American Journal of Emergency Medicine 33 (2015) 1115.e5–1115.e7
Contents lists available at ScienceDirect
American Journal of Emergency Medicine journal homepage: www.elsevier.com/locate/ajem
Case Report
Wearing the mask of ST-elevation myocardial infarction: postpericardiotomy syndrome☆,☆☆ a r t i c l e
i n f o
Article history: Received 21 January 2015 Accepted 23 January 2015
a b s t r a c t Introduction: Postpericardiotomy syndrome (PPS) is an inflammatory process, affecting 15% to 20% of patients, after surgery involving pleura, pericardium, or both. The role of electrocardiogram (ECG) in diagnosing PPS is uncertain because ECG is rarely normal (especially after cardiac surgery). We report a case of PPS that presented initially with localized ST-segment elevation and also discuss proposed mechanisms. Clinical case: A 60-year-old White man presented to the emergency department (ED) after having chest pain, shortness of breath, and palpitation for approximately 2 hours. Patient had known coronary artery disease, status postcoronary artery bypass graft a month earlier with a graft to right coronary artery, and 2 grafts to marginal arteries. In the ED, ECG revealed localized ST-segment elevations in leads II, III, and aVF. Coronary angiography did not reveal significant coronary artery stenosis, and all the grafts were found to be patent. Following ECG showed PR depression along with diffuse ST elevation consistent with pericarditis. Patient was started on nonsteroidal anti-inflammatory drugs and colchicine with significant improvement of his symptoms in a few days. Discussion: In our patient, injury or surgical manipulation to the area perfused by right coronary artery might have initiated a process, initially localized to the inferior wall with subsequent diffuse involvement of the entire pericardium. The presentation of our patient shortly after the development of chest pain and availability of 2 ECGs a few minutes apart may have shed light on the pathophysiology of PPS. © 2015 Elsevier Inc. All rights reserved.
Postpericardiotomy syndrome (PPS) is an inflammatory process, affecting 15% to 20% of patients, after surgery involving pleura, pericardium, or both [1]. Postpericardiotomy syndrome is also presumed to have an autoimmune pathogenesis triggered by an initial damage of pericardial and/or pleural mesothelial cells caused by trauma [2]. Postpericardiotomy syndrome has been reported after myocardial infarction and as an unusual complication after percutaneous coronary [3] or intracardiac interventions, such as pacemaker leads insertion [4] or radiofrequency ablation [5,6]. Unfortunately, the role of electrocardiogram (ECG) in diagnosing PPS is uncertain because ECG is rarely normal especially after cardiac surgery. We present a case of PPS presented initially with localized ST-segment elevation and also discuss proposed mechanisms. A 60-year-old white man presented to the emergency department after having chest pain, shortness of breath, and palpitation for about 2 hours. Medical history was significant for hypertension, diabetes mellitus, hyperlipidemia, and coronary artery disease, status post coronary artery bypass graft (CABG) a month earlier with a graft to right coronary artery and 2 grafts to marginal arteries. On physical examination, the patient was afebrile, heart rate was 84 beats per minute, and blood pressure was 136/78 mm Hg. He did not have tenderness to palpation over the chest. Cardiac auscultation revealed normal heart sounds without murmurs or rub. There was no jugular venous distension, pulmo-
☆ Funding source: none. ☆☆ Conflict of interest: none.
0735-6757/© 2015 Elsevier Inc. All rights reserved.
