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Cardiac tuberculosis with multiple intracardiac masses: A case report
Cardiac Tuberculosis With Multiple Intracardiac Masses: A Case Report ¨ zer, MD, Kudret Aytemir, MD, Elif Sade, Aytekin Oto, MD, Sercan Aksoy, MD, Necla O Hu¨seyin Engin, MD, Lale Tokgo¨zog˘lu, MD, FESC, FACC, and Ali Oto, MD, FESC, FACC, Ankara, Turkey
In this report, clinical, echocardiographic, and pathologic findings of a patient with multiple masses caused by tuberculosis both in the left and right side of the heart are presented. After antituberculosis treatment some of the masses disappeared
T
uberculosis of the heart is very rare, and it is becoming even less frequent because of better control of tuberculosis during the last couple of decades. In this report a case of cardiac tuberculosis with multiple masses in the left atrium (LA), left ventricle (LV), and right atrium (RA) is presented, and several aspects of the involvement of the heart are discussed.
CASE REPORT A 25-year-old female patient was admitted to our hospital with complaints of dyspnea and abdominal swelling. Her history revealed abdominal pain and diarrhea episodes for 1 year. She had been diagnosed and treated for typhoid fever during this period without any benefit. Recently, she noticed facial and abdominal swelling, edema in the legs, anorexia, and weight loss. Moreover, she developed exertional dyspnea, orthopnea, cough, and white sputum. She was found to have a right-sided pleural effusion by examination and on chest radiograph, and she was referred to our hospital for further evaluation. From her family history it was learned that she had an uncle who was treated for tuberculosis. On physical examination, the pulse was 62 bpm, blood pressure was 110/70 mm Hg, and temperature was 38.4°C. There were several lymph node enlargements in the neck region, and jugular venous distension was apparent. The lung and heart examination showed fine rales on the right base of the lungs and a mild mitral regurgitation murmur. She also ¨ ., K.A., E.S., L.T., From the Departments of Cardiology (N.O A.O.), Radiology (A.O.), and Oncology (S.A., H.E.), Hacettepe University, School of Medicine. ¨ zer, Ziraat Mah, 14. Sok, 8/1, 06110, Reprint requests: Necla O Ankara, Turkey (E-mail: [email protected]). Copyright 2002 by the American Society of Echocardiography. 0894-7317/2002/$35.00 ⫹ 0 27/4/119846 doi:10.1067/mje.2002.119846
756
and some became smaller. Although an intracardiac mass caused by tuberculosis is very rare, it should be considered in the list of masses detected by echocardiography. (J Am Soc Echocardiogr 2002;15: 756-8.)
had hepatomegaly and bilateral pitting pretibial edema. Laboratory analysis revealed an elevated sedimentation rate of 41 mm/h and mild anemia (hemoglobin: 10.7 g/dL, mean corpuscular volume: 78 fL, hematocrit: 31.8%). There were no specific findings in the other laboratory analysis. An electrocardiogram revealed no significant findings. A pleural tap was performed, and cytologic examination revealed lymphocytes and polymorphonuclear leukocytes; culture was negative. The transthoracic echocardiography showed multiple masses in the RA, LA (Figures 1, A, and 2, A), and left ventricular apex. There was also a mild pericardial effusion. Transesophageal echocardiography showed that the mass in the RA was extending from the superior vena cava to the inferior vena cava (Figure 3), and there were also multiple masses in the LA and LV. Computed tomography of the abdomen revealed a mass invading the whole mediastinum, pericardium, and superior vena cava, as well as enlarged hepatic veins and inferior vena cava, hepatomegaly with a diffuse contrast enhancement, ascites, and pleural thickening over the bases of the lungs. Magnetic resonance imaging of the heart showed a mass starting from the cardiac apex and surrounding the whole heart with continuity along the superior vena cava and aortic root. The intracardiac masses showed round, nodular characteristics. A right atrial mass was extending from the anterolateral surface of the RA and showed indentation to the right atrial cavity (Figure 4). The mass also invaded the left ventricular wall. The RA and inferior vena cava were markedly dilated. There was also slight dilatation in the LA. A thoracotomy was performed and a mass invading the inferior vena cava, RA, and anterior wall of LV was seen. Frozen biopsy was taken from the mass invading the RA and revealed a granulomatous disease consistent with tuberculosis, and multiple excisional biopsies from the superior vena cava, left subclavian lymph node enlargement, and heart were obtained. Pathologic examination revealed caseating, granulomatous inflammation typical for tuberculosis. A microbiologic culture and polymerase
Journal of the American Society of Echocardiography Volume 15 Number 7
¨ zer et al O
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Figure 1 A, Parasternal long-axis view showing masses in left atrium. B, Parasternal long-axis view after 4-month antituberculosis treatment. AO, Aorta; LV, left ventricle; LA, left atrium.
