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Tuberculous Pericardial Effusion After Coronary Artery Bypass Graft
Ann Thorac Surg 2006;82:1519 –21
CASE REPORT TULADHAR ET AL TB PERICARDIAL EFFUSION AFTER CABG
1519
distal to the tumor should be performed. This assures adequate venous drainage for cardiopulmonary bypass. Long-term surveillance with magnetic resonance imaging and computed tomographic scan of the chest and abdomen, and echocardiography is necessary to detect early recurrence. Anti-estrogen therapy may decrease the likelihood of recurrence [4].
References 1. Whitlash SP, Meyer RL. Recurrent endometrial stromal sarcoma resembling intravenous leiomyomatosis. Gynecol Oncol 1987;28:121– 8. 2. Mikami Y, Demopoulos RI, Boctor F, et al. Low-grade endometrial stromal sarcoma with intracardiac extension. Pathol Res Prac 1999;195:501– 8. 3. Kocica MJ, Vranes MR, Kostic D, et al. Intravenous leiomyomatosis with extension into the heart: rare or underestimated? J Thorac Cardiovasc Surg 2005;130:1724 – 6. 4. Parikh J, Lesseps A. Intravenous leiomyomatosis. J Obstet Gynaecol 2000;20;439 – 40. 5. Phillips MR, Bower TC, Orszulak TA, Hartman LC. Intracardiac extension of an intracaval sarcoma of endometrial origin. Ann Thorac Surg 1995;59:742– 4. 6. Moorjani N, Kuo J, Ashley S, Hughes G. Intravenous uterine leiomyosarcomatosis with intracardiac extension. J Card Surg 2005;20:382–5.
Tuberculous Pericardial Effusion After Coronary Artery Bypass Graft Sampurna M. Tuladhar, MRCS, Mahdad Noursadeghi, MRCP, PhD, Joseph J. Boyle, MRCPath, PhD, Jon S. Friedland, FRCP, PhD, and Philip Hornick, FRCS (CTh), PhD Departments of Cardiac Surgery, Infectious Disease, and Histopathology, Hammersmith Hospital, London, Department of Immunology & Molecular Pathology, University College London, Windeyer Building, London, United Kingdom
We describe a case of a recurrent pericardial effusion after coronary artery bypass grafting. This was initially Accepted for publication Feb 7, 2006. Address correspondence to Dr Hornick, Department of Cardiac Surgery, National Heart and Lung Institute, Imperial College, 2nd Floor, B Block, Hammersmith Campus, Du Cane Rd, London, W12 0NN, UK; e-mail: [email protected].
© 2006 by The Society of Thoracic Surgeons Published by Elsevier Inc
considered to be due to post-pericardiotomy syndrome, but was later treated empirically as tuberculosis. After definitive surgery for this condition, pericardial histology and immunohistochemistry confirmed the diagnosis of tubercular pericarditis. At 4-months follow-up, while continuing anti-tuberculous therapy and corticosteroids, the patient showed consistent improvement without further recurrence of his pericardial effusion. Local reactivation of tuberculosis after pericardiotomy has not been previously reported and merits careful consideration in population groups in which tuberculosis is highly endemic. (Ann Thorac Surg 2006;82:1519 –21) © 2006 by The Society of Thoracic Surgeons
T
uberculosis (TB) constitutes a significant world health burden. Although less common in the developed world, its rising incidence has been of increasing concern. It is well known that TB represents a common cause of pericardial effusion in population subgroups at risk. This report outlines a unique case whereby a patient undergoing coronary artery bypass grafting developed a recurrent post-pericardiotomy effusion due to reactivation of dormant TB. A 47-year-old Indian man, who has resided in the United Kingdom for more than 30 years, underwent elective coronary artery bypass grafting (CABG) for ischemic heart disease. He had no past history of TB. At the time of surgery, he had been well with no antecedent symptoms. He had a normal preoperative assessment including chest roentgenogram, full blood count, and renal and liver biochemistry. At operation, no pericardial abnormalities were noted and there was no effusion. He was discharged fit and well on postoperative day 10. During the ensuing 3-month period he presented twice with exertional breathlessness. At these times he was afebrile with no leukocytosis or rise in his C-reactive protein. However, on each occasion, a computed tomographic scan and transthoracic echocardiography revealed a significant pericardial collection that was completely drained using minimally invasive methods providing full symptomatic improvement. Six weeks after discharge, he again presented with a large compromising pericardial effusion. On this occasion, a large pericardial window 0003-4975/06/$32.00 doi:10.1016/j.athoracsur.2006.02.059
FEATURE ARTICLES
Fig 3. (A) Resected specimen and immunohistochemical stains for (B) CD10 (endometrial stromal cells) and (C) H caldesmon (smooth muscle differentiation).