nary rales, or dependent edema. Initial ECG in the emergency department revealed localized ST-segment elevation in leads II, III, and aVF (Fig. 1A), and serum troponin I level was normal (b 0.01 ng/mL; reference, b 0.09 ng/mL). Because patient had recent CABG, graft occlusion was suspected, and immediate cardiac catheterization was performed for possible myocardial revascularization. Coronary angiography (Fig. 2) did not demonstrate significant obstructive coronary disease, and all grafts were found to be patent. On laboratory tests, patient had leukocytosis (15 400 k/mm3; reference, b11 000 k/mm3), elevated C-reactive protein (4.32 mg/dL; reference, b0.72 mg/dL), and erythrocyte sedimentation rate (25 mm/h; reference, b15 mm/h); urine drug screen and antinuclear antibody profile were negative. Echocardiography (Fig. 3) revealed moderate pericardial effusion, normal left ventricular ejection fraction with no regional wall motion abnormalities. Serial measurements of troponin I levels remained within normal limits. An unnoticed ECG obtained 13 minutes after the first, showed PR depression along with diffuse ST elevation consistent with pericarditis (Fig. 1B). In addition, diffuse ST-segment elevation was more prominent in the subsequent ECG (Fig. 4), which was obtained few hours later. Patient was placed on nonsteroidal anti-inflammatory drugs and colchicine with significant improvement and subsequent resolution of his symptoms. ST elevations can be seen in other conditions that include large pneumothorax, hyperkalemia, Osborne waves, acute myocarditis, certain cardiac tumors, myocardial contusion, aortic dissection, left ventricular aneurysm, stress cardiomyopathy, and the normal variant referred to as “early repolarization” [7-9]. All these clinical conditions were ruled
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R.C. Patel et al. / American Journal of Emergency Medicine 33 (2015) 1115.e5–1115.e7
Fig. 1. Electrocardiograms. A, The patient’s initial ECG showed localized ST elevation in leads II, III, and aVF with subtle PR-segment depression. B, Following ECG, 13 minutes later, demonstrating diffuse ST-segment elevation with PR-segment depression.
out in our patient. The patient had localized ST-segment elevation, resembling inferior wall ST-elevation myocardial infarction, secondary to PPS. There is limited understanding and knowledge of the pathogenesis of PPS. Dressler [2] introduced the theory of immune response against autoantigens released after myocardial necrosis in the setting of myocardial infarction. Later, elevated antiheart antibodies in patients with
PPS were demonstrated [10,11]. Factors such as the period between the trigger event and the onset of symptoms, response to the antiinflammatory, and recurrence after the withdrawal of the steroids support an immune-mediated mechanism. Our patient demonstrated diagnostic challenge to differentiate between PPS and myocardial infarction because of localized ST elevation. We propose that, in patients with history of CABG or percutaneous
Fig. 2. Coronary angiogram demonstrated. A, White and blue arrows showing SVG grafts to OM1 and OM2, respectively. B, Red and yellow arrows showing native RCA and patent SVG graft to distal RCA. SVG, saphenous vein graft; OM, obtuse marginal artery; RCA, right coronary artery.
R.C. Patel et al. / American Journal of Emergency Medicine 33 (2015) 1115.e5–1115.e7
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Rajendrakumar C. Patel, MD, MsPH ⁎ Hemant Goyal, MD Department of Internal Medicine, Mercer University School of Medicine Macon, GA ⁎Corresponding author. Department of Internal Medicine, 707 Pine Street, Macon, GA 31201 Tel.: +1 478 301 5824; fax: +1 478 301 5825 E-mail address: [email protected] Ahmed I. Shah, MD Jalal K. Ghali, MD Cardiology Division, Mercer University School of Medicine, Macon, GA
http://dx.doi.org/10.1016/j.ajem.2015.01.048 References
Fig. 3. Echocardiography showing moderate pericardial effusion.
coronary intervention, who present with chest pain and ST elevation, it would be reasonable to repeat an ECG in 10 to 15 minutes if it can be done in the window period recommended by the guidelines for the management of ST-elevation myocardial infarction to avoid potentially unnecessary cardiac catheterization. In our patient, injury or surgical manipulation to the area perfused by right coronary artery might have initiated a process, initially localized to the inferior wall with subsequent diffuse involvement of the entire pericardium. We also propose that the initial insult in PPS is localized to the region of injury or surgical manipulation that subsequently spreads and becomes generalized. The presentation of our patient shortly after the development of chest pain and availability of 2 ECGs few minutes apart may have shed light on the pathophysiology and progression of PPS.
