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Ann Thorac Surg 2003;76:1457-1464
© 2003 The Society of Thoracic Surgeons
a Division of Cardiothoracic Surgery, San Diego, California, USA
b Department of Anesthesia, San Diego, California, USA
c Division of Pulmonary and Critical Care Medicine, UCSD Medical Center, San Diego, California, USA
* Address reprint requests to Mr Jamieson, Cardiothoracic Surgery, UCSD Medical Center, 200 West Arbor Drive, San Diego, CA 92103, USA.
e-mail: sjamieson{at}ucsd.edu
Presented at the Thirty-ninth Annual Meeting of The Society of Thoracic Surgeons, San Diego, CA, Jan 31–Feb 2, 2003.
Abstract
BACKGROUND: The incidence of pulmonary hypertension resulting from chronic thrombotic occlusion of the pulmonary arteries is significantly underestimated. Although medical therapy for the condition is supportive only, surgical therapy is curative. Our pulmonary endarterectomy program was begun in 1970, and 188 patients were operated on in the subsequent 20 years. With the increased recognition of the disease and the success of operative therapy, however, more than 1,400 operations have been done since 1990 at our center.
METHODS: The safety and efficacy of the operation was assessed with changes made through increased experience. We examined in detail the results of our last 500 consecutive patients.
RESULTS: Median sternotomy, cardiopulmonary bypass, profound hypothermia, and circulatory arrest were found to be essential to the success of the operation. All occluding material could be removed at operation. We currently believe that there is no degree of embolic occlusion within the pulmonary vascular tree that is inaccessible and no degree of right ventricular impairment or any level of pulmonary vascular resistance that is inoperable. With shorter cardiac arrest periods and the use of a cooling jacket to the head, cerebral impairment has been eliminated. The pulmonary artery pressures and pulmonary vascular resistance in a recent cohort of 500 patients is examined. The mortality rate for the operation has been reduced steadily, and was 22 of the last 500 patients operated on (4.4%).
CONCLUSIONS: The operation is considered curative and therefore greatly superior to transplantation for this condition. Current techniques of operation make the procedure relatively safe.
Medical therapy for pulmonary hypertension caused by pulmonary vascular occlusion is generally unsatisfactory and palliative. Therapy by pulmonary endarterectomy offers a surgical cure, yet this procedure is not commonly applied.
This operation is a technically demanding yet highly successful treatment for pulmonary hypertension that is caused by chronic pulmonary thromboembolic disease. Proper patient selection, meticulous surgical technique, and careful postoperative management have now clearly shown that it is an effective therapy. A true endarterectomy (not an embolectomy) of all affected parts of the lung is essential. Circulatory arrest is fundamental for the visibility necessary to clear all affected areas of the pulmonary vasculature.
Although pulmonary transplantation is still used in some centers for patients with thromboembolic disease, we consider that treatment to be outdated. In good hands, the endarterectomy operation has a lower operative mortality rate than lung transplantation, it can be done electively without the wait for a donor, and the long-term problems associated with rejection and immunosuppressive drugs are eliminated. In addition, the mortality rate for transplantation (and especially double lung transplantation) as a therapeutic strategy should include patients on the waiting list and is therefore much higher than is generally reported.
Pulmonary endarterectomy appears to be permanently curative. However, probably fewer than 2,500 of these operations have been performed, and most of them (1,500 cases) were done at the University of California San Diego (UCSD). The recent experience using this procedure at UCSD provides the basis of this report.
Patients and methods
Patient selection
The first pulmonary thromboendarterectomy operation at UCSD was done in 1970 [1], and 188 operations were carried out in the ensuing 20 years. The program has grown steadily since 1990, and 1,580 patients had been operated on by December 2002. Patients are referred nationally and internationally to this center, and the number of referrals increases yearly, indicating an increased awareness of the disease and the effectiveness of therapy rather than an increased incidence. The clinical presentation of the patients varied, from patients with dyspnea on exertion but otherwise well to patients transferred by air ambulance in respiratory failure with florid right heart failure and ascites. At least half the patients did not have a history of deep venous thrombosis, and many gave no history of pulmonary embolism, thus contributing to the difficulty in diagnosis.
