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Bronchoalveolar Lavage in Acute Hypersensitivity Pneumonitis Caused by Sulfasalazine
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infarction complicated by right to left shunt. J Am Cardioll983; 1:554-57 Meyers SN, Shapiro JE, Barresi ~ DeBoer AA, Pavel OJ, Gracey DR, et ale Right atrial myxoma with right to left shunting and mitral valve prolapse. Am J Med 1977; 62:308-14 Valdes-Cruz LM, Pieroni DR, Roland}A, Varghese PJ. Echocardiographic detection of intracardiac right-to-Ieft shunts following peripheral vein injections. Circulation 1976; 54:558-62 Stinson EB, Griepp RB, Bieber C~ Shumway NE. Hemodynamic observations after orthotopic transplantation of the canine heart. J Thorac Cardiovasc Surg 1972; 63:344-52 Stinson EB, Tecklenberg PL, Hollingsworth JF, Jones K~ Sloane R, Rahmoeller G. Changes in left ventricular mechanical and hemodynamic function during acute rejection of orthotopically transplanted hearts in dogs. J Thorac Cardiovasc Surg 1974; 68:783-91 Stinson EB, Caves PK, Griepp RB, Oyer PE, Rider AK, Shumway NE. Hemodynamic observations in the early period after human heart transplantation. J Thorac Cardiovasc Surg 1975; 69: 264-70 Stinson EB, Griepp RB, Dong E, Shumway NE. Results of human heart transplantation at Stanford University. 1hmsplant Proc 1971; 3:337-42 Samet ~ Fritts H~ Fishman ~ Coumand A. The blood volume in heart disease. Medicine 1957; 36(2):211-34 Feldschuh J, Enson Y. Prediction of the normal blood volume: relation of blood volume to body habitus. Circulation 1977; 56: 605-12 Wheeler WE, Rubis LJ, Jones C~ Harrah JD. Etiology and prevention of topical cardiac hypothermia-induced phrenic nerve injury during cardiac surgery. Chest 1985; 88:680-83 Hagen PI: SholzDG, EdwardsWD. Incidence and size of patent foramen ovale during the first ten decades of life: an autopsy study of 965 normal hearts. Mayo Clio Proc 1984; 59:17-20
Bronchoalveolar Lavage in Acute Hypersensitivity Pneumonitis Caused by Sulfasalazine* ~ Valcke, M.D.; R. Pauwels, M.D., F.C.C.~; M. Van Der Straeten, M.D.
and
Sulfasalazine has been reported to induce pulmonary eosinophilia and hypersensitivity with symptoms of dyspnea and fever. We present the results of bronchoalveolar lavage in a patient with acute sulfasalazine-induced hypersensitivity pneumonitis. The lavage specimen showed a significant inftux of eosinophils.
