Asian Cardiovasc Thorac Ann 2007;15:229-233
© 2007 Asia Publishing EXchange Ltd
Thromboendarterectomy for Severe Chronic Thromboembolic Pulmonary Hypertension
Keiichi Ishida, MD,
Masahisa Masuda, MD
Department of Cardiovascular Surgery, National Hospital Organization Chiba Medical Center, Chiba, Japan
For reprint information contact: Keiichi Ishida, MD Tel: 81 43 251 5311 Fax: 81 43 255 1675 Email: keiichi-ishida{at}pro.odn.ne.jp, Department of Cardiovascular Surgery, National Hospital Organization Chiba Medical Center, Tsubakimori 4-1-2, Chuouku, Chiba 260-8606, Japan.
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ABSTRACT
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Pulmonary thromboendarterectomy is a curative surgical procedure for chronic thromboembolic pulmonary hypertension. The aim of this study was to clarify whether severe hemodynamic compromise affects surgical outcome. We studied 19 patients who underwent pulmonary thromboendarterectomy and compared 11 with pulmonary vascular resistance < 1,000 dyne·s·cm–5 (group 1) and 8 with pulmonary vascular resistance > 1,000 dyne·s·cm–5 (group 2). Mean pulmonary artery pressure and pulmonary vascular resistance decreased significantly after surgery in both groups. The incidence of postoperative complications did not differ between groups; however, one patient in group 2 died of multiorgan failure. The overall mortality rate was 5.3%, and the rate in group 2 was 13%. Our results indicate that preoperative hemodynamic compromise does not affect surgical outcome. Patients with high pulmonary vascular resistance can be treated effectively by thromboendarterectomy, with acceptable morbidity and mortality.
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INTRODUCTION
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Chronic thromboembolic pulmonary hypertension (CTEPH) is caused by recurrent thromboembolism and incomplete resolution of thromboembolic pulmonary vascular occlusion associated with acute pulmonary embolism. In the majority of patients with acute pulmonary embolism, the thrombi resolve rapidly and substantially, but it has been reported that 4% of patients develop CTEPH during 2 years of follow-up.1 Without intervention, the late prognosis of patients with CTEPH is poor and proportional to the degree of pulmonary hypertension at the time of diagnosis.2,3 Riedel and colleagues2 demonstrated that the 3-year survival rate among patients with mean pulmonary artery pressure (PAP) above 30 mm Hg was 30%, and the 5-year survival rate among patients with mean PAP above 50 mm Hg was 10%. While medical therapy using anticoagulants, thrombolytic agents, or vasodilators is ineffective and associated with a poor prognosis, surgical treatment by pulmonary thromboendarterectomy has proven effective and has become the standard therapeutic approach for CTEPH. Pulmonary thromboendarterectomy can substantially and permanently reduce PAP and pulmonary vascular resistance (PVR), and relieve clinical symptoms.4,5 A survival rate of 75% at 6 years or more was reported in a follow-up study of patients who underwent pulmonary thromboendarterectomy; 93% of these patients were in New York Heart Association (NYHA) functional class I or II.6 With increased PVR, PAP rises further, right ventricular function is impaired, and the symptoms progressively worsen after a "honeymoon period" of relatively minor symptoms.7 One of the most important concerns in the treatment of CTEPH is whether patients with severe hemodynamic compromise are candidates for pulmonary thromboendarterectomy. Therefore, we compared surgical outcomes of patients with preoperative PVR greater and less than 1,000 dyne·s·cm–5 to determine whether hemodynamically compromised patients could benefit from this procedure.
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PATIENTS AND METHODS
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Nineteen patients with CTEPH underwent pulmonary thromboendarterectomy in National Hospital Organization Chiba Medical Center between April 2002 and March 2006. Surgery was indicated for patients who had PVR > 300 dyne·s·cm–5, mean PAP > 30 mm Hg, NYHA class 
II, and the presence of central disease on a computed tomography scan. Eight patients (42%) had deep vein thrombus and 5 (26%) had coagulation abnormalities: antiphospholipid antibody syndrome in 3, protein S deficiency in 1, and protein C deficiency in 1. The patients were divided into 2 groups: 11 with pulmonary vascular resistance < 1,000 dyne·s·cm–5 (group 1) and 8 with pulmonary vascular resistance > 1,000 dyne·s·cm–5 (group 2).
