Free
Case Reports  |   July 2001
Regional Pericarditis Mimicking Myocardial Infarction
Author Affiliations & Notes
  • George Youssef, M.D.
    *
  • Sameh Khouzam, M.D.
  • Juraj Sprung, M.D., Ph.D.
  • Denis L. Bourke, M.D.
    §
  • * Resident in Anesthesiology, Division of Anesthesiology and Critical Care Medicine, † Resident in Internal Medicine, Department of Internal Medicine, The Cleveland Clinic Foundation. ‡ Associate Professor of Anesthesiology, Department of Anesthesiology, Mayo Foundation. § Professor of Anesthesiology, Department of Anesthesiology, University of Maryland School of Medicine.
  • Received from the Division of Anesthesiology and Critical Care Medicine and the Department of Internal Medicine, The Cleveland Clinic Foundation, Cleveland, Ohio; the Department of Anesthesiology, Mayo Foundation, Rochester, Minnesota; and the Department of Anesthesiology, University of Maryland School of Medicine, Baltimore, Maryland.
Article Information
Case Reports
Case Reports   |   July 2001
Regional Pericarditis Mimicking Myocardial Infarction
Anesthesiology 7 2001, Vol.95, 261-264. doi:
Anesthesiology 7 2001, Vol.95, 261-264. doi:
ACUTE pericarditis is generally considered simple to diagnose because of its characteristic diffuse ST-segment elevation. In contrast, acute myocardial infarction typically presents with more localized ST-segment changes. 1 
We describe a patient who presented for emergency surgery with marked ST-segment elevation in the inferolateral leads, suggestive of acute myocardial ischemia and infarction. However, a thorough diagnostic workup ruled out myocardial injury, and further evaluation suggested that the patient’s electrocardiographic pattern was caused by a regional or localized pericarditis. Regional pericarditis has only been described in the postinfarction setting 2–4 and in a case in which the ST-segment elevation was initially more pronounced in the anterior leads but later evolved to generalized ST-segment elevation with a mild enzyme increase. 5 
Case Report
A 46-yr-old man with abdominal free air shown by computed tomography scan was scheduled to undergo emergency exploratory laparotomy. One month previously, he had undergone kidney and pancreas transplantations as a result of insulin-dependent diabetes and end-stage renal disease.
In the operating room, after applying standard monitoring, the electrocardiograph showed ST-segment elevation in leads II, III, and aVF. There was no dysrhythmia. The patient denied chest pain and was hemodynamically stable (blood pressure, 125/90 mmHg; heart rate, 89 beats/min). A twelve-lead electrocardiograph showed ST-segment elevation in leads II, III, aVF, and V4–V6in addition to tall, peaked T waves in V2–V4(fig. 1). The laboratory report showed a serum potassium concentration of 7.2 mEq/l, a hematocrit of 25%, a creatinine concentration of 1.4 mg/dl, a bicarbonate concentration of 24 mEq/l, and a serum glucose concentration of 103 mg/dl. Other laboratory results were unremarkable.
Fig. 1. Electrocardiogram showing marked ST-segment elevation predominantly in inferior leads (II, III, aVF) and lateral leads (V4–V6). Also, peaked, tall, symmetric T waves are present in V2–V4. PR-segment depression is present in several leads and lateral leads (I, aVL).
Fig. 1. Electrocardiogram showing marked ST-segment elevation predominantly in inferior leads (II, III, aVF) and lateral leads (V4–V6). Also, peaked, tall, symmetric T waves are present in V2–V4. PR-segment depression is present in several leads and lateral leads (I, aVL).
Fig. 1. Electrocardiogram showing marked ST-segment elevation predominantly in inferior leads (II, III, aVF) and lateral leads (V4–V6). Also, peaked, tall, symmetric T waves are present in V2–V4. PR-segment depression is present in several leads and lateral leads (I, aVL).
×
Surgery was postponed to correct hyperkalemia and to investigate the electrocardiographic results. After treatment, when the serum potassium concentration decreased to 5.5 mEq/l, the T waves returned to normal, but the ST-segment elevation persisted. A bedside two-dimensional transthoracic echocardiogram that evaluated all the sixteen segments of the left ventricle showed hyperdynamic ventricles with no segmental wall motion abnormality and no signs of pericardial effusion. The serum troponin T concentration was 0.02 ng/ml (normal, 0.00–0.10 ng/ml), and three sets of creatine phosphokinase enzymes drawn at 8-h intervals were all within normal limits. The electrocardiographic pattern (fig. 1) was analyzed more closely. Despite the local nature of the ST-segment changes, the pattern was otherwise consistent with pericarditis. The ST-segment elevation was concave and was accompanied by upright T waves, PR depression, and reciprocal changes in aVR and V1. The patient’s clinical course and the electrocardiographic analysis suggested that the electrocardiographic changes in this patient were caused by regional pericarditis.
