Dressler’s Syndrome

I. What every physician needs to know.

Dressler’s syndrome has been described as a late pericardial complication following an acute myocardial infarction (MI). It usually develops weeks to months after the initial infarction, and rarely within the first week post-MI. It is characterized by the development of inflammation of the pericardium as well as other serosa. This syndrome has also been called post-acute MI syndrome,and late post-MI pericarditis, post-cardiac injury syndrome, and post-pericardiotomy syndrome.

The etiology of the development of Dressler’s syndrome has been thought to be an autoimmune process. Cardiac tissue injury after an MI causes exposure and release of cardiac antigens of actin and myosin into circulation. This then triggers antibody formation. These antigen-antibody complexes then deposit in the pericardium as well as other serosa due to molecular mimicry causing an inflammatory reaction. The incidence of this syndrome is very low with reports of 1-7% prior to the reperfusion era. Since then, the incidence has markedly diminished to less than 0.5% according to some reports.

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Since the syndrome was first identified by Dressler in 1956, the term has been applied in various permutations from the original scenario. Examples include situations that involve disruption of the pericardium – such as coronary artery bypass surgery, trauma, pacemaker insertion – with eventual signs and symptoms of pericarditis. However, the purest definition is the original described by Dressler- as a late complication of myocardial infarction – and will be the one used for this chapter.

II. Diagnostic Confirmation: Are you sure your patient has Dressler's?

Dressler’s syndrome is largely a clinical diagnosis with no reported clinical, laboratory or radiographic criteria required to establish the diagnosis. Clinical manifestations include a latency period after acute MI, pleuritic chest pain, a pericardial friction rub, malaise, fever, and a tendency of recurrence of symptoms. Laboratory data may reveal a leukocytosis and elevation in inflammatory markers. Electrocardiogram (EKG) changes with pericarditis may be seen. Imaging studies may reveal pericardial and pleural effusions as well as thickening of the pericardium.

A. History Part I: Pattern Recognition:

1. Onset of symptoms developing in the latency period associated with this syndrome

2. Pleuritic chest pain

3. Pericardial friction rub

4. Fever

B. History Part 2: Prevalence:

The incidence of this syndrome is very low with reports of 1-7% prior to the reperfusion era. Since then, the incidence has markedly diminished further to less than 0.5% according to some reports. In one study (Shahar A et al, 1990) of 201 patients with acute MI who had undergone thrombolysis, no patient showing clinical signs of reperfusion developed Dressler’s. However, more recently there has been at least one case report of Dressler’s syndrome after successful reperfusion, suggesting that the syndrome is still a possibility or perhaps underdiagnosed.

It has been reported that Dressler’s is more frequent after larger infarctions, particularly anterior and inferior infarctions, as well as infarctions with complicated in-hospital courses.

C. History Part 3: Competing diagnoses that can mimic Dressler's.

Peri-infarction pericarditis or early post infarct pericarditis

Peri-infarction pericarditis can be distinguished from Dressler’s syndrome mainly in the temporal relationship to the inciting MI. Peri-infarction pericarditis commonly occurs within the first 3-4 days of the MI and is a result of direct extension of inflammation to the pericardium in the region of the MI from damaged myocardial tissue.

Other causes of pericarditis

Includes infectious, uremic, neoplastic, systemic autoimmune diseases, and radiation induced causes.

D. Physical Examination Findings.

A pericardial friction rub is the classic physical exam finding reported with Dressler’s, which is the same as that of other causes of acute pericarditis. A notable difference in Dressler’s is that the rub may be audible for 7-10 days, rather than being very transient. It has been shown that in patients with acute pericarditis, up to 85% will have an audible friction rub at some point in the course of their disease.

Sometimes pleural rubs can also be auscultated when the pleura are involved. This can be distinguished from pericardial rubs by asking the patient to halt respirations. The pleural rub will be absent with suspension of respirations while pericardial rubs will still be present.