Figure 2 A, Parasternal short-axis view of mass in right atrium. B, Parasternal short-axis view after 4-month antituberculosis treatment. RV, Right ventricle; AO, aorta; RA, right atrium; LA, left atrium.
chain reaction confirmed the diagnosis of mycobacterium tuberculosis infection. Antituberculosis treatment was started (isoniazid, rifampin, ethambutol, and pyrazinamide for 2 months; later isoniazid and rifampin were continued). She was seen monthly after therapy, and at the fourth month of treatment the patient’s general condition was improved. Echocardiographic examination showed that the masses in the LA had almost totally disappeared, and the mass in the RA was very small compared with the beginning state (Figures 1, B, and 2, B).
DISCUSSION The most interesting findings from our patient were multiple masses in the LA, RA, aortic root, and left ventricular apex caused by tuberculosis. Tuberculosis may affect the heart in several ways. It may be seen primarily in the heart without involvement of any other organ in the body, or it may complicate typical tuberculous disease elsewhere. All 3 layers of the heart may be affected from the disease process. Pericardial involvement caused by tuberculosis may be in the form of pericardial
effusion, pericarditis, cardiac tamponade, constrictive pericarditis, and pericardial mass.1-6 In the endemic areas, the most common cause of constrictive pericarditis is tuberculosis.7,8 In some cases of constrictive pericarditis, myocardial and pericardial involvement of varying degrees were also demonstrated.9,10 Tuberculous myocardial lesions, however, are extremely rare and usually diagnosed at autopsy.11,12 The myocardium is usually affected by direct extension, or less often by retrograde lymphatic drainage from tuberculous mediastinal nodes. Infection via the hematogenous route may also develop in miliary disease. Three distinct forms of myocardial involvement are recognized: nodular tubercles (tuberculomas) of the myocardium, miliary tubercles of the myocardium, and an uncommon diffuse infiltrative type.13 Although myocardial tuberculosis is usually diagnosed incidentally at necropsy, it may produce cardiac arrhythmias, such as supraventricular arrhythmias,12 atrioventricular block,14,15 ventricular tachycardia, and ventricular fibrillation.16 A patient with an obstructive, tumor-like mass is much less common.17,18 Cases of pseudoaneurysm formation19 and sudden cardiac death20,21 caused by the rupture
¨ zer et al 758 O
Journal of the American Society of Echocardiography July 2002
REFERENCES
Figure 3 Transesophageal echocardiographic view of mass in right atrium.
Figure 4 Magnetic resonance imaging of masses in heart.
of myocardial tuberculoma were also reported. Tuberculosis of the heart may also cause restrictive cardiomyopathy and differential diagnosis of these patients from those with constrictive pericarditis caused by tuberculosis is very difficult.22 The differential diagnosis of cardiac tuberculosis includes other granulomatous disorders, such as sarcoidosis, granulomatous giant cell myocarditis, syphilitic gummas, fungal infections, rheumatic fever, rheumatoid arthritis, metastatic tumors containing giant cells (such as osteosarcoma and Hodgkin’s disease), and abscesses.23 Our experience suggests that tuberculous involvement of the heart should be on the list of intrapericardial masses shown by echocardiography, particularly in the endemic areas.
