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Pericardial complications of myocardial infarction

Pericardial complications of myocardial infarction
Literature review current through: Jan 2024.
This topic last updated: Jun 15, 2022.

INTRODUCTION — Following a myocardial infarction (MI), patients are at risk for a variety of cardiac complications. Many complications are mechanical (eg, papillary muscle rupture, left ventricular free wall rupture, ventricular septal defect) and are related to the location and extent of myocardial injury, while other post-MI complications are immunologic, inflammatory, or iatrogenic.

Three major types of pericardial complications can occur in patients following an MI:

Early infarct-associated pericarditis (often termed peri-infarction pericarditis)

Post- MI pericardial effusion (with or without tamponade), including hemopericardium (due to myocardial rupture)

Post-cardiac injury syndrome, including post-MI (Dressler) syndrome

Each of these complications is related to infarct size as well as location and, as will be described below, has declined in incidence in the early revascularization era [1-3]. The clinical manifestations, diagnosis, and management of pericardial complications of MI will be presented here. Details of the non-pericardial complications of MI are discussed separately. (See "Acute myocardial infarction: Mechanical complications" and "Prognosis and treatment of cardiogenic shock complicating acute myocardial infarction" and "Left ventricular aneurysm and pseudoaneurysm following acute myocardial infarction".)

ANATOMY AND PHYSIOLOGY

Normal anatomy — The normal pericardium consists of two layers: a fibrous parietal layer and the visceral layer, a monolayer lining the surface of the cardiac chambers. The parietal layer forms a closed sac with the visceral layer. The pericardium is reflected from the pulmonary veins and caval vessels as they enter the heart. The parietal pericardium has attachments to the sternum and to the diaphragm [4]. Normally, a small amount of serous fluid (less than 25 to 50 mL) is contained within the pericardial sac.

Physiology of cardiac tamponade — In cardiac tamponade, the primary abnormality is compression of the cardiac chambers due to increased pericardial pressure. The pericardium has a modest degree of elasticity; but once its elastic limit is reached, the heart must compete with the intrapericardial fluid for the relatively fixed total intrapericardial volume. Very little additional fluid needs to accumulate to produce cardiac tamponade once the pericardium can no longer stretch. As cardiac tamponade progresses, the cardiac chambers become smaller, further compromising the cardiac output.

A full discussion of the physiology of cardiac tamponade is presented separately. (See "Cardiac tamponade", section on 'Pathophysiology'.)

PERI-INFARCTION PERICARDITIS — Acute pericarditis may complicate the course of an acute MI [5]. Peri-infarction pericarditis (PIP) usually occurs soon following the MI and is transient and self-limited. One study of MI without reperfusion found that 68 percent of audible pericardial rubs were heard on day 1 or 2, 85 percent were audible for less than three days, and persistence of the rub was rare [5].

Epidemiology of PIP — The incidence of PIP appears to have decreased among patients with ST-elevation MI (STEMI) initially following the widespread use of fibrinolytic therapy and, subsequently, mechanical reperfusion therapy. Historically, pericarditis was reported in approximately 5 percent of STEMI patients treated with fibrinolytic agents versus 12 to 20 percent in those not receiving fibrinolytic (or mechanical) reperfusion therapy [1,2,5]. In the era of primary reperfusion with percutaneous coronary intervention (PCI), the incidence of PIP has continued to decline. Among a registry of 6282 Israeli patients with STEMI between 2000 and 2013 (in which two-thirds of patients underwent primary reperfusion therapy, predominantly with PCI), only 76 patients (1.2 percent) developed PIP [6]. Patients who developed PIP more often had left ventricular ejection fraction <50 percent and had significantly higher troponin levels, but there was no significant difference in death or recurrent MI compared with patients without PIP.

The impact of reperfusion on the incidence of PIP is consistent with other observations suggesting that the appearance of a friction rub in the first two or three days after an acute MI is strongly associated with larger infarct size, as manifested by higher levels of cardiac biomarkers, lower ejection fraction, more frequent anterior location of the MI, and increased in-hospital and one-year mortality [1,2,5], although the mortality data are in apparent disagreement with the Israeli registry data cited above [6].

