| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
Ann Thorac Surg 1999;68:1770-1776
© 1999 The Society of Thoracic Surgeons
a Division of Cardiothoracic Surgery, University of California, San Diego, California, USA
b Division of Pulmonary and Critical Care Medicine, University of California, San Diego, California, USA
Address reprint requests to Dr Jamieson, Division of Cardiothoracic Surgery (8892), University of California, San Diego, 200 West Arbor Dr, San Diego, CA 92103-8892
e-mail: sjamieson{at}ucsd.edu
Presented at the Thirty-fifth Annual Meeting of The Society of Thoracic Surgeons, San Antonio, TX, Jan 25–27, 1999.
 |
Abstract |
|---|
 Top Abstract IntroductionPatients and methodsResultsCommentReferences |
|---|
Methods. Since 1990, 13 of 870 (1.5%) patients underwent reoperative PTE at our institution. These 7 men and 6 women (mean age 38.6 years) were contrasted with the most recent 225 patients (111 men, 114 women, mean age 52.7 years) who underwent primary PTE for whom complete hemodynamic data are available. The preoperative evaluation of all patients was similar. Pulmonary hemodynamic data and outcome measures were compared between groups.
Results. Of 13 reoperated patients: 69% (9/13) had their primary operation at another institution, 54% (7/13) initially underwent unilateral PTE, 38% (5/13) had identifiable coagulation disorders, 38% (5/13) had ineffective caval filtration, 31% (4/13) had suboptimal anticoagulation management, and 31% (4/13) had complete unilateral pulmonary artery obstruction. The mean interval to reoperation was 5.2 years (range 0.7 to 10.9 years). All control patients underwent bilateral PTE using hypothermic circulatory arrest. Operative mortality was 7.7% (1/13) with reoperation vs 8.4% (19/225) in controls. No difference (p = NS) was observed between groups in the preoperative pulmonary artery pressure (PAP) or pulmonary vascular resistance; however, the control group had a significantly (p < 0.05) greater reduction in the postoperative PAP (46/19, mean 28 mm Hg vs 59/23, mean 35 mm Hg) and PVR (271 ± 172 vs 399 ± 154 dynes/s/cm-5) compared with the redo group. No substantial difference in morbidity or functional outcomes was observed between groups.
Conclusions. Reoperative PTE can be performed with a perioperative risk comparable with primary PTE, although the improvement in pulmonary hemodynamics is not as favorable. Bilateral primary operation, effective caval filtration, and vigilant anticoagulant management would prevent the need for most reoperative PTEs.
|
Introduction |
|---|
|
TopAbstractIntroductionPatients and methodsResultsCommentReferences |
|---|
Our institution has been engaged in a program for the surgical management of chronic thromboembolic pulmonary hypertension since 1970. In that interval, over 1,100 pulmonary thromboendarterectomies (PTE) have been performed, although the majority (n = 910) have been performed by two surgeons (S.W.J. and D.P.K.) at our facility within the past decade [5–9]. The success with surgical intervention in this group of difficult patients has been substantial, with a mortality of 6.4% in the last 500 cases performed, and with 95% of surviving patients in New York Heart Association (NYHA) class I or II at 1 year postoperatively [10]. The natural history of patients with chronic thromboembolic pulmonary hypertension after PTE remains unclear, although our experience suggests that relatively few patients develop recurrent disease.
Despite 5%–10% of patients having a defined coagulation abnormality, such as lupus anticoagulant, protein C deficiency, antithrombin III deficiency, or heparin-induced platelet antibody, the vast majority of cases of thromboembolic pulmonary hypertension are due to "spontaneous" thromboembolism. Additionally, although we have previously documented a greater risk for recurrent thromboembolic pulmonary hypertension with unilateral PTE and unilateral PA obstruction [11], the risk factors for recurrent disease and the selection criteria for reoperation remain poorly defined. Likewise, analogous to other reoperative cardiac operation procedures [12, 13], it might be anticipated that a second PTE entails greater risk than the initial operation, although the extent of that risk remains unclear. Similarly, it can not be presumed that normal pulmonary blood flow and resistance, ie, the functional outcome, would be restored in all instances, although this is currently unsubstantiated.
