Background: Pulmonary hypertension associated with chronic congestive heart failure posses a significant risk of morbidity and death after heart transplantation. Isolated observations suggest that chronic ventricular unloading may lead to normalization of pulmonary pressures and thus render a patient likely to be a heart transplant candidate.
Methods: This study is a retrospective analysis of 9 heart failure patients with secondary pulmonary hypertension (transpulmonary gradient [TPG] > 15 mm/Hg). Two were treated with a pulsatile left ventricular assist device (LVAD) and 7 with an axial-flow LVAD.
Results: After LVAD support, mean pulmonary artery pressure decreased from 39 +/- 7 to 31 +/- 5 mm Hg, and the TPG decreased from 19 +/- 3 to 13 +/- 4 mm Hg (p < 0.01). The 1-year Kaplan-Meier survival curve for patients with pre-LVAD TPG > 15 mm Hg vs those with TPG < 15 mm Hg showed no difference in survival (p = 0.6). This finding was supported by analysis of a large multi-institutional cohort obtained from the Organ Procurement and Transplantation Network database, where no differences in survival were found in the same groups.
Conclusions: Pulmonary hypertension that is secondary to congestive heart failure, as defined by a TPG > 15 mm Hg can be reversed by the use of pulsatile and axial-flow LVADs; furthermore, post-transplant survival for patients with secondary pulmonary hypertension treated with an LVAD was no different than for those without pulmonary hypertension who received LVAD support.
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http://dx.doi.org/10.1016/j.healun.2009.05.030 | DOI Listing |
Schizophrenia (Heidelb)
December 2024
Department of Psychiatry, University of Helsinki and Helsinki University Hospital, Helsinki, Finland.
Schizophrenia (SZ), schizoaffective disorder (SZA), bipolar disorder (BD), and psychotic depression (PD) are associated with premature death due to preventable general medical comorbidities (GMCs). The interaction between psychosis, risk factors, and GMCs is complex and should be elucidated. More research particularly among those with SZA or PD is warranted.
View Article and Find Full Text PDFBMJ Open
December 2024
Clinical Research Department, Ignacio Chávez National Heart Institute, Mexico City, Mexico
Objectives: To investigate clinical characteristics, symptom profile, testing practices, treatment patterns and quality of life (QoL) among patients with pulmonary arterial hypertension (PAH) in Latin America.
Design: Data from the Adelphi Real World PAH Disease Specific Programme, a cross-sectional survey with retrospective data collection.
Setting: University/teaching hospital, regional centres, private practices and government institutions in Argentina, Brazil, Colombia and Mexico.
J Pediatr Surg
December 2024
Section of Pediatric Surgery, C.S. Mott Children's Hospital, Michigan Medicine, Ann Arbor, MI, USA. Electronic address:
Introduction: Timing of repair for infants with congenital diaphragmatic hernia (CDH) requiring extracorporeal life support (ECLS) remains controversial. Approaches include early repair on ECLS, late repair on ECLS, or repair after ECLS decannulation; all have potential risks and benefits. To mitigate risk and maximize benefit, our group developed an individualized hybrid model in 2016 in which approach is based on prenatal risk stratification.
View Article and Find Full Text PDFEchocardiography
January 2025
Department of Cardiology, Nanjing First Hospital, Nanjing Medical University, Nanjing, Jiangsu, China.
Objectives: Numerous studies have demonstrated impaired right ventricular (RV) synchronicity in pulmonary arterial hypertension (PAH). However, few studies have focused on connective tissue disease (CTD)-associated PAH. This study evaluates RV dyssynchrony and its prognostic value in CTD-associated PAH.
View Article and Find Full Text PDFPLoS One
December 2024
Division of Medical Biochemistry, Tohoku Medical and Pharmaceutical University, Sendai, Japan.
The vascular endothelium is vital for cardio-pulmonary homeostasis and, thus, plays a crucial role in preventing life-threatening lung diseases. The transcription factor GATA2 is essential for hematopoiesis and maintaining vascular integrity. Heterozygous mutations in GATA2 can lead to a primary immunodeficiency syndrome with pulmonary manifestations.
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