S
ulfasalazine is a chemical combination of 5-aminosalicylic acid, a salicylate analogue, and sulfapyridine, a sulfonamide, linked by an azo bond. It is primarily used as an oral agent in the treatment of inflammatory bowel disease.' Adverse reactions with sulfasalazine are common, occurring in approximately 20 percent of patients taking the drug. Pulmonary hypersensitivity reactions, however, seldom have been reported. We describe a case of sulfasalazine-induced
hypersensitivity pneumonitis in a patient taking the drug for inflammatory bowel disease associated with reactive arthritis. Bronchoalveolar lavage (BAL) demonstrated a marked increase in the percentage of eosinophils and a slight increase in the number of lymphocytes. CASE REPORT
A 4O-ye8l'-Old non-smoking man had a three-year history of arthralgia of the left knee joint. Rheumatologic investigations, including arthroscopy and ileocoloscopy with removal of specimens for biopsy, revealed the diagnosis ofa reactive arthritis with chronic synovitis associated with inflammatory bowel disease. He never experienced, however, any gastrointestinal complaints. At that time, the chest radiograph was normal. 1reatment with sulfasa1azine was initiated in a dosage of 500 mg twice a day for four days and subsequently increased to 1,()()() mg twice a day. Ten days later, the patient developed malaise, lethargy, loss of energy and anorexia, followed by an irritating dry cough, dyspnea on exertion, chest tightness, night sweats and fever up to 38.5°C. On admission, his bodytemperature was 37. goC, the pulse was regular at 88 beatslmin, and the blood pressure was 115170 mm Hg. There were no abnormal auscultatory findings on examination of the chest. Laboratory values included a white blood cell count of 11.300/cu mm, with 51 percent neutrophils, 31 percent lymphocytes, 13 percent monocytes and 5 percent eosinophils. The total eosinophil count was 9161cu mm (normally 50 to 250Icu mm). The erythrocyte sedimentation rate (ESR) was 38 mm in 1 h. Skin prick tests with the most common inhalant allergens were positive for Dermatophtlgoides pteronf/ssinus and Alternaria tenuis. Total 19E was 11 IU/ml. No precipitating antibodies to common antigens causing hypersensitivity pneumonitis could be demonstrated. There was no rise in antibody titer to common respiratory viruses. Roentgenograms of the chest showed bilateral acinar infiltrates, principally in both lung apices, bilateral pleural reaction with obliteration of the costodiaphragmatic sinus on both sides, and accentuation of interstitial markings with Kerley-B lines. Pulmonary function tests revealed a moderate resbictive reduction in lung volumes with a single-breath carbon monoxide diffusing capacity of 82 percent of predicted value. Capillary blood gas analysis revealed a pH of 7.39, a Po. of 58 mm Hg and a Pco, of 40 mm Hg. Fiberoptic bronchoscopy, performed on the day of admission showed moderate bronchial inflammation. Bronchoalveolar lavage (five times a 5O-ml aliquot of sterile saline solution) was performed in the right middle lobe. The totalcell count was 2.56 X 10' cells/l00 ml lavage fluid. Differential cell analysis of the pooled liquid from the last four washings revealed 37 percent eosinophils, 38 percent alveolar macrophages, 10 percent neutrophils, 1 percent basophils and 14percent lymphocytes (88 percent T-Iymphocytes, 5 percent B-lymphocytes, and an OKT4-0IIT8 ratio of 2.32). Discontinuation of the sulfasalazme therapy promptly was followed by a marked symptomatic improvement and a disappearance of all radiographic and functional abnormalities within one week. The eosinophil count remained elevated at 430Icu mm. DISCUSSION
*From the Department of Respiratory Diseases, University Hospital, Ghent, Belgium. . Reprint requests: Dr. Pauwels, Department ofRespiratoru Diseases, Academic Hospital, B-9000 Ghent, Belgium
Although sulfasalazine treatment commonly is used in inflammatory bowel disease, and a high incidence of nonrespiratory side effects is observed, only ten well documented cases of pulmonary injury due to sulfasalazine treatment have been reported. Fibrosing alveolitis is the most severe pulmonary complication and has been reported twice,2.3 including one patient with a fatal outcome," the other also showing bronchiolitis obliterans. 2 Hypersensitivity pneumonitis is the most common pulmo-
