Pulmonary hypertension often complicates mitral valve disease with disabling symptoms. It has been associated with increased perioperative mortality during mitral valve replacement(1,2). Improvement of pulmonary hemodynamics with epoprostenol perioperatively may lead to better surgical outcomes. Though these patients will tend to show improvement in their pulmonary hemodynamics over time after valve replacement, these values rarely return to normal(3). Furthermore, pulmonary artery and capillary endothelin-1 (ET-1) levels have been shown to be elevated in these patients and remain elevated even after valve replacement(4). Since endothelin is known to play a role in the vascular remodeling characteristic of this disease, the ET-1 receptor antagonist bosentan may be useful in the management of these patients after surgery.
A 57 year old female with a history of mitral valve regurgitation from rheumatic heart disease was admitted for progressive shortness of breath. Her dyspnea had worsened so that she could no longer perform her activities of daily living. On admission she underwent right heart catheterization which demonstrated pulmonary artery pressures (PAP) at systemic levels. Subsequently epoprostenol therapy was initiated with significant improvement in pulmonary vascular resistance (PVR) and cardiac output (CO) as shown in Table 1Table 1:
Preoperative HemodynamicsDose (ng/kg/min)Blood PressurePAPPVRPCWPCOPre-op No TherapyNA119/40102/32515274.4Pre-op On Therapy10112/3455/20153206.1
PCWP –pulmonary capillary wedge pressure. She then underwent placement of a St. Jude mechanical valve, was maintained on epoprostenol in the immediate post operative period and then weaned over the next few days. Her post operative course was complicated only by an episode of atrial flutter and she electively underwent cardioversion. After transfer to the floor she was started on bosentan and was discharged. Her response to therapy was followed by serial echocardiographic estimates of right ventricular systolic pressure (RVSP) as shown in Figure 1. At her three month follow up her symptoms had much improved and she was planning to return to work. Pulse oximetry demonstrated desaturation into the 80’s during a six minute walk test. At her six month visit she was working fulltime and her pulse oximetry dropped barely below 90% during her six minute walk. At one year after valve replacement and initiation of bosentan she was able to perform her activities of daily living without dyspnea.
Long standing mitral valve disease can be complicated by significant elevations in pulmonary artery pressure which can reach systemic levels. These patients are usually significantly disabled at this stage. Mitral valve replacement alone will lead to some improvement in PAP and symptoms over time, however, there may be increased mortality in the perioperative period compared to patients without pulmonary hypertension(1,2). The use of a selective pulmonary vasodilator like epoprostenol can lead to rapid improvement in pulmonary hemodynamics and is easily titratable so that it can be adjusted during surgery and in the intensive care unit. This may lead to improved outcomes in mitral valve surgery. It is known that ET-1 is involved in the pathogenesis of pulmonary hypertension and it is possible to block its effects with the receptor antagonist bosentan. The observation that ET-1 is elevated in this patient population suggests that its blockade may lead to improvement in long term outcomes. This is a promising treatment since mitral valve replacement alone does not appear to fully reverse the hemodynamic consequences of long standing disease.
Mitral valve disease is often accompanied by significant pulmonary hypertension. This may lead to increased perioperative mortality. The use of epoprostenol to acutely improve pulmonary hemodynamics during this period may lead to better surgical outcomes. The transition to bosentan at discharge may improve long term outcomes.
B.L. Sandifer, None.