57-Year-Old Man With Atypical Chest Pain

Abstract

A 57-year-old man presented to the emergency department with a 10-day history of intermittent, sharp chest pain that was partially alleviated in the upright position and by leaning forward. Associated symptoms included dyspnea on exertion that preceded his chest pain. He reported no orthopnea, paroxysmal nocturnal dyspnea, orthostatic symptoms, fever, or chills. His medical history was remarkable for provoked deep venous thrombosis, for which he completed treatment with anticoagulation 4 months previously. There was no history of hyperlipidemia, diabetes mellitus, hypertension, or tobacco or alcohol use. The only notable family history was early coronary artery disease in both parents. On arrival at the emergency department, his heart rate was 75 beats/min and his blood pressure was 124/94 mm Hg. His chest pain, initially rated as 4 on a 10-point scale, resolved fully with sublingual nitroglycerin. Cardiac examination revealed mild tenderness to palpation with a regular rate and rhythm. No notable murmurs, rubs, gallops, jugular venous distention, or rales were present. Initial laboratory evaluation revealed the following (reference ranges provided parenthetically): hemoglobin, 16.4 g/dL (13.2-16.6 g/dL); white blood cell count, 7.0 × 109/L (3.4-9.6 × 109/L); platelet count, 187 × 109/L (135-317 × 109/L); creatinine, 0.9 mg/dL (0.74-1.35 mg/dL); sodium, 140 mmol/L (135-145 mmol/L); potassium, 4.2 mmol/L (3.6-5.2 mmol/L); 0- and 3-hour troponin T, 0.38 and 0.34 ng/mL (≤0.04 ng/mL), respectively; erythrocyte sedimentation rate, 3 mm/h (0-22 mm/h); and C-reactive protein (CRP), 3.5 mg/L (≤8.0 mg/L). Electrocardiography (ECG) revealed diffuse ST-segment elevation and PR-segment depression in leads II, III, aVF, and V2 through V6 with concomitant PR-segment elevation in lead aVR. Chest radiography was negative for any acute pathology.1.Based on the available clinical data, which one of the following is the most likely underlying etiology of this patient's chest pain?a.ST-elevation myocardial infarction (STEMI)b.Pulmonary embolismc.Acute pericarditisd.Aortic dissectione.Cardiac tamponade ST-elevation myocardial infarction usually presents with typical angina, persistent, typically regional, ST-elevation on ECG, and troponin release.1O'Gara P.T. Kushner F.G. Ascheim D.D. et al.2013 ACCF/AHA guideline for the management of ST-elevation myocardial infarction: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines.Circulation. 2013; 127 ([published correction appears in Circulation. 2013;128(25):e481]): e362-e425Crossref PubMed Scopus (780) Google Scholar For a diagnosis of STEMI, the troponin level must be considerably increased or decreased and the ECG must show a 1-mm ST elevation in contiguous chest or limb leads. In leads V2 through V3, a 2-mm or 1.5-mm ST elevation in contiguous leads is required in men and women, respectively.2Thygesen K. Alpert J.S. Jaffe A.S. et al.Third universal definition of myocardial infarction.Circulation. 2012; 126: 2020-2035Crossref PubMed Scopus (2376) Google Scholar Diffuse ST elevation that does not correlate with a specific coronary artery territory is not consistent with STEMI. Pulmonary embolism causes pleuritic chest pain, dyspnea, and, occasionally, elevated troponin levels. However, pulmonary embolism does not characteristically present with diffuse ST elevation. Rather, tachycardia and nonspecific ST-segment and T-wave changes predominate.3Stein P.D. Terrin M.L. Hales C.A. et al.Clinical, laboratory, roentgenographic, and electrocardiographic findings in patients with acute pulmonary embolism and no pre-existing cardiac or pulmonary disease.Chest. 1991; 100: 598-603Abstract Full Text Full Text PDF PubMed Scopus (619) Google Scholar Our patient's pleuritic chest pain that improved in the upright position while leaning forward and diffuse ST elevation were most consistent with acute pericarditis. Diagnosis of acute pericarditis requires 2 of the following: typical pericardial chest pain, pericardial rub, diffuse ST elevation or PR depression, or new or worsening pericardial effusion.4Adler Y. Charron P. Imazio M. et al.ESC Scientific Document Group. 