1520
CASE REPORT TULADHAR ET AL TB PERICARDIAL EFFUSION AFTER CABG
Ann Thorac Surg 2006;82:1519 –21
FEATURE ARTICLES
Fig 1. (A) Hematoxylin and eosin, pericardium, with macrophage and epithelioid cell granuloma containing giant cells. (B) High power view of granuloma containing Langhans-type giant cell (nuclei at one end, open arrowhead). (C) Immunohistochemistry for tuberculosis (TB)-specific antigens. Sections were rabbit affinity-adsorbed antibodies specific to Mycobacterium TB (anti-MTB polyclonal, Novocastra plc, Newcastle, UK) were incubated according to the manufacturer’s instructions and were developed with immunoperoxidase and di-amino-benzidine (brown). This procedure will detect not only intact bacilli but TB-specific epitopes derived from proteolytic degradation (eg, in lysosomes or in antigen-presentation pathways). (D) Immunohistochemistry controls. (Main image ⫽ negative control [pre-immune rabbit serum] corresponding to C). Inset: TB-IHC (immunohistochemistry) on positive control tissue containing known AAFBs (acid-alcohol-fast bacilli), showing immunopositive TB bacillus (arrow) and macrophages immunopositive for TB-antigen (red arrowhead) (scalebars ⫽ distance indicated).
was fashioned together with insertion of a pericardial drain. Tissue and pericardial fluid specimens were collected for histology, immunohistochemistry, and microbiology. Despite the absence of any constitutional symptoms, and an anergic 10-unit Mantoux skin test, in view of the recurrent effusions and his ethnicity, the risk of TB was considered to be sufficiently high to warrant empirical anti-TB treatment. Therefore he was started on combination therapy with Rifater (Aventis Pharma, Kent, UK), comprising a daily dose of 720 mg of rifampin, 300 mg of isonaizid and 1.8 g of pyrazinamide, together with 400 mg/day of moxifloxacin (ethambutol not used due to color blindness) and corticosteroids (80 mg prednisolone). This presumptive diagnosis of TB was supported by histologic examination of the resected pericardial tissue, which showed epithelioid cell granuloma with Langhans-type giant cells. The epithelioid granulomas were immunohistochemically positive with a polyclonal antibody specific to mycobacterium TB (anti-MTB polyclonal, Novocastra plc, Newcastle, UK) (Fig 1). After a 10-day inpatient stay, the pericardial drainage decreased to minimal amounts, the drain was removed, and the patient was discharged home on treatment as described. He has since completed 4 months of regular follow-up and has remained well without any recurrence of his pericardial effusion. His treatment has continued with a view to 6-months therapy, plus a gradual reduction of his corticosteroid dose during this time.
