Review Article :
Gharacholou S Michael, Vaca-Cartagena F Bryan,
Parikh P Pragnesh, Pollak M Peter and Bruce J Charles Peri-Myocardial Infarction Pericarditis (PMIP), or epistenocardiac pericarditis, has been considered a relatively benign condition occurring within a few days after Myocardial Infarction (MI). Although the condition usually does not require specific treatment, the finding of a pericardial friction rub in the post-MI patient does prompt a careful review of post-MI symptoms and test results, including dysrhythmia recordings, Electro-Cardio Grams (EKG), and the Transthoracic Echocardiogram (TTE) to exclude potentially life threatening post-MI mechanical complications such as free wall rupture. The auscultatory findings of a pericardial rub often represent a teaching opportunity for house staff and students, yet given the self-limited course of PMIP, very little is known regarding the mechanism, biology, imaging findings, and management strategy in patients with and without symptoms. We review the current understanding of PMIP for clinicians caring for post-MI patients. The pericardium is
functionally a dual layer sac of outer fibrous and inner serosal (visceral)
layer that contains the heart and normally less than 50 mL of pericardial fluid
[1]. The outer fibrous layer is in continuity with the great vessels above and
with the diaphragm below and is in direct contact with many mediastinal
structures such as the pleura, bronchi, esophagus, and rib costal cartilage.
Measuring less than 1mm in thickness, the pericardium is composed of collagen,
elastic fibers, fibroblasts, and mesothelial cell layers
along the parietal and serosal pericardium [1]. Regardless of etiology, injury
to the pericardium generally results in a non-specific response with generation
of fluid and inflammatory cells with formation of fibrinous adhesions during
convalescence. The cardiac and pericarditic injury syndromes, often referred
to as Post-Cardiac
Injury Syndromes (PCIS), are categorized into PMIP, Post-Pericardiotomy Syndrome (PPS), and
post-traumatic pericarditis. It is postulated that PMIP and PPS have a similar
biologic basis, evoking an antibody response to cardiac cellular components and
contractile proteins. However, this response is perhaps magnified in PPS owing
to greater tissue injury following cardiac surgery. Immune complexes trigger
inflammatory responses in the pericardium [2,3]. Post- traumatic etiologies include iatrogenic and
non-iatrogenic factors. The most common iatrogenic culprits are percutaneous
cardiac procedures such as pacemaker lead insertion, cardiac ablation
procedures, percutaneous coronary interventions, endomyocardial biopsies, and
structural heart procedures. Non-iatrogenic factors include trauma to the chest
wall or aortic dissection. Post-infarction etiologies are grouped by timing,
with early (<7 days post MI) involvement consistent with PMIP while a
delayed (>7 days to months) involvement consistent with Dressler syndrome (late or
delayed pericarditis). First described in 1956 by William Dressler, the delayed
post infarction syndrome may present with symptoms similar to those with acute
idiopathic pericarditis including pleuritic chest discomfort or pain across the
trapezius ridge, fever, and signs of a pericardial friction rub [4]. The European Society of Cardiology has proposed diagnostic
criteria for PCIS when at least 2 of the 5 following criteria are met: 1) fever
without alternative explanation, 2) pericarditic or pleuritic chest pain, 3)
pericardial or pleural friction rub, 4) pericardial effusion and/or 5)
pleural effusion with elevated C-reactive protein [5]. Regardless of etiology,
the typical EKG findings of PCIS include widespread ST-segment elevation often
sparing aVR and V1 along with PR segment depression. However, these EKG changes
are dynamic, evolving over time and ultimately normalize. There may be associated findings on chest X-ray demonstrating
a pleural effusion or a pericardial effusion on TTE. Pericardial effusions are
usually small without increased intrapericardial pressures and tamponade
physiology. However, ongoing inflammation necessitates serial clinical and TTE
examinations to determine whether the pericardial effusion is enlarging and
requires pericardiocentesis. Treatment of symptomatic patients usually involves
anti-inflammatory medications (aspirin 650 mg every 6 to 8 hours or ibuprofen
600mg every 8 hours) for 7 to 10 days. There is general consensus that aspirin
is the preferred anti-inflammatory in patients post MI, rather than ibuprofen
and other Non-Steroidal
Anti-Inflammatory Drugs (NSAIDs). Patients with contraindications to aspirin
or NSAIDs (severe renal insufficiency, allergies, GI bleeding, or oral
anticoagulants) may be treated with low-dose glucocorticoids (<0.5
mg/kg/day) for 2 to 4 weeks with slow and gradual tapering. In the Investigation on Colchicine
for Acute Pericarditis (ICAP) study, which included 20% (n=48 patients) of
patients with post-cardiotomy pericarditis, the addition of colchicine to
anti-inflammatory therapy significantly reduced the primary outcome of
incessant/recurrent pericarditis (16.7% vs 37.5%; RRR 0.55, 95% CI 0.30-0.72)
[6]. There were no serious adverse events related to colchicine, which had a
similar side effect profile to placebo. PMIP, or epistenocardiac pericarditis, shares some
characteristics to Dressler syndrome but also has notable differences. It has
been suggested that the incidence of PMIP has declined in the era of
reperfusion therapy and may only affect approximately 1% of those with
ST-elevation myocardial infarction [7]. Since PMIP is more likely to occur
after transmural MI, the EKG findings of pericarditis may be masked by the EKG