572
SALIn Acute Hyper8ensttIvIt Pneumonitis (\WCke, Pauwels, \1InDer Sttaeten)
nary Injury induced by sulfasalazine, eight cases being reported in the English-language literature.r'" The onset usually is acute and unrelated to cumulative dose of the drug or to duration of therapy" Symptoms of the syndrome include dyspnea, cough, chest tightness and chest pain, night sweats and fever, frequently without significant auscultatory chest findings.4-lO Usually there is peripheral eosinophilia and an elevated ESR.4-1O Chest radiography reveals bilateral patchy acinar or reticular infiltrates, mainly peripheral.S'" The most common abnormality of pulmonary function is an obstructive pattern with decreased carbon monoxide transfer factor:8 Challenge tests demonstrated that the sulfapyridine portion of sulfasalazine causes the hypersensitivity reaction. 4.5 The prognosis of sulfasalazine-induced hypersensitivity pneumonitis is generally excellent with complete recovery on discontinuation of the drug. 4-10 Corticosteroids may hasten the recovery but are seldom indicated. The only published report of transbronchiallung biopsy performed in a patient with sulfasalazine-induced hypersensitivity pneumonitis showed interstitial pneumonitis and slight fibrosis but no tissue eosinophilia. 8 To our knowledge, our study is the first report of bronchoalveolar lavage in sulfasalazine-induced hypersensitivity pneumonitis. Bronchoalveolar lavage analysis showed a marked influx of eosinophils and a moderate increase in the numbers of the lymphocytes and basophils. These findings support an immunologic pathogenesis of the disease, rather than direct toxicity of the drug. A predominantly eosinophilic pattern of BAL Huid points to eosinophilic lung disease. However, the exact immunologic mechanisms by which sulfasalazine induces eosinophilic pneumonia remain unknown. The association of the acute respiratory disease with the intake of sulfasalazine and the complete disappearance of all respiratory abnormalities after cessation of the drug provides evidence that the eosinophilic lung infiltrate in our patient should be regarded as a hypersensitivity reaction to sulfasalazine. REFERENCES 1 Peppercorn MA. Sulfasalazine: pharmacology, clinical use, toxicity and related new drug development. Ann Intern Med 1984; 3:377-86 2 Williams l: Eidus L, Thomas E Fibrosing alveolitis, bronchiolitis obliterans and sulfasalazine therapy. Chest 1982; 81:766-68 3 Davies 0, Mac Farlance A. Fibrosing alveolitis and treabnent with sulfasalazine. Gut 1974; 15:185-88 4 Jones GR, Malone OMS. SulfasaJazine induced lung disease. Thorax 1972; 27:713-17 5 Thomas ~ Seaton A, Edwards J. Respiratory disease due to sulfasalazine. Clin Allergy 1974; 4:41-47 6 Constantinidis KA. Eosinophilic pneumonia: an unusual side effect of therapy with salicylazosulfapyridine. Chest 1976; 70:315-16 7 Berliner S, Neeman A, Shoenfeld \: Eldar M, Rousso I, Kadish U, et al. Salazopyrine induced eosinophilic pneumonia. Respiration 1980; 39:119-20 8 Yaffe BH, Korelitz BI. Sulfasalazine pneumonitis. Am J Gastroenterol 1983; 78:493-94 9 Wang KK, Bowyer BA, Fleming CR, Schroeder K. Pulmonary infiltrates and eosinophilia associated with sulfasalazine. Mayo Clin Proc 1984; 59:343-46 10 Auerbuch M, Halpern Z, Hallak A, Topilsky M, Levo ~ Sulfasalazine pneumonitis. Am J Gastroenteroll985; 80:343-45
Flecalnlde-Induced Sustained Ventricular Tachycardia Successfully Treated with Lldocalne* Jerry L. Bauman, Phama.D.; JoseGallastegui, M.D.; Seth R. Tanenbaum, M.D.; and Robert J. Hariman, M.D. A 69-year-old man had new sustained ventricular tachycar-
dia caused by 8ecainide which promptly responded to intravenous lidocaine therapy. Discontinuation of the lidocaine infusion resulted in the reappearance of ventricular tachycardia which again immediately terminated after lidocaine was given. In this case, lidocaine effectively reversed the proarrhythmic etTects of 8ecainide.