The purpose of this study was to analyze our experience with patients undergoing repeat PTE to determine the specific risk factors for the development of recurrent disease, the selection criteria for reoperation, the relative risk for reoperation, and the functional outcome after reoperative PTE.
|
Patients and methods |
|---|
|
TopAbstractIntroductionPatients and methodsResultsCommentReferences |
|---|
Our routine preoperative evaluation for all patients with suspected chronic thromboembolic pulmonary hypertension has been reported previously [5–10]. In brief, this assessment entails a comprehensive medical history and physical examination; chest radiograph and electrocardiogram, pulmonary function studies, and arterial blood gas analysis; transthoracic echocardiography; radionuclide perfusion and ventilation scans; screening for recognized coagulation abnormalities; and right heart catheterization and pulmonary angiography [5, 6]. Although magnetic resonance imaging, computed tomography, and bronchial angiography can contribute important diagnostic information, at present, they lack sufficient resolution to detect disease originating at the origin of the segmental pulmonary artery branches. Accordingly, these modalities are not routinely utilized in our institution to determine operative candidacy. Fiberoptic pulmonary angioscopy is reserved for those patients (approximately 20%) with equivocal angiographic features of chronic thromboembolic disease [14].
In the absence of a precedent concerning repeat PTE, we reasoned that if the current angiogram demonstrated limited disease proximal to the origin of the segmental pulmonary arteries, deteriorating pulmonary hemodynamics could only be attributed to the progression of distal small vessel disease not accessible at reoperation. Accordingly, we believed that the most useful assessment when considering repeat PTE was a qualitative comparison of the current pulmonary angiogram with that preceding the primary operation (Fig 1). Patients excluded following this evaluation were considered for pulmonary transplantation.
|
|
The mean ± standard deviation are tabulated for all continuous variables. The unpaired Student’s t test, paired Student’s t test, and 
2 test were utilized for statistical analysis. A p value less than 0.05 was considered significant.
This study was performed under the auspices of the Institutional Review Board of the University of California, San Diego.
|
Results |
|---|
|
TopAbstractIntroductionPatients and methodsResultsCommentReferences |
|---|
|
|
None of the reoperated patients experienced a documented deep venous thrombosis or clinically recognized pulmonary embolism after their initial operation, although patient 3, with tricuspid endocarditis, suffered a paradoxical cerebral embolism. Despite documented chronic thromboembolic pulmonary disease, 5 of 13 (38%) redo patients had ineffective caval filtration. Caval filtration was never performed in patients 1, 2, or 3 before the recurrence of symptoms, while in patient 11, the caval filter was malpositioned, and in patient 9, occluded by thrombus.
Four of 13 (31%) redo patients had suboptimal anticoagulation management after the primary PTE, at variance with our established policy of lifelong anticoagulation of patients with this disease. Warfarin was discontinued within 2 years of operation in 2 patients (nos. 3 and 6), while in 2 additional patients (nos. 5 and 13), therapeutic prolongation of the INR was not adequately sustained.
Five of 13 patients (38%) in the reoperated cohort had a defined abnormality of coagulation. While this incidence is higher than in the reference group (22%), this difference was not statistically significant, nor was there a predominant coagulation defect among reoperated patients.
Notably, 4 patients (31%) in the reoperated series had complete unilateral occlusion of the pulmonary arteries, compared with only 16 of 225 patients (7%) in the control group, which represented a significantly higher incidence (p < 0.01). Postoperative radionuclide perfusion scans demonstrated variable improvement in the 12 surviving reoperated patients. No flow was reestablished in patients 6 or 12, minimal flow in patient 7, whereas only patient 9 demonstrated a significant improvement in flow to the unilaterally occluded lung after reoperation. The low incidence (25%) of reperfusion in these 4 patients is comparable with our previously reported experience of absent reflow (8 of 16, 50%) among primarily operated patients presenting with complete unilateral pulmonary artery obstruction [11].