2015 ESC guidelines for the diagnosis and management of pericardial diseases: the Task Force for the Diagnosis and Management of Pericardial Diseases of the European Society of Cardiology (ESC); endorsed by: the European Association for Cardio-Thoracic Surgery (EACTS).Eur Heart J. 2015; 36: 2921-2964Crossref PubMed Scopus (1044) Google Scholar Typical pericardial chest pain is acute, retrosternal, and pleuritic and improves with upright positioning and leaning forward.4Adler Y. Charron P. Imazio M. et al.ESC Scientific Document Group. 2015 ESC guidelines for the diagnosis and management of pericardial diseases: the Task Force for the Diagnosis and Management of Pericardial Diseases of the European Society of Cardiology (ESC); endorsed by: the European Association for Cardio-Thoracic Surgery (EACTS).Eur Heart J. 2015; 36: 2921-2964Crossref PubMed Scopus (1044) Google Scholar Radiation to the arms and neck is common. In particular, pain in the left or right trapezius ridge is quite common as bilateral phrenic nerves course through the anterior pericardium.4Adler Y. Charron P. Imazio M. et al.ESC Scientific Document Group. 2015 ESC guidelines for the diagnosis and management of pericardial diseases: the Task Force for the Diagnosis and Management of Pericardial Diseases of the European Society of Cardiology (ESC); endorsed by: the European Association for Cardio-Thoracic Surgery (EACTS).Eur Heart J. 2015; 36: 2921-2964Crossref PubMed Scopus (1044) Google Scholar Aortic dissection most commonly is associated with abrupt, intense, and stabbing chest pain. Electrocardiography typically reveals nonspecific ST-segment T-wave changes. However, if the dissection involves the coronary ostia, ECG evidence of ischemia and troponin elevation may be seen.5Hiratzka L.F. Bakris G.L. Beckman J.A. et al.2010 ACCF/AHA/AATS/ACR/ASA/SCA/SCAI/SIR/STS/SVM guidelines for the diagnosis and management of patients with thoracic aortic disease: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines, American Association for Thoracic Surgery, American College of Radiology, American Stroke Association, Society of Cardiovascular Anesthesiologists, Society for Cardiovascular Angiography and Interventions, Society of Interventional Radiology, Society of Thoracic Surgeons, and Society for Vascular Medicine.Circulation. 2010; 121 ([published correction appears in Circulation. 2010;122(4):e410]): e266-e369Crossref PubMed Scopus (1917) Google Scholar Cardiac tamponade presents with jugular venous distention, pulsus paradoxus, and muffled heart sounds. Although tamponade can occur in patients with pericarditis, it is more commonly seen in pericarditis associated with a specific etiology such as tuberculosis or malignancy.4Adler Y. Charron P. Imazio M. et al.ESC Scientific Document Group. 2015 ESC guidelines for the diagnosis and management of pericardial diseases: the Task Force for the Diagnosis and Management of Pericardial Diseases of the European Society of Cardiology (ESC); endorsed by: the European Association for Cardio-Thoracic Surgery (EACTS).Eur Heart J. 2015; 36: 2921-2964Crossref PubMed Scopus (1044) Google Scholar Our patient was admitted to the hospital for further management of a working diagnosis of acute pericarditis.2.Which one of the following is the most appropriate initial treatment strategy for this patient?a.Prednisone and morphineb.Ibuprofen and intrapericardial lidocainec.Colchicine and pericardiectomyd.Aspirin and colchicinee.Anakinra and intravenous immunoglobulin (IVIG) Corticosteroids are not recommended as first-line therapy for acute pericarditis because of associated high recurrence rates.6Imazio M. Brucato A. Cumetti D. et al.Corticosteroids for recurrent pericarditis: high versus low doses; a nonrandomized observation.Circulation. 2008; 118: 667-671Crossref PubMed Scopus (185) Google Scholar However, corticosteroids may be considered in cases of refractory pericarditis, autoimmune pericarditis, or in patients with contraindications to nonsteroidal anti-inflammatory drugs (NSAIDs) or colchicine.4Adler Y. Charron P. Imazio M. et al.ESC Scientific Document Group. 2015 ESC guidelines for the diagnosis and management of pericardial diseases: the Task Force for the Diagnosis and Management of Pericardial Diseases of the European Society of Cardiology (ESC); endorsed by: the European Association for Cardio-Thoracic Surgery (EACTS).Eur Heart J. 2015; 36: 2921-2964Crossref PubMed Scopus (1044) Google Scholar, 6Imazio M. Brucato A. Cumetti D. et al.Corticosteroids for recurrent pericarditis: high versus low doses; a nonrandomized observation.Circulation. 