changes of an evolving MI. Thus, a pericardial friction rub may be the only
diagnostic clue to its presence. Indeed, since the typical pyramidal infarction
zone of the myocardium has its base at the endocardium and apex at the
epicardium, adjacent to the visceral pericardium, it is less
likely to produce diffuse ST elevations as seen in Dressler syndromes [8]. Pericardial friction rubs are characteristically dynamic,
subtle, change with underlying pericardial insult, and rarely persist beyond a
few days. A study of auscultatory and phonocardiographic recordings by an
experienced examiner identified that the majority of pericardial friction rubs
are composed of 3 components: atrial systole, ventricular systole, and protodiastole
(immediately after S2), rather than biphasic to-and-fro as had been originally
characterized [9]. Rubs have a qualitative characteristic of grating or
scratching, and may on rare occasions be palpable [9]. Due to the fleeting
nature of rubs and limitations of auscultation to detect pericarditis, PMIP has
been increasingly incidentally identified using Cardiac Magnetic Resonance (CMR) early
after acute MI. Evidence for pericardial inflammation can be appreciated on
late gadolinium enhancement early after acute MI, often adjacent to the region
of infarct (Figure 1). In a study of 189 patients undergoing CMR 2 to 5 days after
primary PCI for acute ST-segment elevation MI, 31% of patients had pericardial
inflammation with the majority (60%) of inflammation located in the infarct
zone confirmed on late gadolinium enhancement [10]. Interestingly, diffuse
involvement was present in 28% of those with pericardial inflammation. Those with
pericardial inflammation had larger infarct size, more microvascular
obstruction, and higher levels of CRP, as compared to those without
inflammation. At 4 month follow up CMR, pericardial abnormalities had resolved
in 80% of patients. Indeed, advanced cardiac imaging suggests that PMIP is likely
more common than initially appreciated, with identification of subclinical
PMIP. Since most of these abnormalities show resolution in follow up, further
research is needed to determine the prognostic significance of pericardial
inflammation in post-acute MI. Figure 3
illustrates various degrees of pericardial involvement with late pericaridits
and PMIP as compared to normal pericardium.
Although Imazio et al observed that the incidence of atrial
fibrillation/atrial flutter (AF/AFL) in patients with acute pericarditis ranges
from 4 -7%, pericardial inflammation may not be independently associated with
incident AF/AFL since affected patients were typically older [11].
Nevertheless, some patients with pericarditis develop AF without traditional
clinical risk factors for AF (Figure 2A
and 2B). Furthermore, in an analysis of patients with acute coronary syndrome from
several large clinical trials, the incidence of AF was approximately 7% [12].
Unfortunately, the incidence of PMIP or Dresslers was not reported in this
study, raising the question whether post infarction pericarditis may have
contributed in part to the observed rates of AF [12]. Table 1 compares and contrasts early PMIP with late pericarditis
(Dressler syndrome). Table 1: Comparison between PMIP and
Dressler Syndrome. The general approach to patients with PMIP, diagnosed
clinically or by advanced cardiac imaging, is usually supportive and no
specific therapy is recommended since symptoms and signs usually resolve
without intervention. For symptomatic patients, acetaminophen 650 mg scheduled
every 6 to 8 hours for up to 10 days is useful. If patients remain symptomatic,
aspirin 650 mg every 6 to 8 hours can be initiated with tapering once symptoms
improve, usually after 7 to 10 days. Of note, there is a potential bleeding
risk with high dose aspirin in the post PCI patient and is not recommended in
patients on ticagrelor since it reduces drug efficacy [13]. Colchicine may be considered as an adjunct to reduce
recurrence risk. This recommendation is based on practice guideline
recommendations for acute idiopathic pericarditis and limited data [5,6]. Non-steroidal medications (NSAIDs)
are generally avoided in post MI patients since observational studies have
documented increased cardiovascular risk and events (MI and stroke) in patients
with known heart disease [14]. Corticosteroids are also generally avoided in
the post MI patient due to propensity for fluid retention, hypertension, and
their adverse effect on atherosclerotic vascular disease. Advanced imaging with CMR has identified both localized and
generalized pericardial enhancement in PMIP. This observation suggests that pericardial
involvement post MI is likely more common than previously thought since the
clinical findings of pericarditis alone may be subtle and go unnoticed. Further
research is needed to establish whether the finding of pericardial enhancement
in PMIP has prognostic significance since clinically diagnosed PMIP generally
has a benign and self-limited course. We thank Michael A. King, senior medical illustrator in the
division of biomedical and scientific visualization at Mayo Clinic Rochester,
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USA, Tel: 904-953-7278, E-mail: gharacholou.shahyar@mayo.edu Gharacholou SM, Vaca-Cartagena FB, Parikh PP,
Pollak PM and Bruce CJ. Peri-myocardial infarction pericarditis: Current
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Dressler syndrome, Corticosteroids.Peri-Myocardial Infarction Pericarditis: Current Concepts
Abstract
Full-Text
Pericardial
Anatomy
Cardiac-Pericardial
Injury Syndromes
Peri-Myocardial Infarction Pericarditis
Treatment
Future
Directions
Acknowledgments
References
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