NT-proBNP can be used to detect right ventricular systolic dysfunction in pulmonary hypertension

Blyth, Kevin G.; Groenning, Bjoern A.; Mark, Patrick B.; Martin, Thomas N.; Foster, John E.; Steedman, Tracey; Morton, J.; Dargie, Henry J.; Peacock, Andrew J.

doi:10.1183/09031936.00095606

Cited by 103 publications

(85 citation statements)

References 51 publications

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“…Brain natriuretic peptide changes are correlated with RV strain and RVEF measured by CMR, and the brain natriuretic peptide differences found in our study further support our CMR fi ndings. [17][18][19] In an earlier study, RVEF change difference between survivors and nonsurvivors in PAH was 8%, further illustrating that the difference found in our study is clinically meaningful. 20 Sex differences have been well documented in diseases of the left ventricle.…”

Section: Discussionsupporting

confidence: 53%

The Right Ventricle Explains Sex Differences in Survival in Idiopathic Pulmonary Arterial Hypertension

Jacobs

Veerdonk²,

Trip³

et al. 2014

Chest

181

150

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Pulmonary arterial hypertension (PAH) is a rare disease characterized by obstructive lesions of the small pulmonary vessels, leading to increased pulmonary artery pressure (PAP), right-sided heart failure, and death within several years. 1,2 Despite the advent of improved therapies, outcome remains poor. 3,4 Prognosis correlates with severity of right ventricular (RV) structure and function. 2,5 More recently, male sex was identifi ed as an independent predictor of mortality. [6][7][8][9][10] Men treated with endothelin receptor antagonists had less 6-min walk distance (6MWD) improvement. 11 The cause of these sex differences is unknown; however, a distinct vascular and/or RV response to medical therapies is one possibility. Considering the need for improved treatments and "personalized therapy," Background: Male sex is an independent predictor of worse survival in pulmonary arterial hypertension (PAH). This fi nding might be explained by more severe pulmonary vascular disease, worse right ventricular (RV) function, or different response to therapy. The aim of this study was to investigate the underlying cause of sex differences in survival in patients treated for PAH. Methods: This was a retrospective cohort study of 101 patients with PAH (82 idiopathic, 15 heritable, four anorexigen associated) who were diagnosed at VU University Medical Centre between February 1999 and January 2011 and underwent right-sided heart catheterization and cardiac MRI to assess RV function. Change in pulmonary vascular resistance (PVR) was taken as a measure of treatment response in the pulmonary vasculature, whereas change in RV ejection fraction (RVEF) was used to assess RV response to therapy. Results: PVR and RVEF were comparable between men and women at baseline; however, male patients had a worse transplant-free survival compared with female patients ( P 5 .002). Although male and female patients showed a similar reduction in PVR after 1 year, RVEF improved in female patients, whereas it deteriorated in male patients. In a mediator analysis, after correcting for confounders, 39.0% of the difference in transplant-free survival between men and women was mediated through changes in RVEF after initiating PAH medical therapies. Conclusions: This study suggests that differences in RVEF response with initiation of medical therapy in idiopathic PAH explain a signifi cant portion of the worse survival seen in men.

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Section: Discussionsupporting

confidence: 53%

The Right Ventricle Explains Sex Differences in Survival in Idiopathic Pulmonary Arterial Hypertension

Jacobs

Veerdonk²,

Trip³

et al. 2014

Chest

181

150

View full text Add to dashboard Cite

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“…8,16 One study found that NT-pro-BNP negatively correlated with right-ventricular ejection fraction and that it identifies patients with pulmonary hypertension and right-ventricular systolic dysfunction. 17 Our COPD patients had a slightly and nonsignificantly higher NT-pro-BNP than our healthy subjects, both at rest and during exercise. Therefore, cardiac factors may not contribute to exercise intolerance in patients with mild to moderate COPD.…”

Section: Discussionmentioning

confidence: 99%

Cardiac Response and N-Terminal-Pro-Brain Natriuretic Peptide Kinetics During Exercise in Patients With COPD