Survival
The 7.7% (1 of 13) operative mortality among redo patients did not differ (p > 0.05) from the 8.4% (19 of 225) mortality among primary patients in this series, although the previously reported operative mortality in a larger cohort of 500 primary PTE patients was 6.4% (10). The single death among reoperated patients (patient 13) occurred on postoperative day 6, when hypotension from refractory supraventricular tachycardia (SVT) precipitated cardiac arrest. The 1- and 3-year actuarial survival, at a mean follow-up of 3.4 years after reoperation, was 92% and 82%, respectively. One patient (patient 1) died 1.3 years after reoperation of progressive respiratory failure due to preexistent idiopathic pulmonary fibrosis. A second patient (patient 7) with lupus anticoagulant antibody, complete unilateral pulmonary artery obstruction, and minimal reperfusion after reoperation died of progressive right heart failure 4.5 years after repeat PTE. The 1- and 3-year actuarial survival among primarily operated patients was 90% and 81%, respectively.
Pulmonary hemodynamics
The preoperative pulmonary artery pressures (pulmonary artery systolic/diastolic; mean PAP in mm Hg) were equivalent (p = NS) between the redo patients (82 ± 13/31 ± 6; 49 ± 8) and the reference cohort (80 ± 22/31 ± 10; 48 ± 14). Likewise, the preoperative pulmonary vascular resistance (PVR) (dynes/s/cm-5) was similar (p = NS) between the reoperative PTE patients (862 ± 332) and the primary PTE patients (842 ± 431) (Figs 3 and 4; Table 2). In each patient, pulmonary angiography depicted significant obstruction of the central arteries (Fig 1).
|
|
The relative reduction in postoperative PAP between redo patients (59 ± 18/23 ± 8; 35 ± 11) and primary PTE patients (46 ± 16/19 ± 7; 28 ± 9) was greater in the reference cohort (p < 0.01). Similarly, the reduction in PVR observed in the primary PTE patients (271 ± 172) was greater (p < 0.01) than that observed in the redo PTE patients (399 ± 154) postoperatively (Figs 3 and 4; Table 2).
Functional outcome
Eleven of 13 redo patients experienced a functional benefit after their initial PTE, but developed recurrent symptoms of pulmonary hypertension from 6 months to 10 years after the primary operation (mean 2.7 ± 2.8 years). The mean interval to reoperative PTE was 5.2 years ± 2.7 years (range 8 months to 10.9 years). Immediately before the second PTE, the majority of patients were NYHA class III (11 of 13, 85%) or class IV (1 of 13, 8%). The exception was the patient with paradoxical embolism, who was in NYHA class II (Fig 5).
|
Surgical management
Indicative of the greater difficulties encountered during repeat PTE, the cumulative duration of circulatory arrest (45 ± 19 vs 35 ± 14 minutes, p < 0.05), and the aortic cross-clamp time (127 ± 14 vs 97 ± 41 minutes, p < 0.01) were prolonged in the reoperated patients. The duration of cardiopulmonary bypass was also prolonged (249 ± 51 vs 225 ± 50 minutes), although not significantly (p > 0.05).
Notwithstanding the increased technical challenge of repeat PTE, substantial chronic thromboembolic material was recovered in each patient (Fig 2). The type of disease encountered in reoperative cases was different than that typically encountered in our primarily operated series. Among redo patients, 5 of 13 (38%) had type 1 disease (partially organized central thrombus proximal to organized distal thrombus), and 8 of 13 patients (62%) had type 2 disease (organized thrombus proximal to the origin of the segmental artery). In contrast, although type 2 disease predominates (70%) among primarily operated patients, only 10% historically demonstrate type 1 disease [15].