2008; 118: 667-671Crossref PubMed Scopus (185) Google Scholar If corticosteroids are utilized, the starting dose should be low to moderate (ie, prednisone at 0.2-0.5 mg/kg per day or equivalent), with the initial dose continued until resolution of symptoms and CRP normalization.4Adler Y. Charron P. Imazio M. et al.ESC Scientific Document Group. 2015 ESC guidelines for the diagnosis and management of pericardial diseases: the Task Force for the Diagnosis and Management of Pericardial Diseases of the European Society of Cardiology (ESC); endorsed by: the European Association for Cardio-Thoracic Surgery (EACTS).Eur Heart J. 2015; 36: 2921-2964Crossref PubMed Scopus (1044) Google Scholar Tapering should be done slowly and may require several months.4Adler Y. Charron P. Imazio M. et al.ESC Scientific Document Group. 2015 ESC guidelines for the diagnosis and management of pericardial diseases: the Task Force for the Diagnosis and Management of Pericardial Diseases of the European Society of Cardiology (ESC); endorsed by: the European Association for Cardio-Thoracic Surgery (EACTS).Eur Heart J. 2015; 36: 2921-2964Crossref PubMed Scopus (1044) Google Scholar Of note, corticosteroids should be avoided in the management of post–myocardial infarction pericarditis because use in this setting is associated with increased risk of mechanical complications and myocardial infarction. Opioid analgesics do not treat the underlying inflammatory mechanism responsible for pain in pericarditis. Ibuprofen and colchicine both have been utilized as effective monotherapy for acute pericarditis.7Lill L.S. Treatment of acute and recurrent idiopathic pericarditis.Circulation. 2013; 127: 1723-1726Crossref PubMed Scopus (52) Google Scholar However, intrapericardial lidocaine and pericardiectomy are not indicated as first-line treatment for acute pericarditis. Intrapericardial lidocaine may be used in patients requiring pericardiocentesis. Pericardiectomy is usually only considered after extensive unsuccessful trials of medical therapy.4Adler Y. Charron P. Imazio M. et al.ESC Scientific Document Group. 2015 ESC guidelines for the diagnosis and management of pericardial diseases: the Task Force for the Diagnosis and Management of Pericardial Diseases of the European Society of Cardiology (ESC); endorsed by: the European Association for Cardio-Thoracic Surgery (EACTS).Eur Heart J. 2015; 36: 2921-2964Crossref PubMed Scopus (1044) Google Scholar The combination of an NSAID and colchicine is recommended as first-line therapy for acute pericarditis. This combination has been found to improve clinical efficacy and reduce recurrences.8Alabed S. Cabello J.B. Irving G.J. Qintar M. Burls A. Colchicine for pericarditis.Cochrane Database Syst Rev. 2014; : CD010652PubMed Google Scholar Aspirin is the NSAID of choice for pericarditis when acute coronary syndrome (ACS) remains in the differential diagnosis (ie, with substantial troponin elevation as in our patient) because other NSAIDs are associated with increased risk of mechanical complications in ACS.1O'Gara P.T. Kushner F.G. Ascheim D.D. et al.2013 ACCF/AHA guideline for the management of ST-elevation myocardial infarction: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines.Circulation. 2013; 127 ([published correction appears in Circulation. 2013;128(25):e481]): e362-e425Crossref PubMed Scopus (780) Google Scholar Anakinra, an interleukin 1 inhibitor, and IVIG are often utilized only in cases of steroid-dependent pericarditis refractory to colchicine and NSAIDs. Both are fast-acting and effective treatments for pericarditis. However, recurrences of pericarditis after discontinuation of anakinra and IVIG are not uncommon.4Adler Y. Charron P. Imazio M. et al.ESC Scientific Document Group. 