Clinical presentation and diagnosis of PIP — The presence of a pericardial friction rub is diagnostic of PIP. Pleuritic chest pain and especially pain in one or both trapezius ridges is also consistent with the diagnosis. By contrast to acute pericarditis occurring in other settings, electrocardiographic (ECG) findings in patients with suspected PIP may be less obvious and dependent upon the ECG changes caused by the MI.

PIP can present in a variety of ways. The major clinical manifestations of PIP include (see "Acute pericarditis: Clinical presentation and diagnosis", section on 'Clinical features'):

Chest pain – Typically sharp, pleuritic, and centrally located; the pain is improved by sitting up and leaning forward.

Pericardial friction rub – A superficial scratchy or squeaking sound best heard with the diaphragm of the stethoscope over the left sternal border; the rub is frequently intermittent and may be difficult to appreciate, but is diagnostic when present.

ECG changes – New widespread ST elevation and/or PR depression which extend beyond a typical anatomic regional boundary.

Pericardial effusion – Most effusions are small and not hemodynamically significant [7].

The typical ECG changes seen with other presentations of pericarditis are often overshadowed by the changes due to the MI. However, ST segments that remain elevated, with persistence of upright T waves, may suggest PIP or early onset post-cardiac injury syndrome (PCIS), as may T waves that rapidly become upright after being inverted initially [8,9].

The diagnosis of PIP is often suspected based on a history of characteristic pleuritic chest pain within days post-MI, and confirmed if a pericardial friction rub is present. It is not unusual for PIP to be asymptomatic, with only a pericardial rub signaling its presence. Additional testing, which typically includes blood work, chest radiography, electrocardiography, and echocardiography, can support the diagnosis but is frequently normal or unrevealing. (See "Acute pericarditis: Clinical presentation and diagnosis", section on 'Diagnosis'.)

While the absence of pericardial effusion by echocardiography does not exclude PIP, echocardiography should be performed in patients suspected of having PIP specifically to evaluate for the presence of a pericardial effusion which may be related to other potential post-MI complications. While most PIP effusions are small, patients with effusions greater than 10 mm in width are at significantly increased risk of free wall rupture or may have already had a rupture that is subacute and contained [10,11]. Blood that has coagulated within the pericardial space has a distinct appearance of floating "jelly." It is often difficult to identify the location of a rupture, and transesophageal echocardiography with the use of contrast and color flow imaging may be helpful in identifying the site. (See 'Post-MI pericardial effusion' below and "Acute myocardial infarction: Mechanical complications", section on 'Rupture of the left ventricular free wall'.)

Management of PIP — Our approach to patients with PIP, which is usually self-limited, includes avoidance of antiinflammatory drugs for 7 to 10 days after an acute MI (other than once daily aspirin as prescribed for secondary prevention following the MI). For patients with significant symptoms who require analgesia, acetaminophen may be employed as initial treatment. If this does not suffice, and for rare patients who remain symptomatic after the initial 7 to 10 days, we recommend aspirin 650 mg every six to eight hours rather than other nonsteroidal antiinflammatory drugs (NSAIDs) or glucocorticoids.

In contrast with viral or acute idiopathic pericarditis, treatment with routine antiinflammatory therapy is generally avoided in patients with PIP. There is no evidence that any antiinflammatory drug favorably alters its outcome. Accordingly, the 2013 guidelines of the American College of Cardiology Foundation (ACCF) and the American Heart Association (AHA) gave NSAIDs (other than aspirin) and glucocorticoids a class III recommendation (harmful) in this setting [12]. We agree with these recommendations.

In contrast to post-cardiac injury syndromes, there is no published experience with the use of colchicine in PIP, in large measure reflecting the fact that so few cases persist long enough to warrant consideration of treatment other than aspirin. It is possible that apparently persistent cases of PIP represent a transition to a post-cardiac injury syndrome. In such unusual cases, based on indirect evidence of the efficacy of colchicine in the treatment of pericarditis from other etiologies, a trial of colchicine may be warranted. (See "Acute pericarditis: Treatment and prognosis", section on 'Colchicine' and "Recurrent pericarditis", section on 'Colchicine'.)