1. Afzal A, Keohane M, Keeley E, Borzak S, Callender CW, Iannuzzi M. Myocarditis and pericarditis with tamponade associated with disseminated tuberculosis. Can J Cardiol 2000;16:519-21. 2. Schwartz AB, Mitchell RS, Higgins CB, Lipton MJ, Klausner SC. Invasive calcific constrictive pericarditis simulating a left ventricular mass. Am Heart J 1986;112:861-3. 3. Sauleda S, Permanyer MG, Soler SJ. Tuberculous pericarditis: ten-year experience with a prospective protocol for diagnosis and treatment. J Am Coll Cardiol 1988;11:724-8. 4. Fowler NO. Tuberculous pericarditis. JAMA 1991;266:99-103. 5. Atar S, Chiu J, Forrester JS, Siegel RJ. Bloody pericardial effusion in patients with cardiac tamponade: is the cause cancerous, tuberculous, or iatrogenic in the 1990’s? Chest 1999;116:1564-9. 6. Komsuoglu B, Goldeli O, Kulan K, Gedik Y. Tuberculous pericarditis in north-east Turkey: an echocardiographic study. Acta Cardiol 1994;49:157-63. 7. Blake S, Bonar S, O’Neil H, Hanly P, Drury I, Flanagan M, et al. Aetiology of chronic constrictive pericarditis. Br Heart J 1983;50:273. 8. Cameron J, Oesterle SN, Baldwin JC, Hancock EW. The etiologic spectrum of constrictive pericarditis. Am Heart J 1987;113:354. 9. Dave T, Narula JP, Chopra P. Myocardial and endocardial involvement in tuberculous constrictive pericarditis: difficulty in biopsy distinction from endomyocardial fibrosis as a cause of restrictive heart disease. Int J Cardiol 1990;28:245-51. 10. Talwar KK, Narula JP, Chopra P. Myocarditis and myocardial interstitial fibrosis in constrictive pericarditis—an extended pathological spectrum. Int J Cardiol 1990;29:241-3. 11. Pomerance A. Tuberculoma of the interventricular septum. Br Heart J 1963;25:412-4. 12. Kapoor OP, Mascarenhas E, Rananaware MM, Gadgil RK. Tuberculoma of the heart: report of 9 cases. Am Heart J 1973;86:334-40. 13. Horn H, Saphir O. The involvement of the myocardium in tuberculosis: a review of the literature and report of three cases. Am Rev Tuberc 1935;32:492-506. 14. Menon BT, Rao CKP. Tuberculosis of the myocardium causing complete heart block. Am J Pathol 1945;21:1193-7. 15. Wren C, Stovin PGI. Isolated interventricular septal tuberculoma causing complete heart block. Thorax 1982;37:149-50. 16. Behr G, Palin HC, Temperly JM. Myocardial tuberculosis. Br Med J 1977;1(6066):951. 17. Rawis WJ, Shuford WH, Logan WD, Hurst JW, Schland RC. Right ventricular outflow tract obstruction produced by a myocardial abscess in a patient with tuberculosis. Am J Cardiol 1968;21:738-45. 18. Kinare SG. Interesting facts of cardiovascular tuberculosis. Indian J Surg 1975;37:144-51. 19. Halim MA, Mercer EN, Guinn GA. Myocardial tuberculoma with rupture and pseudoaneurysm formation—successful surgical treatment. Br Heart J 1985;54:603-4. 20. Wallis PJ, Branfoot AC, Emerson PA. Sudden death due to myocardial tuberculosis. Thorax 1984;39:155-6. 21. Kirsten K, Schaedel C. Sudden death due to myocardial tuberculosis. Thorax 1985;40:799. 22. Bali HK, Wahi S, Sharma BK, Anand IS, Datta BN, Wahi PL. Myocardial tuberculosis presenting as restrictive cardiomyopathy. Am Heart J 1990;120:703-6. 23. Ferrans VJ, Rodriguez ER, McAllister HA Jr. Granulomatous inflammation of the heart. Heart Vessels Suppl 1985;1:262-70.