2015 ESC guidelines for the diagnosis and management of pericardial diseases: the Task Force for the Diagnosis and Management of Pericardial Diseases of the European Society of Cardiology (ESC); endorsed by: the European Association for Cardio-Thoracic Surgery (EACTS).Eur Heart J. 2015; 36: 2921-2964Crossref PubMed Scopus (1044) Google Scholar On admission, our patient began treatment with colchicine and high-dose aspirin. Echocardiography to further evaluate suspected acute pericarditis revealed subtle hypokinesis of the lateral left ventricular apex with no signs of pericardial effusion, valvular disease, or heart failure. Shortly after admission, the 6-hour troponin level had increased to 0.47 ng/mL. The patient continued to have intermittent sharp chest pain, which improved after nitroglycerin administration.3.Which one of the following is the most appropriate next diagnostic step?a.Cardiac computed tomography (CT)b.Cardiac magnetic resonance imaging (MRI)c.Activate the STEMI alert for emergent left-sided heart catheterization with intravenous heparin and clopidogrel loadingd.Stress echocardiographye.No further diagnostic testing necessary Cardiac CT is a valuable tool in the evaluation of acute pericarditis. Although cardiac CT may be a reasonable consideration, it is not the best first choice given the necessary radiation exposure. Additionally, in the setting of elevated troponin level in a patient in whom a coronary etiology has not been excluded as the source, the need for iodine contrast agent may contribute to a higher risk of renal injury.4Adler Y. Charron P. Imazio M. et al.ESC Scientific Document Group. 2015 ESC guidelines for the diagnosis and management of pericardial diseases: the Task Force for the Diagnosis and Management of Pericardial Diseases of the European Society of Cardiology (ESC); endorsed by: the European Association for Cardio-Thoracic Surgery (EACTS).Eur Heart J. 2015; 36: 2921-2964Crossref PubMed Scopus (1044) Google Scholar Cardiac MRI provides a comprehensive anatomic and functional evaluation when pericardial or myocardial disease is being considered.9Bogaert J. Francone M. Cardiovascular magnetic resonance in pericardial diseases.J Cardiovasc Magn Reson. 2009; 11: 14Crossref PubMed Scopus (151) Google Scholar Although not necessary in all cases of pericarditis, cardiac MRI is particularly useful in cases of pericarditis with extension to the myocardium (ie, myopericarditis) because it has the ability to characterize the extent of myocardial abnormalities and distinguish ischemic heart disease from nonischemic etiologies including myocarditis.4Adler Y. Charron P. Imazio M. et al.ESC Scientific Document Group. 2015 ESC guidelines for the diagnosis and management of pericardial diseases: the Task Force for the Diagnosis and Management of Pericardial Diseases of the European Society of Cardiology (ESC); endorsed by: the European Association for Cardio-Thoracic Surgery (EACTS).Eur Heart J. 2015; 36: 2921-2964Crossref PubMed Scopus (1044) Google Scholar The use of cardiac MRI in further risk stratification of pericardial disease is based on institutional availability and expertise and should not otherwise be routinely performed.4Adler Y. Charron P. Imazio M. et al.ESC Scientific Document Group. 2015 ESC guidelines for the diagnosis and management of pericardial diseases: the Task Force for the Diagnosis and Management of Pericardial Diseases of the European Society of Cardiology (ESC); endorsed by: the European Association for Cardio-Thoracic Surgery (EACTS).Eur Heart J. 2015; 36: 2921-2964Crossref PubMed Scopus (1044) Google Scholar Our patient's clinical presentation was most consistent with acute myopericarditis (ie, pericarditis with troponin elevation). Therefore, cardiac MRI was determined to be the most appropriate next test because this modality can distinguish between ischemic and nonischemic myocardial injury. Intermittent pleuritic chest pain lasting more than a week with diffuse ST elevation and PR depression on ECG is not consistent with STEMI. Therefore, activation of the STEMI alert for emergent left-sided heart catheterization is not indicated at this time. Use of heparin for suspected ACS in the setting of concomitant acute pericarditis is controversial because heparin may precipitate hemorrhagic tamponade in this setting, although this is not uniformly seen.10Imazio M. Cecchi E. Demichelis B. et al.Indicators of poor prognosis of acute pericarditis.Circulation. 