Antiplatelet and anticoagulation therapy — Antiplatelet therapy is part of the standard management of all patients with acute MI, both to minimize intracoronary thrombus formation and following percutaneous coronary intervention. In addition, anticoagulation is indicated in selected patients. There is a theoretical concern that antiplatelet and anticoagulant therapy might promote the development of a hemorrhagic pericardial effusion in patients with PIP. However, such a relationship has never been established, and the risk-benefit ratio overwhelmingly favors the continuation of aspirin, as well as anticoagulants, if the latter are indicated. These recommendations for antiplatelet and anticoagulant therapy are most applicable to patients with the usual small PIP effusions. It is prudent to be alert to the possibility of development of a hemorrhagic effusion, especially if anticoagulant therapy is used.

Another concern is whether PIP-associated pericardial effusions could be worsened in patients receiving thrombolytic therapy for acute MI. One analysis of patients with acute MI treated with thrombolytics reported that 40 of 810 developed PIP [2]. However, cardiac tamponade did not occur clinically in any patient who developed a friction rub, suggesting that any worsening of effusions is not clinically significant. (See "Aspirin for the secondary prevention of atherosclerotic cardiovascular disease" and "Antithrombotic therapy for elective percutaneous coronary intervention: General use".)

The management of antiplatelet and anticoagulant therapy in acute MI patients with larger effusions due to PIP or other causes is discussed below.

POST-MI PERICARDIAL EFFUSION — Pericardial effusion is common in the early course of transmural MI. Most are associated with PIP; clinically significant post-MI pericardial effusions leading to signs and symptoms of cardiac tamponade remain rare, particularly in the era of primary reperfusion therapy.

Epidemiology — Serial echocardiographic studies before the era of widespread reperfusion therapy showed that pericardial effusion occurs in approximately one-third of cases of acute ST-elevation MI (STEMI) [13-18]. In a review of 330 such patients, 83 (25 percent) had a pericardial effusion on the third day, more than one-half of whom did not have a pericardial friction rub [14]. In a subsequent study of 193 patients with STEMI during the percutaneous coronary intervention era, pericardial effusion (mean pericardial effusion volume 32 mL) was identified by cardiac magnetic resonance imaging (MRI) in 59 percent, with cardiac MRI being more sensitive than echocardiography in detecting effusion [7]. The major risk factor for development of a pericardial effusion was poor hemodynamic function (presumably reflecting larger infarct size). At one-year follow-up, pericardial effusion was resolved in most patients, and none required pericardiocentesis.

Post-MI pericardial effusions are most often minimal or small (<10 mm). As with peri-infarction pericarditis (PIP), however, an effusion post-MI is associated with higher morbidity and mortality [15,17]. In a retrospective study of 228 consecutive patients (48 percent treated with thrombolysis or primary percutaneous revascularization) who developed post-MI pericardial effusions that were moderate-to-large in size (10 mm or greater), 30-day mortality was higher (43 percent) compared with those with smaller effusions or no effusion (10 and 6 percent, respectively) [11].

Clinical presentation and diagnosis — Patients with a post-MI pericardial effusion are usually asymptomatic, and the accrual of pericardial fluid is typically self-limited.

The presence of a post-MI pericardial effusion is often identified incidentally when an echocardiogram is performed for other reasons (eg, evaluation of left ventricular function post-MI, etc). The rate of resorption is surprisingly slow, with one echocardiographic study reporting a prevalence of persistent pericardial effusion at one day, three days, 10 days, three months, and six months of 17, 25, 21, 11, and 8 percent respectively [17]. A small number of effusions persisted beyond one year.