Wang

Xiao

et al. 2011

Respir Care

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BACKGROUND: COPD increases the risk of cardiovascular problems. Dyspnea on exertion can be associated with COPD or heart failure or both. N-terminal-pro-brain natriuretic peptide (NT-pro-BNP) is a marker of cardiac dysfunction, and exercise testing can identify subtle heart abnormalities. OBJECTIVE: To determine whether cardiac dysfunction adds to the mechanism of dyspnea caused primarily by impaired lung function in patients with mild to moderate COPD. METHODS: With 19 COPD patients and 10 healthy control subjects we measured physiologic variables and collected venous blood samples before and during incremental and constant-work-rate exercise, and measured NT-pro-BNP. RESULTS: Peak oxygen uptake and constant-work exercise time were significantly lower in the COPD group than in the control group (16 ؎ 4 mL/min/kg vs 19 ؎ 6 mL/ min/kg, P ‫؍‬ .04, and 7.8 ؎ 6.5 min vs 14.8 ؎ 7.3 min, P ‫؍‬ .02). Between the groups there were no significant differences in anaerobic threshold, oxygen pulse (oxygen uptake divided by heart rate), or heart-rate reserve (difference between predicted and measured maximum heart rate). Both at rest and during constant-work exercise, NT-pro-BNP was not significantly higher in the COPD group than in the control group. In the COPD patients there was no significant correlation between constant-work exercise time and NT-pro-BNP at rest or during exercise. CONCLUSIONS: Heart failure did not contribute to exercise intolerance in patients with mild to moderate COPD.

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“…Previous studies have not used this biomarker as outcome measure in PH associated with lung disease. In IPAH, NT-proBNP has been shown to correlate with RV function [39] and changes in serial NT-proBNP with treatment have been shown to predict survival [40]. In COPD, NT-proBNP has been shown to predict outcome following acute exacerbations of airways disease [41][42][43], identify those with concurrent left ventricular dysfunction [42,44] and function as a screening tool for PH in COPD [45].…”

Section: Discussionmentioning

confidence: 99%

Severe pulmonary hypertension in lung disease: phenotypes and response to treatment

et al. 2015

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Pulmonary hypertension (PH) due to lung disease (World Health Organization (WHO) group 3) is common, but severe PH, arbitrarily defined as mean pulmonary artery pressure ⩾35 mmHg is reported in only a small proportion. Whether these should be treated as patients in WHO group 1 (i.e. pulmonary arterial hypertension) with PH-targeted therapies is unknown.We compared the phenotypic characteristics and outcomes of 118 incident patients with severe PH and lung disease with 74 idiopathic pulmonary arterial hypertension (IPAH) patients, all treated with pulmonary vasodilators.Lung disease patients were older, more hypoxaemic, and had lower gas transfer, worse New York Heart Association functional class and lower 6-min walking distance (6MWD) than IPAH patients. Poorer survival in those with lung disease was driven by the interstitial lung disease (ILD) cohort.In contrast to IPAH, where significant improvements in 6MWD and N-terminal pro-brain natruiretic peptide (NT-proBNP) occurred, PH therapy in severe PH lung disease did not lead to improvement in 6MWD or functional class, but neither was deterioration seen. NT-proBNP decreased from 2200 to 1596 pg·mL −1 ( p=0.015). Response varied by lung disease phenotype, with poorer outcomes in patients with ILD and emphysema with preserved forced expiratory volume in 1 s. Further study is required to investigate whether vasodilator therapy may delay disease progression in severe PH with lung disease. @ERSpublications Treatment of severe pulmonary hypertension associated with lung disease can improve or stabilise noninvasive outcomes

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NT-proBNP can be used to detect right ventricular systolic dysfunction in pulmonary hypertension

Cited by 103 publications

References 51 publications

The Right Ventricle Explains Sex Differences in Survival in Idiopathic Pulmonary Arterial Hypertension

The Right Ventricle Explains Sex Differences in Survival in Idiopathic Pulmonary Arterial Hypertension

Cardiac Response and N-Terminal-Pro-Brain Natriuretic Peptide Kinetics During Exercise in Patients With COPD

Severe pulmonary hypertension in lung disease: phenotypes and response to treatment

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