I
n addition to successfully suppressing arrhythmogenic foci, antiarrhythmic drugs may also paradoxically precipitate new rhythm disturbances or worsen existing arrhythmias.P Indeed, antiarrhythmic agents have been causally related to out-of-hospital cardiac arrest in patients who do not have underlying sustained ventricular tachycardia or ventricular fibrillation. 1 Flecainide is a new type IC antiarrhythmic agent recently approved for the treatment of serious ventricular arrhythmias. The proarrhythmic potential of 8ecainide has received considerable attention in the medical literature. 3.4 However, there is little information regarding the therapeutic approach to patients with flecainide-induced arrhythmias. We report a case of new sustained ventricular tachycardia related to Hecainide therapy which terminated immediately after intravenous administration of lidocaine. CASE REPORT A 69-year-old black man was admitted to the University of Illinois Hospital for numerous episodes of palpitations associated with mild dizziness. An ambulatory Holter recording prior to admission showed sinus bradycardia with preexcited ventricular complexes and occasional episodes of a slightly irregular rhythm with wide QRS complexes (rate 120 bpm, 9 beats maximum). On admission, physical examination was not remarkable. Blood pressure was 146190 mm Hg. Laboratory examination revealed normal findings except for a blood urea nitrogen value of 31 mgldl and a serum creatinine concentration of 2.2 mg/dl, Chest roentgenogram revealed a nonnal heart size. Ejection fraction by gated nuclear angiography was 51 percent 1\velve-lead ECG showed sinus bradycardia (rate 56 bpm) with evidence of ventricular preexcitation. Electrocardiographic monitoring for 48 hours revealed occasional premature ventricular complexes and several episodes of a selfterminating wide QRS tachycardia (four to nine beats) (Fig lA). Intravenous and oral procainamide failed to suppress recurrences of this rhythm, and the patient was subsequently taken to the electrophysiology laboratory. During this study, nonsustained ventricular tachycardia was confirmed as the cause of the wide QRS tachycardia (Fig 2A) and the effective refractory period of the accessory atrioventricular pathway was determined to be 200 ms. Oral flecainide, 100 mg twice daily, was started (48 hours after the *From the Departments of Pharm89' Practice and Medicine, Section of Cardiology, University of Illinois at Chicago.
~nt requem: Dr. Bauman, University of lUinois College PMrmtICfJ, 833 Wood Street, Chicago, 60612
CHEST I 92 I 3 I SEPTEMBER, 1987
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infarction complicated by right to left shunt. J Am Cardioll983; 1:554-57 Meyers SN, Shapiro JE, Barresi ~ DeBoer AA, Pavel OJ, Gracey DR, et ale Right atrial myxoma with right to left shunting and mitral valve prolapse. Am J Med 1977; 62:308-14 Valdes-Cruz LM, Pieroni DR, Roland}A, Varghese PJ. Echocardiographic detection of intracardiac right-to-Ieft shunts following peripheral vein injections. Circulation 1976; 54:558-62 Stinson EB, Griepp RB, Bieber C~ Shumway NE. Hemodynamic observations after orthotopic transplantation of the canine heart. J Thorac Cardiovasc Surg 1972; 63:344-52 Stinson EB, Tecklenberg PL, Hollingsworth JF, Jones K~ Sloane R, Rahmoeller G. Changes in left ventricular mechanical and hemodynamic function during acute rejection of orthotopically transplanted hearts in dogs. J Thorac Cardiovasc Surg 1974; 68:783-91 Stinson EB, Caves PK, Griepp RB, Oyer PE, Rider AK, Shumway NE. Hemodynamic observations in the early period after human heart transplantation. J Thorac Cardiovasc Surg 1975; 69: 264-70 Stinson EB, Griepp RB, Dong E, Shumway NE. Results of human heart transplantation at Stanford University. 1hmsplant Proc 1971; 3:337-42 Samet ~ Fritts H~ Fishman ~ Coumand A. The blood volume in heart disease. Medicine 1957; 36(2):211-34 Feldschuh J, Enson Y. Prediction of the normal blood volume: relation of blood volume to body habitus. Circulation 1977; 56: 605-12 Wheeler WE, Rubis LJ, Jones C~ Harrah JD. Etiology and prevention of topical cardiac hypothermia-induced phrenic nerve injury during cardiac surgery. Chest 1985; 88:680-83 Hagen PI: SholzDG, EdwardsWD. Incidence and size of patent foramen ovale during the first ten decades of life: an autopsy study of 965 normal hearts. Mayo Clio Proc 1984; 59:17-20
Bronchoalveolar Lavage in Acute Hypersensitivity Pneumonitis Caused by Sulfasalazine* ~ Valcke, M.D.; R. Pauwels, M.D., F.C.C.~; M. Van Der Straeten, M.D.