Exploratory laparotomy for intestinal perforation was performed the next day, with an uneventful perioperative course. ST-segment elevation gradually resolved during the subsequent week (fig. 2).
Fig. 2. Electrocardiogram showing nonspecific ST-segment changes in inferior leads (II, III, aVF).
Fig. 2. Electrocardiogram showing nonspecific ST-segment changes in inferior leads (II, III, aVF).
Fig. 2. Electrocardiogram showing nonspecific ST-segment changes in inferior leads (II, III, aVF).
×
Discussion
The classic diagnostic triad of acute pericarditis includes specific electrocardiographic abnormalities, chest pain, and pericardial friction rub. 1 Chest pain, when present, can be confused with that of myocardial infarction. The chest pain of pericarditis, however, is usually constant and can be relieved by sitting up and leaning forward. Further, pericardial friction rub, when present, is often evanescent and can be overlooked. Therefore, the frequency of pericarditis is thought to be underestimated. 6 
The electrocardiographic changes of acute pericarditis typically evolve through four stages. 1,7,8 Stage 1 lasts several days to 2 weeks and is characterized by widespread concave ST-segment elevation, usually less than 5 mm, with reciprocal depression in leads over the areas not bounded by the pericardial–myocardial interface, aVR and V1. 4 The ST-segment elevation is believed to reflect the abnormal repolarization caused by injury of the superficial myocardium or a superficial myocarditis. Except for leads aVR and V1, the PR segment is usually depressed, likely reflecting abnormal atrial repolarization caused by inflammation. 7 PR depression is nearly as sensitive and specific for acute pericarditis as the more familiar ST-segment changes. 9 During stage 2, lasting several days to weeks, the ST and PR segments both return toward isoelectric status. Stage 3 usually begins around the third week and may last for several weeks, during which T waves may become inverted. Finally, during stage 4, there is a gradual resolution of any T-wave changes.
Distinguishing acute pericarditis from myocardial infarction can be problematic. In acute pericarditis, ST-segment elevation is usually seen in most of the leads. If ST-segment elevation is localized to a few leads, pericarditis can be confused with acute myocardial infarction. 9,10 However, ST-segment elevation observed during the acute injury stage of myocardial infarction is convex, whereas ST-segment elevation during acute pericarditis is usually concave. In addition, myocardial infarction is usually distinguished by the presence of Q waves and T-wave inversion associated with ST-segment elevation. In acute pericarditis, Q waves are absent and T-wave inversion occurs days to weeks later, after the ST segments have returned to normal. 1 
In the current patient, ST-segment elevation was registered predominantly in the inferolateral leads, mimicking an inferolateral wall myocardial infarction. More detailed electrocardiographic analysis in the patient showed that although the changes were regional, they were typical of pericarditis—that is, absence of Q waves, concave ST-segment elevation with reciprocal changes in aVR and V1, upright T waves, and typical PR depression. Further, myocardial infarction was ruled out by normal serum cardiac enzymes and by a two-dimensional transthoracic echocardiogram that showed no signs of regional wall motion abnormality. Although ST-segment elevation can be associated with hyperkalemia, it is unlikely in this patient because ST-segment elevation persisted after the potassium concentration decreased to the normal range and the peaked T waves returned to normal morphology.
This is a rare instance of regional pericarditis mimicking inferolateral myocardial infarction with no evidence of an underlying myocardial infarction. Regional pericarditis has been described in several previous instances; however, these cases are somewhat different from the current case. 2–5 
In one case of atypical pericarditis, marked (greater than 5 mm), localized ST-segment elevation in the anterior precordial leads mimicked acute myocardial infarction. 5 Myocardial infarction was considered unlikely on the basis of lack of symptoms, a two-dimensional echocardiogram showing no significant localized wall motion abnormalities, and only a slight increase in the peak creatine phosphokinase MB. However, the following day, the ST-segment elevation became more generalized, and a new pericardial friction rub became audible. Further, subsequent studies ruled out acute myocardial infarction. In this case of pericarditis, the initial presentation was that of an atypical regional pericarditis.
