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Variant Angina Pectoris Due to Coronary Artery Spasm
of radiation therapy. However, the rapid increase in size of the mass was highly suggestive of lymphomas. Sonography might have been helpful in discriminating cystic from solid lesions. Since no inflammatory reaction was noted in the mediastinum of our patient, the acute respiratory obstruction following a meal containing a large amount of fat could have been precipitated by the increased amount of lymph in the thoracic duct required by absorption of chylomicrons.
1 Shields TW (ed): General Thoracic Surgery. Philadelphia, Lea & Febiger, 1972, p 914 2 Emerson GL: Supradiaphragmatic thoracic dust cyst. N Engl J Med 242:575, 1950 3 Bakst AA: Blind supradiaphragmatic thoracic duct cyst. Am Surg 140:250, 1954 4 Thomas MJ, Sawyer PW, Taylor FH, et al: Thoracic duct cyst of the mediastinum. Lancet 1:579.1966
Variant Angina Pectoris Due to Coronary Artery spasm* Dariush Owlia, M.D.;OO Rauindra Prabhu, M.D.;' Pierce, M.D.;" Peter V. Stoughton, M.D.;t Kanakaiahnavara R. Shankar, M.D.; and Alfredo Nfno, M.D.OO
John A.
The syndrome of variant angina pectoris and normal coronary arteries with intermittent spontaneous spasm, so-called variant of the variant, is probably more common than realized. Spasm commonly occurs in the right coronary artery with speclc ECG findings. Ambnlatory ECG monitoring and coronary angiograpby are likely to uncover more cases of coronary artery spasm.
sion, peptic ulcer and emotional lability was admitted to Hartford Hospital on March 7, 1973, for severe intermittent recurrent precordial pain of six months' duration, associated with numbness in both forearms and severe dvs~nea. Pain . and dyspnea were not effort-related, and her symptoms were relieved by walking or nitroglycerin therapy. On the day of admission, shortly after breakfast, she began having paroxysms of chest pain and dyspnea unrelieved by several nitroglycerin tablets. Findings in the initial physical examination were within normal limits, and the ECG showed slight ST-T changes. The serial ECGs failed to show any evidence of acute myocardial infarction, severe bradycardia, or A-V block. AU routine laboratory studies including repeated enzyme determinations were normal. On the sixth day after admission, the patient complained of severe precordial pain, and an ECG made at that time showed ST elevation in the inferior leads (Fig la). However, an ECG made two hours later showed return of the ST segment to normal (Fig l b ) . Again, serial ECGs and enzyme determinations did not reveal myocardial infarction. She had three more such documented episodes of transient i n i w current in the inferior leads. Rinzmetal's variant angina with critical atherosclerotic narrowing of proximal right coronary artery was clinically suspected. Coronary arteriography was performed on March 16, 1973, by Sones' method. A n ECG taken just before the arteriography showed injury current in the inferior leads without chest pain, but,this subsided in a few minutes. Left ventriculogram was performed first and was found to be normal. The patient was then given nitroglycerin 0.4 mg sublingually and left coronary injections were made in three projections. The artery was normal. The patient was then given another nitroglycerin tablet and right coronary injections were made. The first two injections revealed a dominant right coronary artery, which was entirely normal. The third injection showed a long segment of spasm beginning about 2 cm from the tip of the catheter, which tapered distally to about 80
-
T
he syndrome of angina pectoris and coronary artery disease has an infinite variety of presentations. The classic manifestation of coronary atherosclerosis is Heberden's angina and myocardial infarction. A variant of this syndrome was described by Prinzmetal in which the attacks of angina are precipitated by temporary increase in the tonus of a large narrowed Recently, a variant form of angina due to coronary artery spasm in the absence of coronary atherosclerosis was described.415 We have encountered two such cases.