2007; 115: 2739-2744Crossref PubMed Scopus (258) Google Scholar Stress echocardiography is contraindicated in patients with increasing troponin levels suggestive of myocardial injury. Idiopathic pericarditis with no predictors of poor prognosis may be managed with empiric anti-inflammatory medications and outpatient monitoring.4Adler Y. Charron P. Imazio M. et al.ESC Scientific Document Group. 2015 ESC guidelines for the diagnosis and management of pericardial diseases: the Task Force for the Diagnosis and Management of Pericardial Diseases of the European Society of Cardiology (ESC); endorsed by: the European Association for Cardio-Thoracic Surgery (EACTS).Eur Heart J. 2015; 36: 2921-2964Crossref PubMed Scopus (1044) Google Scholar However, an increasing troponin level demands that ACS remains in the differential diagnosis. These patients require inpatient monitoring and further risk stratification with serial troponin evaluation, echocardiography, and consideration of further imaging (such as cardiac MRI) in the proper clinical setting. The patient underwent cardiac MRI, which revealed a subacute transmural infarction of the left ventricular apex with associated anterior, apical, and septal hypokinesis. There was also enhancement of the adjacent pericardium.4.Given the cardiac MRI and echocardiographic findings, which one of the following coronary vessels is most likely to be affected in this patient?a.Left anterior descending coronary artery (LAD)b.Left circumflex coronary arteryc.Multiple coronary arteriesd.Left main coronary artery (LMCA)e.Right coronary artery (RCA) Although considerable overlap in coronary distribution can occur, hypokinesis of the septum, apex, and anterior regions of the left ventricle is characteristic of an LAD occlusion.11Cerqueira M.D. Weissman N.J. Dilsizian V. et al.American Heart Association Writing Group on Myocardial Segmentation and Registration for Cardiac Imaging. Standardized myocardial segmentation and nomenclature for tomographic imaging of the heart: a statement for healthcare professionals from the Cardiac Imaging Committee of the Council on Clinical Cardiology of the American Heart Association.Circulation. 2002; 105: 539-542Crossref PubMed Scopus (5284) Google Scholar Lateral left ventricular hypokinesis may be seen with occlusion of the left circumflex artery. However, the lateral left ventricular myocardium has substantial blood supply overlap, and lateral hypokinesis is more typical of multiple territories of ischemia.11Cerqueira M.D. Weissman N.J. Dilsizian V. et al.American Heart Association Writing Group on Myocardial Segmentation and Registration for Cardiac Imaging. Standardized myocardial segmentation and nomenclature for tomographic imaging of the heart: a statement for healthcare professionals from the Cardiac Imaging Committee of the Council on Clinical Cardiology of the American Heart Association.Circulation. 2002; 105: 539-542Crossref PubMed Scopus (5284) Google Scholar Because the LMCA is the common source of both the left circumflex coronary artery and the LAD, hypokinesis can be seen in anterior, lateral, and apical left ventricular distributions with LMCA occlusion.11Cerqueira M.D. Weissman N.J. Dilsizian V. et al.American Heart Association Writing Group on Myocardial Segmentation and Registration for Cardiac Imaging. Standardized myocardial segmentation and nomenclature for tomographic imaging of the heart: a statement for healthcare professionals from the Cardiac Imaging Committee of the Council on Clinical Cardiology of the American Heart Association.Circulation. 2002; 105: 539-542Crossref PubMed Scopus (5284) Google Scholar Occlusion of the RCA most commonly involves hypokinesis of the inferior segments of the left ventricle. Moreover, proximal RCA disease is more likely to be associated with severe right ventricular dysfunction.11Cerqueira M.D. Weissman N.J. Dilsizian V. et al.American Heart Association Writing Group on Myocardial Segmentation and Registration for Cardiac Imaging. Standardized myocardial segmentation and nomenclature for tomographic imaging of the heart: a statement for healthcare professionals from the Cardiac Imaging Committee of the Council on Clinical Cardiology of the American Heart Association.Circulation. 