Comment The development of a late pericardial effusion with variable clinical symptoms such as fever, chest pain,
and malaise after coronary artery bypass surgery is commonly ascribed to postcardiac injury syndrome, a term that includes post-pericardiotomy syndrome and Dressler syndrome [1]. Indeed, Tsang and colleagues [2] noted that of 209 hemodynamically significant late pericardial effusions, just more than one third were considered to be due to postcardiac injury syndrome, with anticoagulation causing a hemopericardium in the remaining cases. Although postcardiac injury syndrome can still be of a recurrent nature, such recurrences need to be considered with utmost concern and also warrant a thorough investigation, particularly in the context of TB. In general, TB pericardial effusions are relatively uncommon in developed countries, and there are no reports after pericardiotomy. Sagrista-Sauleda and colleagues [3] studied 322 patients with pericardial effusions for a 6-year period and found TB as a cause in only 2%. Nevertheless, increasing international migration has increased the risks. The incidence of TB has been rising by 25% in England for the last 10 years with 2 in 5 cases found in London and 7 in 10 being from an ethnic minority background [4]. Tuberculous pericarditis usually spreads from the lungs, mediastinal nodes, or bony structures, but can also spread through the hematogenous route. It may sometimes be associated with an effusion. Progression commonly leads to a constrictive pericarditis. The mortality rate in untreated acute effusive tuberculous pericarditis approaches 85% [5]. Identification of Mycobacterium TB in pericardial fluid or tissue, or the presence of caseous granulomas in histologic examination of pericardial tissue establishes the diagnosis [5]. Finding acid-alcohol-fast bacilli (AAFB) within the granuloma is conclusive, but insensitive. In
CASE REPORT MASSOUDY ET AL AORTOCORONARY SHUNTING AS ACUTE REPERFUSION STRATEGY
contrast, TB immunohistochemistry is both sensitive and specific [6]. This is probably because antibodies detect not just intact bacilli, but also epitopes that are generated from the processing of killed bacteria. In addition, even in isolated broth suspensions of mycobacteria, immunohistochemistry is several fold more sensitive than AAFB [6]. Thus, TB immunohistochemistry may differentiate between TB and other causes of epitheloid cell granulomas (eg, sarcoidosis). Our TB immunohistochemistry was confirmed by positive control tissue that confirmed the antibodies were positively stained identifiable bacilli in addition to more diffuse staining of the granuloma macrophages. Once diagnosed with TB, patients are treated with anti-TB therapy for a period of 6 months. Controversy remains regarding the use of steroids in TB pericarditis. Nevertheless, systematic review of the literature, especially trial data from South Africa, indicates that they may have a role in nonresolving effusions [7]. Cardiopulmonary bypass [8] and surgery are known to be immunosuppressive. We postulate that this immunosuppression led to reactivation of tubercular pericarditis causing large recurrent pericardial effusions until appropriate anti-TB treatment was initiated. A high index of suspicion and early investigation is required in recurrent pericardial effusions after cardiac surgery, especially in immigrant populations. Although immunohistochemistry is a very sensitive and novel mode of diagnosis, treatment with anti-TB drugs and steroids may need to be started empirically and will help to prevent long-term complications.
References 1. Khan AH. The post cardiac injury syndromes. Clin Cardiol 1992;15:67–72. 2. Tsang TS, Barnes ME, Hayes SN, et al. Clinical and echocardiographic characteristics of significant pericardial effusions following cardiothoracic surgery and outcomes of echoguided pericardiocentesis for management: Mayo Clinic experience, 1979-1998. Chest 1999;116:322–31. 3. Sagrista-Sauleda J, Merce J, Permanyer-Miralda G, SolerSoler J. Clinical clues to the causes of large pericardial effusion. Am J Med 2000;109:95–101. 4. Stopping tuberculosis in England: an action plan from the Chief Medical Officer. Department of Health, Oct 2004. Available at: http://www.dh.gov.uk/PublicationsAndStatistics/Publications/ PublicationsPolicyAndGuidance/PublicationsPolicyAndGuidance Article.html. Accessed December 30, 2005. 5. Maisch B, Seferovic PM, Ristic AD, et al. Guidelines on the diagnosis and management of pericardial diseases executive summary; the Task force on the diagnosis and management of pericardial diseases of the European Society Of Cardiology. Eur Heart J 2004;25:587– 610. 6. Ulrichs T, Lefmann M, Reich M, et al. Modified immunohistological staining allows detection of Ziehl-Neelsen-negative Mycobacterium tuberculosis organisms and their precise localization in human tissue. J Pathol 2005;205:633– 40. 7. Ntsekhe M, Wiysonge C, Volmink JA, Commerford PJ, Mayosi BM. Adjuvant corticosteroids for tuberculous pericarditis: promising, but not proven. Q J Med 2003;96:593–9. 8. Markewitz A, Faist E, Lang S, Endres S, Fuchs D, Reichart B. Successful restoration of cell-mediated immune response after cardiopulmonary bypass by immunomodulation. J Thorac Cardiovasc Surg 1993;105:15–24. © 2006 by The Society of Thoracic Surgeons Published by Elsevier Inc