and
Sulfasalazine has been reported to induce pulmonary eosinophilia and hypersensitivity with symptoms of dyspnea and fever. We present the results of bronchoalveolar lavage in a patient with acute sulfasalazine-induced hypersensitivity pneumonitis. The lavage specimen showed a significant inftux of eosinophils.
S
ulfasalazine is a chemical combination of 5-aminosalicylic acid, a salicylate analogue, and sulfapyridine, a sulfonamide, linked by an azo bond. It is primarily used as an oral agent in the treatment of inflammatory bowel disease.' Adverse reactions with sulfasalazine are common, occurring in approximately 20 percent of patients taking the drug. Pulmonary hypersensitivity reactions, however, seldom have been reported. We describe a case of sulfasalazine-induced
hypersensitivity pneumonitis in a patient taking the drug for inflammatory bowel disease associated with reactive arthritis. Bronchoalveolar lavage (BAL) demonstrated a marked increase in the percentage of eosinophils and a slight increase in the number of lymphocytes. CASE REPORT
A 4O-ye8l'-Old non-smoking man had a three-year history of arthralgia of the left knee joint. Rheumatologic investigations, including arthroscopy and ileocoloscopy with removal of specimens for biopsy, revealed the diagnosis ofa reactive arthritis with chronic synovitis associated with inflammatory bowel disease. He never experienced, however, any gastrointestinal complaints. At that time, the chest radiograph was normal. 1reatment with sulfasa1azine was initiated in a dosage of 500 mg twice a day for four days and subsequently increased to 1,()()() mg twice a day. Ten days later, the patient developed malaise, lethargy, loss of energy and anorexia, followed by an irritating dry cough, dyspnea on exertion, chest tightness, night sweats and fever up to 38.5°C. On admission, his bodytemperature was 37. goC, the pulse was regular at 88 beatslmin, and the blood pressure was 115170 mm Hg. There were no abnormal auscultatory findings on examination of the chest. Laboratory values included a white blood cell count of 11.300/cu mm, with 51 percent neutrophils, 31 percent lymphocytes, 13 percent monocytes and 5 percent eosinophils. The total eosinophil count was 9161cu mm (normally 50 to 250Icu mm). The erythrocyte sedimentation rate (ESR) was 38 mm in 1 h. Skin prick tests with the most common inhalant allergens were positive for Dermatophtlgoides pteronf/ssinus and Alternaria tenuis. Total 19E was 11 IU/ml. No precipitating antibodies to common antigens causing hypersensitivity pneumonitis could be demonstrated. There was no rise in antibody titer to common respiratory viruses. Roentgenograms of the chest showed bilateral acinar infiltrates, principally in both lung apices, bilateral pleural reaction with obliteration of the costodiaphragmatic sinus on both sides, and accentuation of interstitial markings with Kerley-B lines. Pulmonary function tests revealed a moderate resbictive reduction in lung volumes with a single-breath carbon monoxide diffusing capacity of 82 percent of predicted value. Capillary blood gas analysis revealed a pH of 7.39, a Po. of 58 mm Hg and a Pco, of 40 mm Hg. Fiberoptic bronchoscopy, performed on the day of admission showed moderate bronchial inflammation. Bronchoalveolar lavage (five times a 5O-ml aliquot of sterile saline solution) was performed in the right middle lobe. The totalcell count was 2.56 X 10' cells/l00 ml lavage fluid. Differential cell analysis of the pooled liquid from the last four washings revealed 37 percent eosinophils, 38 percent alveolar macrophages, 10 percent neutrophils, 1 percent basophils and 14percent lymphocytes (88 percent T-Iymphocytes, 5 percent B-lymphocytes, and an OKT4-0IIT8 ratio of 2.32). Discontinuation of the sulfasalazme therapy promptly was followed by a marked symptomatic improvement and a disappearance of all radiographic and functional abnormalities within one week. The eosinophil count remained elevated at 430Icu mm. DISCUSSION