Large pericardial effusions sufficient to cause cardiac tamponade and its associated signs and symptoms (eg, hypotension, tachycardia, elevated venous pressure, dyspnea, chest discomfort or fullness, etc) are rare. Data from a combined clinical trials database of over 100,000 patients with a STEMI who were treated with fibrinolytic therapy found an incidence of isolated (no ventricular septal rupture, no acute mitral regurgitation) cardiac tamponade of 0.85 percent during the initial hospitalization [19]. Potential mechanisms of cardiac tamponade in patients with a post-MI pericardial effusion include:

Pericardial involvement with hemorrhagic pericarditis

Transmural infarction resulting in free wall rupture (see "Acute myocardial infarction: Mechanical complications", section on 'Rupture of the left ventricular free wall')

Iatrogenic coronary artery perforation during percutaneous coronary intervention (see "Periprocedural complications of percutaneous coronary intervention", section on 'Perforation')

The physical findings associated with cardiac tamponade, while helpful if present, are neither sensitive nor specific enough to confirm the diagnosis. Beck triad, the combination of low arterial blood pressure, elevated venous pressure, and muffled heart sounds, while useful, is present in only a minority of cases of acute cardiac tamponade [20]. Physical findings such as sinus tachycardia, even in the absence of frank hypotension, may indicate significant hemodynamic compromise from cardiac tamponade and serve as an indication for pericardiocentesis if a diagnosis of cardiac tamponade is confirmed. (See "Cardiac tamponade", section on 'Diagnosis'.)

The presence of a pericardial effusion on two-dimensional echocardiography with evidence of cardiac chamber collapse, exaggerated mitral-tricuspid respiratory flow variation, or dilation of the inferior vena cava is diagnostic for cardiac tamponade in the setting of acute MI. (See "Pericardial effusion: Approach to management".)

Management of post-MI pericardial effusion — The optimal management of post-MI pericardial effusion varies depending upon the etiology of the effusion as well as the presence or absence of symptoms felt to be related to the effusion.

For patients with a post-MI pericardial effusion that is suspected to be related to a mechanical complication (ie, free wall rupture), urgent/emergency surgical repair is typically required for any chance of survival. (See "Acute myocardial infarction: Mechanical complications", section on 'Management'.)

For patients with a pericardial effusion and no suspected mechanical complication who are symptomatic due to cardiac tamponade, definitive treatment requires drainage of the pericardial fluid, which is almost always accomplished percutaneously.

For patients with a pericardial effusion and no suspected mechanical complication who have an incidental pericardial effusion with no evidence of cardiac tamponade, no specific therapy is required.

The risk of developing a small to moderate size post-MI pericardial effusion is not increased with the use of fibrinolytic agents, heparin, aspirin, and other antiplatelet agents. Anticoagulation has not been reported to alter the frequency, size, or time course to resolution of pericardial effusion [17,18]. There is virtually no evidence to guide the use of antiplatelet therapy in patients with a large pericardial effusion. However, for most patients with PIP and a large pericardial effusion, we do not routinely modify antiplatelet therapy. However, we do monitor the size of the pericardial effusion with repeat echocardiograms and clinically follow the patient's hemodynamic status to assess for signs of cardiac tamponade. Follow-up for large pericardial effusions is discussed in greater detail separately. (See "Cardiac tamponade" and "Pericardial effusion: Approach to management", section on 'Large effusions'.)

With respect to anticoagulation (eg, warfarin, heparin, or direct oral anticoagulants [DOACs]), the presence of a large effusion or early tamponade requires consideration of less aggressive treatment. The 2013 ACCF/AHA guidelines recommended that anticoagulation should be immediately discontinued if a pericardial effusion develops or increases [12]. We discontinue anticoagulation for effusions exceeding one centimeter in maximum width and for effusions that increase by more than three millimeters in width.