Patients accepted for operation included those with pulmonary hypertension and evidence of thromboembolic disease on pulmonary angiography. In general, pulmonary vascular resistance was higher than 300 dynes · second-1 · cm-5 and in some cases was more than 2,000 dynes · second-1 · cm-5. This group of patients, spanning ages 8 to 86 years, reflects a broad clinical range. On one side of the spectrum, young patients with dyspnea on exertion have been accepted for operation to remove unilateral pulmonary artery thromboembolic disease. On the other side of the spectrum, we now accept high-risk patients who have vascular disease in subsegmental pulmonary vessels only, as well as patients presenting with advanced multisystem organ failure from cardiovascular collapse.
Contraindications were limited only to conditions judged to be unrelated to pulmonary hypertension or deep venous thrombosis that were likely to independently limit patient survival in the near future. The expansion of patient population considered acceptable for this operation is based largely on accumulated surgical experience, improved operative technique, and a multidisciplinary approach to postoperative care.
Operative technique
Coronary angiography was performed in all patients more than 45 years old. A Greenfield inferior vena cava filter is always placed preoperatively.
The operation has been described in detail [2]. The essential features are that a median sternotomy incision is made, with cardiopulmonary bypass enabling hypothermia to 20°C. During the precardiopulmonary bypass period, the head is wrapped in a circulating cold-water blanket (Polar Care; Breg, Inc., Vista, CA). Water, maintained at approximately 4°C, is circulated through this blanket by an electrical pump. This system, originally designed as a knee-wrap for orthopedic and physical medicine purposes, is easily applied to the head. It contains a thermometer within the fluid circulation system for confirmation of adequate blanket cooling, as well as a flow control dial.
After the institution of cardiopulmonary bypass, the patient is cooled, and vents are placed in both the pulmonary artery and the right upper pulmonary vein. The right pulmonary artery is exposed between the aorta and superior vena cava and mobilized within the pericardial reflection. The pleura are not entered on either side. The aorta is cross-clamped, and antegrade cold cardioplegia is administered. Additional myocardial protection is then provided by the use of a cooling jacket, and no further cardioplegia is administered during the arrest period.
An incision is made in the right pulmonary artery and continued into the right lower lobe. Any thrombus encountered, be it loose or organized and attached to the vessel wall, is now removed. The endarterectomy cannot be performed in the presence of thrombus because it obscures the plane and prevents collapse of the endarterectomized specimen, hindering distal exposure. Circulatory arrest is begun when bronchial back bleeding obscures good visualization.
Excellent visibility of the entire vascular tree can now be obtained with appropriate positioning of the incision and the patient. Once the endarterectomy plane is developed, gentle traction with forceps while sweeping away the outer vessel wall layer will result in the progressive withdrawal of the endarterectomy specimen. The endarterectomy is performed primarily with a long miniature sucker with a rounded tip [2]. As each lobar branch appears it is grasped individually, and the specimen is withdrawn until each segmental vessel branches again. Each of these subsegmental specimens is then removed.
Removal of each lobar and then segmental branch makes subsequent distal dissection easier. If a large mass of endarterectomized tissue begins to obscure visibility, it is excised. The entire specimen can thus be removed progressively for a length of approximately 20 cm (Fig 1). All mechanically occluding material can be removed with these techniques, and visibility can be obtained in subsegmental vessels. The term "surgically accessible thrombus" is no longer appropriate, because the plane can be raised, with experience, even at segmental and subsegmental levels. Although pulmonary vascular resistance does not always decrease to normal levels postoperatively, provided a full endarterectomy has been performed, residual pulmonary hypertension is caused by secondary damage to the vessel at the arteriolar and capillary levels, not by residual embolic material.
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Postoperative care is similar to that of routine open heart operations, except that aggressive diuresis is instituted to remove fluid in the third space that accumulated as a result of prolonged bypass and hypothermia and to reduce the incidence of pulmonary edema [2]. Nitric oxide and other pulmonary vasodilating agents have not been used routinely and should not be necessary if the mechanical obstruction has been removed.
A cohort of 500 consecutive patients (numbers 1,000 to 1,500 in our series) operated on between July 22, 1998 and July 11, 2002 were analyzed in detail for hemodynamic data and survival.
Statistical analysis
Results are summarized as mean ± standard deviation or n (%). Tympanic, bladder, and rectal temperatures were compared using one-way analysis of variance. The association between preoperative and postoperative pulmonary vascular resistance (PVR) and mortality rate was assessed using an exact likelihood ratio test. Paired Student's t tests were performed to identify significant changes in hemodynamic and other variables. Statistical tests were two-sided and assumed a 5% level of significance. Software used for the data and statistical analyses included Axis Clinical Software, Inc, JMP 5.0 (SAS Institute Inc., Cary, NC) and StatXact-5 Release 5.0.3 (Cytel Software Corporation, ).
Results
There is undoubtedly a learning curve for the operation. The operative mortality rate was 17% for the first 200 patients in the beginning of the UCSD series (1970 to 1990). Changes were made in the operative technique in 1990 [3], and the perioperative mortality rate has since steadily declined, to 8.8% for the 500 individuals who had the operation between 1994 and 1998, and to 4.4% for the 500 patients operated on between 1998 and 2002.
The cohort of 500 consecutive patients was analyzed in detail for hemodynamic data and survival. Patients in this group ranged in age from 8 to 84 years (median, 52 years), with a slight preponderance of males (256 of 500 patients, 51.2%). Duration of preoperative symptoms ranged from 6 months to 25 years. Only 229 patients (45%) gave a history of prior deep venous thrombosis, and 150 (30%) had no history suggestive of pulmonary embolism.
Mean cardiopulmonary bypass time was 218.7 ± 40.5 minutes. The mean cardiac arrest time was 88 ± 24.6 minutes, and the mean circulatory arrest time was 35.7 ± 11.9 minutes (19.8 ± 8.0 minutes for the right side and 15.8 ± 6.3 minutes for the left side).
The effect of the cooling jacket on tympanic membrane temperature was measured in 55 patients. Temperatures were measured at the commencement of circulatory arrest; the mean tympanic membrane temperature was 15.1 ± 1.1°C, rectal 20.8 ± 1.5°C, and bladder 19.8 ± 1.1°C. The difference between tympanic membrane temperature and that measured in the bladder or rectum was apparent in all cases and was statistically significant (p < 0.0001).
Tricuspid annuloplasty was not performed, even when severe tricuspid regurgitation was documented preoperatively. Two patients had a tricuspid valve replacement for leaflet structural damage caused by past endocarditis. One patient had an aortic valve replacement; one patient with an absent pulmonary valve had a pulmonary valve replacement. Thirty-six of 500 (7%) patients had concomitant coronary artery operation.
The median stay in the intensive care unit was 96 hours, and the median number of days the patients were intubated was 1 ± 9.6 (longest, 86 days). The median length of hospital stay postoperatively was 10 days.
Twenty-two of 500 patients died (either in the hospital or within 30 days of discharge) for an overall mortality rate of 4.4%. Death was related to residual high pulmonary pressures in 17 of 22 patients (77%). In 18 patients who died, the preoperative PVR was higher than 1,000 dynes · second-1 · cm-5, making the mortality rate for patients with this degree of preoperative impairment 10.1% (18 of 179 patients). In individuals in whom the preoperative PVR was less than 1,000 dynes · second-1 · cm-5, the mortality rate was 1.3% (4 of 309 patients, p < 0.0001). The degree of postoperative residual PVR most strongly correlated with mortality rate. Patients with a postoperative PVR higher than 500 dynes · second-1 · cm-5 had a mortality rate of 30.6% (15 of 49 patients), whereas individuals with a postoperative PVR less than 500 had a mortality rate of 0.9% (4 of 434 patients, p = < 0.0001).
