Heart-Lung Transplantation

Dr. Robin proposes that the problem of increasing asthma mortality be addressed with considerable urgency This is being done by the Asthma Mortality Task Force, a collaborative project of the American Academy of Allergy and Immunology and the American Thoracic Society A Workshop was held in November 1986 to bring together epidemiologists, pathologists, physiologists, clinicians, pharmacologists and behavioralists from academia, clinical medicine and industry to review the evidence relating to asthma mortality The proceedings of the Workshop have been published." The Task Force now takes on the much harder job of putting into effect the recommendations of the Workshop, mostly relating to the need for further information in specific areas and for education of health professionals and the lay public. The important message for the practicing physician is that patients with asthma can die from their disease as well as with their disease. The challenge is to identify the asthmatic at greatest risk. We need to know more before we can do this with accuracy Meanwhile, we should keep in mind that all asthmatic patients are potentially vulnerable and all anti-asthma medications have some risk. It is also worth remembering that we, as physicians, are responsible for the reliability of mortality statistics. I would be remiss if I did not emphasize that undertreatment rather than overtreatment has repeatedly been indicted as the probable cause of the "epidemic" of asthma deaths that occurred in the United Kingdom in the 1960s.5•9 It is almost certain that this is still the case. Failure of the patient and physician to recognize a deteriorating clinical condition and overreliance on inhalers creates a potentially fatal scenario. The solution is increased education of health professionals, their patients and the patients' families. A twopronged attack which includes more research to complete the information base and more education to raise awareness is therefore indicated. As pulmonologists, we have an opportunity and responsibility to take on this task. A. Sonia Buist, M.D. Portland Professor of Medicine and Acting Head, Pulmonary and Critical Care Medicine Division, Oregon Health Sciences University REFERENCES

1 Sly R. Increases in deaths from asthma. Ann Allergy 1984; 53:205

2 Sly R. Effects of treatment on mortality from asthma. Ann Allergy 1986; 56:207-12 3 Sears MR. Why are deaths from asthma increasing? Eur J Respir Dis 1986; 69(SuppI147):175-81 4 Paulozzi LJ, Coleman JJ, Buist AS. A recent increase in asthma mortality in the northwestern United States. Ann Allergy 1986; 56:392-95 5 Benatar SR. Fatal asthma. N Eng}J Med 1986; 314:423-29 6 Esdaile JM. Asthma mortality-How high is up? And is it up?

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(editorial). Chest 1987; 91:640-42 7 Gross NJ. What is this thing called love?-Or, defining asthma (editorial), Am Rev Respir Dis 1980; 121:203-04 8 Barger LW, Vollmer WM, Felt R, Buist AS. Further investigation into the recent increase in asthma death rates: a review of 41 asthma deaths in Oregon in 1982. Ann Allergy 1988; 60:31-40 9 Sheffer AL, Buist AS, eds, Proceedings of the Asthma Mortality Task Force. J Allergy Clin Immunoll987; 80:[Suppl]No. 3, Part 2.

Heart-Lung Transplantation Since 1981, more than 250 patients have undergone heart-lung transplantation for a variety of indications. The majority of patients have had pulmonary vascular disease either due to primary pulmonary hypertension or congenital heart disease. In this issue of Chest (see page 644) Jones, Higgenbottam, and Wallwork report successful heart-lung transplantation for a patient with cystic fibrosis. The symptomatic and functional improvements have been remarkable, and in up to 16 months of follow-up there has been no sign of the recurrence of lung disease. These results are very encouraging, and are consistent with the presence of relatively normal secretory function in the bronchial epithelium of the transplanted lung. Although the authors point out that follow-up is short, it is probable that there will be no recurrence of the typical cystic fibrosis lung disease in the transplant recipients, and their long-term survival will be similar to other patients with heart-lung transplants in the absence of nonpulmonary complications of their disease. To help predict the survival of patients receiving heart-lung transplants for cystic fibrosis, it would be helpful to review the experience for other indications. In a recent survey, 19 centers around the world have performed heart-lung transplantation in 255 patients.' Approximately 80 percent of the patients had either primary pulmonary hypertension or congenital heart disease. Twenty percent of patients had a variety of illnesses characterized as primarily diffuse lung disease, and several patients received retransplants. The overall one-year survival in these patients has been 60 percent, with a five-year survival of 20 percent. The overall mortality both early and late for patients with primary pulmonary hypertension or congenital heart disease has been 41 percent. For the patients with primary lung disease, the overall mortality is presently 58 percent. The two longest living patients (the first two patients in the Stanford series") survived, respectively, for five years and two months, dying of unrelated causes and with relatively normal cardiopulmonary histology at autopsy, and five years and 11 months, dying of multisystem failure after staphylococcal pneumonia. The high operative mortality of approximately 25 Editorials