In this report, clinical, echocardiographic, and pathologic findings of a patient with multiple masses caused by tuberculosis both in the left and right side of the heart are presented. After antituberculosis treatment some of the masses disappeared
T
uberculosis of the heart is very rare, and it is becoming even less frequent because of better control of tuberculosis during the last couple of decades. In this report a case of cardiac tuberculosis with multiple masses in the left atrium (LA), left ventricle (LV), and right atrium (RA) is presented, and several aspects of the involvement of the heart are discussed.
CASE REPORT A 25-year-old female patient was admitted to our hospital with complaints of dyspnea and abdominal swelling. Her history revealed abdominal pain and diarrhea episodes for 1 year. She had been diagnosed and treated for typhoid fever during this period without any benefit. Recently, she noticed facial and abdominal swelling, edema in the legs, anorexia, and weight loss. Moreover, she developed exertional dyspnea, orthopnea, cough, and white sputum. She was found to have a right-sided pleural effusion by examination and on chest radiograph, and she was referred to our hospital for further evaluation. From her family history it was learned that she had an uncle who was treated for tuberculosis. On physical examination, the pulse was 62 bpm, blood pressure was 110/70 mm Hg, and temperature was 38.4°C. There were several lymph node enlargements in the neck region, and jugular venous distension was apparent. The lung and heart examination showed fine rales on the right base of the lungs and a mild mitral regurgitation murmur. She also ¨ ., K.A., E.S., L.T., From the Departments of Cardiology (N.O A.O.), Radiology (A.O.), and Oncology (S.A., H.E.), Hacettepe University, School of Medicine. ¨ zer, Ziraat Mah, 14. Sok, 8/1, 06110, Reprint requests: Necla O Ankara, Turkey (E-mail: [email protected]). Copyright 2002 by the American Society of Echocardiography. 0894-7317/2002/$35.00 ⫹ 0 27/4/119846 doi:10.1067/mje.2002.119846
756
and some became smaller. Although an intracardiac mass caused by tuberculosis is very rare, it should be considered in the list of masses detected by echocardiography. (J Am Soc Echocardiogr 2002;15: 756-8.)
had hepatomegaly and bilateral pitting pretibial edema. Laboratory analysis revealed an elevated sedimentation rate of 41 mm/h and mild anemia (hemoglobin: 10.7 g/dL, mean corpuscular volume: 78 fL, hematocrit: 31.8%). There were no specific findings in the other laboratory analysis. An electrocardiogram revealed no significant findings. A pleural tap was performed, and cytologic examination revealed lymphocytes and polymorphonuclear leukocytes; culture was negative. The transthoracic echocardiography showed multiple masses in the RA, LA (Figures 1, A, and 2, A), and left ventricular apex. There was also a mild pericardial effusion. Transesophageal echocardiography showed that the mass in the RA was extending from the superior vena cava to the inferior vena cava (Figure 3), and there were also multiple masses in the LA and LV. Computed tomography of the abdomen revealed a mass invading the whole mediastinum, pericardium, and superior vena cava, as well as enlarged hepatic veins and inferior vena cava, hepatomegaly with a diffuse contrast enhancement, ascites, and pleural thickening over the bases of the lungs. Magnetic resonance imaging of the heart showed a mass starting from the cardiac apex and surrounding the whole heart with continuity along the superior vena cava and aortic root. The intracardiac masses showed round, nodular characteristics. A right atrial mass was extending from the anterolateral surface of the RA and showed indentation to the right atrial cavity (Figure 4). The mass also invaded the left ventricular wall. The RA and inferior vena cava were markedly dilated. There was also slight dilatation in the LA. A thoracotomy was performed and a mass invading the inferior vena cava, RA, and anterior wall of LV was seen. Frozen biopsy was taken from the mass invading the RA and revealed a granulomatous disease consistent with tuberculosis, and multiple excisional biopsies from the superior vena cava, left subclavian lymph node enlargement, and heart were obtained. Pathologic examination revealed caseating, granulomatous inflammation typical for tuberculosis. A microbiologic culture and polymerase
Journal of the American Society of Echocardiography Volume 15 Number 7
¨ zer et al O
757
Figure 1 A, Parasternal long-axis view showing masses in left atrium. B, Parasternal long-axis view after 4-month antituberculosis treatment. AO, Aorta; LV, left ventricle; LA, left atrium.