1521
Aortocoronary Shunting During Off-Pump Coronary Artery Bypass Surgery as Acute Reperfusion Strategy in ST-Elevation Myocardial Infarction Parwis Massoudy, MD, Matthias Thielmann, MD, Andras Szabo, MD, Ivan Aleksic, MD, Eva Kottenberg-Assenmacher, MD, Jenno Szolnoki, MD, and Heinz Jakob, MD Department of Thoracic and Cardiovascular Surgery, West German Heart Center Essen; Department of Anesthesiology and Intensive Care Medicine, University Hospital Essen, Essen, Germany; Department of Cardiac Surgery, University Hospital Szeged, Szeged, Hungary
We report the case of a 43-year-old patient with acute ST-segment elevation anterior myocardial infarction who underwent off-pump coronary artery bypass grafting. To reduce the duration of ongoing myocardial ischemia, acute reperfusion of the infarcted coronary artery was achieved using an aortocoronary shunt, thereby perfusing the occluded left anterior descending artery. Under the protection of the aortocoronary shunt, the left internal thoracic artery was harvested and was thereafter anastomosed to the left anterior descending artery. The patient had an uneventful postoperative recovery. (Ann Thorac Surg 2006;82:1521–3) © 2006 by The Society of Thoracic Surgeons
C
oronary artery bypass grafting in acute myocardial infarction is known to be performed at a considerably increased perioperative risk. Mortality depends on the timing after transmural infarction. In a large retrospective study, investigating over 30,000 patients having undergone coronary artery bypass grafting after transmural myocardial infarction, perioperative mortality was described to be highest (14.2%) when coronary artery bypass grafting was performed within the first 6 hours after the ischemic event. When coronary artery bypass grafting was delayed for 4 to 7 days, perioperative mortality was reduced to 3.8% and could further be reduced when the delay was 8 to 14 days (2.9%) [1]. On the other hand, if the patient is at acute risk and the myocardium can be salvaged, quick reperfusion of the infarcted vessel is warranted. When reperfusion of an occluded coronary artery occurred at 40 minutes, transmyocardial necrosis was reported to be 38 ⫾ 4%. When reperfusion occurred at 6 hours, transmyocardial necrosis was reported to be 71 ⫾ 7% [2]. A 43-year-old man with a history of arterial hypertension and hyperlipidemia presented with an acute anterior Accepted for publication Feb 2, 2006. Address correspondence to Dr Massoudy, West German Heart Center Essen, University Hospital, Department of Thoracic and Cardiovascular Surgery, Hufelandstr. 55, Essen, 45147 Germany; e-mail: [email protected].
0003-4975/06/$32.00 doi:10.1016/j.athoracsur.2006.02.008
FEATURE ARTICLES
Ann Thorac Surg 2006;82:1521–3
CASE REPORT TULADHAR ET AL TB PERICARDIAL EFFUSION AFTER CABG
1519
distal to the tumor should be performed. This assures adequate venous drainage for cardiopulmonary bypass. Long-term surveillance with magnetic resonance imaging and computed tomographic scan of the chest and abdomen, and echocardiography is necessary to detect early recurrence. Anti-estrogen therapy may decrease the likelihood of recurrence [4].
References 1. Whitlash SP, Meyer RL. Recurrent endometrial stromal sarcoma resembling intravenous leiomyomatosis. Gynecol Oncol 1987;28:121– 8. 2. Mikami Y, Demopoulos RI, Boctor F, et al. Low-grade endometrial stromal sarcoma with intracardiac extension. Pathol Res Prac 1999;195:501– 8. 3. Kocica MJ, Vranes MR, Kostic D, et al. Intravenous leiomyomatosis with extension into the heart: rare or underestimated? J Thorac Cardiovasc Surg 2005;130:1724 – 6. 4. Parikh J, Lesseps A. Intravenous leiomyomatosis. J Obstet Gynaecol 2000;20;439 – 40. 5. Phillips MR, Bower TC, Orszulak TA, Hartman LC. Intracardiac extension of an intracaval sarcoma of endometrial origin. Ann Thorac Surg 1995;59:742– 4. 6. Moorjani N, Kuo J, Ashley S, Hughes G. Intravenous uterine leiomyosarcomatosis with intracardiac extension. J Card Surg 2005;20:382–5.
Tuberculous Pericardial Effusion After Coronary Artery Bypass Graft Sampurna M. Tuladhar, MRCS, Mahdad Noursadeghi, MRCP, PhD, Joseph J. Boyle, MRCPath, PhD, Jon S. Friedland, FRCP, PhD, and Philip Hornick, FRCS (CTh), PhD Departments of Cardiac Surgery, Infectious Disease, and Histopathology, Hammersmith Hospital, London, Department of Immunology & Molecular Pathology, University College London, Windeyer Building, London, United Kingdom
We describe a case of a recurrent pericardial effusion after coronary artery bypass grafting. This was initially Accepted for publication Feb 7, 2006. Address correspondence to Dr Hornick, Department of Cardiac Surgery, National Heart and Lung Institute, Imperial College, 2nd Floor, B Block, Hammersmith Campus, Du Cane Rd, London, W12 0NN, UK; e-mail: [email protected].