percent can be attributed in most cases to multisystem failure, often triggered by excessive postoperative bleeding complications. The patients remain at risk for frequent pulmonary infections both early and late after transplantation, and in the intermediate and late phases there is a continually increasing incidence of obliterative bronchiolitis. 3 The accumulating evidence suggests that this latter complication is primarily due to rejection," but may be triggered by viral infection." Until this complication can be detected early and either reversed or held in check, the intermediate and longterm results after heart-lung transplantation will continue to be disappointing. Since the routine use of triple drug therapy which includes cyclosporine, prednisone and azathioprine, this complication may be less frequent. Due to increased awareness, patients are followed more closely for a decline in pulmonary function, and receive an increase in immunosuppression if obliterative bronchiolitis is proven. As we develop better understanding of this process, overall Iongte rm results can only improve. Since heart-lung transplantation has been successful in diffuse lung disease, there is reason to believe that bilateral en bloc lung transplantation could also be used for this indication, and may be preferable. In many of the patients with cystic fibrosis, cardiac function is reasonably well maintained. Depending upon the degree of pulmonary hypertension and right ventricular hypertrophy, the heart could be saved or could be used as a donor heart for cardiac transplantation if heart-lung transplantation is performed. A recent report of successful bilateral lung transplantation is an encouraging development. 6 Since a bilateral lung transplant allows the donor heart to be available for another patient requiring heart transplantation, better cooperation in sharing donors would provide for transplants in a larger number of patients. It is not clear yet whether the intermediate and longterm complication of obliterative bronchiolitis will develop in the bilateral lung transplant, but there is no reason to suspect that it would not be present. Although heart-lung transplantation therapy is difficult and complicated, and the present intermediate and longterm results are not as good as for heart transplantation alone, the remarkable functional improvement in the patient reported by Higgenbottam and associates, and in other patients, encourages many centers to continue. At least for many years to come, there will be no other alternative therapy for patients with end-stage disease due to cystic fibrosis. Broce A Reitz, M.D., F.C.C.P. Baltimore Cardiac Surgeon-in-Charge, The Johns Hopkins Hospital.

REFERENCES 1 Griffith B. Personal communication 2 Reitz BA, Wallwork JL, Hunt SA, Pennock JL, Billingham ME, Oyer PE, et ale Heart-lung transplantation: successful therapy for patients with pulmonary vascular disease. N Eng} J Med 1982; 306:557-64 3 Burke CM, Theodore J, Dawkins KD, Yousem SA, Blank N, Billingham ME, et ale Post-transplant obliterative bronchiolitis and other late lung sequelae in human heart-lung transplantation. Chest 1984; 86:824-29 4 Harjula A, Baldwin JC, Glanville AR, Tazelaar HD, Oyer PE, Stinson EB, et ale HLA antigen compatibility in heart-lung transplantation (abstract) J Heart Transplant 1986; 5:375 5 Burke CM, Glanville AR, Macoviak jA, O'Connell BM, Tazelaar HD, Baldevin JC, et ale The spectrum of cytomegalovirus infection following human heart-lung transplantation. J Heart Transplant 1986; 5:267-71 6 Cooper JD, Pearson FG, Patterson GA, Toad TRJ, Ginsberg RJ, Goldberg M, et ale Technique of successful lung transplantation in humans. J Thoracic and Cardiovasc Surg 1987; 93:173-81

Thin-Section CT and the Solitary Pulmonary Nodule Less is more. Andrea del Sarto (1855) Robert Browning large series of resected solitary pulmonary Several nodules (SPN) have shown that granuloma ac-

counts for about 50 percent of cases, and bronchogenic carcinoma for another 30 percent.' Since the majority of SPNs which are not granulomas are carcinoma, identification of a SPN as a granuloma is important. A SPN can be diagnosed as a granuloma if a dense nidus of calcification, laminated calcification, or diffuse calcification is identified on low kilovoltage spot films or conventional tomograms. If spot films or tomograms are unrevealing, computed tomography (CT) may demonstrate benign calcification because CT is 10-20 times more sensitive to density differences than chest radiography 2 Standard chest CT examinations, eg, staging of bronchogenic carcinoma, are performed using 8-10 mm thick slices. The key to CT detection of calcification in SPN is obtaining 1.5-5 mm thick slices, ie, thin-section CI: through the SPN. Thin-section CT avoids partial volume averaging of surrounding lung (-1,000 Hounsfield units) with a diffusely calcified SPN (+ 200 to 300 Hounsfield units), which reduces the CT density of the SPN so that it no longer appears calcified. Using thin-section CI: 50 percent of SPNs not seen to be calcified on spot films or conventional tomography can be shown to be diffusely calcified. 3.4 In this issue of Chest (see page 595) Naidich et al, report a new and useful finding in thin-section CT of SPNs. The authors describe the "positive bronchus" sign-a bronchus leading to or contained within a SPN CHEST I 93 I 3 I MARCH. 1988

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