scholarly journals Exercise-Induced Pulmonary Hypertension: How to Define, Diagnose, and Treat At-Risk Patients

2021 ◽  
Vol 20 (1) ◽  
Author(s):  
Brandon Shokoples ◽  
Kevin Comeau

Introduction Pulmonary hypertension is a devastating disease with a rapid progression of symptoms leading to high patient mortality. It is characterized by high blood pressure in the pulmonary vasculature and poor pulmonary perfusion, resulting in patient fatigue, dyspnea, and syncope, especially upon physical exertion. A sub-clinical form of pulmonary hypertension also exists which is referred to as exercise induced pulmonary hypertension, where patients display normal resting hemodynamic properties but abnormal pulmonary responses to exercise. Discussion Recent evidence suggests early intervention and treatment of pulmonary hypertension can improve patient outcomes. However, there is a lack of clinical evidence supporting effective treatments for exercise induced pulmonary hypertension (EIPH), arguably the earliest stage of pulmonary hypertension. This is due in part to the removal of EIPH from official guidelines such as the European Respiratory Society in 2008. EIPH was removed from clinical guidelines due to a lack of consensus on the definition and standardized testing procedures for diagnosing EIPH. Emerging evidence suggests that exercise testing following a standardized protocol of stress echocardiography or right heart catheterization of patients may allow for the classification of EIPH as a mean pulmonary artery pressure/cardiac output slope > 3 mmHg/L/min, and/or mean pulmonary artery pressure > 30 mmHg with a pulmonary vascular resistance > 3 Wood Units. Conclusion Providing evidence for a consensus definition of EIPH, along with a validated, standardized testing procedure, will hopefully foster the progression of research on EIPH and further the development of treatments and improve patient outcomes for people with pulmonary hypertension.

2020 ◽  
Vol 10 (2) ◽  
pp. 204589402091583 ◽  
Author(s):  
Reza S. Pratama ◽  
Anggoro B. Hartopo ◽  
Dyah W. Anggrahini ◽  
Vera C. Dewanto ◽  
Lucia K. Dinarti

Uncorrected atrial septal defect undergoes right ventricle chronic volume overload which may lead to pulmonary hypertension and Eisenmenger Syndrome. The soluble suppression of tumorigenicity-2 is a left ventricle strain biomarker; however, its role in right ventricle strain is unclear. This study aimed to investigate the implication of serum soluble suppression of tumorigenicity-2 in adult uncorrected atrial septal defect. This was a cross-sectional study. We enrolled 81 adult uncorrected secundum atrial septal defect patients. Clinical and hemodynamic data were collected. Serum samples were withdrawn from the pulmonary artery during right heart catheterization. Serum soluble suppression of tumorigenicity-2 and NT-proBNP levels were measured. Subjects were divided into three groups based on clinical and hemodynamic severity. The correlation of soluble suppression of tumorigenicity-2 with patients' data and comparison among groups were analyzed. A p value <0.05 was considered statistically significant. Results showed that, there were significant correlations between serum soluble suppression of tumorigenicity-2 and mean pulmonary artery pressure ( r = 0.203, p = 0.035) and right ventricle end-diastolic diameter ( r = 0.203, p <0.05). Median serum soluble suppression of tumorigenicity-2 level was incrementally increased from group I (atrial septal defect and no-pulmonary hypertension), group II (left-to-right atrial septal defect and pulmonary hypertension), to group III (Eisenmenger Syndrome): (17.4 ng/mL, 21.8 ng/mL, and 29.4 ng/mL, respectively). A post-hoc analysis showed that serum soluble suppression of tumorigenicity-2 level was significantly different between groups I and III ( p = 0.01). Serum N terminal pro brain natriuretic peptide (NT-proBNP) level was consistently associated with worse clinical and hemodynamic parameters. No correlation was found between serum soluble suppression of tumorigenicity-2 and NT-proBNP level. In conclusion, serum soluble suppression of tumorigenicity-2 level had significant positive correlation with mean pulmonary artery pressure and right ventricle end-diastolic diameter in uncorrected secundum atrial septal defect patients. Higher serum soluble suppression of tumorigenicity-2 level was associated with the presence of pulmonary hypertension and Eisenmenger Syndrome in uncorrected secundum atrial septal defect patients.


2013 ◽  
Vol 65 (4) ◽  
pp. 1074-1084 ◽  
Author(s):  
Christopher J. Valerio ◽  
Benjamin E. Schreiber ◽  
Clive E. Handler ◽  
Christopher P. Denton ◽  
John G. Coghlan

PLoS ONE ◽  
2010 ◽  
Vol 5 (12) ◽  
pp. e15670 ◽  
Author(s):  
Fikret Er ◽  
Stefan Ederer ◽  
Amir M. Nia ◽  
Evren Caglayan ◽  
Kristina M. Dahlem ◽  
...  

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