© 2006 by The Society of Thoracic Surgeons Published by Elsevier Inc
considered to be due to post-pericardiotomy syndrome, but was later treated empirically as tuberculosis. After definitive surgery for this condition, pericardial histology and immunohistochemistry confirmed the diagnosis of tubercular pericarditis. At 4-months follow-up, while continuing anti-tuberculous therapy and corticosteroids, the patient showed consistent improvement without further recurrence of his pericardial effusion. Local reactivation of tuberculosis after pericardiotomy has not been previously reported and merits careful consideration in population groups in which tuberculosis is highly endemic. (Ann Thorac Surg 2006;82:1519 –21) © 2006 by The Society of Thoracic Surgeons
T
uberculosis (TB) constitutes a significant world health burden. Although less common in the developed world, its rising incidence has been of increasing concern. It is well known that TB represents a common cause of pericardial effusion in population subgroups at risk. This report outlines a unique case whereby a patient undergoing coronary artery bypass grafting developed a recurrent post-pericardiotomy effusion due to reactivation of dormant TB. A 47-year-old Indian man, who has resided in the United Kingdom for more than 30 years, underwent elective coronary artery bypass grafting (CABG) for ischemic heart disease. He had no past history of TB. At the time of surgery, he had been well with no antecedent symptoms. He had a normal preoperative assessment including chest roentgenogram, full blood count, and renal and liver biochemistry. At operation, no pericardial abnormalities were noted and there was no effusion. He was discharged fit and well on postoperative day 10. During the ensuing 3-month period he presented twice with exertional breathlessness. At these times he was afebrile with no leukocytosis or rise in his C-reactive protein. However, on each occasion, a computed tomographic scan and transthoracic echocardiography revealed a significant pericardial collection that was completely drained using minimally invasive methods providing full symptomatic improvement. Six weeks after discharge, he again presented with a large compromising pericardial effusion. On this occasion, a large pericardial window 0003-4975/06/$32.00 doi:10.1016/j.athoracsur.2006.02.059
FEATURE ARTICLES
Fig 3. (A) Resected specimen and immunohistochemical stains for (B) CD10 (endometrial stromal cells) and (C) H caldesmon (smooth muscle differentiation).
1520
CASE REPORT TULADHAR ET AL TB PERICARDIAL EFFUSION AFTER CABG
Ann Thorac Surg 2006;82:1519 –21
FEATURE ARTICLES
Fig 1. (A) Hematoxylin and eosin, pericardium, with macrophage and epithelioid cell granuloma containing giant cells. (B) High power view of granuloma containing Langhans-type giant cell (nuclei at one end, open arrowhead). (C) Immunohistochemistry for tuberculosis (TB)-specific antigens. Sections were rabbit affinity-adsorbed antibodies specific to Mycobacterium TB (anti-MTB polyclonal, Novocastra plc, Newcastle, UK) were incubated according to the manufacturer’s instructions and were developed with immunoperoxidase and di-amino-benzidine (brown). This procedure will detect not only intact bacilli but TB-specific epitopes derived from proteolytic degradation (eg, in lysosomes or in antigen-presentation pathways). (D) Immunohistochemistry controls. (Main image ⫽ negative control [pre-immune rabbit serum] corresponding to C). Inset: TB-IHC (immunohistochemistry) on positive control tissue containing known AAFBs (acid-alcohol-fast bacilli), showing immunopositive TB bacillus (arrow) and macrophages immunopositive for TB-antigen (red arrowhead) (scalebars ⫽ distance indicated).
