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ENDOBRONCHIAL TUBERCULOSIS Digitalization is necessary when congestive heart failure and auricular fibrillation develop. The discontinuation of digitalis prior to closure of the defect or any cardiopulmonary bypass procedure, is well known. Both the morbidity as well as the mortality can be greatly reduced by meticulous control of the patient's metabolic state whenever possible. Angiocardiography should be perlormed to exclude other lesions.H-1 6 Several thoracic centers have reported successful closure of postinfarction interventricular septal defects.U-18 But these do not include the four subaortic ruptures. Boicourt et al 19 studied the healing of the infarcted myocardium. They concluded that the minimum time for repair of the acquired interventricular septal defect and associated aneurysm is eight weeks after the myocardial infarction. The best surgical results are obtained when attempts to close the defects are delayed after the third month. Trinkle et al 20 were also of the same opinion. A deterioration in the patient's condition may not allow this idea to hold. 1 Gregg DE, Fisher LC: Circulation, Section 2. Baltimore, Williams and Williams, 1963 2 Abrams LD, Evans DW, Howarth FH: Coronary artery -right ventricular fistula treated surgically. Br Heart J 29:132, 1967 3 Nunn DB, Thrower WD, Boone JA, et al: Coronary arteriovenous fistula simulating patient ductus arteriosus. Am Surg 28:476, 1962 4 Schwartz H, Canelli FR: Spontaneous rupture of papillary muscle of the left ventricle: a clinical syndrome. Am Heart J 40:354, 1950 5 Bailey OT, Rickman JB: Rupture of mitral chordae tendineae. Am Heart J 28:578, 1944 6 Latham PM: Lectures on Clinical Medicine Comprising Diseases of the Heart. (Vol 2) London, Brown Green and Longman, 1846 7 Swithinbank JM: Perforation of the interventricular septum in myocardial infarction. Br Heart J 21:562, 1959 8 Sanders RJ, Neubuerger liT, Ravin A: Rupture of papillary muscles: occurrence of rupture of the posterior muscle in posterior myocardial infarction. Dis Chest 31:316, 1957 9 Stirling GA: Hypertensive disease in Jamaican necropsy material. Br Med J 1:1173, 1960 10 Robertson WB: Some Factors influencing the development of atherosclerosis. A survey in Jamaica, West Indies. J Atherosclerosis Res 2:79, 1962 11 Hayes J: Personal communication 12 Malone RGS, Parkes WE: Rupture of the interventricular septum. Br Heart J 17:448, 1955 13 Cahill F, Cahill F, Flood F: Rupture of the infarcted ventricular septum. Report of a case with unusual phonocardiographic and electrocardiographic findings. Am Heart J 64:686, 1962 14 Partington T, Somerville J, Holmes-Sellors T, et al: Rupture of the ventricular septum from myocardial infarction: haemodynamic response to surgical treatment. Thorax 24:118, 1969 15 Honey M, Belcher JR, Hasan M, et al: Successful early repair of acquired ventricular septal defect after myocardial infarction. Br Heart 29:453, 1967 16 Rawlins MD, Mendel D, Braimbridge MV: Ventricular

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septal defect and mitral regurgitation secondary to myocardial infarction. Br Heart J 34:322, 1972 Cooley DA, Belmonte BA, Zeis LB: Surgical repair of ruptured interventricular septum following acute myocardial infarction. Surgery 41:930, 1957 Collis JL, Mackinnon J, Raison JCA, et al: Repair of acquired interventricular septal defect following myocardial infarction. The Lancet 11:172, 1962 Boicourt OW, Ritzmann LW, Chase JD: Rupture of the infarcted interventricular septum: Surgical repair with survival. Circulation 26:1321, 1962 Trinkle JK, Furman RE, Orr JA: Myocardial infarctectomy and repair of ruptured ventricular septum during acute stage of infarction. J Thorac Cardiovasc Surg 63: 193-5, 1972 Schlappi JC, Landall DG: Perforation of the infarcted interventricular septum. Am Heart J 47:432, 1954

Endobronchial Tuberculosis* David ]. Pierson, M.D.,•• S. Lahhminaravan, M.B.t and Thomas L. Petty, M.D., F.C.C.P.t

An elderly woman presented with incapacitating chronic: congb. Routine chest 6Jms and full-chest tomograms showed no abnormaHty, but bronchoscopy revaled diffuse inflammation of the trachea IUid bronchi and her sputum contained Mycobacterium tubercuiOIIIs in large numbers. Antituberculosis tbenpy was followed by res. lotion of symptoms and broncboscopic abnormaHties.

Tuberculous involvement of the bronchial tree was J. recognized as early as 1694, when Morton1 reported the ulceration of broncholiths into the bronchi of tuberculosis patients. Since its original description, endobronchial tuberculosis has been the subject of numerous reports, as chronicled by Smart. 2 In most reported cases, however, this entity has occurred in the setting of extensive parenchymal or nodal disease, and the possibility of its presence without radiographically demonstrable lesions has not been emphasized. 8 We have recently studied a patient with extensive tracheobronchial tuberculosis, in whom no radiologic evidence of pulmonary involvement could be found.

CASE REPoRT A 75-year-old Caucasian housewife was admitted to the hospital for evaluation of chronic cough. Aside from mild adult-onset diabetes and essential hypertension, the patient had been healthy throughout her life and denied exposure to tuberculosis. A hacking cough developed four years prior to admission. This was initially nonproductive, but gradually became productive of small amounts of whitish sputum. She consulted several internists and an allergist, who evaluated her with chest radiographs, skin tests for allergens, and •From the Department of Medicine, University of Colorado Medical Center, Denver. ..Clinical Fellow in Pulmonary Diseases. tSenior Clinical Fellowl Division of Pulmonary Diseases. tAssociate Professor ot Medicine and Head, Division of Pulmonary Diseases. Reprint requests: Dr. Pierson, University of Colorado Medical Center, Denver 80220

538 routine pulmonary function tests, all of which were normal. A two-month trial of prednisone therapy produced no change in her symptoms, and treatment was continued with antihistamines, bronchodilators, and antibiotics. The patient continued to complain of cough, but was not otherwise symptomatic. Specifically, she denied weight loss, fever, night sweats, hemoptysis, or dyspnea. Over the year prior to admission the cough became progressively more intractable, with worsening on exertion, and the patient took a variety of medications without relief. Eight months prior to admission, she was hospitalized for elective cholecystotomy, which was completed without complication. During another hospitalization four months prior to admission for further evaluation of her cough, the patient received further laboratory studies, including complete blood count, sputum bacterial cultures, and chest radiographs, all of which were normal. Another four-week course of prednisone produced no benefit. On admission to Colorado General Hospital, the patient complained of cough productive of one-fourth cup of whitish sputum per day, and continued to deny other symptoms. The cough interfered with eating, with normal conversation, and with sleep. Physical examination revealed a healthy-appearing elderly woman whose vital signs were normal. Examination of the chest revealed mild dorsal kyphosis and occasional scattered bilateral inspiratory rhonchi, but was otherwise unremarkable. The remainder of the examination was entirely normal. Laboratory data included normal hemoglobin, hematocrit, white blood cell count and differential, urinalysis, serum electrolytes, biochemical screen, intravenous pyelogram, and upper gastrointestinal series. Fasting glucose was 120 mg per 100 mi. Intermediate strength PPD-Tween showed 25 mm induration at 48 hours. Examination of the patient's sputum revealed more than 100 acid-fast bacilli per high-power field. Posteroanterior and ·lateral chest radiographs showed diffuse osteoporosis, compression factures of the 8th and 12th thoracic vertebrae, and a rounded density in the posterior left chest consistent with a Bochdalek's hernia. The heart, great vessels, and lung parenchyma were normal. Whole chest tomograms in posteroanterior and lateral projections showed no evidence of adenopathy or infiltrates. Fiberoptic bronchoscopy on the third hospital day revealed the hypopharynx and vocal cords to be normal. The mucosa of the trachea and bronchi, examined to the segmental level, was diffusely and uniformly erythematous and thickened, with blunting of the carina and partial airway collapse on expiration. No discrete ulcerations or nodules were seen, although minute whitish plaques were scattered diffusely over the entire mucosa (Fig la). The patient was begun on isoniazid, 300 mg daily, ethambutol, 1600 mg (25 mg/kg) daily, and .. rifampin, 600 mg

PIERSON, LAKSHMINARAYAN, PETTY daily. Her sputum cultures revealed typical Mycobacterium tuberculosis with full susceptibility to these three drugs. Over the first four weeks of therapy her cough diminished markedly, and by the time of discharge on the 95th hospital day she was asymptomatic. Repeat bronchoscopy on the 40th hospital day, after 36 days of triple therapy, showed marked clearing of the mucosal erythema and absence of the previously noted white plaques (Fig lb). Again, no mass lesions, ulceration, or mucosal irregularity were seen. The patient's sputum became culture-negative on the 55th hospital day, although sputum smears were positive for small numbers of bacilli intermittently until the 81st hospital day. Since discharge from the hospital, the patient has remained symptom-free. She received rifampin daily for three months; isoniazid and ethambutol will be continued for a total of two years. DISCUSSION

This patient's active tuberculosis went undiagnosed despite frequent medical examinations over a period of several years. During this time, she received corticosteroid therapy and a variety of other medications, was active socially, and underwent both pulmonary function testing and a surgical procedure under general anesthesia. Repeatedly negative chest radiographs throughout the course of her illness undoubtedly contributed to the delay in establishing the correct diagnosis. Tuberculous involvement of the tracheobronchial tree has classically been described to begin with localized areas of erythema, and to progress with local granuloma formation and ulceration to eventual fibrosis and stenosis of airways. 4 No ulcerations or other localized lesions were visualized in this patient, and the extensive erythema, probably exacerbated by her frequent cough, was more diffuse than has usually been described. Endobronchial tuberculosis has been thought to develop by the following mechanisms, either singly or in combinations: 2 1) extension from the lungs by direct infiltration; 2) implantation of organisms from infected sputum; 3) hematogenous spread; 4) lymphatic spread; and 5) by primary infection of the bronchial mucosa. In our patient, no definite statement can be made regarding pathogenesis. Because of the very large numbers of organisms shed, and the duration of therapy required to convert the sputum to negative, a continuous source of infection, either from diffuse infection of bronchial mucosa or from a small, radiologically undetectable caseous focus, seems likely. Active chronic pulmonary tuberculosis with normal

FIGURE la ( left ) : Bronchoscopic view of carina and mainstem bronchi prior to treatment, showing diffuse mucosal erythema. FIGURE lb (right): View at bronchoscopy after 36 days of antituberculous therapy. Erythema has resolved.