2002; 105: 539-542Crossref PubMed Scopus (5284) Google Scholar Given concern about an evolving subacute myocardial infarction, cardiac catheterization was obtained. It revealed distal occlusion of the LAD that was also accompanied by a high-grade stenosis of the proximal LAD. A drug-eluting stent was subsequently placed in the proximal LAD lesion with excellent results.5.Which one of the following is the most likely cause of this patient's clinical presentation?a.Type 2 myocardial infarction in the setting of acute pericarditisb.Takotsubo cardiomyopathy in the setting of acute pericarditisc.Post–cardiac injury syndrome (PCIS)d.Viral myopericarditise.Acute STEMI Type 2 myocardial infarction occurs secondary to a myocardial oxygen supply-and-demand mismatch not attributable to an acute primary coronary thrombotic event (ie, ACS). Typical causes of type 2 myocardial infarction include hypovolemia, tachycardia, sepsis, respiratory failure, coronary vasospasm, and anemia.2Thygesen K. Alpert J.S. Jaffe A.S. et al.Third universal definition of myocardial infarction.Circulation. 2012; 126: 2020-2035Crossref PubMed Scopus (2376) Google Scholar Type 2 myocardial infarction is unlikely in the absence of a non–ACS-related supply-and-demand mismatch. Takotsubo cardiomyopathy is a transient, often stress-induced condition of midsegment and apical left ventricular dysfunction in the absence of obstructive coronary disease or pheochromocytoma. Patients present with chest pain similar to that in ACS, ST elevation, and troponin release.12Prasad A. Lerman A. Rihal C.S. Apical ballooning syndrome (Tako-Tsubo or stress cardiomyopathy): a mimic of acute myocardial infarction.Am Heart J. 2008; 155: 408-417Crossref PubMed Scopus (1285) Google Scholar Magnetic resonance perfusion imaging typically does not identify coronary-specific perfusion abnormalities or late gadolinium enhancement. These features help distinguish Takotsubo cardiomyopathy from myocardial infarction or other inflammatory processes.12Prasad A. Lerman A. Rihal C.S. Apical ballooning syndrome (Tako-Tsubo or stress cardiomyopathy): a mimic of acute myocardial infarction.Am Heart J. 2008; 155: 408-417Crossref PubMed Scopus (1285) Google Scholar Takotsubo cardiomyopathy remains a diagnosis of exclusion and requires angiography to demonstrate the absence of obstructive epicardial coronary disease or the presence of left ventricular dysfunction that is discordantly worse than the extent of epicardial coronary disease.12Prasad A. Lerman A. Rihal C.S. Apical ballooning syndrome (Tako-Tsubo or stress cardiomyopathy): a mimic of acute myocardial infarction.Am Heart J. 2008; 155: 408-417Crossref PubMed Scopus (1285) Google Scholar Post–cardiac injury syndrome is an overarching term that refers to a group of inflammatory, likely autoimmune-mediated, pericardial syndromes that includes post–myocardial infarction pericarditis. Diagnostic criteria for post–myocardial infarction pericarditis are similar to those for acute pericarditis. However, prior injury (ie, myocardial infarction or trauma) to the myocardium, pericardium, or both is required.13Imazio M. Hoit B.D. Post-cardiac injury syndromes: an emerging cause of pericardial diseases.Int J Cardiol. 2013; 168: 648-652Abstract Full Text Full Text PDF PubMed Scopus (151) Google Scholar In most cases of post–myocardial infarction pericarditis, ECG will reveal evidence of pericarditis as well as previous ischemic injury such as Q waves or poor R-wave progression.14Oliva P.B. Hammill S.C. Talano J.V. T wave changes consistent with epicardial involvement in acute myocardial infarction: observations in patients with a postinfarction pericardial effusion without clinically recognized postinfarction pericarditis.J Am Coll Cardiol. 1994; 24: 1073-1077Crossref PubMed Scopus (18) Google Scholar However, these changes are not always seen, as in our patient. Our patient met diagnostic criteria for acute pericarditis and had cardiac catheterization and MRI evidence of myocardial infarction, making post–myocardial infarction pericarditis the most likely diagnosis. Because troponin levels can remain elevated up to 2 weeks after myocardial infarction, the elevated troponin level in our patient was likely due to a previous myocardial infarction and possibly myocardial extension of the post–myocardial infarction pericarditis.2Thygesen K. Alpert J.S. Jaffe A.S. et al.Third universal definition of myocardial infarction.Circulation. 