A 64-year-old white housewife with a history of hyperten*From Hartford Hospital, Hartford. Conn. and Ottawa Civic Hospital, Ottawa. "The Cardiology Section. Department of Medicine, Hartford Hospital. tuniversity of Ottawa Cardiac Unit, Ottawa Civic Hospital. Reprint requests: Dr. Owl&, Hartford Hospital, Hartford 06115
CHEST, 67: $, JUNE, 1975
FIGURE1a (left).(Case 1) ECG taken during chest pain showing injury current in inferior leads. l b (right) ECG repeated after relief of chest pain showing resolution of injury current in inferior leads.
VARIANT ANGINA PECTORIS DUE TO CORONARY ARTERY SPASM 727
the right coronary ostium, and injections -showed diffuse spasm, with a threadlike lumen throughout its course. Administration of nitroglycerin sublingually produced relief of pain and retumed ST segment to normal (Fig 3b). A repeated injection of the right coronary artery showed complete disappear,ance of the spasm, and the entire vessel was free of atherosclerosis. Followup over the subsequent two years indicates minimal improvement in his symptoms on therapy with longacting nitrites and propranolol.
percent obstruction at the acute margin (Fig 2a). The patient had no pain and ST segment elevation was not observed in lead 2, which was being monitored. She was immediately given another nitroglycerin tablet. The spasm persisted through the next injection, but disappeared completely in the third injection made a few minutes later (Fig 2b). The course after arteriography was uneventful. She was discharged a few days later on isosorbide dinitrate (Isordil) therapy sublingually, and followup six months after discharge from the hospital indicated that the patient is doing well symptomatically.
Coronary artery spasm has long been suspected as a source of angina pectoris.6 The important difference between the syndrome described by Prinzrnetall and the present one is that in the former, a preexistent, critical, atherosclerotic lesion is noted, whereas, in the latter no such lesion is identified. This syndrome of variant angina pectoris and normal coronary arteries with intermittent spontaneous spasm, the so-called variant of the ~ a r i a n t ,is~ probably more common than realized. It is conceivable that some and perhaps many of the cases of angina pectoris and myocardial infarction reported in the absence of demonstrable coronary artery disease may be due to coronary artery spasm. If the spasm is mild, it is likely to produce only T wave changes; but if it is severe and prolonged, it could be associated with injury pattern or infarction. The etiology of the spasm is only speculative. Alpha and adrenergic receptors have recently been identified in the coronary arteries of man.' Stimulation of a recep.tors produces vasoconstric@onand B receptor stimulation produces 'vasodilation. Whether alteration in the tone of the receptors would produce spasm of a large artery is speculative. Administration of propranolol may be contraindicated in these cases because of unopposed a stimulation, with resultant vasoconstri~tion.~~~ It is of interest to note that most of the cases of coronary artery spasm so far reported, including ours, have involved the right coronary artery. The tendency of this coronary artery to go into spasm during selective injections is greater than that of the left coronary artery.g*10This may be due to some anatomic differences such as the presence of sphincterlike muscles at
A 36-year-old man ( a designer for a computer company) was admitted to Ottawa Civic Hospital for elective coronary angiography. For several years prior to admission, he gave a history of precordial pain, with radiation to the left shoulder and arm. The pain occurred infrequently in the beginning, but in the six months prior to the study he had one or two attacks a week. He described no relation to exercise, emotions or cold, and the pains occurred mostly at rest. Physical examination revealed no abnormalities. A resting ECC and double Master's two-step exerise ECC were normal. AU routine laboratory studies yielded negative results. Coronary angiography was performed by Judkin's technique. The left ventriculogram was performed first and was normal. The left coronary injections were made and at this time he complained of severe chest pain. At the same time, ST segment elevation was observed in lead 2, which was
FIGURE3a (upper). ( Case 2 ) ECC (lead 2 ) during chest pain showing injury current. 3b (lower)ECC (lead 2) following relief of chest pain, with resolution of injury current.
FIGURE 2a (upper). (Case 1)Right coronary angiogram ( RAO view) showing severe spasm of middle portion. 2b (lower) Right coronary angiogram (RAO view) showing total relief of spasm of middle portion.