Figure 2 A, Parasternal short-axis view of mass in right atrium. B, Parasternal short-axis view after 4-month antituberculosis treatment. RV, Right ventricle; AO, aorta; RA, right atrium; LA, left atrium.
chain reaction confirmed the diagnosis of mycobacterium tuberculosis infection. Antituberculosis treatment was started (isoniazid, rifampin, ethambutol, and pyrazinamide for 2 months; later isoniazid and rifampin were continued). She was seen monthly after therapy, and at the fourth month of treatment the patient’s general condition was improved. Echocardiographic examination showed that the masses in the LA had almost totally disappeared, and the mass in the RA was very small compared with the beginning state (Figures 1, B, and 2, B).
DISCUSSION The most interesting findings from our patient were multiple masses in the LA, RA, aortic root, and left ventricular apex caused by tuberculosis. Tuberculosis may affect the heart in several ways. It may be seen primarily in the heart without involvement of any other organ in the body, or it may complicate typical tuberculous disease elsewhere. All 3 layers of the heart may be affected from the disease process. Pericardial involvement caused by tuberculosis may be in the form of pericardial
effusion, pericarditis, cardiac tamponade, constrictive pericarditis, and pericardial mass.1-6 In the endemic areas, the most common cause of constrictive pericarditis is tuberculosis.7,8 In some cases of constrictive pericarditis, myocardial and pericardial involvement of varying degrees were also demonstrated.9,10 Tuberculous myocardial lesions, however, are extremely rare and usually diagnosed at autopsy.11,12 The myocardium is usually affected by direct extension, or less often by retrograde lymphatic drainage from tuberculous mediastinal nodes. Infection via the hematogenous route may also develop in miliary disease. Three distinct forms of myocardial involvement are recognized: nodular tubercles (tuberculomas) of the myocardium, miliary tubercles of the myocardium, and an uncommon diffuse infiltrative type.13 Although myocardial tuberculosis is usually diagnosed incidentally at necropsy, it may produce cardiac arrhythmias, such as supraventricular arrhythmias,12 atrioventricular block,14,15 ventricular tachycardia, and ventricular fibrillation.16 A patient with an obstructive, tumor-like mass is much less common.17,18 Cases of pseudoaneurysm formation19 and sudden cardiac death20,21 caused by the rupture
¨ zer et al 758 O
Journal of the American Society of Echocardiography July 2002
REFERENCES
Figure 3 Transesophageal echocardiographic view of mass in right atrium.
Figure 4 Magnetic resonance imaging of masses in heart.
of myocardial tuberculoma were also reported. Tuberculosis of the heart may also cause restrictive cardiomyopathy and differential diagnosis of these patients from those with constrictive pericarditis caused by tuberculosis is very difficult.22 The differential diagnosis of cardiac tuberculosis includes other granulomatous disorders, such as sarcoidosis, granulomatous giant cell myocarditis, syphilitic gummas, fungal infections, rheumatic fever, rheumatoid arthritis, metastatic tumors containing giant cells (such as osteosarcoma and Hodgkin’s disease), and abscesses.23 Our experience suggests that tuberculous involvement of the heart should be on the list of intrapericardial masses shown by echocardiography, particularly in the endemic areas.
