Misdiagnosis of Acute Pericarditis: Preventing Unnecessary PCI

Amal Mattu, MD


September 22, 2009


The distinction between acute pericarditis and acute myocardial infarction (AMI) is a difficult one. Clinically, both presentations cause chest pain that is often described as severe in nature. In addition, classic, textbook descriptions of the conditions (eg, pleuritic, positional pain radiating to the trapezius ridge in pericarditis; substernal pressure radiating to the left jaw/neck/arm in AMI) are often absent in real patients. Electrocardiographic (ECG) findings are often similar, with both conditions producing ST-segment elevation. The overall result is that many patients with acute pericarditis are mistakenly diagnosed with ST-segment myocardial infarction (STEMI) and are sent for primary percutaneous coronary intervention (PCI), ie, angioplasty or stent placement. Larson and colleagues[1] recently reported that 18.7% of patients who were sent for primary PCI for presumed STEMI and found to have no culprit lesion were later diagnosed with pericarditis or myocarditis. Complicating matters further is the fact that anticoagulation or thrombolysis for presumed STEMI can be dangerous in patients with acute pericarditis[2] because these medications increase the chance that a pericardial effusion may develop into a hemorrhagic tamponade. During my career, I have known of 2 patients with acute pericarditis who developed pulseless electrical activity and died from hemorrhagic tamponade after they were treated for presumed STEMI with thrombolytics. Clearly, a greater understanding of both the overlapping as well as the distinguishing features of acute pericarditis vs AMI is needed.

Frequency and Predictors of Urgent Coronary Angiography in Patients With Acute Pericarditis

Salisbury AC, Olalla-Gomez C, Rihal CS, et al
Mayo Clin Proc. 2009;84:11-15

Acute Pericarditis: Appendicitis of the Heart?

Bainey KR, Bhatt DL
Mayo Clin Proc. 2009;84:5-6 (editorial accompanying Salisbury AC, et al article)


This study and the accompanying editorial present important information that helps us compare and contrast acute pericarditis with AMI. Salisbury and colleagues attempted to determine the frequency of urgent PCI in patients with acute pericarditis; in other words, the authors sought to evaluate patients with pericarditis who were mistakenly diagnosed with AMI and sent for urgent PCI. The clinical characteristics of those patients who were referred for PCI were also evaluated. Between January 2000 and December 2006, 238 patients with a final diagnosis of acute pericarditis were identified, 40 (16.8%) of whom were referred for PCI. Of the total group, 146 patients (61.3%) had ST-segment elevation and 92 (38.7%) did not. Not surprisingly, PCI was performed in many more of the ST-segment elevation group (24.7%) than in the non-ST-segment elevation group (4.3%). Statistical analysis revealed that the factors associated with a higher likelihood for urgent PCI included the typical anginal-type description of chest pain, ST-segment elevation on ECG, history of previous PCI, elevated troponin, diaphoresis, and male sex.


In comparing the ST-segment elevation group with the non-ST-segment elevation group, some interesting results were revealed, many of which were highlighted in the accompanying editorial:

  1. In terms of clinical features, 49.6% of patients reported that their pain was positional, and 68.9% reported that their pain was pleuritic. These numbers are clearly less than what is commonly taught. Complicating matters further, 12.2% of patients complained of pain that was consistent with typical angina.

  2. There appear to be significant sex differences with acute pericarditis. Almost twice as many men were diagnosed with pericarditis than women (157 vs 81). Men constituted 81.5% of the patients with ST-segment elevation, whereas women accounted for 58.7% of the non-ST-segment elevation group. Looking at the numbers another way, men diagnosed with pericarditis demonstrated ST-segment elevation in 76% of cases, whereas women diagnosed with pericarditis demonstrated ST-segment elevation in only 33% of cases. One must wonder whether there is a physiologic reason why women are less likely to develop ST-segment elevation in acute pericarditis.

  3. Patients in the ST-segment elevation group were less likely than patients in the non-ST-segment elevation group to report a history of viral illness (32.2% vs 46.7%) and less likely to have a friction rub (12.3% vs 27.2%). Of note, both of these "classic" features are uncommon.

  4. Elevated troponin levels were found in 15.8% of the ST-segment elevation group and 7.6% of the non-ST-segment elevation group (12.6% of patients overall). This difference was not statistically significant, but it is important to be aware that acute pericarditis is often associated with elevated troponin levels, further complicating diagnostic certainty. Other studies have demonstrated even higher rates of positive troponin at admission, including one study that reported a 23.7% incidence of positive troponin levels at the time of admission.[3]

  5. Pericardial effusion was common in patients: 38.1% of patients in the ST-segment elevation group and 73.5% of patients in the non-ST-segment elevation group had effusions. This difference between the 2 groups may not be a huge surprise when one considers that larger effusions tend to reduce voltage, including the magnitude of ST-segment elevation. Although the authors did not comment on the size of the effusions, the editorial discusses a study in which 60% of patients with acute pericarditis presented with effusions: 80% being mild, 10% being moderate, and 10% being severe in size.[4]

  6. What about that classic "pulsus paradoxus" that the inpatient physicians always ask us about? The researchers noted a positive pulsus paradoxus in only 1 of the 146 patients in the ST-segment elevation group and in only 3 of the 92 patients in the non-ST-segment elevation group. (Remember that a lot of patients in this latter group did have pericardial effusions).

The researchers reminded us of the limitations of a retrospective study, not the least of which is that the "definition of acute pericarditis relied heavily on the opinion and diagnosis of the treating physician." Nevertheless, this study serves as an excellent reminder to all of us that (1) acute pericarditis must remain in the differential diagnosis for any patient with chest pain, with or without ST-segment elevation; (2) neither patients with STEMI nor patients with acute pericarditis can be relied on to present "classically"; and (3) given the frequency with which patients with acute pericarditis present with pericardial effusions, the use of bedside ultrasound in any patient with chest pain may be enormously helpful. Finally, just as there is an appropriate "false-laparotomy rate" for patients with presumed appendicitis, it may be appropriate to accept a "false-catheterization rate" for patients with acute pericarditis, despite our best efforts and knowledge.