CHEST, 67: 6, JUNE, 1975
the orifice of the right coronary a r t e ~ y . ~ ? l l W e believe that intermittent coronary artery. spasm as the cause of angina pectoris in the absence of atherosclerotic coronary artery disease is a definite entity. Holter monitoring a n d coronary angiography during t h e attacks of pain may b e fruitful in establishing the diagnosis.
1 Prinzmetal MD, Kennamer R, Merliss R, et al: Angina pectoris 1: A variant form of angina pectoris. Preliminary report. Am J Med 27: 375, 1959 2 Prinzmetal M, Ekmekci A, Kennamer R, et al: Variant form of angina pectoris. Previously undelineated syndrome. JAMA 174:1974, 1960 3 Silvermann ME, Flamm MD: Variant angina pectoris: Anatomic and prognostic implications. Ann Intern Med 75:339, 1971 4 Cheng TO, Bashour T, Kelser GA Jr, et al: Variant angina of Prinzmetal with normal coronary arteriogriuns: A variant of the variant. Circulation 37:476, 1973 5 Oliva PD, Potts DE, Pluss RG: Coronary arterial spasm in Prinzmetal angina. N Engl J Med 288:745, 1973 6 White PD: Coronary artery spasm. N Engl J Med 288: 1355, 1973 7 Andersson R, Holmberg S, Svedmyr N, et al: Adrenergic a and j3 receptors in coronary vessels in man. An in oitro study. Acta Med Scand 191:241, 1972 8 Malindzak GA Jr, VanDyke AH, Green HD, et al: a and j3 adrenergic receptors in coronary vascular bed. Arch Int Pliarmacodyn Ther 197: 112, 1972 9 Demany MA, Tambe A, Zimmerman HA: Coronary arterial spasm. Chest 53:714, 1968 10 O'Reilly RJ, Spellberg RD, King TW: Recognition of proximal right coronary artery spasm during coronary arteriography. Radiology 95: 305, 1970 11 Bouchek RJ, Takeshita R, Brady AH: Intimal hypertrophy in coronary arteries and considerations of the papillary muscle arteries (man). Anat Rec 153:243,1965
Pulmonary Sarcoidosis Presenting as Bronchogenic carcinoma* Jerome C . A m t t , Jr., M.D.OOand Hurst B. Hatch, Jr., M.D., F.C.C.P.
Massive pulmonary fibrosis simulating bronchogenic carcinoma on chest roentgenograms, planigrams and bronchograms is a d i i c t l y unusual manifestatioo of sarcoidosis. Bronchial stenosis can result from any of three types of bronchial involvement: compression of the major bronchi by enlarged perihilar nodes, sarcoid lesions in the bronchial wall, and diffuse bronchial constriction 'From the Department of Internal Medicine, Sedion on Pulmonary Disease, Alton Ochsner Medical Foundation and Ochsner Clinic, New Orleans. "Presently at Elkins, West Virginia. Re rint requests: Dr. Amett, 1514 J d e r s o n Highway, New 0 r L a n s 70121
CHEST, 67: 6, JUNE, 1975
associated with massive fibrosis. The symptoms produced by sarcoidosis can be quite similar to those commonly associated with bnmchogenic carcinoma, and when combiied with suspicions findings on chest roentgenograms, planigrams, and bronchograms, can lead to a strong clinical suspicion of carcinoma. Since the two diseases can co-exist in the same patient, diagnostic thoracotomy is usually required even with a prior diagnmis of sarcoidosis.
T
he pulmonary fibrosis seen in patienis with advanced sarcoidosis can roentgenographically simulate pulmonary tuberculosis, idiopathic pulmonary fibrosis, congestive heart failure, pulmonary involvement with scleroderma, rheumatoid lung, pneumoconiosis, or lymphangitic carcinoma.' T h e presence of a mass lesion simulating bronchogenic carcinoma is distinctly unusual. W e report a case where massive fibrosis suggested bronchogenic carcinoma on chest roentgenogram, a t bronchoscopy, and on bronchograms.