Regional pericarditis has also been described in the post–myocardial infarction setting. 2–4 Further, acute abdominal disorders (e.g.  , pancreatitis, cholecystitis, hepatitis, and peritonitis) have been reported to cause electrocardiographic patterns mimicking pericarditis. ST-segment elevation observed in patients with gastrointestinal emergencies can be difficult to distinguish from acute myocardial infarction. 11 Additionally, similar electrocardiographic findings are not uncommon after cardiac surgery. Finally, vasospastic angina may present with localized ST-segment changes similar to those we describe; however, they are typically accompanied with clinical symptoms (chest pain) or signs (dysrhythmias). 12 
In the current patient, pericarditis mimicked inferolateral wall myocardial infarction. This case shows that localized ST-segment changes in the absence of symptoms and signs of myocardial infarction can be consistent with a diagnosis of pericarditis and that a two-dimensional echocardiogram is an invaluable aid to rapid diagnosis.
References
Alexander RW, Schlant RC, Fuster V: The Heart. New York, McGraw-Hill, 1998, pp 2169–74
Oliva PB, Hammill SC, Edwards WD: The electrocardiographic diagnosis of regional pericarditis in acute inferior myocardial infarction. Eur Heart J 1993; 14: 1683–9Oliva, PB Hammill, SC Edwards, WD
Oliva PB, Hammill SC, Edwards WD: Electrocardiographic diagnosis of postinfarction regional pericarditis. Circulation 1993; 88: 896–904Oliva, PB Hammill, SC Edwards, WD
Oliva PB, Hammill SC: The clinical distinction between regional postinfarction pericarditis and other causes of postinfarction chest pain. Clin Cardiol 1994; 17: 471–8Oliva, PB Hammill, SC
Jain A:“Tombstone” anterior ST-segment elevations secondary to acute pericarditis: The role of two-dimensional echocardiogram. Clin Cardiol 1997; 20: 404–6Jain, A
Surawicz B, lasseter KC: Electrocardiogram in pericarditis. Am J Cardiol 1970; 26: 471–4Surawicz, B lasseter, KC
Spodick DH: Diagnostic electrocardiographic sequences in acute pericarditis: Significance of PR segment and PR vector changes. Circulation 1973; 48: 575–80Spodick, DH
Teh BS, Walsh J, Bell AJ, Walker SJ, Kilpatrick D: Electrical current paths in acute pericarditis. J Electrocardiol 1993; 26: 291–300Teh, BS Walsh, J Bell, AJ Walker, SJ Kilpatrick, D
Hancock WE: Acute myocardial infarction or pericarditis. Hosp Pract (Off Ed) 1992; 27: 25–6Hancock, WE
Braunwald E: A Textbook of Cardiovascular Medicine. Philadelphia, WB Saunders, 1997, pp 1482–3
Ryan ET, Pak PH, DeSanctis RW: Myocardial infarction mimicked by acute cholecystitis. Ann Inter Med 1992; 116: 218–20Ryan, ET Pak, PH DeSanctis, RW
Sprung J, Lesitsky MA, Jagetia A, Tucker C, Saffian M, Gottlieb A: Cardiac arrest caused by coronary spasm in two patients during recovery from epidural anesthesia. Reg Anesth 1996; 21: 253–60Sprung, J Lesitsky, MA Jagetia, A Tucker, C Saffian, M Gottlieb, A
Fig. 1. Electrocardiogram showing marked ST-segment elevation predominantly in inferior leads (II, III, aVF) and lateral leads (V4–V6). Also, peaked, tall, symmetric T waves are present in V2–V4. PR-segment depression is present in several leads and lateral leads (I, aVL).
Fig. 1. Electrocardiogram showing marked ST-segment elevation predominantly in inferior leads (II, III, aVF) and lateral leads (V4–V6). Also, peaked, tall, symmetric T waves are present in V2–V4. PR-segment depression is present in several leads and lateral leads (I, aVL).
Fig. 1. Electrocardiogram showing marked ST-segment elevation predominantly in inferior leads (II, III, aVF) and lateral leads (V4–V6). Also, peaked, tall, symmetric T waves are present in V2–V4. PR-segment depression is present in several leads and lateral leads (I, aVL).
×
Fig. 2. Electrocardiogram showing nonspecific ST-segment changes in inferior leads (II, III, aVF).
Fig. 2. Electrocardiogram showing nonspecific ST-segment changes in inferior leads (II, III, aVF).
Fig. 2. Electrocardiogram showing nonspecific ST-segment changes in inferior leads (II, III, aVF).
×