An inferior vena cava filter was inserted in all patients preoperatively. All patients underwent the standardized surgical technique described by the University of California at San Diego (UCSD) group.8 A median sternotomy was made, and cardiopulmonary bypass was instituted. While the patient was cooled to 20°C, the right pulmonary artery was exposed between the aorta and the superior vena cava. When the body temperature reached 20°C, an aortic cross clamp was applied and antegrade cold cardioplegia was administered with topical cooling using ice slush. An incision was made in the right pulmonary artery and fresh or organized thrombus was removed. Circulatory arrest was started to ensure adequate visualization by interrupting back-bleeding from the bronchial arteries. Once the proper thromboendarterectomy plane was identified between the intima and the fibrotic embolic material, endarterectomy specimens were grasped gently with forceps, and distal and circumferential dissections were performed while sweeping away the outer vessel layer with a sucker. Circulatory arrest was limited to 20 min, and reperfusion was carried out for a minimum of 10 min. Following thromboendarterectomy of the right pulmonary artery, the left side was treated in the same way. After completion of the thromboendarterectomy, cardiopulmonary bypass was re-instituted, and the patient was rewarmed. We did not routinely repair tricuspid regurgitation. Hemodynamics were assessed by right-sided heart catheterization preoperatively in all patients, and at one month postoperatively in survivors. Right atrial pressure, PAP, and pulmonary capillary wedge pressure were measured. Cardiac output was determined by thermodilution, and PVR was calculated.
Results are expressed as mean ± standard deviation or as a percentage. Hemodynamic and operative variables were compared between the groups using the Mann-Whitney U test. Pre- and postoperative hemodynamic variables were compared using the Wilcoxon signed rank test. Discrete variables were analyzed using Fisher’s exact test. A value of p < 0.05 was considered to be statistically significant.
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RESULTS
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Patient characteristics are summarized in Table 1
. The ages of the patients ranged from 20 to 70 years. Patients in group 2 had a longer duration of illness and relatively more were in NYHA functional class III or IV than those in group 1. Pre- and postoperative hemodynamic indices are listed in Table 2. Preoperative PVR ranged from 319 to 1,698 dyne·s·cm–5, and PAP ranged from 23 to 71 mm Hg. Two patients had PVR < 500 dyne·s·cm–5, and one had PVR > 1,500 dyne·s·cm–5; 7 patients had mean PAP > 50 mm Hg. Postoperatively, mean PAP and PVR decreased significantly and cardiac index increased compared to the preoperative levels in both groups. The mean decreases in mean PAP and PVR were significantly greater in group 2 than group 1, although the mean increase in cardiac index did not differ between groups. Operative parameters are shown in Table 3. Thromboendarterectomy on the right side took longer than on the left side; these variables were similar in both groups. Postoperative complications are listed in Table 4. The incidence of complications did not differ between groups. Six patients developed postoperative persistent pulmonary hypertension, defined as PVR > 500 dyne·s·cm–5, immediately after surgery. One patient with preoperative PVR of 1,089 dyne·s·cm–5 could not be weaned from cardiopulmonary bypass and needed percutaneous cardiopulmonary support due to severe persistent pulmonary hypertension and right ventricular failure. This patient subsequently died of multiorgan failure. In 2 other patients, PVR did not decrease after surgery: pre- to postoperative changes were 1,292 to 1,168 dyne·s·cm–5; and 960 to 982 dyne·s·cm–5. Postoperative pulmonary angiography showed insufficient removal of obstruction to reduce PAP and PVR. These patients required prolonged ventilatory support. In the other 3 patients, postoperative right heart catheterization showed further reduction of PVR. Pulmonary hemorrhage was observed in 3 patients in group 2; however, the hemorrhage was not massive or fatal in any of them, although one suffered from persistent hemoptysis. Six patients developed reperfusion pulmonary edema, defined as radiographic evidence of infiltrates involving the endarterectomized pulmonary segments, and hypoxia necessitating ventilatory support for more than 4 days. In addition, one patient with postoperative persistent pulmonary hypertension developed severe reperfusion pulmonary edema associated with profound alveolar flooding. The one death in group 2 accounted for the overall hospital mortality rate of 5.3% (13% in group 2).