[1] Finkelstein Y, Shemesh J, Mahlab K, Abramov D, Bar-El Y, Sagie A, et al. Colchicine for the prevention of postpericardiotomy syndrome. Herz 2002;27:791–4. [2] Dressler W. The Postmyocardial infarction syndrome. Arch Intern Med 1959;103:28–42. [3] Holmes Jr DR, Nishimura R, Fountain R, Turi ZG. Iatrogenic pericardial effusion and tamponade in the percutaneous intracardiac intervention era. J Am Col Card Cardiovasc Interv 2009;2:705–17. [4] Cevik C, Wilborn T, Corona R, Schanzmeyer E, Nugeni K. Post-cardiac injury syndrome following transvenous pacemaker insertion: a case report and review of the literature. Heart Lung Circ 2009;18:379–83. [5] Haegeli LM, Kotschet E, Byrne J, Adam DC, Lockwood EE, Leather RA, et al. Cardiac injury after percutaneous catheter ablation for atrial fibrillation. Europace 2008;10:273–5. [6] Cappato R, Calkins H, Chen SA, Davies W, Lesaka Y, Kalman J, et al. Worldwide survey on the methods, efficacy, and safety of catheter ablation for human atrial fibrillation. Circulation 2005;111:1100–5. [7] Wagner GS, Macfarlene P, Wellens H, Josephson M, Gorgels A, Mirvis DM, et al. AHA/ ACCF/HRS recommendations for the standardization and interpretation of the electrocardiogram. Part VI: acute ischemia/infarction A scientific statement from the American Heart Association Electrocardiography and Arrythmias Committee, Council on Clinical Cardiology; the American College of Cardiology Foundation. J Am Coll Cardiol 2009;53(11):1003–11. [8] Praserthdam W, Robinson M, Gamp P, Amsterdam EA. “Door-to-chest-tube” time? Am J Med 2010;123:598–600. [9] Wang K, Asinger RW, Marriott HJ. ST- segment elevation in conditions other than acute myocardial infarction. N Eng J Med 2003;349:2128–35. [10] Ritter G. Are we missing something? What is really the postcardiotomy syndrome? South Med J 2006;99:206–7. [11] Robinson J, Brigden W. Immunological studies in the postcardiotomy syndrome. Br Med J 1963;5359:706–9.
Fig. 4. ECG, few hours later, showing prominent diffuse ST-segment elevation with PR-segment depression.
Contents lists available at ScienceDirect
American Journal of Emergency Medicine journal homepage: www.elsevier.com/locate/ajem
Case Report
Wearing the mask of ST-elevation myocardial infarction: postpericardiotomy syndrome☆,☆☆ a r t i c l e
i n f o
Article history: Received 21 January 2015 Accepted 23 January 2015
a b s t r a c t Introduction: Postpericardiotomy syndrome (PPS) is an inflammatory process, affecting 15% to 20% of patients, after surgery involving pleura, pericardium, or both. The role of electrocardiogram (ECG) in diagnosing PPS is uncertain because ECG is rarely normal (especially after cardiac surgery). We report a case of PPS that presented initially with localized ST-segment elevation and also discuss proposed mechanisms. Clinical case: A 60-year-old White man presented to the emergency department (ED) after having chest pain, shortness of breath, and palpitation for approximately 2 hours. Patient had known coronary artery disease, status postcoronary artery bypass graft a month earlier with a graft to right coronary artery, and 2 grafts to marginal arteries. In the ED, ECG revealed localized ST-segment elevations in leads II, III, and aVF. Coronary angiography did not reveal significant coronary artery stenosis, and all the grafts were found to be patent. Following ECG showed PR depression along with diffuse ST elevation consistent with pericarditis. Patient was started on nonsteroidal anti-inflammatory drugs and colchicine with significant improvement of his symptoms in a few days. Discussion: In our patient, injury or surgical manipulation to the area perfused by right coronary artery might have initiated a process, initially localized to the inferior wall with subsequent diffuse involvement of the entire pericardium. The presentation of our patient shortly after the development of chest pain and availability of 2 ECGs a few minutes apart may have shed light on the pathophysiology of PPS. © 2015 Elsevier Inc. All rights reserved.