During the time of study, 17 additional patients who had pulmonary endarterectomy were excluded from this series. These patients did not have thromboembolic pulmonary disease; rather 9 were found to have pulmonary artery neoplasia (angiosarcoma), 6 had pulmonary arteritis (diagnosed by microscopy) with stricture formation, and 2 had fibrosing mediastinitis. In all these patients, because of atypical appearances on angiography, the correct diagnosis was suspected but not proven before operation. One patient of these 17 (6%) died.
We previously described a method of patient classification based on the location and morphology of thromboembolic and vascular wall disease found at the time of operation [2, 4]. The results of operation correlated with the classification type, as confirmed in this series. In this cohort of 500 patients, 187 (37.4%) were type 1—fresh or organized clot in the main or lobar pulmonary arteries; 245 (49%) were type 2—intimal thickening and fibrosis without visible thrombus; 60 (12%) were type 3—fibrosis, intimal webbing, and thickening within distal segmental arteries only (no visible thrombus); and 8 (1.6%) were type 4—microscopic distal arteriolar vasculopathy. Type 4 patients represent a group with pulmonary hypertension not directly related to pulmonary embolism and are not benefited by pulmonary endarterectomy [2]. Table 1 shows the hemodynamics and results for all patients overall and as classified by type.
Comment
Unappreciated incidence
Pulmonary hypertension as a result of pulmonary embolism is an unappreciated but major cause of morbidity and mortality. Its incidence is difficult to calculate because of the uncertainty regarding the frequency of acute pulmonary embolism and the proportion of patients with acute pulmonary emboli in whom embolic residua fail to resolve. In 1975, Dalen and Alpert [5] calculated that pulmonary embolism resulted in 630,000 symptomatic episodes in the United States, making it about half as common as acute myocardial infarction and three times more common than cerebrovascular accidents. They also estimated that pulmonary embolism caused approximately 200,000 deaths yearly in the United States (the sole contributing cause of death in 100,000 and the major contributing cause in another 100,000) and as such was the third most frequent cause of death. However, the true incidence of acute pulmonary embolism is unknown because many (if not most) of the episodes are asymptomatic.
Because emboli resolve completely in most patients, it is unclear why some individuals progress to chronic pulmonary hypertension. Approximately 10% of patients with chronic thromboembolic pulmonary hypertension have a coagulation abnormality, such as protein S or C deficiency, whereas a smaller cohort have defects in the fibrinolytic system [2]. In addition, some cases may be caused by repetitive pulmonary emboli, in situ propagation of a clot into branch pulmonary vessels, or embolization of partially organized thrombus. In many patients, chronic pulmonary hypertension may be a combination of these factors. The pathologic progression from acute embolism to end-stage pulmonary hypertension is therefore thought to be a multifactorial process that occurs over months to years. Failure of the initial embolus to resolve can also lead to secondary vasculopathy within the arterioles of the lung, resulting in microvascular muscular thickening and occlusion, similar to that seen in primary pulmonary hypertension and Eisenmenger syndrome [2, 4, 6]
Whatever the incidence of acute pulmonary emboli, chronic thromboembolic pulmonary hypertension is estimated to result after only 1% to 5% of all cases of acute pulmonary embolism [2, 7, 8]. However, the chronic disease process, even when established and symptomatic, is commonly unrecognized because of the nonspecific nature of the two major symptoms, effort dyspnea and fatigue, and the fact that physical findings may be elusive until right heart failure supervenes. Autopsy series concentrating specifically on pulmonary artery pathology found that 30% of cases had gross evidence of recurrent emboli and an additional 34% had stigmata of partial resolution [2]. Calculations extrapolated from mortality rates and the random incidence of major thrombotic occlusion found at autopsy could support a estimate that more than 100,000 people in the United States currently suffer from pulmonary hypertension that could be relieved by operation.
