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Ann Thorac Surg 1996;62:1253-1254
© 1996 The Society of Thoracic Surgeons
Department of Medicine, Washington University School of Medicine, St. Louis, Missouri
Recognition of chronic organized thromboemboli as a cause of sustained pulmonary hypertension and the development of a surgical approach to the disease have been major steps in establishing chronic thromboembolic pulmonary hypertension as one of the few potentially curable causes of pulmonary hypertension [1–3]. Increasing experience with this disease at a number of centers now indicates that we can successfully treat many of these patients by thromboendarterectomy after selection by appropriate diagnostic evaluations. As with most diseases, we still have many unanswered questions, some of which have emerged from our ability to remove the obstructing material. The article in this issue by Hartz and colleagues [4] suggests some of these important questions.
We do not know why the vast majority of patients presenting with this problem do not have normal resolution of their acute thrombotic obstruction. Only a minority have identifiable procoagulant tendencies, most commonly the presence of antiphospholipid antibodies. The remainder have no known risk factors and are the subject of active investigation, although studies to date have not identified defects in blood vessel-related lytic mechanisms [5].
Some problems raised by the surgical treatment have become clear with time. The unusual neuropsychiatric abnormalities that patients may experience postoperatively are related to total time of circulatory arrest [6] and are probably caused by cerebral edema and related metabolic changes. Although distressing, these changes are transient.
The most troubling postoperative management problems have been related to postoperative ventilatory insufficiency, usually associated with persistent hypoxemia, elevated pulmonary artery pressure, elevated pulmonary vascular resistance, and reperfusion edema. These problems are probably multifactorial in origin, but we need to isolate factors that may predict outcome from this complex group of patients. Hartz and colleagues [4] found in their series of 34 patients that operative mortality was associated with high preoperative pulmonary artery pressure (mean, 62.1 mm Hg) and high preoperative pulmonary vascular resistance (mean, 1,512 dynes•s•cm-5). These findings are interesting and suggest that severity of disease may affect outcome. Daily and associates [3], however, in their series of 127 patients, did not find preoperative hemodynamic measurements to be predictors of outcome. Instead they found that a failure to lower pulmonary vascular resistance postoperatively by more than 50% was a predictor of mortality as was longer time of complete circulatory arrest. These factors seem to suggest that the inability to remove sufficient obstructing material or difficulty in removing the material with subsequent vascular damage may have been factors in survival. Because Hartz and colleagues observed incomplete removal of obstructing material in 6 of 8 autopsy cases, inadequate relief of obstruction may be a factor in this current series as well.
It is particularly interesting that a graded analysis of pulmonary artery obstruction and relief of obstruction in Daily and associates' series suggested no correlation between the percentage of material removed and the postoperative change in pulmonary vascular resistance. One interpretation of the findings in both these series is that the distal microvasculature may be an important factor in outcome, a factor that cannot necessarily be predicted from our preoperative evaluation. It was long assumed that the vascular bed distal to the obstruction was patent and even atrophic because of lack of flow. We know that the distal bed is actually supplied by an extensive network of bronchial collateral vessels and is usually far from stagnant. Bronchial flow may account for more than 25% of cardiac output in chronic pulmonary artery obstruction [7]. We also now know that the obstructed vascular bed demonstrates changes consistent with pulmonary hypertension [8], although it is not exposed to high flow or high pressure. In an animal model of chronic pulmonary artery obstruction, Bloom and I [9] have found that similar changes can be induced and that these changes (intimal fibrosis, medial hypertrophy, plexiform lesions) are associated with signs of endothelial injury. We have also found that they can be prevented in the animal model by treatment with heparin, probably related to heparin's antiproliferative effect rather than to its antithrombotic properties. These changes suggest that reperfusion edema may simply be the unmasking of an already injured bed by the establishment of normal flow rates and subsequent leakage.
These remodeling changes are reversible in many patients, because reperfusion edema is generally self-limited and lung scan perfusion patterns slowly return toward normal over a period of months after successful thromboendarterectomy. We do not know if the duration of pulmonary artery obstruction or the severity of pulmonary hypertension influences the severity of these postobstructive changes. These will be important questions to answer.
It also appears that some patients may fail to experience a postoperative decrease in pulmonary vascular resistance because of microvascular obstruction related to old thrombi in situ or an arteritis. Patients with procoagulant tendencies and those with systemic lupus erythematosis may fall into this category. We are currently examining data from such patients.
At the present time, we can only continue to search for preoperative predictors of unacceptable mortality. Until we know more, thromboendarterectomy still offers the best hope for cure of a life-threatening disease. Increased community awareness of the problem as a cause of unexplained dyspnea is also important and can lead to earlier detection and treatment before severe pulmonary hypertension and disability develop. For now, patient selection for thromboendarterectomy still needs to be based on assessment of surgical accessibility by angiography (and angioscopy when appropriate) and consideration of comorbid disease.
Footnotes
Address reprint requests to Dr Shure, Pulmonary and Critical Care Medicine, Barnes-Jewish Hospital North, 216 S Kingshighway, St Louis, MO 63110.
References
Related Article
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  P. Mares, T. B. Gilbert, E. M. Tschernko, M. Hiesmayr, M. Muhm, A. Herneth, S. Taghavi, W. Klepetko, I. Lang, and W. Haider Pulmonary Artery Thromboendarterectomy: A Comparison of Two Different Postoperative Treatment Strategies Anesth. Analg., February 1, 2000; 90(2): 267 - 267. [Abstract] [Full Text] [PDF]
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 S. K. Kolvekar, G. J. Peek, A. W. Sosnowski, R. K. Firmin, R. S. Hartz, and M. J. Davies Extracorporeal Membrane Oxygenator for Pulmonary Embolism Ann. Thorac. Surg., September 1, 1997; 64 (3): 883 - 884. [Full Text]
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