2012; 126: 2020-2035Crossref PubMed Scopus (2376) Google Scholar Myopericarditis is diagnosed in patients meeting diagnostic criteria for acute pericarditis who have concomitant troponin elevation. In developed countries, the most common etiology of myopericarditis is a viral infection.4Adler Y. Charron P. Imazio M. et al.ESC Scientific Document Group. 2015 ESC guidelines for the diagnosis and management of pericardial diseases: the Task Force for the Diagnosis and Management of Pericardial Diseases of the European Society of Cardiology (ESC); endorsed by: the European Association for Cardio-Thoracic Surgery (EACTS).Eur Heart J. 2015; 36: 2921-2964Crossref PubMed Scopus (1044) Google Scholar Although our patient met criteria for myopericarditis, the established left ventricular hypokinesis and LAD stenosis were not consistent with viral myopericarditis but rather post–myocardial infarction pericarditis with persistent troponin elevation from a previous myocardial infarction and possibly myocardial extension of the post–myocardial pericarditis. Pleuritic chest pain lasting more than 1 week with diffuse ST elevation on ECG that does not correlate with a specific coronary artery territory is not consistent with acute STEMI.1O'Gara P.T. Kushner F.G. Ascheim D.D. et al.2013 ACCF/AHA guideline for the management of ST-elevation myocardial infarction: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines.Circulation. 2013; 127 ([published correction appears in Circulation. 2013;128(25):e481]): e362-e425Crossref PubMed Scopus (780) Google Scholar Although acute STEMI can be a nidus for pericardial inflammation in PCIS, pericarditis associated with PCIS typically develops over days to weeks and not in the acute setting.4Adler Y. Charron P. Imazio M. et al.ESC Scientific Document Group. 2015 ESC guidelines for the diagnosis and management of pericardial diseases: the Task Force for the Diagnosis and Management of Pericardial Diseases of the European Society of Cardiology (ESC); endorsed by: the European Association for Cardio-Thoracic Surgery (EACTS).Eur Heart J. 2015; 36: 2921-2964Crossref PubMed Scopus (1044) Google Scholar Our patient was continued on anti-inflammatory treatment for post–myocardial infarction pericarditis as well as standard treatment for the drug-eluting stent placed in his proximal LAD. Post–myocardial infarction pericarditis is an inflammatory, likely autoimmune-mediated, subset of the broader disease group known as PCIS.13Imazio M. Hoit B.D. Post-cardiac injury syndromes: an emerging cause of pericardial diseases.Int J Cardiol. 2013; 168: 648-652Abstract Full Text Full Text PDF PubMed Scopus (151) Google Scholar Post–myocardial infarction pericarditis is much less common in the present era of primary percutaneous intervention. In fact, less than 5% of patients will present with peri-infarction pericarditis.13Imazio M. Hoit B.D. Post-cardiac injury syndromes: an emerging cause of pericardial diseases.Int J Cardiol. 2013; 168: 648-652Abstract Full Text Full Text PDF PubMed Scopus (151) Google Scholar However, the incidence is higher in patients with delayed presentation. The pathogenesis of post–myocardial infarction pericarditis is thought to be an autoimmune phenomenon instigated by myocardial necrosis with subsequent pericardial damage.13Imazio M. Hoit B.D. Post-cardiac injury syndromes: an emerging cause of pericardial diseases.Int J Cardiol. 2013; 168: 648-652Abstract Full Text Full Text PDF PubMed Scopus (151) Google Scholar Clinical features include an initial ACS presentation followed by pleuritic chest pain days to weeks after the ACS. Diagnostic criteria for post–myocardial infarction pericarditis are similar to those for acute pericarditis. However, identification of prior pericardial or myocardial injury such as demonstration of transmural infarction on cardiac MRI is also necessary.13Imazio M. Hoit B.D. Post-cardiac injury syndromes: an emerging cause of pericardial diseases.Int J Cardiol. 2013; 168: 648-652Abstract Full Text Full Text PDF PubMed Scopus (151) Google Scholar The ECG in post–myocardial infarction pericarditis will typically show evidence of pericarditis as well as previous ischemic injury such as Q waves or poor R-wave progression.14Oliva P.B. Hammill S.C. Talano J.V. T wave changes consistent with epicardial involvement in acute myocardial infarction: observations in patients with a postinfarction pericardial effusion without clinically recognized postinfarction pericarditis.J Am Coll Cardiol. 