Chronic pulmonary hypertension from thrombotic disease carries a poor prognosis, which is proportional to the severity of pulmonary hypertension. Reidel and colleagues [9] followed up 147 patients with pulmonary hypertension with serial right heart studies and pulmonary arteriograms, and they found that patients with mean pulmonary artery pressure more than 30 mm Hg had a 30% 5-year survival rate. Those with pressures more than 50 mm Hg had a 10% survival rate at 5 years. These findings were confirmed by a more recent study [10].
Treatment
Medical therapy with anticoagulant drugs, thrombolytic agents, or vasodilator drugs has not been shown to affect the prognosis [2]. However, the lungs are unique in that embolization uncommonly results in tissue necrosis (because of the bronchial circulation); therefore, subsequent endarterectomy of occluded pulmonary vessels allows the distal pulmonary tissue to be recruited once more to assist in gas exchange. Surgical therapy is curative, and with few exceptions [11] is regarded as permanent. Long-term outcome after pulmonary thromboendarterectomy has also been studied by our group. In 308 patients (mean age, 56 years [range, 19 to 89 years]) with a mean of 3.3 ± 2.7 years since the operation (range, 1 to 16 years), survival, functional status, quality of life, and the subsequent use of medical help were assessed. Survival after pulmonary thromboendarterectomy was 75% at 6 years or more. Ninety-three percent of the patients were found to be in New York Heart Association class I or II [12].
Historical perspective of surgical treatment
Trendelenburg described an operative approach for acute pulmonary embolism in 1908 [13] using inflow occlusion. However, success with this operation was rare, and a significant milestone in the application of acute pulmonary embolectomy was the use of cardiopulmonary bypass to allow a careful and more thorough approach, as first described by Cooley and associates in 1961 [14].
The entity of chronic occlusion of the pulmonary arteries was not recognized until its description at autopsy in 1928 by Lungdahl [15]. A review in 1956 stated, "it is probable that no more than 200 cases of the syndrome have been reported in the medical literature to date" [7]. In any event, the impression at that time was that chronic thrombotic occlusion was not amenable to surgical correction.
Carroll [16] described the first operation on a patient with chronic thrombotic occlusion of the pulmonary arteries. The patient underwent a left thoracotomy at Johns Hopkins Hospital in January 1948 by Dr Alfred Blalock. The left pulmonary artery was found to be small, with proximal occlusion, although aspiration with a needle produced red blood. The artery was divided and found to contain organized thrombus. No attempt was made to relieve the obstruction, and the situation was thought to be inoperable. The patient was discharged from the hospital unimproved.
In May 1962, Dr Charles Hufnagel operated on probably the first patient in whom the diagnosis was made preoperatively, and successful correction was achieved [17]. The operation showed that extensive, well-organized thrombi, which obstructed major pulmonary vessels for months to years, could be removed successfully. Furthermore, the reclaimed lung areas were shown to be able to accept safely the sudden return of blood flow and to resume adequate respiratory function. In 1984, Chitwood and colleagues [18] reviewed the world's literature and found 85 cases managed surgically, with a mortality rate of 22%.
In 1970, Nina Braunwald performed the first operation at UCSD [1]. This patient was a 67-year-old human whose operation was done through a right lateral thoracotomy; cardiopulmonary bypass was used. The patient was discharged from the hospital and returned to full activity.
Moser and Braunwald observed that the patient had a "two compartment pulmonary vascular bed." The open pulmonary arteries probably had advanced changes of pulmonary hypertension, but the closed vascular bed, which had never been exposed to high pressures, had retained normal structure. In this patient the thromboembolism was known to have been present for 10 years or more, and this was the first documentation of the ability to remove such material and to achieve long-term patency at operation. The pulmonary vascular resistance decreased from 1208 to 640 dynes · second-1 · cm-5, and the patient was discharged well.