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DISCUSSION
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Pulmonary vascular resistance indicates the degree of pulmonary vascular occlusion. Therefore, patients with a high PVR are considered to be more severely ill. Indeed, the majority of our patients with PVR > 1,000 dyne·s·cm–5 were in NYHA class III or IV. Nevertheless, the decreases in PVR and mean PAP were significantly greater in patients with PVR > 1,000 dyne·s·cm–5 than in those with a lower PVR. This result shows that more severely compromised patients benefited more from the surgical procedure than those less compromised. Although the majority of our patients showed substantial hemodynamic improvement after surgery, 6 developed pulmonary hypertension immediately after surgery. Persistent pulmonary hypertension, caused by pulmonary vasoconstriction and incomplete removal of obstruction, leads to right heart failure and multiorgan failure, and is the major cause of death after pulmonary thromboendarterectomy. Jamieson and colleagues9 demonstrated that this complication accounted for 77% of the mortality, and that patients with postoperative PVR > 500 dyne·s·cm–5 had a mortality rate of 30.6%, whereas those with PVR < 500 dyne·s·cm–5 had a mortality rate of 0.9%. In the present study, the incidence of this complication was similar in both groups. However, persistent pulmonary hypertension, mainly due to inadequate thromboendarterectomy, occurred in 3 patients who had preoperative PVR > 900 dyne·s·cm–5. In the case of particular patients with preoperative high PVR, persistent pulmonary hypertension due to inadequate thromboendarterectomy was severe and difficult to manage. Indeed, 2 patients needed prolonged ventilatory support and one needed percutaneous cardiopulmonary support; the latter died of multiorgan failure.
Reperfusion pulmonary edema and pulmonary hemorrhage are the major complications after pulmonary thromboendarterectomy. The incidence of reperfusion pulmonary edema ranges from 8% to 36%.10–12 We used the definition of reperfusion pulmonary edema as hypoxia requiring ventilatory support for more than 4 days, and radiographic evidence of infiltrates involving the endarterectomized pulmonary segments.11 This occurred in 6 (32%) of our patients. The severity of reperfusion pulmonary edema is variable, and failure to reduce PAP exacerbates this complication. One patient with postoperative persistent pulmonary hypertension due to inadequate thromboendarterectomy also developed severe reperfusion pulmonary edema associated with profound alveolar flooding. Pulmonary hemorrhage, which is caused by endarterectomy in a deeper plane, occurs in 18% of patients.13 This complication affected 3 (16%) of our patients who had preoperative PVR > 1,000 dyne·s·cm–5, although it was not massive or fatal in any of them. We found no significant difference in the incidence of these complications between the 2 groups, possibly due to the small numbers. However, the fact that patients with preoperative high PVR developed a severe form of these complications more often suggests that preoperative high PVR is a risk factor for severe complications associated with high mortality rates.
It has been demonstrated that preoperative severe pulmonary hypertension and high PVR are associated with operative mortality. Hartz and colleagues13 reported that patients with mean PAP > 50 mm Hg and PVR > 1,100 dyne·s·cm–5 had 40% operative mortality. The UCSD group indicated that patients with preoperative PVR > 1,000 dyne·s·cm–5 or systolic PAP > 100 mm Hg had a mortality rate of approximately 10%, whereas those with lower PVR and PAP had mortality rates of 1.3% and 3.5%, respectively.9,10 On the other hand, D’Armini and colleagues12 found that severity of preoperative pulmonary hypertension had no impact on mortality or surgical success. In our study, patients with PVR > 1,000 dyne·s·cm–5 had a mortality rate of 13%, whereas there was no mortality among those with lower PVR. However, we found that PVR > 1,000 dyne·s·cm–5 was unrelated to postoperative mortality, possibly because of the small number of patients in this study. The mortality rate in patients undergoing thromboendarterectomy ranges from 4% to 23%.9,12–14 The lowest mortality rate of 4% was reported by the group at UCSD, which has the most experience with this procedure.9 Mortality rates reported by other groups are around 10%. Our group has previously reported a hospital mortality rate of 18% in patients who underwent surgery between 1985 and 2001.15 With increased surgical experience and refinement of operative and postoperative management, we were able to reduce the perioperative mortality to an acceptable level, currently 5.3%.
It was concluded that marked hemodynamic improvement can be achieved by performing pulmonary thromboendarterectomy to treat severely compromised patients, with acceptable mortality and morbidity rates. Surgical success may depend on the feasibility of thromboendarterectomy of the segmental pulmonary arteries, and not on the degree of PVR. The UCSD group indicated that patients with microscopic distal vasculopathy without visible thromboembolic disease have higher mortality rates and thus may not be candidates for pulmonary thromboendarterectomy.9 We believe that the location and extent of the proximal thromboembolic obstruction, assessed by computed tomography, are the most critical determinants of operability.
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ABSTRACT
INTRODUCTION