Postpericardiotomy syndrome (PPS) is an inflammatory process, affecting 15% to 20% of patients, after surgery involving pleura, pericardium, or both [1]. Postpericardiotomy syndrome is also presumed to have an autoimmune pathogenesis triggered by an initial damage of pericardial and/or pleural mesothelial cells caused by trauma [2]. Postpericardiotomy syndrome has been reported after myocardial infarction and as an unusual complication after percutaneous coronary [3] or intracardiac interventions, such as pacemaker leads insertion [4] or radiofrequency ablation [5,6]. Unfortunately, the role of electrocardiogram (ECG) in diagnosing PPS is uncertain because ECG is rarely normal especially after cardiac surgery. We present a case of PPS presented initially with localized ST-segment elevation and also discuss proposed mechanisms. A 60-year-old white man presented to the emergency department after having chest pain, shortness of breath, and palpitation for about 2 hours. Medical history was significant for hypertension, diabetes mellitus, hyperlipidemia, and coronary artery disease, status post coronary artery bypass graft (CABG) a month earlier with a graft to right coronary artery and 2 grafts to marginal arteries. On physical examination, the patient was afebrile, heart rate was 84 beats per minute, and blood pressure was 136/78 mm Hg. He did not have tenderness to palpation over the chest. Cardiac auscultation revealed normal heart sounds without murmurs or rub. There was no jugular venous distension, pulmo-
☆ Funding source: none. ☆☆ Conflict of interest: none.
0735-6757/© 2015 Elsevier Inc. All rights reserved.
nary rales, or dependent edema. Initial ECG in the emergency department revealed localized ST-segment elevation in leads II, III, and aVF (Fig. 1A), and serum troponin I level was normal (b 0.01 ng/mL; reference, b 0.09 ng/mL). Because patient had recent CABG, graft occlusion was suspected, and immediate cardiac catheterization was performed for possible myocardial revascularization. Coronary angiography (Fig. 2) did not demonstrate significant obstructive coronary disease, and all grafts were found to be patent. On laboratory tests, patient had leukocytosis (15 400 k/mm3; reference, b11 000 k/mm3), elevated C-reactive protein (4.32 mg/dL; reference, b0.72 mg/dL), and erythrocyte sedimentation rate (25 mm/h; reference, b15 mm/h); urine drug screen and antinuclear antibody profile were negative. Echocardiography (Fig. 3) revealed moderate pericardial effusion, normal left ventricular ejection fraction with no regional wall motion abnormalities. Serial measurements of troponin I levels remained within normal limits. An unnoticed ECG obtained 13 minutes after the first, showed PR depression along with diffuse ST elevation consistent with pericarditis (Fig. 1B). In addition, diffuse ST-segment elevation was more prominent in the subsequent ECG (Fig. 4), which was obtained few hours later. Patient was placed on nonsteroidal anti-inflammatory drugs and colchicine with significant improvement and subsequent resolution of his symptoms. ST elevations can be seen in other conditions that include large pneumothorax, hyperkalemia, Osborne waves, acute myocarditis, certain cardiac tumors, myocardial contusion, aortic dissection, left ventricular aneurysm, stress cardiomyopathy, and the normal variant referred to as “early repolarization” [7-9]. All these clinical conditions were ruled
1115.e6
R.C. Patel et al. / American Journal of Emergency Medicine 33 (2015) 1115.e5–1115.e7
Fig. 1. Electrocardiograms. A, The patient’s initial ECG showed localized ST elevation in leads II, III, and aVF with subtle PR-segment depression. B, Following ECG, 13 minutes later, demonstrating diffuse ST-segment elevation with PR-segment depression.
out in our patient. The patient had localized ST-segment elevation, resembling inferior wall ST-elevation myocardial infarction, secondary to PPS. There is limited understanding and knowledge of the pathogenesis of PPS. Dressler [2] introduced the theory of immune response against autoantigens released after myocardial necrosis in the setting of myocardial infarction. Later, elevated antiheart antibodies in patients with
PPS were demonstrated [10,11]. Factors such as the period between the trigger event and the onset of symptoms, response to the antiinflammatory, and recurrence after the withdrawal of the steroids support an immune-mediated mechanism. Our patient demonstrated diagnostic challenge to differentiate between PPS and myocardial infarction because of localized ST elevation. We propose that, in patients with history of CABG or percutaneous
Fig. 2. Coronary angiogram demonstrated. A, White and blue arrows showing SVG grafts to OM1 and OM2, respectively. B, Red and yellow arrows showing native RCA and patent SVG graft to distal RCA. SVG, saphenous vein graft; OM, obtuse marginal artery; RCA, right coronary artery.