Drs Daily, Utley, and Dembitsky, who together performed the next 187 cases in the UCSD series in the 20 years between 1970 and 1989, made progressive modifications of the surgical technique, including the use of a median sternotomy and hypothermic circulatory arrest. Two of the authors of this paper did the subsequent 1,400 cases.
Improvements in technique
In 1993, the first 323 patients in the UCSD series were described [3]. Changes had been made in the surgical management of the cohort comprising the last 150 patients in that group, which improved results, with more expeditious removal of occluding material and shorter circulatory arrest times. These changes included more proximal incisions, an approach to the right side beneath the superior vena cava rather than above it, and avoidance of more than one arteriotomy on each side. The method of raising the endarterectomy plane posteriorly and leaving normal pulmonary artery in the region of the incision resulted in less leakage from suture lines.
When we compared circulatory arrest times in the 150 patients operated on between November 1989 and March 1992 with the 100 immediately preceding patients operated on between October 1987 and October 1989, we found a reduction in circulatory arrest times from a mean of 59.16 ± 23.03 minutes to 36.46 ± 16.60 minutes (p < 0.0001). The mortality rate decreased from 17.0% to 8.7%.
In the present series, the mean circulatory arrest time was 36 ± 11.89 minutes. The mortality rate was 4.4%. Although the circulatory arrest times have remained the same, the mortality rate has gradually decreased. The mortality rate for the entire 1,500 cases in our experience was 7.5%, compared with 6.7% for the last 1,000. We have progressively accepted more complicated patients for operation, including patients in whom it is clear that thromboembolic disease is only part of the pulmonary hypertension they present. Operation on more distal disease (type 3) [2, 4] is more time-consuming and requires longer periods on bypass but is still able to restore the pulmonary circulation.
Neurologic injury preventing extubation and normal patient recovery is no longer seen with this operation. Although reasons for this are multifactorial, we believe that a substantive advance in cerebral protection during pulmonary endarterectomy is the use of the cooling jacket placed around the head. This head-wrap had been used in more than 1,000 pulmonary endarterectomies at our institution without complication, and it provides even cooling to the surface of the cranium, particularly in the posterior location. It is easier to apply circumferentially than ice bags and has not been associated with skin necrosis, as has been seen with other topical cooling modalities.
The largest risk factor for operation remains the degree of operability as assessed by PVR. A high PVR without gross changes on angiogram signifies secondary vasculopathy –an inoperable change and a degree of postoperative pulmonary hypertension that will likely hinder recovery. The mortality rate was 30.6% when the residual PVR was higher than 500 dynes · second-1 · cm-5 but only 0.9% when it was below this level. This disease represents not direct thromboembolic occlusion, but rather vascular obstruction at the capillary level, be this a reflection of primary pulmonary hypertension or changes in the pulmonary vascular bed as a result of redirection of pressure or flow as a result of mechanical obstruction in the closed bed. Interestingly, this observation was made by Moser and Braunwald after their first San Diego case in 1971 [1]. Current studies in the laboratory may provide insight into the molecular pathogenesis of these changes [6, 19].
Acknowledgments
Cleonice Gordon and David Garcia were invaluable in data analysis. Reena Deutsch assisted in the statistical analysis. Reena Deutsch is funded by General Clinical Research Center grant National Institutes of Health M01 RR00827.
Discussion
DR CHRISTOPHER G. MCGREGOR (Rochester, MN): First of all, I would like to thank the authors for sending me the manuscript in a timely fashion. I would like to congratulate Dr Jamieson and his team for the development of the world's leading pulmonary endarterectomy practice, which is testimony not only to your surgical skill but to the organization of the team approach to the management of this demanding disease. In this paper the authors have demonstrated progressive excellence in outcomes of pulmonary endarterectomy, establishing the gold standard for both surgical mortality rate and hemodynamic outcomes.