was fashioned together with insertion of a pericardial drain. Tissue and pericardial fluid specimens were collected for histology, immunohistochemistry, and microbiology. Despite the absence of any constitutional symptoms, and an anergic 10-unit Mantoux skin test, in view of the recurrent effusions and his ethnicity, the risk of TB was considered to be sufficiently high to warrant empirical anti-TB treatment. Therefore he was started on combination therapy with Rifater (Aventis Pharma, Kent, UK), comprising a daily dose of 720 mg of rifampin, 300 mg of isonaizid and 1.8 g of pyrazinamide, together with 400 mg/day of moxifloxacin (ethambutol not used due to color blindness) and corticosteroids (80 mg prednisolone). This presumptive diagnosis of TB was supported by histologic examination of the resected pericardial tissue, which showed epithelioid cell granuloma with Langhans-type giant cells. The epithelioid granulomas were immunohistochemically positive with a polyclonal antibody specific to mycobacterium TB (anti-MTB polyclonal, Novocastra plc, Newcastle, UK) (Fig 1). After a 10-day inpatient stay, the pericardial drainage decreased to minimal amounts, the drain was removed, and the patient was discharged home on treatment as described. He has since completed 4 months of regular follow-up and has remained well without any recurrence of his pericardial effusion. His treatment has continued with a view to 6-months therapy, plus a gradual reduction of his corticosteroid dose during this time.
Comment The development of a late pericardial effusion with variable clinical symptoms such as fever, chest pain,
and malaise after coronary artery bypass surgery is commonly ascribed to postcardiac injury syndrome, a term that includes post-pericardiotomy syndrome and Dressler syndrome [1]. Indeed, Tsang and colleagues [2] noted that of 209 hemodynamically significant late pericardial effusions, just more than one third were considered to be due to postcardiac injury syndrome, with anticoagulation causing a hemopericardium in the remaining cases. Although postcardiac injury syndrome can still be of a recurrent nature, such recurrences need to be considered with utmost concern and also warrant a thorough investigation, particularly in the context of TB. In general, TB pericardial effusions are relatively uncommon in developed countries, and there are no reports after pericardiotomy. Sagrista-Sauleda and colleagues [3] studied 322 patients with pericardial effusions for a 6-year period and found TB as a cause in only 2%. Nevertheless, increasing international migration has increased the risks. The incidence of TB has been rising by 25% in England for the last 10 years with 2 in 5 cases found in London and 7 in 10 being from an ethnic minority background [4]. Tuberculous pericarditis usually spreads from the lungs, mediastinal nodes, or bony structures, but can also spread through the hematogenous route. It may sometimes be associated with an effusion. Progression commonly leads to a constrictive pericarditis. The mortality rate in untreated acute effusive tuberculous pericarditis approaches 85% [5]. Identification of Mycobacterium TB in pericardial fluid or tissue, or the presence of caseous granulomas in histologic examination of pericardial tissue establishes the diagnosis [5]. Finding acid-alcohol-fast bacilli (AAFB) within the granuloma is conclusive, but insensitive. In
CASE REPORT MASSOUDY ET AL AORTOCORONARY SHUNTING AS ACUTE REPERFUSION STRATEGY
contrast, TB immunohistochemistry is both sensitive and specific [6]. This is probably because antibodies detect not just intact bacilli, but also epitopes that are generated from the processing of killed bacteria. In addition, even in isolated broth suspensions of mycobacteria, immunohistochemistry is several fold more sensitive than AAFB [6]. Thus, TB immunohistochemistry may differentiate between TB and other causes of epitheloid cell granulomas (eg, sarcoidosis). Our TB immunohistochemistry was confirmed by positive control tissue that confirmed the antibodies were positively stained identifiable bacilli in addition to more diffuse staining of the granuloma macrophages. Once diagnosed with TB, patients are treated with anti-TB therapy for a period of 6 months. Controversy remains regarding the use of steroids in TB pericarditis. Nevertheless, systematic review of the literature, especially trial data from South Africa, indicates that they may have a role in nonresolving effusions [7]. Cardiopulmonary bypass [8] and surgery are known to be immunosuppressive. We postulate that this immunosuppression led to reactivation of tubercular pericarditis causing large recurrent pericardial effusions until appropriate anti-TB treatment was initiated. A high index of suspicion and early investigation is required in recurrent pericardial effusions after cardiac surgery, especially in immigrant populations. Although immunohistochemistry is a very sensitive and novel mode of diagnosis, treatment with anti-TB drugs and steroids may need to be started empirically and will help to prevent long-term complications.