POST-CARDIAC INJURY SYNDROME — The term post-cardiac injury syndrome (PCIS) encompasses postpericardiotomy syndrome, post-percutaneous cardiac procedural pericarditis and, when occurring after MI, Dressler or post-MI syndrome. Patients with post-MI syndrome as well as other forms of PCIS present with signs and symptoms similar to those seen in patients with acute pericarditis and/or pericardial effusion in other clinical settings. The latency period is typically weeks to months post-MI, with rare early presentations within one week post-MI. In such patients, the initial myocardial injury is thought to release as yet unidentified substances that initiate an immune-mediated damage response, possibly similar to the interleukin-1 mediated autoinflammation present in recurrent idiopathic pericarditis. The incidence of post-MI syndrome has markedly declined during the reperfusion era.

The clinical presentation, diagnosis, and management of PCIS, including post-MI syndrome, is presented in detail separately. (See "Post-cardiac injury syndromes".)

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Non-ST-elevation acute coronary syndromes (non-ST-elevation myocardial infarction)" and "Society guideline links: ST-elevation myocardial infarction (STEMI)" and "Society guideline links: Pericardial disease".)

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

Basics topics (see "Patient education: What can go wrong after a heart attack? (The Basics)")

Beyond the Basics topic (see "Patient education: Pericarditis (Beyond the Basics)")

SUMMARY AND RECOMMENDATIONS

Following a myocardial infarction (MI), patients are at risk for a variety of cardiac complications, including three pericardial complications: peri-infarction pericarditis (PIP), post-MI pericardial effusion, and post-cardiac injury syndrome. (See 'Introduction' above.)

PIP occurs soon following the MI and is usually transient and self-limited. The presence of a pericardial friction rub is diagnostic of PIP, while pleuritic chest pain is also consistent with the diagnosis. In contrast to acute pericarditis that occurs in other settings, ECG findings in patients with suspect PIP may be less obvious and modified by the changes seen due to the MI itself. (See 'Clinical presentation and diagnosis of PIP' above.)

Our approach to patients with PIP, which is usually self-limited, is to avoid using antiinflammatory drugs for 7 to 10 days after the acute MI (other than once daily aspirin as prescribed for secondary prevention following the MI). Acetaminophen is recommended for pain. For patients with symptoms who require early antiinflammatory therapy, or patients who remain symptomatic after the initial 7 to 10 days, we recommend aspirin at higher doses rather than other nonsteroidal antiinflammatory drugs or glucocorticoids (Grade 1B). There is insufficient evidence to recommend administration of colchicine in this population. (See 'Management of PIP' above.)

Pericardial effusion is common in the early course of transmural MI. Patients with a post-MI pericardial effusion are typically asymptomatic, and the accrual of pericardial fluid is typically self-limited. However, if pericardial fluid continues to accumulate and intrapericardial pressure rises substantially, signs and symptoms of cardiac tamponade may develop. All patients with suspected cardiac tamponade should undergo echocardiography to assess for the presence and hemodynamic impact of a pericardial effusion. (See 'Clinical presentation and diagnosis' above and "Cardiac tamponade".)

The optimal management of post-MI pericardial effusion varies depending upon the etiology of the effusion as well as the presence or absence of symptoms felt to be related to the effusion. (See 'Management of post-MI pericardial effusion' above.)

For patients with a post-MI pericardial effusion that is suspected to be related to a mechanical complication (ie, free wall rupture), urgent surgical repair is typically required for any chance of survival. (See "Acute myocardial infarction: Mechanical complications", section on 'Management'.)

For patients with a pericardial effusion and no suspected mechanical complication who are symptomatic due to cardiac tamponade, definitive treatment requires drainage of the pericardial fluid, which is almost always accomplished percutaneously. (See "Pericardial effusion: Approach to management".)

For patients with a pericardial effusion and no suspected mechanical complication who have an incidentally found pericardial effusion and no evidence of cardiac tamponade, no specific therapy is required.

The post-cardiac injury syndrome (PCIS), a general term for several related forms of pericarditis, is termed post-MI or Dressler syndrome when it occurs following acute MI. Post-MI syndrome typically has a longer latency period than PIP and is thought to be immune-mediated. Patients present with signs and symptoms similar to those seen in patients with acute pericarditis and/or pericardial effusion in other clinical settings. (See "Post-cardiac injury syndromes".)

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References

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