Pericarditis epistenocardica I30.8.

Pericarditis epistenocardica is an inflammation of the pericardium, which can occur as a complication of an acute myocardial infarction. It begins up to one week after the acute event, usually on the 1st - 3rd day. This form of pericarditis is found exclusively in patients with a large transmural infarction (Pinger 2019)

Since the introduction of reperfusion therapies, pericarditis following myocardial infarction (pericarditis epistenocardica plus Dressler syndrome) has become a rare complication. It now occurs in only < 5% of cases. In the past, this figure was up to 23% (Feola 2015).

Far greater numbers are found in autopsies of patients with a large transmural infarction. Here, up to 40% of cases show evidence of pericarditis epistenocardica (Pinger 2019).

In a transmural infarction, the inflammatory processes of transmural necrosis can transfer the inflammation to the visceral and also to the parietal pericardial leaflet, thus leading to pericarditis epistenocardica (Feola 2015).

In the majority of cases, pericarditis epistenocardica is clinically inapparent. Symptoms of pericarditis are found in only about 5% - 6% of patients (Pinger 2019).

These can consist of the following symptoms:

• circumscribed left thoracic pain
• Occasionally, the pain radiates into the left shoulder, left arm and neck
• sometimes there is also isolated pain along the upper trapezius margin (pathognomonic for irritation of the pericardium)
• the pain is reduced when the posture is bent forward
• the pain increases when lying down, during deep inspiration, occasionally also when coughing or swallowing (Kühl 2004)
• Mostly there is tachycardia
• subfebrile or febrile temperature rise are possible
• Lassitude
• general feeling of illness (Herold 2018)

Echocardiography: In the case of pericardial effusion, it can be detected by echocardiography and its size, location and hemodynamics can be well assessed by echocardiography (Feola 2015). In addition, dysfunction of the myocardium in the infarct area and general dysfunction due to any pericardial constriction can be found.

Chest X-ray: The chest X-ray may show pleural effusion and possibly enlargement of the cardiac silhouette (Feola 2015).

The diagnosis of pericarditis epistenocardica is based on clinical observation, the presence of fever, the pain typical of pleuritis and evidence of pleural effusion (Feola 2015).

Auscultation:

• Pulse-synchronous systolic-diastolic, creaking sound close to the ear, most clearly above the lingula near the sternum (so-called pericardial rubbing)
• Pericardial drift may also be present only passagally
• it intensifies with the inspiration
• there is no change in sound during a breathing break (in contrast to pleural rubbing)
• missing pericardial rubbing does not rule out pericarditis!
• Damping (with simultaneous pericardial effusion) (Erdmann 2009)
• Occasional heart rhythm disturbances (Kaiser 2002)
• Tachycardia (Foris 2019)

ECG

• The ECG shows changes that are difficult to interpret due to the repolarization disorders caused by acute myocardial infarction (Erdmann 2009).
• In the presence of larger effusions, pericarditis epistenocardica can cause a global ST segment elevation and low voltage (Foris 2019).
• However, the classic changes in the ECG due to acute pericarditis do not occur in pericarditis epistenocardica, so that an increase in necrosis could rather be assumed on the basis of the ECG (Feola 2015).

• Dressler's syndrome (only occurs about 1-6 weeks after an acute infarction)
• Re - Infarction (to be distinguished from pericarditis epistenocardica by differential diagnosis:
  • the pain symptoms improve after nitro administration
  • in the ECG there are newly appeared Q-waves
  • a CK-MB reaction can be detected [Erdmann 2009])

Treatment is symptomatic, preferably with ibuprofen, as this also has a beneficial effect on coronary blood flow. Alternatively, acetylsalicylic acid can be given.

Dosage suggestion:

• Ibuprofen: 600mg every 8 h
• Acetylsalicylic acid: 4 x 650 mg / d for 2 - 5 days
• as stomach protection proton pump inhibitor (e.g. cimetidine 200 mg - 400 mg/d)

In pericarditis epistenocardica, corticosteroids can cause thinning of the infarct zone and thus lead to a rupture. Therefore, corticosteroids should be avoided (Maisch 2008).

The mortality rate of patients with pericarditis epistenocardica is not increased compared to patients with transmural myocardial infarction - but without pericarditis epistenocardica (Oddone 1977).

1. Erdmann E (2009) Clinical Cardiology: Diseases of the heart, the circulation and the vessels near the heart. Springer publishing house S 342
2. Feola A et al (2015) Pericarditis epistenocardica or Dressler syndrome? An autopsy case. Case reports in Medicine. Hindawi Publishing Corporation. Article ID 215340
3. Foris L A et al (2019) Dressler syndrome. StatPearls Publishing LLC. PubMed PMID: 28723017
4. Herold G et al (2018) Internal Medicine Herold Verlag 235, 252
5. Kaiser H et al (2002) Cortisone therapy: Corticoids in clinic and practice. Georg Thieme publishing house S 256
6. Kühl H P et al (2004) Acute and chronic constrictive pericarditis. The internist 45: 574
7. Maisch B et al (2008) New possibilities for the diagnosis and therapy of pericarditis. The internist 49: 17-26
8. Oddone a et al (1977) Pericarditis epistenocardica as a marker of extensive myocardial infarction. Clinical, electrocardiographic and enzymatic study. G Ital Cardiolog 8: 760-769
9. Pinger S et al (2019) Repetitorium Kardiologie: For clinic, practice, specialist examination. German Medical Publisher S 590