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COMPLETE LEFT CORONARY ARTERY OBSTRUCTION chest radiographs must be exceedingly uncommon. Several cases of culture-proved puhnonary tuberculosis with negative chest films have been reported," however, these cases were detected within a few weeks or months of documented tuberculin conversion, and epidemiologic studies have demonstrated that recovery of viable M tuberculosis is often possible in individuals who have just converted their tuberculin tests, if pulmonary secretions are cultured frequently enough." The numbers of organisms recovered and the duration of symptoms both indicate the unlikelihood of recent infection in this instance. This case, in which highly infectious, active tuberculosis was present with normal chest radiographs and whole-chest tomography, points out the need to consider this diagnosis in any patient with chronic cough. While a negative chest film makes tuberculosis less likely, it does not rule it out, particularly in an individual with predisposing factors or in whom routine diagnostic procedures have failed to identify the cause of a chronic cough. ACKNOWLEDGMENT: The authors wish to thank Dr. Roger S. Mitchell for his critical review of the manuscript.

1 Morton R: Phthisiologica. London, 1694 2 Smart J: Endobronchial tuberculosis. Br J Tuberc and Dis Chest 45:61-68, 1951 3 Birkelo CC, Poznak LA: The radiologic findings in tracheobronchial tuberculosis. Dis Chest 11:26-35, 1945 4 Richards WF: Tracheobronchial tuberculosis. In Modem Practice in Tuberculosis. (Sellors TH, Livingston JL eds) London, Butterworth & Co, 1952, Vol 2, pp 15-43 5 Schmidek HH, Hardy MA: Pulmonary tuberculosis with normal chest radiographs: Report of eight cases. Canad Med Ass J 97:178-180,1967 6 Kent DC, Reid D, Sokolowski ]W, et al: Tuberculin conversion: The iceberg of tuberculous pathogenesis. Arch Environ Health 14:580-584, 1967

atherosclerotic disease of the main left coroOcclusive nary artery (LCA) before its bifurcation into the

left anterior descending (LAD) and left circumfiex coronary (LCF) arteries has been reported in 10 percent of patients with angiographic evidence of coronary atherosclerosis. I Although complete ostial narrowing by luetic aortitis and total LCA obstruction by intimal dissection with coronary catheters have been described, LCA atherosclerotic obstruction with no distal filling of the LCA branches in living man has rarely been reported.v? This report presents angiographic evidence of complete LCA occlusion and indicates the serious prognostic implications of such a lesion. CASE REPoRT

A 47-year-old caucasian man with known type IV hyperlipoproteinemia was referred to the Hospital of the University of Pennsylvania for coronary angiography. At age 42 years, he was hospitalized with an acute myocardial infarction after several months of angina pectoris. The patient was unable to return to work because of severe angina provoked by exertion, exposure to cold, and by meals, and was treated with isosorbide dinitrate and nitroglycerin. Crescendo angina requiring 20 nitroglycerin tablets/day culminated in a second myocardial infarction at age 45 years. One year prior to his catheterization at the Hospital of the University of Pennsylvania he was hospitalized for an anteroseptal myocardial infarction and was informed he had a ventricular aneurysm; he was told he had had cardiac arrest requiring resuscitation in the ambulance. Two months before angiography he was hospitalized with "coronary insufficiency" and was discharged on isosorbide dinitrate, propranolol, chlordiazepoxide and nitroglycerin, which he used 6-8 times/day for treatment and prophylaxis. At the time of catheterization, he admitted to dyspnea on exertion in addition to his exertional and nocturnal angina, which was characterized as a retrostemal pain with radiation to the neck and arms,

Complete Left Coronary Artery Obstruction * Kenneth L. Kershbaum, M.D., Joel H. Manchester. M.D. and James C. Shelburne. M.D.

A case of angiograpbicaJly documented complete left c0ronary artery (LCA) obstruction is presented. Complete occlusion of the main LeA is associated with a poor prognosis, and patients with this lesion shonld be considered for immediate emergency coronary bypass graft surgery. ·From the Cardiopulmonary Division, Department of Medicine, University of Pennsylvania School of Medicine Philaddpma. ' This study was supported by U.S. Public Health Service Grant HL05239. Reprint requests: Dr. Manchester, Hospital, University of

Pennsylvania, Philadelphia 19104

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FIGURE 1. Single frame from a 35 mm coronary cineangiogram of the left coronary artery in left anterior oblique position. Arrow indicates occluded main left coronary artery (LCA).