Preoperative Evaluation of Pulmonary Function

that a different distn"bution could have been seen with broadening of the palette of PiM subtypes with Ml and M5.e Independent of this, it would have been advisable to acquaint ourselves more closely with the biochemical properties of electrophoretic variants. The functional changes of the primary structure alone can hardly be the sole factor of pathologic action. A change in the tertiary structure can also be influenced by an inductive effect, for instance, the binding energy of the neuramine acid and therefore the splitting of the ester bord, and thus lead to a different biological action. An indication of this can be the split change of the Pi. Presently we are informed concerning the structure of the pathogenic Pi variant z1,s and se,10 as well as some of the problems of microheterogeneity.11.12 The question of the connection between structure and biological activity is still open. In the phenotypes V, S, T or Y, Z the Pi values are not larger than M1, M 3 , M2; however, Z and S have been assumed to be pathologic. K. Beneze, Ph.D.; and G. Frohmann, M.D., F.C.C.P., lmtitut and Poliklinik Arbeitsmedizin, University of Munich, Munich, Gennany

REFERENCES 1 Cox DW, Johnson AM, Fagerhol MK. Report of nomenclature meeting for a.1-Antitrypsin. Human Genet 1980; 53:429-33 2 Frants RR, Eriksson AW. Reliable classification of six PiM subtypes by separator isoelectric focusing. Hum Hered 1978; 28:201-09 3 Beneze K, Sabatke L. Fast a.1-antitrypsin phenotyping for the differentiation of PiMM-Subtypes. J Clin Chem Clin Biochem 1980; 18:13-16 4 Beneze K. Vergleich von Triigerampholyten bei der Phiinotypisierung von a.1-Antitrypsin nach isoelektrischer Fokussierung in Polyacrylamidgelen. In: Radola B. J. ed: Elektrophorese: Selfedition forum der Technischen Universitiit Miinchen. Miinchen, 1980: 218-24 5 Constans J, Vian M, Gonaillard C. PiM4 : An additional PiM subtype. Human Genet 1980; 55:119-21 6 Weidinger S. Alpha,-antitrypsin (A1-AT): Darstellung mittels Diinnschicht-Isoelektrischerfokussierung und Immunflxation. In: Radola B.J., ed.: Elektrophorese-forum der Technischen Universitiit Miinchen. Miinchen 1980, 303-08 7 Jeppsson JO. Amino acid substitution g]u-lys in a.1-antitrypsin PiZ. FEBS Letters 1976; 65:195-97 8 Yoshida AJ, Lieberman J, Gaidules L, Ewing C. Molecular abnormality of human alpha1-antitrypsin variant ( PiZZ) associated with plasma activity deficiency. Proc Nat Acad Sci (USA) 1976; 73:1324-48 9 Jeppsson JO, Laurell CB, Fagerhol M. Properties of isolated human a.1-antitrypsin of pi types M, S, and Z. Eur J Biochem 1978; 83:143-53 10 Yoshida A, Swing C, Wessels M, Lieberman J, Gaidulis L. MolecuJar abnormality of PS variant of human alpha1antitrypsin. Am J Hum Genet 1977; 29:233-39 11 Yoshida A, Taylor JCh, van den Brock MGM. Structural difference between the normal PiM1 and the common PiM 2 variant of human a.1-antitrypsin. Am J Hum Genet 1979; 31:564-68 12 Arnaud Ph, Gianazza E, Righetti PG, Fudenberg HH. In: Radola BJ ed: Electrophoresis '79. Berlin-New York: W. de Gruyter, 1980, 151-63 13 Kueppers, F, Christopherson MJ. Alpha1 -antitrypsin: Further genetic heterogeneity revealed by isoelectric focusing. Am J Hum Genet 1978; 30:359-65