1. Afzal A, Keohane M, Keeley E, Borzak S, Callender CW, Iannuzzi M. Myocarditis and pericarditis with tamponade associated with disseminated tuberculosis. Can J Cardiol 2000;16:519-21. 2. Schwartz AB, Mitchell RS, Higgins CB, Lipton MJ, Klausner SC. Invasive calcific constrictive pericarditis simulating a left ventricular mass. Am Heart J 1986;112:861-3. 3. Sauleda S, Permanyer MG, Soler SJ. Tuberculous pericarditis: ten-year experience with a prospective protocol for diagnosis and treatment. J Am Coll Cardiol 1988;11:724-8. 4. Fowler NO. Tuberculous pericarditis. JAMA 1991;266:99-103. 5. Atar S, Chiu J, Forrester JS, Siegel RJ. Bloody pericardial effusion in patients with cardiac tamponade: is the cause cancerous, tuberculous, or iatrogenic in the 1990’s? Chest 1999;116:1564-9. 6. Komsuoglu B, Goldeli O, Kulan K, Gedik Y. Tuberculous pericarditis in north-east Turkey: an echocardiographic study. Acta Cardiol 1994;49:157-63. 7. Blake S, Bonar S, O’Neil H, Hanly P, Drury I, Flanagan M, et al. Aetiology of chronic constrictive pericarditis. Br Heart J 1983;50:273. 8. Cameron J, Oesterle SN, Baldwin JC, Hancock EW. The etiologic spectrum of constrictive pericarditis. Am Heart J 1987;113:354. 9. Dave T, Narula JP, Chopra P. Myocardial and endocardial involvement in tuberculous constrictive pericarditis: difficulty in biopsy distinction from endomyocardial fibrosis as a cause of restrictive heart disease. Int J Cardiol 1990;28:245-51. 10. Talwar KK, Narula JP, Chopra P. Myocarditis and myocardial interstitial fibrosis in constrictive pericarditis—an extended pathological spectrum. Int J Cardiol 1990;29:241-3. 11. Pomerance A. Tuberculoma of the interventricular septum. Br Heart J 1963;25:412-4. 12. Kapoor OP, Mascarenhas E, Rananaware MM, Gadgil RK. Tuberculoma of the heart: report of 9 cases. Am Heart J 1973;86:334-40. 13. Horn H, Saphir O. The involvement of the myocardium in tuberculosis: a review of the literature and report of three cases. Am Rev Tuberc 1935;32:492-506. 14. Menon BT, Rao CKP. Tuberculosis of the myocardium causing complete heart block. Am J Pathol 1945;21:1193-7. 15. Wren C, Stovin PGI. Isolated interventricular septal tuberculoma causing complete heart block. Thorax 1982;37:149-50. 16. Behr G, Palin HC, Temperly JM. Myocardial tuberculosis. Br Med J 1977;1(6066):951. 17. Rawis WJ, Shuford WH, Logan WD, Hurst JW, Schland RC. Right ventricular outflow tract obstruction produced by a myocardial abscess in a patient with tuberculosis. Am J Cardiol 1968;21:738-45. 18. Kinare SG. Interesting facts of cardiovascular tuberculosis. Indian J Surg 1975;37:144-51. 19. Halim MA, Mercer EN, Guinn GA. Myocardial tuberculoma with rupture and pseudoaneurysm formation—successful surgical treatment. Br Heart J 1985;54:603-4. 20. Wallis PJ, Branfoot AC, Emerson PA. Sudden death due to myocardial tuberculosis. Thorax 1984;39:155-6. 21. Kirsten K, Schaedel C. Sudden death due to myocardial tuberculosis. Thorax 1985;40:799. 22. Bali HK, Wahi S, Sharma BK, Anand IS, Datta BN, Wahi PL. Myocardial tuberculosis presenting as restrictive cardiomyopathy. Am Heart J 1990;120:703-6. 23. Ferrans VJ, Rodriguez ER, McAllister HA Jr. Granulomatous inflammation of the heart. Heart Vessels Suppl 1985;1:262-70.