A 53-year-old white farmer from Texas was referred to the Ochsner Medical Center in December, 1973 for evaluation of a mass lesion in his left upper lobe demonstrated on chest roentgenogram. He had smoked approximately six cigars daily for the ten years between 1946 and 1956. In 1956 a "spot" had been discovered in the lower left lung field on chest roentgenogram, which was no longer present on repeat study one year later. A routine chest roentgenogram in 1969 had revealed a diffuse interstitial infiltrate predominantly in the upper half of both lung fields. He remained asymptomatic, and a repeat study in 1971 revealed no change in the infiltrate. Evaluation at another hospital had included a left scalene node biopsy which had revealed a noncaseating granulomatous adenitis. Upon.admission, the patient reported malaise with a persistent nonproductive cough for the preceding six months, but he denied dyspnea, wheezing, chest pain, hemoptysis, fever, or weight loss. Auscultation of the lungs revealed a prolonged expiratory phase without rales or wheezes. There was no adenopathy or finger clubbing. Skin tests for tuberculosis, histoplasmosis, and mumps were negative. The chest roentgenogram revealed diffuse interstitial changes with a marked prominence of the left upper lobe hilus, suggesting a mass lesion, with radiation of fibrotic strands toward the periphery (Fig 1 ) . Tomograms revealed stenosis of the apicoposterior segment bronchus of the left upper lobe. Pulmonary function studies revealed a pure restrictive impairment, with the vital capacity 76 percent of predicted, the FEVl 83 percent of predicted, and the maximum breathing capacity 111percent of predicted. The resting alveolar-arterial oxygen gradient was elevated to 28 mm Hg, and the resting arterial oxygen pressure was normal (77 mm H g ) , with no change on exercise. Fiberoptic bronchoscopy revealed stenosis of the apicoposterior and anterior segmental bronchi of the left upper lobe, with normal-appearing mucosa. Brush biopsies of the segmental bronchi were negative for malignancy, and multiple washings were negative for fungi and acid-fast bacilli. A bronchogram showed a persistent filling defect of the anterior segment bronchus, with definite narrowing of the apicoposterior segment bronchus ( Fig 2 ) .
PULMONARY SARCOlDOSlS PRESENTING AS CARCINOMA 723
1 Shields TW (ed): General Thoracic Surgery. Philadelphia, Lea & Febiger, 1972, p 914 2 Emerson GL: Supradiaphragmatic thoracic dust cyst. N Engl J Med 242:575, 1950 3 Bakst AA: Blind supradiaphragmatic thoracic duct cyst. Am Surg 140:250, 1954 4 Thomas MJ, Sawyer PW, Taylor FH, et al: Thoracic duct cyst of the mediastinum. Lancet 1:579.1966
Variant Angina Pectoris Due to Coronary Artery spasm* Dariush Owlia, M.D.;OO Rauindra Prabhu, M.D.;' Pierce, M.D.;" Peter V. Stoughton, M.D.;t Kanakaiahnavara R. Shankar, M.D.; and Alfredo Nfno, M.D.OO
John A.
The syndrome of variant angina pectoris and normal coronary arteries with intermittent spontaneous spasm, so-called variant of the variant, is probably more common than realized. Spasm commonly occurs in the right coronary artery with speclc ECG findings. Ambnlatory ECG monitoring and coronary angiograpby are likely to uncover more cases of coronary artery spasm.