CHEST, 80: 2, AUGUST, 1981

Preoperative Evaluation of Pulmonary Function To the Editor: With the advent of noninvasive radionuclide methods of determining regional perfusion and ventilation, there has been increasing interest in evaluating preoperatively the patient who requires pulmonary resection. I have followed recent publications, including the one by Ali et al. (Chest 1980, 77:337-342) who have discovered that following pneumonectomy, pulmonary regional and overall pulmonary functions are relatively stable, and that following subtotal pulmonary resection, there is a severe decrease in pulmonary function which gradually improve with time. They state that "the quantitative evaluation of the late functional recovery has not been documented before." I have1,2 shown that following pulmonary resection of seven segments or less, patients suffered restrictive changes which were almost identical, but postpneumonectomy patients, especially those who developed contralateral hyperinflation, do not demonstrate this effect. 1•2 Almost all patients recovered from restrictive effects in approximately six weeks, in a very predlctable manner. I also note that Boysen's editorial (Chest 1980, 77:6-7), still places reliance on ventilatory tests in screening patients. We have found that ventilatory tests are of no greater help than clinical impressions in prognostication. Our continued experience supports om original findings& which indicate that mean pulmonary artery pressures correlate best with prognosis. Thus far, scintiscanning appears to offer little more than bronchospirometry, being preferred because it is noninvasive. The data of Ali et al, indicate that the technique is not accurate enough to rely upon where subtotal resection is planned. Daoid V. Pecora, M.D., F.C.C.P., Chief, Surgical Seroice, Veterans Administration Medical and Rsgional Of1U;e Center, Wilmington, Delaware

1 Pecora DV. Progressive changes in venti1ati.on following pulmonary resection. Surg Gynec Obstet 1956; 103:45558 2 Pecora DV. Evaluation of cardiopulmonary reserve in candidates for chest surgery. J Thorac Cardiovas Surg 1962; 44:60-66 3 Pecora DV, Hohenberger M. Effects of postpneumonectomy distention on pulmonary compliance and vascu1ar resistance. Am Surgeon 1979; 45:797-01

To the Editor: Dr. Pecora has commented about our discovery that following pneumonectomy, pulmonary regional and overall pulmonary functions are relatively stable. I refer Dr. Pecora to Table 3 of our paper published in Chest (1975; 68:292), which shows that we were the first group to present and publish data emphasizing the stability of regional pulmonary function following pneumonectomy. Dr. Pecora's quotation of our statement is incomplete. The sentence in our paper reads "Although this short term discrepancy between the physiologic and anatomic loss following partial pulmonary resection has been noticed by other investigators,11 to our knowledge, the quantitative evaluation of the late functional recovery has not been documented

COMMUNICATIONS TO THE EDITOR 249

before." Of course, Dr. Pecora's work could have been additionally referenced at that stage of our paper and we regret this oversight However, the previous publications were concerned with lung resection in patients who had pulmonary tuberculosis. These patients usually have healthy contralateral lungs. Our paper presents data on .regional pulmonary function in lung cancer where the incidence of concomitant obstructive lung disease in the non-tumor-bearing lung parenchyma is a significant complicating factor. We are fully aware of the relative inaccuracy of our predictions for the outcome of smaller resections compared to pneumonectomy. This has been clearly stated in both the abstract and the body of our paper. Finally, we support and agree with Dr. Boysen's editorial in Ched and we feel that the great majority of thoracic surgeons. when given the choice, would prefer to augment their clinical impressions with physiologic data. M.K. AU, M.D., F.C.C.P., Aasociate Pro/6UOI' of Medldne, and M.S. Ewer, M.D., Aui8tant Profeuor of Medicine, of Tam S11atem The Cancer Center, Houafon

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Self-terminating Torsades de Pointes or Holter Conversion 7 To the Editor: Undoubtedly, the case of "Holter auto-thumping" for termination of presumed quinidine-induced ventricular tachycardia was read with some interest and great amusement (Chen 1980; 78:674). There is, however, a mo.re plausible explanation for the patient's cardioversion based upon an analysis of the case history and ECG rhythm strips. It is clear from such analysis that the patient has a prolonged qr interval at the time of his normal sinus rhythm, undoubtedly related to quinidine therapy, followed by the degeneration to an arrhythmia characteri7.ed by an alternating pattern of electrical polarity where the QRS complexes appear to spiral around the isoelectric line. These features assure that the patient, in fact, experienced a classic episode of toraadea de pointu, (TDP) as described by Dessertenne et a11 in 1966 and which was recently reviewed by Smith and Gallagher.• The importance of this diatinction is that TOP is usually self-terminating after a couple seconds to minutes, and this is for apparent cardioversion without the the probable aid of standard resuscitation in this patient. In addition, since TOP is rarely converted successfully by standard methods of cardioversion,• it is hardly plausible that the "Holter autothump" was responsible. Alas, we must await further investigations and case reports to assess the role of the Holter monitor as a therapeutic modality. Frederlclc T. Zugibe, ]r. M.D. Unloenitv of Bocheder Schoola of

