Conference: 2008 International PHA Conference and Scientific Sessions
Release Date: 06.20.2008
Presentation Type: Abstracts
Hurewitz A.N., Bartlett M., Schubach S.
Department of Medicine and Department of Cardiothoracic Surgery, Winthrop University Hospital, Mineola, NY, USA
BACKGROUND: The course of prolonged mitral regurgitation or aortic stenosis is often complicated by progressive pulmonary hypertension (PH) and a risk of right heart strain. A portion of the PH can be attributed to an elevated left ventricular end-diastolic pressure (LVEDP) and/or an elevated left atrial pressure. However, pulmonary arterial remodeling also contributes to the PH and this can persist after surgical repair or replacement of the damaged heart valve. With new advanced therapies for PH there is increasing interest in studying this population of patients.
METHODS: This pilot study is a retrospective chart review of 93 consecutive patients undergoing valve repair or replacement at an academic medical center. Data collected included age, sex, type of surgery, preoperative and initial intraoperative right heart catheterization (RHC) and postoperative RHC obtained immediately before the catheter was removed. The transpulmonary gradient (TPG) was calculated from the difference between pulmonary artery diastolic (PAD) pressure and pulmonary wedge pressure (PCW); LVEDP was obtained during preoperative left heart catheterization. Cardiac index was determined by thermodilution. PH is defined as a mean PA pressure (mPAP) > 24 mmHg. Data are expressed as mean±standard deviation and are compared using paired or unpaired t-testing.
RESULTS: Forty two patients with aortic valve disease (group A) had baseline mPAP = 33±11 mmHg; most patients in this group (88%) had mPAP > 24 mmHg. Fifty one patients with mitral valve disease (group M) had mPAP = 28±10 mmHg and of these 57% had PH. Pulmonary pressures were significantly higher in group M than in group A (p < 0.008). TPGs were also significantly higher in group M (12±5 mmHg) than in group A (3±7 mmHg); LVEDPs were elevated in both (group A=23±11 mmHg; group M=20±8 mmHg).
Following aortic valve surgery, mPAP decreased from 28 to 21 mmHg (delta -6.5); p=0.0017. Following mitral valve surgery mPAP decreased from 34 to 27 mmHg (delta -6.2); p=0.0006. Sixty percent of patients in group M had persistent PH in the first few days after surgery whereas only 32% with aortic valve surgery had persistent PH.
CONCLUSIONS: PH is a common finding in patients with either aortic valve disease or mitral valve disease although it occurred more frequently in the latter group. Patients with mitral disease are more likely to develop higher transpulmonary pressure gradients. Following valve surgery both groups showed a modest reduction in mPAP but persistent PH was common, especially in the mitral valve group. How often and how long it takes for this residual PH to resolve needs to be addressed and will require long term prospective hemodynamic monitoring of these patients.