*From the Department of Respiratory Diseases, University Hospital, Ghent, Belgium. . Reprint requests: Dr. Pauwels, Department ofRespiratoru Diseases, Academic Hospital, B-9000 Ghent, Belgium
Although sulfasalazine treatment commonly is used in inflammatory bowel disease, and a high incidence of nonrespiratory side effects is observed, only ten well documented cases of pulmonary injury due to sulfasalazine treatment have been reported. Fibrosing alveolitis is the most severe pulmonary complication and has been reported twice,2.3 including one patient with a fatal outcome," the other also showing bronchiolitis obliterans. 2 Hypersensitivity pneumonitis is the most common pulmo-
572
SALIn Acute Hyper8ensttIvIt Pneumonitis (\WCke, Pauwels, \1InDer Sttaeten)
nary Injury induced by sulfasalazine, eight cases being reported in the English-language literature.r'" The onset usually is acute and unrelated to cumulative dose of the drug or to duration of therapy" Symptoms of the syndrome include dyspnea, cough, chest tightness and chest pain, night sweats and fever, frequently without significant auscultatory chest findings.4-lO Usually there is peripheral eosinophilia and an elevated ESR.4-1O Chest radiography reveals bilateral patchy acinar or reticular infiltrates, mainly peripheral.S'" The most common abnormality of pulmonary function is an obstructive pattern with decreased carbon monoxide transfer factor:8 Challenge tests demonstrated that the sulfapyridine portion of sulfasalazine causes the hypersensitivity reaction. 4.5 The prognosis of sulfasalazine-induced hypersensitivity pneumonitis is generally excellent with complete recovery on discontinuation of the drug. 4-10 Corticosteroids may hasten the recovery but are seldom indicated. The only published report of transbronchiallung biopsy performed in a patient with sulfasalazine-induced hypersensitivity pneumonitis showed interstitial pneumonitis and slight fibrosis but no tissue eosinophilia. 8 To our knowledge, our study is the first report of bronchoalveolar lavage in sulfasalazine-induced hypersensitivity pneumonitis. Bronchoalveolar lavage analysis showed a marked influx of eosinophils and a moderate increase in the numbers of the lymphocytes and basophils. These findings support an immunologic pathogenesis of the disease, rather than direct toxicity of the drug. A predominantly eosinophilic pattern of BAL Huid points to eosinophilic lung disease. However, the exact immunologic mechanisms by which sulfasalazine induces eosinophilic pneumonia remain unknown. The association of the acute respiratory disease with the intake of sulfasalazine and the complete disappearance of all respiratory abnormalities after cessation of the drug provides evidence that the eosinophilic lung infiltrate in our patient should be regarded as a hypersensitivity reaction to sulfasalazine. REFERENCES 1 Peppercorn MA. Sulfasalazine: pharmacology, clinical use, toxicity and related new drug development. Ann Intern Med 1984; 3:377-86 2 Williams l: Eidus L, Thomas E Fibrosing alveolitis, bronchiolitis obliterans and sulfasalazine therapy. Chest 1982; 81:766-68 3 Davies 0, Mac Farlance A. Fibrosing alveolitis and treabnent with sulfasalazine. Gut 1974; 15:185-88 4 Jones GR, Malone OMS. SulfasaJazine induced lung disease. Thorax 1972; 27:713-17 5 Thomas ~ Seaton A, Edwards J. Respiratory disease due to sulfasalazine. Clin Allergy 1974; 4:41-47 6 Constantinidis KA. Eosinophilic pneumonia: an unusual side effect of therapy with salicylazosulfapyridine. Chest 1976; 70:315-16 7 Berliner S, Neeman A, Shoenfeld \: Eldar M, Rousso I, Kadish U, et al. Salazopyrine induced eosinophilic pneumonia. Respiration 1980; 39:119-20 8 Yaffe BH, Korelitz BI. Sulfasalazine pneumonitis. Am J Gastroenterol 1983; 78:493-94 9 Wang KK, Bowyer BA, Fleming CR, Schroeder K. Pulmonary infiltrates and eosinophilia associated with sulfasalazine. Mayo Clin Proc 1984; 59:343-46 10 Auerbuch M, Halpern Z, Hallak A, Topilsky M, Levo ~ Sulfasalazine pneumonitis. Am J Gastroenteroll985; 80:343-45