Complications
Despite the inherent risks of reoperative cardiac procedures, the incidence and nature of complications encountered in this reoperative series was comparable with those experienced after primary operation (Table 2). Two of 13 reoperated patients (15%) required reexploration for perioperative hemorrhage, significantly greater than the 2% (5 of 225) incidence of reexploration among primarily operated patients (p < 0.01). Four reoperated patients (31%) experienced significant perioperative rhythm disturbances (sinus node dysfunction in 1, and supraventricular tachycardia in 3 patients), nearly threefold greater than the incidence of arrhythmias experienced in the reference population (29 of 225, 13%; p < 0.05). Additionally, the incidence of reperfusion injury (6 of 13; 46% vs 75 of 225; 33%), the duration of mechanical ventilation (9.8 ± 12.3 days vs 5.1 ± 12.1 days), and the length of intensive care unit stay (11 ± 12.5 days vs 6.6 ± 12.7 days) was greater in reoperated patients, although none of these differences was statistically significant (p > 0.05 for all comparisons). Although 3 reoperated patients required more than 20 days of assisted ventilation, including patient 8, who was supported with extracorporeal carbon dioxide removal (ECCO2R) for 6 days, no patient in the reoperated series succumbed to respiratory failure.
|
Comment |
|---|
|
TopAbstractIntroductionPatients and methodsResultsCommentReferences |
|---|
The team at the University of California, San Diego Medical Center has benefited from an institutional experience of more than 1,100 PTE cases since the inception of this program in 1970 [7–9, 18]. While accumulating this experience, we have had the opportunity to consider reoperation for patients initially managed here as well as at other institutions. The purpose of this study was to determine the risk factors for recurrent thromboembolic disease, the selection criteria for reoperation, the relative risk of repeat PTE, and the functional benefit derived from reoperative PTE.
Generally, reoperative cardiac surgery is accompanied by a higher perioperative risk and reduced functional outcome compared with the equivalent primary procedure [12, 13]. Accordingly, an appreciation of the factors, technical and others, that may contribute to an unsatisfactory outcome after the primary operation can only serve to improve the results of primary operation and limit the likelihood that subsequent procedures will be necessary. Additionally, because PTE is almost invariably lethal whenever a significant improvement in pulmonary blood flow is not achieved, the selection criteria for reoperative PTE warrants particular scrutiny.
Seven of the 13 patients in this series initially underwent a unilateral primary operation, yet at reoperation, each of these 7 patients had significant bilateral chronic thromboembolic disease, as we found substantial thromboembolic material in the contralateral side of the prior surgery in these redo patients. In the comparison cohort of 225 patients, in whom bilateral pulmonary artery exploration was performed regardless of the preoperative findings, only 6 of 225 patients (2.7%) exhibited true unilateral disease. Accordingly, we believe that unilateral PTE for bilateral disease poses a substantial risk for early recurrence of symptomatic pulmonary hypertension.
Less certain were the possible causes of recurrent symptomatic pulmonary hypertension in those 6 patients who initially underwent bilateral PTE using our present technique, which employs profound hypothermia and circulatory arrest. While none of those patients had experienced a clinical episode consistent with recurrent deep venous thrombosis or pulmonary embolism, it must be recalled that thromboembolic events are clinically occult in the majority of patients [19]. Additionally, the possibility of in situ thrombosis of portions of the previously endarterectomized proximal vascular bed cannot be excluded by present means [20]. Each of the patients in the reoperated series, except patient 8, had at least one recognized risk factor for recurrent disease, eg, coagulation disorder, poor anticoagulation management, ineffective caval filtration, or complete unilateral PA obstruction, that could have predisposed to a thrombotic or embolic event. While it can be argued that differentiation between these two possibilities is of academic interest only, the essential observation remains that scrupulous prophylaxis may have eliminated the need for reoperation in these patients.
The validity of our initially empiric selection criteria, based predominantly on the pulmonary angiogram, appears to be verified by the outcomes achieved in this small sample of patients. In each instance, at operation, we were able to identify a suitable plane of dissection and extract significant chronic thromboembolic material from both lungs, even when the prior operation was bilateral (Fig 2). Though the improvement in pulmonary blood flow was not as great as could be accomplished in primarily operated patients (Figs 3 and 4), the majority of reoperated patients experienced some sustained increment in functional class (Fig 5). Notwithstanding the difficulties encountered at reoperation, and despite higher perioperative morbidity, these benefits were attained without incurring a substantially greater mortality than in primarily operated patients. While the benefits identified among those patients with complete unilateral pulmonary artery obstruction suggest that this cohort should undergo reoperation with only limited expectations, we believe that reoperation with this caveat is preferable to either pulmonary transplantation or inexorable right heart failure and premature death.
