Acute Pericarditis

The Scope

  • Visceral and Parietal layers of the pericardium – in between these layers is the pericardial space
  • Typically, there is up to 50mL of fluid in the space
  • On autopsy, 1 – 6 % of people have evidence of pericarditis
  • Up to 5% of patients that complain of chest pain, but do NOT have MI, may have pericarditis

The Causes

  • 90% – idiopathic or viral
  • 10% other: bacterial infection, tuberculosis, post-MI (often transmural), secondary to aortic dissection (if blood leaks into the pericardium), blunt or sharp chest trauma, neoplastic invasion, radiation exposure, uremia, post-thoracotomy, auto-immune, drug reaction
  • With the advent of coronary reperfusion, post-MI pericarditis is less common
  • Autoinflammatory disorders: Tumor necrosis factor Receptor–Associated Periodic Syndrome (TRAPS) and familial Mediterranean fever can cause repeated bouts of pericarditis

The Consequences

  • Cardiac Tamponade
  • Constrictive Pericarditis
  • Recurrent Pericarditis (up to 30%)
  • Myocarditis: present in up to 30% of idiopathic pericarditis

The Diagnosis

Based on at least two of the following – typical chest pain, pericardial friction rub, typical electrocardiographic changes, and pericardial effusion.

  • Differential: esophageal disorders, costochondritis, acute MI, aortic dissection, pulmonary embolus, gastritis/PUD
  • History:
    • Chest pain, usually retrosternal, sudden, and pleuritic.
    • Worse when supine, better when sitting upright and leaning forward. Can radiate to neck, arms, etc.
    • TIP: if pain radiates to the trapezius, consider pericarditis, because the phrenic nerve (which innervates parts of the pericardium) runs through this muscle. This is virtually pathognomonic.
  • Physical exam:
    • Fever: temperature above 38.5°C suggests that a specific cause is present (i.e. purulent pericarditis)
    • Friction rub: present in up to 85% of patients. High-pitched, squeaky, and best heard at the left sternal border with the patient leaning forward.
      • Present throughout the respiratory cycle (differs from pleural rubs, which stop when the patient holds their breath)
      • TIP: friction rubs can vary in intensity from moment to moment, so the exam can be different based on the time.
    • Hypotension, tachycardia, and elevated JVP: Beck’s Triad! Suggestive of cardiac tamponade.
      • Pulsus Paradoxus: see here for information on how to perform this evaluation
      • 15% of idiopathic pericarditis
      • Up to 60% of malignant, purulent, or tuberculous pericarditis
  • Electrocardiography:
    • Classic: diffuse, ST-segment elevation and PR depression – present in up to 80% of patients with pericarditis
    • 4 phases:
      • Stage I: diffuse, concave ST-segment elevation and PR depression. Stage II: normalization of the ST and PR segments
      • Stage III: diffuse T-wave inversions
      • Stage IV: normalization of the T-waves
    • ST-elevation MI v Pericarditis
      • ST-segments are concave (as opposed to the convex or dome-shaped ST-elevations seen in MI)
      • Ratio of ST-segment elevation to T-wave amplitude in lead V6 > 0.24 suggests acute pericarditis
    • Pericarditis table 2
  • CXR: apparent cardiomegaly may suggest a large effusion, but a small, rapidly accumulating effusion can be clinically significant without being apparent on XR. Important to rule out pulmonary or mediastinal disease.
  • Laboratory testing:
    • Inflammatory markers: ESR, CRP – often elevated, but do not provide significant insight regarding the etiology of the pericarditis.
    • WBC count: if significantly elevated, could suggest purulent pericarditis
    • H/H: anemia could suggest chronic inflammatory condition or malignancy
    • Troponin: elevated in 35-50% of patients with pericarditis. Typically, elevation of troponin does not suggest poor prognosis, though persistent elevation may be due to true myocarditis.
    • Testing for ANA, RF, complements, etc. should be guided by history and exam – they should not be ordered in all cases of pericarditis.
  • Echocardiography: helps to determine if there is a pericardial effusion, tamponade, or systolic dysfunction. Left-ventricular dysfunction is uncommon. Large effusions (> 20mm in width on echo) are more likely to cause tamponade, but smaller, rapidly accumulating effusions can cause tamponade without enlarging the silhouette on XR, giving additional reason for prompt echocardiographic evaluation.
  • Cardiac MRI: not typically recommended, but can be helpful in identifying because pericardial thickening, enhanced pericardial gadolinium uptake on MRI, or both support the diagnosis
  • Pericardiocentesis and Biopsy:
    • Indications:
      • Tamponade
      • Known or suspected purulent or or neoplastic effusion
    • Not a strong diagnostic tool: in patients with unknown cause for pericarditis after considering history, imaging, and lab data, pericardiocentesis and pericardial biopsy provided a diagnosis in only ~5% of cases.
    • Lab studies to be sent on pericardial fluid
      • RBC count, WBC count
      • Cytology
      • Gram stain and culture
      • PCR and ADA for TB
      • pH, glucose, LDH, protein: not specifically linked to particular etiologies

pericarditis diagnostic flow

The Treatment

  • Initial bout of pericarditis: 70 to 90% of cases resolve completely
    • NSAIDS: goal is to relieve pain and inflammation; effective in up to 90%
      • Many NSAIDs are effective: can use ASA if known CV disease or recent MI. Ibuprofen is often preferred, due to lower risk of GI side effects.
      • Indomethacin should be avoided in patients with coronary artery disease, since it diminishes coronary blood flow.
      • Patient should also be started on a PPI to reduce the risk of ulcers.
      • 1-2 week course is reasonable
      • Some suggest tapering NSAIDs and guiding therapy based on CRP, but data are lacking
    • Colchicine: significantly reduced the rate of incessant or recurrent pericarditis.
      • ICAP randomized clinical trial: NSAID + (colchicine or placebo)
        • Colchicine, as compared with placebo, resulted in a significantly lower rate of persistent or recurrent pericarditis (17% vs. 38%)
        • Lower rate of persistent symptoms at 72 hours (19% vs. 40%)
        • Effect thought to be mediated blockade of microtubule assembly in white cells
      • 3-month course is reasonable
  • Recurrent pericarditis: more common in women and in TRAPS
    • Prompt reinstitution of NSAID therapy + Colchicine
    • Poor Response
  • Persistent pericarditis: poor response is defined as “continued chest pain necessitating treatment with analgesic agents, fever, or worsening effusion despite at least 1 week of treatment.”
    • Steroids
      • ESC Guidelines (2004): initiate glucocorticoid therapy
      • Observational data: steroids can have high rate of symptom relief – but also an increased rate of recurrence!
      • Steroids appear to reduce the anti-inflammatory effects of colchicine
      • High dose regimens can increase the risk for recurrence
      • If steroids are necessary, it is preferable to use moderate doses (0.2 to 0.5 mg/kg prednisone daily for several weeks)
      • Continue NSAIDs and Colchicine for some time after steroid taper ends
    • Other Immunosuppresants: data is lacking, but there are small studies that suggest the effectiveness of medications like azathioprine, anakinra, IVIG, etc.
    • Pericardiectomy: rarely performed; not consistently effective, (? because visceral pericardium remains, along with remnants of parietal pericardium)

Pericarditis Table 1

References: