertension in patients with parenchymal lung disease referred for dyspnea

2020 ◽  
Vol 10 (1) ◽  
pp. 204589401989191 ◽  
Author(s):  
Richard H. Zou ◽  
William D. Wallace ◽  
S. Mehdi Nouraie ◽  
Stephen Y. Chan ◽  
Michael G. Risbano
Keyword(s):  
Pulmonary Hypertension ◽  
Lung Disease ◽  
Vascular Disease ◽  
Pulmonary Function Tests ◽  
Pulmonary Vascular Disease ◽  
Chronic Obstructive ◽  
Exertional Dyspnea ◽  
Pulmonary Arterial ◽  
Parenchymal Lung Disease ◽  
Parenchymal Lung

Exercise pulmonary hypertension is an underappreciated form of physical limitation related to early pulmonary vascular disease. A low diffusing capacity of lungs for carbon monoxide (DLco) can be seen in patients with resting pulmonary hypertension as well as parenchymal lung disease. It remains unclear whether low DLco% identifies early pulmonary vascular disease. We hypothesize that a reduced DLco% differentiates the presence of exercise pulmonary hypertension in patients with parenchymal lung disease. Fifty-six patients referred for unexplained exertional dyspnea with pulmonary function tests within six months of hemodynamic testing underwent exercise right heart catheterization. Exclusion criteria included resting pulmonary arterial or venous hypertension. Receiver operator characteristic curve determined the optimal DLco% cutoffs based on the presence or absence of parenchymal lung disease. Twenty-one (37%) patients had parenchymal lung disease, most common manifesting as chronic obstructive lung disease or interstitial lung disease. In patients with parenchymal lung disease, a DLco of 46% demonstrated 100% sensitivity and 73% specificity for detecting exercise pulmonary hypertension. In patients without parenchymal lung disease, a DLco of 73% demonstrated 58% sensitivity and 94% specificity for detecting exercise pulmonary hypertension. In both cohorts, DLco% below the optimum cutoffs were associated with higher peak mean pulmonary arterial pressure and peak total pulmonary resistance consistent with the hemodynamic definition of exercise pulmonary hypertension. Patients with a DLco < 46% were more often treated with pulmonary vasodilators and had a trend to higher mortality and lung transplant. DLco% is a simple non-invasive screening test for the presence of exercise pulmonary hypertension in our mixed referral population with progressive exertional dyspnea. DLco < 46% with parenchymal lung disease and DLco < 73% without parenchymal lung disease may play a role in differentiating the presence of pulmonary vascular disease prior to invasive hemodynamic testing.

Polyamines and the development of monocrotaline-induced pulmonary hypertension

1984 ◽  
Vol 247 (4) ◽  
pp. H682-H685 ◽  
Author(s):  
J. W. Olson ◽  
A. D. Hacker ◽  
R. J. Altiere ◽  
M. N. Gillespie
Keyword(s):  
Pulmonary Hypertension ◽  
Vascular Disease ◽  
Ventricular Hypertrophy ◽  
Continuous Treatment ◽  
Pulmonary Vascular Disease ◽  
Decarboxylase Activity ◽  
Rat Lung ◽  
Specific Enzyme ◽  
Irreversible Inhibitor ◽  
Adenosylmethionine Decarboxylase

Previous work in our laboratory has shown that the development of monocrotaline-induced pulmonary vascular disease in rats is preceded by a prolonged activation of lung ornithine decarboxylase (ODC). We now report that significant increases in rat lung adenosylmethionine decarboxylase activity and levels of the diamine putrescine and the polyamines, spermidine and spermine, are produced by a single dose of monocrotaline (MCT). Lung putrescine levels were increased from days 7 through 21, and both spermidine and spermine were first elevated at day 10 following MCT administration. This sustained elevation of lung polyamine levels substantially preceded the development of right ventricular hypertrophy and pulmonary hypertension, which were first evident at days 14 and 16, respectively. Continuous treatment with alpha-difluoromethylornithine, a highly specific enzyme-activated, irreversible inhibitor of ODC activity, prevented the development of MCT-induced pulmonary toxicity. It thus appears that ODC and the polyamines may be important mediators of hypertensive pulmonary vascular disease that develops in response to monocrotaline administration.

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.

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