|
References |
|---|
|
TopAbstractIntroductionPatients and methodsResultsCommentReferences |
|---|
This article has been cited by other articles:
|
|
 |
|
  H. J. Reesink, J. T. Marcus, I. I. Tulevski, S. Jamieson, J. J. Kloek, A. V. Noordegraaf, and P. Bresser Reverse right ventricular remodeling after pulmonary endarterectomy in patients with chronic thromboembolic pulmonary hypertension: Utility of magnetic resonance imaging to demonstrate restoration of the right ventricle J. Thorac. Cardiovasc. Surg., January 1, 2007; 133(1): 58 - 64. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. Peacock, G. Simonneau, and L. Rubin Controversies, Uncertainties and Future Research on the Treatment of Chronic Thromboembolic Pulmonary Hypertension Proceedings of the ATS, September 1, 2006; 3(7): 608 - 614. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H. R. Buller, G. Agnelli, R. D. Hull, T. M. Hyers, M. H. Prins, and G. E. Raskob Antithrombotic Therapy for Venous Thromboembolic Disease: The Seventh ACCP Conference on Antithrombotic and Thrombolytic Therapy Chest, September 1, 2004; 126(3_suppl): 401S - 428S. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. L. Doyle, D. McCrory, R. N. Channick, G. Simonneau, and J. Conte Surgical Treatments/Interventions for Pulmonary Arterial Hypertension: ACCP Evidence-Based Clinical Practice Guidelines Chest, July 1, 2004; 126(1_suppl): 63S - 71S. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. W. Jamieson, D. P. Kapelanski, N. Sakakibara, G. R. Manecke, P. A. Thistlethwaite, K. M. Kerr, R. N. Channick, P. F. Fedullo, and W. R. Auger Pulmonary endarterectomy: experience and lessons learned in 1,500 cases Ann. Thorac. Surg., November 1, 2003; 76(5): 1457 - 1464. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
F. Sakamaki, S. Kyotani, N. Nagaya, N. Sato, H. Oya, and N. Nakanishi Increase in Thrombomodulin Concentrations After Pulmonary Thromboendarterectomy in Chronic Thromboembolic Pulmonary Hypertension Chest, October 1, 2003; 124(4): 1305 - 1311. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 I Cerveri, A M D'Armini, and M Vigano Pulmonary thromboendarterectomy almost 50 years after the first surgical attempts Heart, April 1, 2003; 89(4): 369 - 370. [Full Text] [PDF]
|
|
|
|
 |
|
 M. B. Streiff Vena Caval Filters: A Review for Intensive Care Specialists J Intensive Care Med, March 1, 2003; 18(2): 59 - 79. [Abstract] [PDF]
|
|
|
|
|
|
P. A. Thistlethwaite, M. Mo, M. M. Madani, R. Deutsch, D. Blanchard, D. P. Kapelanski, and S. W. Jamieson Operative classification of thromboembolic disease determines outcome after pulmonary endarterectomy J. Thorac. Cardiovasc. Surg., December 1, 2002; 124(6): 1203 - 1211. [Abstract] [Full Text]
|
|
|
|
 |
|
 P. F. Fedullo, W. R. Auger, K. M. Kerr, and L. J. Rubin Chronic Thromboembolic Pulmonary Hypertension N. Engl. J. Med., November 15, 2001; 345(20): 1465 - 1472. [Full Text] [PDF]
|
|
|
|
|
|
P. A. Thistlethwaite, W. R. Auger, M. M. Madani, S. Pradhan, D. P. Kapelanski, and S. W. Jamieson Pulmonary thromboendarterectomy combined with other cardiac operations: indications, surgical approach, and outcome Ann. Thorac. Surg., July 1, 2001; 72(1): 13 - 18. [Abstract] [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| ANN THORAC SURG | ASIAN CARDIOVASC THORAC ANN | EUR J CARDIOTHORAC SURG |
| J THORAC CARDIOVASC SURG | ICVTS | ALL CTSNet JOURNALS |
