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ECG Quiz Answer

Acute Onset of Chest Pain in a Soccer Player

David S. Ross, MD; Gary Cooper, MD



Return to case presentation.

The ECG (figure 2) shows diffuse ST elevations and PR depressions, which suggest pericarditis. The patient was transferred to the cardiac care unit. He improved slowly on non-steroidal anti-inflammatory drug (NSAID) therapy. Serial cardiac enzymes proved to be unremarkable. An echocardiogram was performed and revealed no significant abnormalities.

[Figure 2]

There are many causes of acute pericarditis. The most common causes include an idiopathic source, viral infection, connective tissue disorder, malignancy, chronic renal failure, bacterial infection, and tuberculosis (1,2). Based on the history, physical, and laboratory data, our differential was limited to an idiopathic or viral cause. We were unable to obtain a history of any recent illness.

Common presenting symptoms include retrosternal pleuritic chest pain, shortness of breath, fever, syncope, and fatigue (1,2). The pain often involves the left trapezius ridge, which may be its only location. Patients will typically sit up to relieve the discomfort. Symptoms are exacerbated in the recumbent position and with deep inspiration. In addition, nausea, vomiting, diaphoresis, and radiating pain may be noted in the history. The pericardium is innervated by the vagus nerve, left recurrent laryngeal nerve, and esophageal plexus, and also has rich sympathetic innervation from the stellate ganglion, first dorsal ganglia, and the cardiac, aortic, and diaphragmatic plexuses (3). Inflammation of the pericardium accounts for these symptoms.

A pericardial friction rub is pathognomonic for acute pericarditis (2). Repeated auscultation is recommended since the rub may be transient or intermittent. Absence of a rub does not exclude the diagnosis (2). Our patient had what we believe was pleuritic chest pain and shortness of breath. A pericardial rub was never appreciated.

An ECG can be the most helpful test when used as an adjunct to the history and physical exam. The most sensitive abnormality is diffuse elevation of the ST segment (2). The ST-segment elevation differs from that associated with myocardial infarction by being evident in more leads (2,4). Also, a highly specific but insensitive sign of acute pericarditis is depression of the PR segment (2). When present, this additional information can be of great help in differentiating acute pericarditis from myocardial infarction.

In addition, one must be able to distinguish acute pericarditis from normal early repolarization. This pattern is most common in teenaged boys and men in their 20s. These individuals differ from pericarditis patients in that the clinical syndrome of pain and dyspnea is absent, PR-segment depression is present in some patients but uncommon, and, most important, the ECG does not, over time, evolve a pattern of return of the ST segment to baseline followed by T-wave inversion (3). A prior ECG can be helpful if available.

Our patient's ECG was classic for acute pericarditis. Most patients with acute pericarditis maintain sinus rhythm, frequently with a degree of sinus tachycardia. Atrial arrhythmia can occasionally be observed. These arrhythmias are secondary to inflammation of the superficial atrial myocardium. Laboratory data are not specific; however, the erythrocyte sedimentation rate and WBC are commonly elevated (1,2).

When the diagnosis is in question, a transthoracic echocardiogram is indicated. When regional wall motion abnormalities are absent in a patient who has chest pain and ECG evidence of epicardial injury, the diagnosis of acute myocardial infarction is very unlikely.

An integral part of the physical examination in patients with pericarditis is detection of any paradoxical pulse and observation of the patient's neck veins. Borderline or low blood pressure, a paradoxical pulse greater than 10 mm Hg, and increasing elevation of the neck veins with inspiration (Kussmaul's sign) strongly suggest cardiac tamponade.

Acute idiopathic or viral pericarditis is normally a self-limited disease that responds to NSAIDs. Details of treatment are beyond the scope of this article. However, agents typically used for treatment have included ibuprofen, parenteral ketorolac, aspirin, and indomethacin. Some experts consider the last a poor treatment choice in those with known coronary artery disease because of its propensity to diminish coronary blood flow (5). Aspirin should not be used in conjunction with other NSAIDs. Addition of colchicine may be helpful for those patients who do not respond to NSAIDs. Prednisone should be considered as a last resort because its use has been associated with difficulty with tapering and recurrence of symptoms. In pericarditis, heparin, IIb/IIIa inhibitors (antiplatelet agents), and thrombolytic agents are contraindicated.

The 26th Bethesda Conference guidelines from the American College of Sports Medicine and the American College of Cardiology on athletes with cardiovascular abnormalities recommend that those who have pericarditis not participate in competitive sports during the acute episode (6). An athlete may return to full activity when there is no longer evidence of active disease by history or physical examination, appropriate blood tests, exercise testing, and an ambulatory 12-lead ECG.


  1. Ilan Y, Oren R, Ben-Chetrit E: Acute pericarditis: etiology, treatment, and prognosis: a study of 115 patients. Jpn Heart J 1991;32(3):315-321
  2. Shabetai R: Acute pericarditis. Cardiol Clin 1990;8(4):639-644
  3. Lorell BH: Pericardial diseases, in Braunwald E (ed): Heart Disease: A Textbook of Cardiovascular Medicine, ed 5. Philadelphia, Saunders, 1997, pp 1478-1534
  4. Kouvaras G, Soufras G, Chronopoulos G, et al: The ST segment axis as a differential diagnostic feature between acute pericarditis and acute inferior myocardial infarction. Angiology 1990;41(3):207-212
  5. Friedman PL, Brown EJ Jr, Gunther S, et al: Coronary vasoconstrictor effect of indomethacin in patients with coronary-artery disease. N Engl J Med 120211;305(20):1171-1175
  6. Maron BJ, Isner JM, McKenna WJ: 26th Bethesda conference: recommendations for determining eligibility for competition in athletes with cardiovascular abnormalities. Task force 3: hypertrophic cardiomyopathy, myocarditis, and other myopericardial diseases and mitral valve prolapse. Med Sci Sports Exerc 1994;26(10 suppl):S261-S267

Dr Ross is director of the Primary Care Sports Medicine Fellowship Program at Methodist Hospitals in Dallas and the University of Texas Southwestern Medical Center in Dallas. He serves as team physician for Dallas Baptist University. Dr Cooper is an associate clinical professor in the Division of Cardiology in the Department of Medicine at the University of Florida in Gainesville. Address correspondence to David S. Ross, MD, Family Practice and Sports Medicine Center, 3500 W Wheatland Rd, Dallas, TX 75237; e-mail to [email protected].