R.C. Patel et al. / American Journal of Emergency Medicine 33 (2015) 1115.e5–1115.e7
1115.e7
Rajendrakumar C. Patel, MD, MsPH ⁎ Hemant Goyal, MD Department of Internal Medicine, Mercer University School of Medicine Macon, GA ⁎Corresponding author. Department of Internal Medicine, 707 Pine Street, Macon, GA 31201 Tel.: +1 478 301 5824; fax: +1 478 301 5825 E-mail address: [email protected] Ahmed I. Shah, MD Jalal K. Ghali, MD Cardiology Division, Mercer University School of Medicine, Macon, GA
http://dx.doi.org/10.1016/j.ajem.2015.01.048 References
Fig. 3. Echocardiography showing moderate pericardial effusion.
coronary intervention, who present with chest pain and ST elevation, it would be reasonable to repeat an ECG in 10 to 15 minutes if it can be done in the window period recommended by the guidelines for the management of ST-elevation myocardial infarction to avoid potentially unnecessary cardiac catheterization. In our patient, injury or surgical manipulation to the area perfused by right coronary artery might have initiated a process, initially localized to the inferior wall with subsequent diffuse involvement of the entire pericardium. We also propose that the initial insult in PPS is localized to the region of injury or surgical manipulation that subsequently spreads and becomes generalized. The presentation of our patient shortly after the development of chest pain and availability of 2 ECGs few minutes apart may have shed light on the pathophysiology and progression of PPS.
[1] Finkelstein Y, Shemesh J, Mahlab K, Abramov D, Bar-El Y, Sagie A, et al. Colchicine for the prevention of postpericardiotomy syndrome. Herz 2002;27:791–4. [2] Dressler W. The Postmyocardial infarction syndrome. Arch Intern Med 1959;103:28–42. [3] Holmes Jr DR, Nishimura R, Fountain R, Turi ZG. Iatrogenic pericardial effusion and tamponade in the percutaneous intracardiac intervention era. J Am Col Card Cardiovasc Interv 2009;2:705–17. [4] Cevik C, Wilborn T, Corona R, Schanzmeyer E, Nugeni K. Post-cardiac injury syndrome following transvenous pacemaker insertion: a case report and review of the literature. Heart Lung Circ 2009;18:379–83. [5] Haegeli LM, Kotschet E, Byrne J, Adam DC, Lockwood EE, Leather RA, et al. Cardiac injury after percutaneous catheter ablation for atrial fibrillation. Europace 2008;10:273–5. [6] Cappato R, Calkins H, Chen SA, Davies W, Lesaka Y, Kalman J, et al. Worldwide survey on the methods, efficacy, and safety of catheter ablation for human atrial fibrillation. Circulation 2005;111:1100–5. [7] Wagner GS, Macfarlene P, Wellens H, Josephson M, Gorgels A, Mirvis DM, et al. AHA/ ACCF/HRS recommendations for the standardization and interpretation of the electrocardiogram. Part VI: acute ischemia/infarction A scientific statement from the American Heart Association Electrocardiography and Arrythmias Committee, Council on Clinical Cardiology; the American College of Cardiology Foundation. J Am Coll Cardiol 2009;53(11):1003–11. [8] Praserthdam W, Robinson M, Gamp P, Amsterdam EA. “Door-to-chest-tube” time? Am J Med 2010;123:598–600. [9] Wang K, Asinger RW, Marriott HJ. ST- segment elevation in conditions other than acute myocardial infarction. N Eng J Med 2003;349:2128–35. [10] Ritter G. Are we missing something? What is really the postcardiotomy syndrome? South Med J 2006;99:206–7. [11] Robinson J, Brigden W. Immunological studies in the postcardiotomy syndrome. Br Med J 1963;5359:706–9.
Fig. 4. ECG, few hours later, showing prominent diffuse ST-segment elevation with PR-segment depression.