sion, peptic ulcer and emotional lability was admitted to Hartford Hospital on March 7, 1973, for severe intermittent recurrent precordial pain of six months' duration, associated with numbness in both forearms and severe dvs~nea. Pain . and dyspnea were not effort-related, and her symptoms were relieved by walking or nitroglycerin therapy. On the day of admission, shortly after breakfast, she began having paroxysms of chest pain and dyspnea unrelieved by several nitroglycerin tablets. Findings in the initial physical examination were within normal limits, and the ECG showed slight ST-T changes. The serial ECGs failed to show any evidence of acute myocardial infarction, severe bradycardia, or A-V block. AU routine laboratory studies including repeated enzyme determinations were normal. On the sixth day after admission, the patient complained of severe precordial pain, and an ECG made at that time showed ST elevation in the inferior leads (Fig la). However, an ECG made two hours later showed return of the ST segment to normal (Fig l b ) . Again, serial ECGs and enzyme determinations did not reveal myocardial infarction. She had three more such documented episodes of transient i n i w current in the inferior leads. Rinzmetal's variant angina with critical atherosclerotic narrowing of proximal right coronary artery was clinically suspected. Coronary arteriography was performed on March 16, 1973, by Sones' method. A n ECG taken just before the arteriography showed injury current in the inferior leads without chest pain, but,this subsided in a few minutes. Left ventriculogram was performed first and was found to be normal. The patient was then given nitroglycerin 0.4 mg sublingually and left coronary injections were made in three projections. The artery was normal. The patient was then given another nitroglycerin tablet and right coronary injections were made. The first two injections revealed a dominant right coronary artery, which was entirely normal. The third injection showed a long segment of spasm beginning about 2 cm from the tip of the catheter, which tapered distally to about 80
-
T
he syndrome of angina pectoris and coronary artery disease has an infinite variety of presentations. The classic manifestation of coronary atherosclerosis is Heberden's angina and myocardial infarction. A variant of this syndrome was described by Prinzmetal in which the attacks of angina are precipitated by temporary increase in the tonus of a large narrowed Recently, a variant form of angina due to coronary artery spasm in the absence of coronary atherosclerosis was described.415 We have encountered two such cases.
A 64-year-old white housewife with a history of hyperten*From Hartford Hospital, Hartford. Conn. and Ottawa Civic Hospital, Ottawa. "The Cardiology Section. Department of Medicine, Hartford Hospital. tuniversity of Ottawa Cardiac Unit, Ottawa Civic Hospital. Reprint requests: Dr. Owl&, Hartford Hospital, Hartford 06115
CHEST, 67: $, JUNE, 1975
FIGURE1a (left).(Case 1) ECG taken during chest pain showing injury current in inferior leads. l b (right) ECG repeated after relief of chest pain showing resolution of injury current in inferior leads.
VARIANT ANGINA PECTORIS DUE TO CORONARY ARTERY SPASM 727
the right coronary ostium, and injections -showed diffuse spasm, with a threadlike lumen throughout its course. Administration of nitroglycerin sublingually produced relief of pain and retumed ST segment to normal (Fig 3b). A repeated injection of the right coronary artery showed complete disappear,ance of the spasm, and the entire vessel was free of atherosclerosis. Followup over the subsequent two years indicates minimal improvement in his symptoms on therapy with longacting nitrites and propranolol.
percent obstruction at the acute margin (Fig 2a). The patient had no pain and ST segment elevation was not observed in lead 2, which was being monitored. She was immediately given another nitroglycerin tablet. The spasm persisted through the next injection, but disappeared completely in the third injection made a few minutes later (Fig 2b). The course after arteriography was uneventful. She was discharged a few days later on isosorbide dinitrate (Isordil) therapy sublingually, and followup six months after discharge from the hospital indicated that the patient is doing well symptomatically.
Coronary artery spasm has long been suspected as a source of angina pectoris.6 The important difference between the syndrome described by Prinzrnetall and the present one is that in the former, a preexistent, critical, atherosclerotic lesion is noted, whereas, in the latter no such lesion is identified. This syndrome of variant angina pectoris and normal coronary arteries with intermittent spontaneous spasm, the so-called variant of the ~ a r i a n t ,is~ probably more common than realized. It is conceivable that some and perhaps many of the cases of angina pectoris and myocardial infarction reported in the absence of demonstrable coronary artery disease may be due to coronary artery spasm. If the spasm is mild, it is likely to produce only T wave changes; but if it is severe and prolonged, it could be associated with injury pattern or infarction. The etiology of the spasm is only speculative. Alpha and adrenergic receptors have recently been identified in the coronary arteries of man.' Stimulation of a recep.tors produces vasoconstric@onand B receptor stimulation produces 'vasodilation. Whether alteration in the tone of the receptors would produce spasm of a large artery is speculative. Administration of propranolol may be contraindicated in these cases because of unopposed a stimulation, with resultant vasoconstri~tion.~~~ It is of interest to note that most of the cases of coronary artery spasm so far reported, including ours, have involved the right coronary artery. The tendency of this coronary artery to go into spasm during selective injections is greater than that of the left coronary artery.g*10This may be due to some anatomic differences such as the presence of sphincterlike muscles at
A 36-year-old man ( a designer for a computer company) was admitted to Ottawa Civic Hospital for elective coronary angiography. For several years prior to admission, he gave a history of precordial pain, with radiation to the left shoulder and arm. The pain occurred infrequently in the beginning, but in the six months prior to the study he had one or two attacks a week. He described no relation to exercise, emotions or cold, and the pains occurred mostly at rest. Physical examination revealed no abnormalities. A resting ECC and double Master's two-step exerise ECC were normal. AU routine laboratory studies yielded negative results. Coronary angiography was performed by Judkin's technique. The left ventriculogram was performed first and was normal. The left coronary injections were made and at this time he complained of severe chest pain. At the same time, ST segment elevation was observed in lead 2, which was
FIGURE3a (upper). ( Case 2 ) ECC (lead 2 ) during chest pain showing injury current. 3b (lower)ECC (lead 2) following relief of chest pain, with resolution of injury current.
FIGURE 2a (upper). (Case 1)Right coronary angiogram ( RAO view) showing severe spasm of middle portion. 2b (lower) Right coronary angiogram (RAO view) showing total relief of spasm of middle portion.
CHEST, 67: 6, JUNE, 1975
the orifice of the right coronary a r t e ~ y . ~ ? l l W e believe that intermittent coronary artery. spasm as the cause of angina pectoris in the absence of atherosclerotic coronary artery disease is a definite entity. Holter monitoring a n d coronary angiography during t h e attacks of pain may b e fruitful in establishing the diagnosis.
1 Prinzmetal MD, Kennamer R, Merliss R, et al: Angina pectoris 1: A variant form of angina pectoris. Preliminary report. Am J Med 27: 375, 1959 2 Prinzmetal M, Ekmekci A, Kennamer R, et al: Variant form of angina pectoris. Previously undelineated syndrome. JAMA 174:1974, 1960 3 Silvermann ME, Flamm MD: Variant angina pectoris: Anatomic and prognostic implications. Ann Intern Med 75:339, 1971 4 Cheng TO, Bashour T, Kelser GA Jr, et al: Variant angina of Prinzmetal with normal coronary arteriogriuns: A variant of the variant. Circulation 37:476, 1973 5 Oliva PD, Potts DE, Pluss RG: Coronary arterial spasm in Prinzmetal angina. N Engl J Med 288:745, 1973 6 White PD: Coronary artery spasm. N Engl J Med 288: 1355, 1973 7 Andersson R, Holmberg S, Svedmyr N, et al: Adrenergic a and j3 receptors in coronary vessels in man. An in oitro study. Acta Med Scand 191:241, 1972 8 Malindzak GA Jr, VanDyke AH, Green HD, et al: a and j3 adrenergic receptors in coronary vascular bed. Arch Int Pliarmacodyn Ther 197: 112, 1972 9 Demany MA, Tambe A, Zimmerman HA: Coronary arterial spasm. Chest 53:714, 1968 10 O'Reilly RJ, Spellberg RD, King TW: Recognition of proximal right coronary artery spasm during coronary arteriography. Radiology 95: 305, 1970 11 Bouchek RJ, Takeshita R, Brady AH: Intimal hypertrophy in coronary arteries and considerations of the papillary muscle arteries (man). Anat Rec 153:243,1965
Pulmonary Sarcoidosis Presenting as Bronchogenic carcinoma* Jerome C . A m t t , Jr., M.D.OOand Hurst B. Hatch, Jr., M.D., F.C.C.P.