I and others in the field would like to acknowledge Dr Jamieson's group for education of colleagues in the United States and overseas about the disease itself, patient selection, and surgical techniques. They have been gracious hosts to many of us in San Diego. In addition, you are to be congratulated not just for the development of the clinical practice but also for developments in the basic laboratory research—by Dr Thistlethwaite and other members of Dr Jamieson's team—in the pathogenesis of chronic thromboembolic pulmonary hypertension. I would like to focus on the specific lessons from this paper regarding the surgical risks for individual patients who undergo pulmonary endarterectomy.
You outlined that a learning curve exists for this operation, with a 17% mortality in the San Diego group in the first 200 patients in the series, decreasing to 4.4% for the last 500 patients. This experience reflects our own smaller experience where the operative mortality rate in our own program decreased from 19% in the first 21 patients operated on before 1997 to 4.6% in the most recent 43 consecutive patients. Hemodynamic outcomes, interestingly, have been almost identical between our own program and the UCSD program, with a dramatic decrease in mean pulmonary artery pressure to a range where we know that prognosis is good.
In your presentation, Dr Jamieson, you stated that major preoperative risk factors included a pulmonary vascular resistance of 1,000, especially in the context of limited angiographic disease, but that preoperative right ventricular function was not a risk factor. Because of the availability of ultrafast computed tomography at our institution, we have been able to develop some unique data confirming that improvement in right ventricular ejection fraction is consistent no matter what the original preoperative calculation is.
As you can see in the slide, right ventricular ejection fraction in a recent cohort of 37 patients improved significantly, from 36% to 51%. Similar improvement occurred across the spectrum of preoperative right ventricular ejection fraction levels. So no matter how low the initial right ventricular ejection fraction was, there is a real possibility for improvement after pulmonary endarterectomy.
Associated with this increase in right ventricular ejection fraction is a decrease in right ventricular end-diastolic volume, from a mean of 254 mL before pulmonary thoracoendarterectomy PTE to 157 mL after the procedure. You also describe the high operative risk when residual pulmonary vascular resistance is greater than 500, especially if only a limited endarterectomy is possible.
I have a number of questions for the speaker. First, can you comment on the wider application of this surgical procedure in terms of appropriate medical and surgical resources, commitment, and number of cases?
Second, do you believe that pulmonary angiography remains absolutely necessary as part of the preoperative evaluation of the patient, or can computed tomography be substituted?
Third, what happens to patients who do have a residual pulmonary vascular resistance greater than 500? How do we follow up these patients?
With the great improvement in outcomes that you have described today, should the threshold in terms of symptoms for recommending pulmonary endarterectomy be changed, ie, lowered, in the setting of significant elevation of a pulmonary vascular resistance as we know that the disease will likely progress and be fatal? In other words, should patients be operated on earlier, if possible, even with limited symptoms?
And finally, is there still a place in rare circumstances for lung transplantation in patients with a pulmonary vascular resistance greater than 1,000 and the presence of limited angiographic disease?
DR ALVAN W. ATKINSON (Raleigh, NC): I have several questions. One, would magnetic resonance imaging be more favorable than computed tomography for staging these patients? Could you give us a little insight on some stratification of risk in terms of magnetic resonance imaging, computed tomography, or angiographic findings?
Would all patients need a filter postoperatively, or is there some selection to that, whether anticoagulation is tolerated or not?
And finally, I know there is a new drug out for treatment of pulmonary hypertension, and I wondered if you have any experience with it preoperatively perioperatively, or postoperatively?
DR JOSEPH E. BAVARIA (Philadelphia, PA): I congratulate you on a fantastic series. We have performed about 200 of those operations since Dr L. Henry Edmunds visited Dr Daily in San Diego during the mid-1980s. One of the things we have noticed in last 5 years or so is that our results are better if there is no significant concomitant pulmonary disease. In other words, we do better if we make sure there is no IPF, chronic obstructive pulmonary disease, or other nonvascular pulmonary diagnosis which will compromise postoperative results. Would you like to comment on your preoperative pulmonary risk evaluation?