1994; 24: 1073-1077Crossref PubMed Scopus (18) Google Scholar However, these ischemic changes are not always seen, as was the case with our patient. For patients presenting with acute pericarditis and myocardial involvement (ie, myopericarditis), inpatient admission is mandatory. Serial troponin evaluation, echocardiography, and consideration of further imaging in the proper clinical context are necessary for further risk stratification.4Adler Y. Charron P. Imazio M. et al.ESC Scientific Document Group. 2015 ESC guidelines for the diagnosis and management of pericardial diseases: the Task Force for the Diagnosis and Management of Pericardial Diseases of the European Society of Cardiology (ESC); endorsed by: the European Association for Cardio-Thoracic Surgery (EACTS).Eur Heart J. 2015; 36: 2921-2964Crossref PubMed Scopus (1044) Google Scholar Cardiac MRI is particularly useful in cases such as ours with marked troponin elevation because this modality can distinguish between ischemic and nonischemic causes of myocardial injury.4Adler Y. Charron P. Imazio M. et al.ESC Scientific Document Group. 2015 ESC guidelines for the diagnosis and management of pericardial diseases: the Task Force for the Diagnosis and Management of Pericardial Diseases of the European Society of Cardiology (ESC); endorsed by: the European Association for Cardio-Thoracic Surgery (EACTS).Eur Heart J. 2015; 36: 2921-2964Crossref PubMed Scopus (1044) Google Scholar The use of advanced cardiac imaging, however, relies on institutional availability and expertise and therefore is not mandated as part of the routine evaluation of inflammatory pericardial disease. For those patients with a high clinical index of suspicion for ACS, left-sided heart catheterization should be obtained to rule out ACS.4Adler Y. Charron P. Imazio M. et al.ESC Scientific Document Group. 2015 ESC guidelines for the diagnosis and management of pericardial diseases: the Task Force for the Diagnosis and Management of Pericardial Diseases of the European Society of Cardiology (ESC); endorsed by: the European Association for Cardio-Thoracic Surgery (EACTS).Eur Heart J. 2015; 36: 2921-2964Crossref PubMed Scopus (1044) Google Scholar The treatment of post–myocardial infarction pericarditis is similar to recommended therapy for acute pericarditis, which includes NSAIDs and colchicine. In particular, high-dose aspirin and colchicine are the preferred treatment for post–myocardial infarction pericarditis, both for short-term and preventive therapy.4Adler Y. Charron P. Imazio M. et al.ESC Scientific Document Group. 2015 ESC guidelines for the diagnosis and management of pericardial diseases: the Task Force for the Diagnosis and Management of Pericardial Diseases of the European Society of Cardiology (ESC); endorsed by: the European Association for Cardio-Thoracic Surgery (EACTS).Eur Heart J. 2015; 36: 2921-2964Crossref PubMed Scopus (1044) Google Scholar Colchicine is typically continued for 3 months, while aspirin duration is dictated by symptom resolution and CRP normalization.4Adler Y. Charron P. Imazio M. et al.ESC Scientific Document Group. 2015 ESC guidelines for the diagnosis and management of pericardial diseases: the Task Force for the Diagnosis and Management of Pericardial Diseases of the European Society of Cardiology (ESC); endorsed by: the European Association for Cardio-Thoracic Surgery (EACTS).Eur Heart J. 2015; 36: 2921-2964Crossref PubMed Scopus (1044) Google Scholar. Nonsteroidal anti-inflammatory drugs other than aspirin are not preferred for treatment of post–myocardial infarction pericarditis because their use may lead to myocardial scar thinning, infarct expansion, and potential adverse outcomes.1O'Gara P.T. Kushner F.G. Ascheim D.D. et al.2013 ACCF/AHA guideline for the management of ST-elevation myocardial infarction: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines.Circulation. 2013; 127 ([published correction appears in Circulation. 2013;128(25):e481]): e362-e425Crossref PubMed Scopus (780) Google Scholar