reason

Medicine and Dentidrr/, Bochater, NetD York

REFEBENca 1 Dessertenne F Coumel PH, Fabiato A. Filbrillation ventriculare et toursades de pointes. Presse Med 1969; 11: 193-

96

S Smith WM, Gallagher JJ. "Les toursades de pointes:" an unusual ventricular arrhythmia. Ann Intem Med 1980; 93: 573-84

250 COllllUllCATIOllS TO THE DITOR

Hepatoma Presenting as a Single Cavitary Lung Mass and Leukemoid Reaction To the Editor: I read with interest the article by Cooper and Hayes published in Ched, Febmary, 1980.1 I recently had the opportunity to see a similar case referred in consultation because of a leukemoid reaction white blood cell count of 40,000 with a platelet count of l,S00,000 and normal hemoglobin of 14 gm. The patient complained of evening fever up tO 39"C associated with night sweats and pleuritic chest pains. On enmjnation, decreased breath sounds were heard in the right lower hemit:horax. A chest x-ray film showed a 2.5 X 3 cm lobulated cavitary lesion in the right lung base. Her alkaline phosphatase level was greater than 500 (normal up to 250), LDH, 557; SGOT, 88; and bilirubin 2.2. Isotope liver scan and CAT scans showed two large defects in the right and left lobe of the liver. A needle biopsy of the liver demonstrated multiple foci of active granulomatous inflammation compatible with micobacterial infection or fungal infection. The patient received a course of antituberculosis therapy with INH, ethambutol and rifampin. The patient's condition continued to deteriorate and she became semioomatose. Her white blood cell count increased to 70,000 and the platelet count to 1,500,000. Her leukocyte alkaline phosphatase was very high ( !15) compatible with a leukemoid reaction. At this time repeat sections of the original liver biopsy were made which revealed a moderately differentiated hepatocellular carcinoma ( hepatoma). The patient expired two weeks after her admission and, unfortunately, an autopsy was not obtained. This case is interesting since it represents the second reported case of a hepatoma presenting as a single cavitary lung mass. Also, the very severe leukemoid reaction and the granulomatous lesions in the liver misled us originally to the presumptive diagnosis of tuberculosis. Hepatomas, as do many other neoplasms, often produce a leukemoid reaction1 and hepatocellular carcinomas have produced secondary polycythemia in a number of reported cases, 8 •' due in some instances to ectopic erythropoietin production.II As in the case reported by Cooper and Hayes,1 our patient had a very high alkaline phosphatase level which probably is the most commonly elevated laboratory test in hepatoma. We wish to emphasize that these interesting tumors could masquerade as polycythemia or even, as in our case, as cavitary pulmonary tuberculosis with liver involvement and severe leukemoid reaction. ]ulM> F. Ochoa, M.D. St. Pet.enburg, F'lorida &prim reqaem: Dr. Ochoa, UIO 16tla Streel North, St. Petenbarg 33105

l\EnmENCES 1 Cooper KR, Hayes JA. Hepatoma presenting as a single cavitary lung mass. Chest 1980; 11 :!40-41 S Robinson WA. Granulocytosis neoplasia. Ann NY Acad

Sci 1974; !30:21! 3 McFachean AJS, Todd D, Tsargk C, Polycythemia in primary carcinoma of the liver. Blood 1958; 13:4!7 4 Davidson CS. Hepatocellular carcinoma and erythrocytosis. Semin Hematol 1976; 13:115 5 Eppatein S. Primary carcinoma of the liver. Am J Med Sci 1964; !47:137

CHEST, 80: 2, AUGUST, 1981