DR ANDREA M. D'ARMINI (Pavia, Italy): Congratulations on your excellent presentation. I have a question. Did you see any difference in outcome based on duration of the disease and how long the patient was classified New York Heart Association class III or IV? Considering the natural progression of chronic thromboembolic pulmonary hypertension to irreversible right cardiac failure, did you see better results in patients with a shorter duration of the disease? If so, could this be a reason to perform this operation in patients still classified as New York Heart Association class II?
DR JAMIESON: I would like to thank you very much for your kind comments. I think we all realize that it is our responsibility to teach what we learn, and we have tried to do this. If any credit is to be given to our effort with this disease, it of course goes to the team, without whom success would not be possible.
With regard to the first question about the wider application of pulmonary endarterectomy in terms of resources and commitment, this is a difficult question because there is definitely a learning curve to the procedure and, unquestionably, a team approach is necessary. Perhaps at least a commitment to the procedure with a minimum volume of 10 or 20 cases a year would be a reasonable objective.
Regarding pulmonary angiography, there is some risk with the procedure but it is not high. We have done probably 5,000 pulmonary angiograms with no mortality and very limited morbidity. There are other techniques, as the subsequent discussant mentioned. I think whether you absolutely need to use angiography really depends on the pulmonary vascular resistance, because the most fundamental risk is to operate on a patient in whom the pulmonary vascular resistance is out of context with the degree of angiographic obstruction. I would suggest, perhaps, as a compromise that if the pulmonary vascular resistance is below 500, it is not absolutely necessary to do an angiogram. Otherwise it probably is, in order to get an exact road map for the technical portions of the procedure and to match the degree of angiographic obstruction with the pulmonary vascular resistance.
With regard to the threshold of when we should be doing pulmonary endarterectomy, I believe absolutely that we should be doing it earlier. We have become increasingly aware of the secondary changes that occur in the pulmonary vascular bed because of increased pressure and flow in the open vessels, and that, of course, is eventually inoperable.
With regard to the place of lung transplantation, we have applied lung transplantation in perhaps half a dozen patients in whom we were not able to get a good result because of type 3 or type 4 disease. I suppose that if patients were clearly at very high risk and the angiographic appearances suggested that they would get limited benefit, then serious consideration of transplantation should be given at that time. Other factors to be weighed in the decision here would be the projected length of time on the waiting list and the likelihood of a suitable donor.
With regard to follow-up, I think follow-up with pulmonary artery pressures could largely be done with echocardiography.
To answer the question about the filter, we believe it is important that all patients have an inferior vena cava filter placed preoperatively.
With regard to the newer drugs coming out for treatment of pulmonary hypertension, these are immensely promising. But of course, this is a mechanical condition. It cannot be treated by angioplasty; it can only be removed by open operation. And you might tide somebody through temporarily and improve the condition somewhat before the operation by using pulmonary vasodilating agents, but in the end the only thing that will help is physical removal of the obstruction.
Dr Bavaria brought up an important question about the comorbidities of the patient, particularly with regard to lung function, and I think the answer depends on the assessment of how much residual lung function will be left once you have a normal vascular supply to the lung.
I am sorry, Dr D'Armini, that we did not have time to discuss in more detail the preoperative status of the patients. However, there is no question that if there is mechanically occluding disease causing pulmonary hypertension, no matter where it is in the pulmonary vascular bed, this can be removed at operation, and delay is not in the patient's interest. I think occluding material can be removed at any time period, even many years after obstruction, and there is ample justification for doing this before the patient becomes severely ill.
References
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W. Klepetko, E. Mayer, J. Sandoval, E. P. Trulock, J.-L. Vachiery, P. Dartevelle, J. Pepke-Zaba, S. W. Jamieson, I. Lang, and P. Corris Interventional and surgical modalities of treatment for pulmonary arterial hypertension J. Am. Coll. Cardiol., June 16, 2004; 43(12_Suppl_S): 73S - 80S. [Abstract] [Full Text] [PDF]
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