References 1. Khan AH. The post cardiac injury syndromes. Clin Cardiol 1992;15:67–72. 2. Tsang TS, Barnes ME, Hayes SN, et al. Clinical and echocardiographic characteristics of significant pericardial effusions following cardiothoracic surgery and outcomes of echoguided pericardiocentesis for management: Mayo Clinic experience, 1979-1998. Chest 1999;116:322–31. 3. Sagrista-Sauleda J, Merce J, Permanyer-Miralda G, SolerSoler J. Clinical clues to the causes of large pericardial effusion. Am J Med 2000;109:95–101. 4. Stopping tuberculosis in England: an action plan from the Chief Medical Officer. Department of Health, Oct 2004. Available at: http://www.dh.gov.uk/PublicationsAndStatistics/Publications/ PublicationsPolicyAndGuidance/PublicationsPolicyAndGuidance Article.html. Accessed December 30, 2005. 5. Maisch B, Seferovic PM, Ristic AD, et al. Guidelines on the diagnosis and management of pericardial diseases executive summary; the Task force on the diagnosis and management of pericardial diseases of the European Society Of Cardiology. Eur Heart J 2004;25:587– 610. 6. Ulrichs T, Lefmann M, Reich M, et al. Modified immunohistological staining allows detection of Ziehl-Neelsen-negative Mycobacterium tuberculosis organisms and their precise localization in human tissue. J Pathol 2005;205:633– 40. 7. Ntsekhe M, Wiysonge C, Volmink JA, Commerford PJ, Mayosi BM. Adjuvant corticosteroids for tuberculous pericarditis: promising, but not proven. Q J Med 2003;96:593–9. 8. Markewitz A, Faist E, Lang S, Endres S, Fuchs D, Reichart B. Successful restoration of cell-mediated immune response after cardiopulmonary bypass by immunomodulation. J Thorac Cardiovasc Surg 1993;105:15–24. © 2006 by The Society of Thoracic Surgeons Published by Elsevier Inc
1521
Aortocoronary Shunting During Off-Pump Coronary Artery Bypass Surgery as Acute Reperfusion Strategy in ST-Elevation Myocardial Infarction Parwis Massoudy, MD, Matthias Thielmann, MD, Andras Szabo, MD, Ivan Aleksic, MD, Eva Kottenberg-Assenmacher, MD, Jenno Szolnoki, MD, and Heinz Jakob, MD Department of Thoracic and Cardiovascular Surgery, West German Heart Center Essen; Department of Anesthesiology and Intensive Care Medicine, University Hospital Essen, Essen, Germany; Department of Cardiac Surgery, University Hospital Szeged, Szeged, Hungary
We report the case of a 43-year-old patient with acute ST-segment elevation anterior myocardial infarction who underwent off-pump coronary artery bypass grafting. To reduce the duration of ongoing myocardial ischemia, acute reperfusion of the infarcted coronary artery was achieved using an aortocoronary shunt, thereby perfusing the occluded left anterior descending artery. Under the protection of the aortocoronary shunt, the left internal thoracic artery was harvested and was thereafter anastomosed to the left anterior descending artery. The patient had an uneventful postoperative recovery. (Ann Thorac Surg 2006;82:1521–3) © 2006 by The Society of Thoracic Surgeons
C
oronary artery bypass grafting in acute myocardial infarction is known to be performed at a considerably increased perioperative risk. Mortality depends on the timing after transmural infarction. In a large retrospective study, investigating over 30,000 patients having undergone coronary artery bypass grafting after transmural myocardial infarction, perioperative mortality was described to be highest (14.2%) when coronary artery bypass grafting was performed within the first 6 hours after the ischemic event. When coronary artery bypass grafting was delayed for 4 to 7 days, perioperative mortality was reduced to 3.8% and could further be reduced when the delay was 8 to 14 days (2.9%) [1]. On the other hand, if the patient is at acute risk and the myocardium can be salvaged, quick reperfusion of the infarcted vessel is warranted. When reperfusion of an occluded coronary artery occurred at 40 minutes, transmyocardial necrosis was reported to be 38 ⫾ 4%. When reperfusion occurred at 6 hours, transmyocardial necrosis was reported to be 71 ⫾ 7% [2]. A 43-year-old man with a history of arterial hypertension and hyperlipidemia presented with an acute anterior Accepted for publication Feb 2, 2006. Address correspondence to Dr Massoudy, West German Heart Center Essen, University Hospital, Department of Thoracic and Cardiovascular Surgery, Hufelandstr. 55, Essen, 45147 Germany; e-mail: [email protected].
0003-4975/06/$32.00 doi:10.1016/j.athoracsur.2006.02.008
FEATURE ARTICLES
Ann Thorac Surg 2006;82:1521–3