Post myocardial infarction pericarditis
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Pericarditis Microchapters |
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Post myocardial infarction pericarditis On the Web |
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American Roentgen Ray Society Images of Post myocardial infarction pericarditis |
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Risk calculators and risk factors for Post myocardial infarction pericarditis |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:
Synonyms and keywords: post MI pericarditis
Overview
Post-Myocardial Infarction Pericarditis, also named peri-infarction pericarditis, is defined as acute pericarditis occurring within 7 days following an acute myocardial infarction.
Historical Perspective
Classification
Pathophysiology
Extension of myocardial infarction to the epicardial surface, which occurs in transmural MI, causes local pericardial inflammation adjacent to the infarction zone with resultant acute fibrinous pericarditis.
Causes
Acute fibrinous pericarditis occurs following transmural myocardial infarction.
Differentiating peri-infarction pericarditis from other Diseases
The chest pain of pericarditis must be differentiated from post-infarction angina and recurrent infarction. Pleuritic nature of pain and/or radiation of pain to either trapezius ridge may help in differentiating PIP from other causes of chest pain following MI.
| Characteristic/Parameter | Pericarditis | Myocardial infarction |
|---|---|---|
| Pain description | Sharp, pleuritic, retro-sternal (under the sternum) or left precordial (left chest) pain. | Crushing, pressure-like, heavy pain. Described as "elephant on the chest". |
| Radiation | Pain radiates to the trapezius ridge (to the lowest portion of the scapula on the back) or no radiation. | Pain radiates to the jaw, or the left or arm, or does not radiate. |
| Exertion | Does not change the pain | Can increase the pain |
| Position | Pain is worse supine or upon inspiration (breathing in) | Not positional |
| Onset/duration | Sudden pain, that lasts for hours or sometimes days before a patient comes to the ER | Sudden or chronically worsening pain that can come and go in paroxysms or it can last for hours before the patient decides to come to the ER |
Epidemiology and Demographics
The incidence of PIP has decreased in recent years due to following the widespread use of fibrinolytic or mechanical reperfusion therapy. Recent studies estimated an incidence of less than 2% among patients with ST-elevation MI.[1]
Risk Factors
Screening
Natural History, Complications, and Prognosis
PIP is usually self-limited in most patients.
Diagnosis
Diagnostic Study of Choice
- Historically, auscultation of pericardial friction rub has been considered as a diagnostic sign of PIP.
- The diagnosis of PIP is also made with the presence of pleuritic chest pain, particularly pain in one or both trapezius ridges.
History and Symptoms
The major clinical manifestations of PIP include:
- Chest pain; typically is centrally-located, sharp, and pleuritic. Pleuritic chest pain is defined as the pain that is worst during deep inspiration and improves by sitting up and leaning forward.
- Pericardial friction rub; although diagnostic for PIP, it may not be heard in all patients. A pericardial friction rub is usually described as a superficial scratchy or squeaking sound which is best heard with the diaphragm of the stethoscope over the left sternal border
- Pericardial effusion.
However, some patients may be asymptomatic and incidental hearing of friction rub may be the only finding in these patients.
Physical Examination
The presence of friction rub on physical examination is diagnostic of PIP.
Laboratory Findings
- Cardiac biomarkers are often elevated in patients with due to recent MI.
- Inflammatory markers, such as CRP, might be elevated.
Electrocardiogram
The typical ECG finding in PIP is new widespread ST elevation and/or PR depression which extends beyond a typical anatomic. However, in contrast to other etiologies of acute pericarditis, ECG findings might be less helpful in the diagnosis of PIP; since the ECG changes caused by recent MI might obscure or alter typical findings of acute pericarditis in the setting of PIP. However, the persistence of ST segments elevation and/or upright T waves, T waves that become upright again after having been inverted, may suggest PIP.[2][3]
X-ray
Chest radiography may reveal the presence of pericardial effusion to support the diagnosis.
Echocardiography or Ultrasound
Echocardiography is a useful imaging modality in assessing the presence of pericardial effusion in patients with PIP. It can also be helpful in differentiating other post-Mi complications as the etiology of pericardial effusion, such as free wall rupture. However, the absence of pericardial effusion does not exclude PIP; and most effusions, if present, are small and not hemodynamically significant.
CT scan
MRI
MRI may be useful in revealing pericardial effusion. Pericardial inflammation, particularly adjacent to the infarction zone, might be detected on late gadolinium enhancement.
Other Imaging Findings
Other Diagnostic Studies
There are no other diagnostic studies associated with [disease name].
Treatment
Medical Therapy
The majority of cases of PIP are self-limited. Acetaminophen may be the initial treatment for patients with significant chest pain. For those with more severe symptoms, and those who continue to have chest pain beyond initial 7-10 days, high-dose aspirin (650 mg every 6 to 8 hours) are preferred over other non- steroidal anti-inflammatory drugs (NSAIDs) and glucocorticoids, which are in class III recommendation according to the 2013 guidelines of the American College of Cardiology Foundation (ACCF) and the American Heart Association (AHA).[4]
NSAIDS and glucocorticoids may interfere with proper myocardial healing and scar formation.
Routine administration of colchicine (along with aspirin) in these patients is still controversial.
Although it has been suggested that antiplatelet and anticoagulant therapy may increase the risk of hemorrhagic pericardial effusion in patients with PIP, currently there is no enough evidence to prohibit administration of aspirin and other anticoagulants in these patients.
Surgery
Primary Prevention
Secondary Prevention
References
- ↑ Lador A, Hasdai D, Mager A, Porter A, Goldenberg I, Shlomo N; et al. (2018). "Incidence and Prognosis of Pericarditis After ST-Elevation Myocardial Infarction (from the Acute Coronary Syndrome Israeli Survey 2000 to 2013 Registry Database)". Am J Cardiol. 121 (6): 690–694. doi:10.1016/j.amjcard.2017.12.006. PMID 29370922.
- ↑ Oliva PB, Hammill SC, Edwards WD (1993). "Electrocardiographic diagnosis of postinfarction regional pericarditis. Ancillary observations regarding the effect of reperfusion on the rapidity and amplitude of T wave inversion after acute myocardial infarction". Circulation. 88 (3): 896–904. doi:10.1161/01.cir.88.3.896. PMID 8353916.
- ↑ Oliva PB, Hammill SC, Talano JV (1994). "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. 24 (4): 1073–7. doi:10.1016/0735-1097(94)90872-9. PMID 7930200.
- ↑ O'Gara PT, Kushner FG, Ascheim DD, Casey DE, Chung MK, de Lemos JA; et al. (2013). "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. 127 (4): e362–425. doi:10.1161/CIR.0b013e3182742cf6. PMID 23247304.