Flecalnlde-Induced Sustained Ventricular Tachycardia Successfully Treated with Lldocalne* Jerry L. Bauman, Phama.D.; JoseGallastegui, M.D.; Seth R. Tanenbaum, M.D.; and Robert J. Hariman, M.D. A 69-year-old man had new sustained ventricular tachycar-
dia caused by 8ecainide which promptly responded to intravenous lidocaine therapy. Discontinuation of the lidocaine infusion resulted in the reappearance of ventricular tachycardia which again immediately terminated after lidocaine was given. In this case, lidocaine effectively reversed the proarrhythmic etTects of 8ecainide.
I
n addition to successfully suppressing arrhythmogenic foci, antiarrhythmic drugs may also paradoxically precipitate new rhythm disturbances or worsen existing arrhythmias.P Indeed, antiarrhythmic agents have been causally related to out-of-hospital cardiac arrest in patients who do not have underlying sustained ventricular tachycardia or ventricular fibrillation. 1 Flecainide is a new type IC antiarrhythmic agent recently approved for the treatment of serious ventricular arrhythmias. The proarrhythmic potential of 8ecainide has received considerable attention in the medical literature. 3.4 However, there is little information regarding the therapeutic approach to patients with flecainide-induced arrhythmias. We report a case of new sustained ventricular tachycardia related to Hecainide therapy which terminated immediately after intravenous administration of lidocaine. CASE REPORT A 69-year-old black man was admitted to the University of Illinois Hospital for numerous episodes of palpitations associated with mild dizziness. An ambulatory Holter recording prior to admission showed sinus bradycardia with preexcited ventricular complexes and occasional episodes of a slightly irregular rhythm with wide QRS complexes (rate 120 bpm, 9 beats maximum). On admission, physical examination was not remarkable. Blood pressure was 146190 mm Hg. Laboratory examination revealed normal findings except for a blood urea nitrogen value of 31 mgldl and a serum creatinine concentration of 2.2 mg/dl, Chest roentgenogram revealed a nonnal heart size. Ejection fraction by gated nuclear angiography was 51 percent 1\velve-lead ECG showed sinus bradycardia (rate 56 bpm) with evidence of ventricular preexcitation. Electrocardiographic monitoring for 48 hours revealed occasional premature ventricular complexes and several episodes of a selfterminating wide QRS tachycardia (four to nine beats) (Fig lA). Intravenous and oral procainamide failed to suppress recurrences of this rhythm, and the patient was subsequently taken to the electrophysiology laboratory. During this study, nonsustained ventricular tachycardia was confirmed as the cause of the wide QRS tachycardia (Fig 2A) and the effective refractory period of the accessory atrioventricular pathway was determined to be 200 ms. Oral flecainide, 100 mg twice daily, was started (48 hours after the *From the Departments of Pharm89' Practice and Medicine, Section of Cardiology, University of Illinois at Chicago.
~nt requem: Dr. Bauman, University of lUinois College PMrmtICfJ, 833 Wood Street, Chicago, 60612
CHEST I 92 I 3 I SEPTEMBER, 1987
of
573