Massive pulmonary fibrosis simulating bronchogenic carcinoma on chest roentgenograms, planigrams and bronchograms is a d i i c t l y unusual manifestatioo of sarcoidosis. Bronchial stenosis can result from any of three types of bronchial involvement: compression of the major bronchi by enlarged perihilar nodes, sarcoid lesions in the bronchial wall, and diffuse bronchial constriction 'From the Department of Internal Medicine, Sedion on Pulmonary Disease, Alton Ochsner Medical Foundation and Ochsner Clinic, New Orleans. "Presently at Elkins, West Virginia. Re rint requests: Dr. Amett, 1514 J d e r s o n Highway, New 0 r L a n s 70121
CHEST, 67: 6, JUNE, 1975
associated with massive fibrosis. The symptoms produced by sarcoidosis can be quite similar to those commonly associated with bnmchogenic carcinoma, and when combiied with suspicions findings on chest roentgenograms, planigrams, and bronchograms, can lead to a strong clinical suspicion of carcinoma. Since the two diseases can co-exist in the same patient, diagnostic thoracotomy is usually required even with a prior diagnmis of sarcoidosis.
T
he pulmonary fibrosis seen in patienis with advanced sarcoidosis can roentgenographically simulate pulmonary tuberculosis, idiopathic pulmonary fibrosis, congestive heart failure, pulmonary involvement with scleroderma, rheumatoid lung, pneumoconiosis, or lymphangitic carcinoma.' T h e presence of a mass lesion simulating bronchogenic carcinoma is distinctly unusual. W e report a case where massive fibrosis suggested bronchogenic carcinoma on chest roentgenogram, a t bronchoscopy, and on bronchograms.
A 53-year-old white farmer from Texas was referred to the Ochsner Medical Center in December, 1973 for evaluation of a mass lesion in his left upper lobe demonstrated on chest roentgenogram. He had smoked approximately six cigars daily for the ten years between 1946 and 1956. In 1956 a "spot" had been discovered in the lower left lung field on chest roentgenogram, which was no longer present on repeat study one year later. A routine chest roentgenogram in 1969 had revealed a diffuse interstitial infiltrate predominantly in the upper half of both lung fields. He remained asymptomatic, and a repeat study in 1971 revealed no change in the infiltrate. Evaluation at another hospital had included a left scalene node biopsy which had revealed a noncaseating granulomatous adenitis. Upon.admission, the patient reported malaise with a persistent nonproductive cough for the preceding six months, but he denied dyspnea, wheezing, chest pain, hemoptysis, fever, or weight loss. Auscultation of the lungs revealed a prolonged expiratory phase without rales or wheezes. There was no adenopathy or finger clubbing. Skin tests for tuberculosis, histoplasmosis, and mumps were negative. The chest roentgenogram revealed diffuse interstitial changes with a marked prominence of the left upper lobe hilus, suggesting a mass lesion, with radiation of fibrotic strands toward the periphery (Fig 1 ) . Tomograms revealed stenosis of the apicoposterior segment bronchus of the left upper lobe. Pulmonary function studies revealed a pure restrictive impairment, with the vital capacity 76 percent of predicted, the FEVl 83 percent of predicted, and the maximum breathing capacity 111percent of predicted. The resting alveolar-arterial oxygen gradient was elevated to 28 mm Hg, and the resting arterial oxygen pressure was normal (77 mm H g ) , with no change on exercise. Fiberoptic bronchoscopy revealed stenosis of the apicoposterior and anterior segmental bronchi of the left upper lobe, with normal-appearing mucosa. Brush biopsies of the segmental bronchi were negative for malignancy, and multiple washings were negative for fungi and acid-fast bacilli. A bronchogram showed a persistent filling defect of the anterior segment bronchus, with definite narrowing of the apicoposterior segment bronchus ( Fig 2 ) .
PULMONARY SARCOlDOSlS PRESENTING AS CARCINOMA 723