E. What diagnostic tests should be performed?

1. What laboratory studies (if any) should be ordered to help establish the diagnosis? How should the results be interpreted?

Markers of inflammation can be elevated in acute pericarditis including white blood cell count, erythrocyte sedimentation rate (ESR), and C-reactive protein (CRP). These tests are of limited use, however, as they do not provide any information on the underlying cause of the pericarditis. Troponin I levels have also been shown to be minimally elevated in acute pericarditis likely due to inflammation of the adjacent epicardium.

Four stages of EKG changes have been described in acute pericarditis:

  • Stage I includes diffuse ST segment elevation and PR segment depression with reciprocal ST segment depression in leads aVR and V1

  • Stage II involves normalization of the ST and PR segments

  • Stage III is characterized by diffuse T wave inversion

  • In stage IV, the EKG changes may normalize or the T wave inversions may persist

In a clinical series, it was shown that 60% of patients with pericarditis had typical EKG changes as described above. It should be noted, however, that in the specific case of Dressler’s syndrome the typical EKG changes of pericarditis may be overshadowed by the EKG changes of a recent MI.

2. What imaging studies (if any) should be ordered to help establish the diagnosis? How should the results be interpreted?

The following imaging studies are not normally indicated in the diagnosis of Dressler’s syndrome; however, they may be useful in the exclusion of a large pericardial effusion or tamponade physiology. They are also used in the evaluation of other causes of acute pericarditis.

The chest X-ray is mostly normal in the setting of acute pericarditis unless there is a significant pericardial effusion.

Transthoracic echocardiogram (TTE) can be used in the setting of acute pericarditis to quickly assess the pericardium and underlying cardiac function. The TTE is usually normal in uncomplicated cases. The presence of a pericardial effusion can help in confirming a diagnosis of acute pericarditis.

Cardiac computed tomography (CCT) as well as magnetic resolution imaging (CMR) are also being increasingly used in the evaluation of acute pericarditis. Both of these imaging modalities can be used in the detection of pericardial effusions but have the added advantage of being used to measure pericardial thickness. Normal thickness is usually 1-2 mm and no more than 4 mm. Increased pericardial thickness can be a feature of acute pericarditis but is not diagnostic. The most sensitive method for the diagnosis of acute pericarditis is delayed enhancement of the pericardium on CMR. Normal pericardium appears black on CMR due to its low water content. Inflamed pericardium has enhanced gadolinium uptake in the delayed phase.

F. Over-utilized or “wasted” diagnostic tests associated with this diagnosis.

Although markers of inflammation are usually elevated in Dressler’s syndrome, these tests are non-specific and do not distinguish the cause of pericarditis.

III. Default Management.

The initial step in making the diagnosis of Dressler’s syndrome is to have a high index of suspicion, and to exclude other complications of acute MI such as reinfarction, ventricular free wall rupture, and pericardial tamponade, as well as other causes of acute pericarditis.

The course of Dressler’s is self-limiting. There is no consensus on the duration of treatment but most cases respond to a course of high dose non-steroidal anti inflammatory drugs (NSAIDS). According to the European Society of Cardiology, ibuprofen (300-800 mg every 6-8 hours initially) is the agent of choice as other nonsteroidal agents can thin the infarction zone. High doses of aspirin (800 mg every 6-8 hours initially) has also been shown to provide relief of symptoms. Corticosteroids have also been shown to relieve symptoms in patients not responding to NSAID therapy; however, corticosteroids should be used with caution as they have been shown to delay myocardial healing. There are reports that colchicine is helpful in patients with recurrent symptoms although there is no definitive evidence at present.

A. Immediate management.

Hospitalization is rarely required in patients with Dressler’s syndrome due to its benign course. It has been reported that patients with acute pericarditis with high-risk features should be hospitalized. These high-risk features include fever, marked leukocytosis, presence of a large pericardial effusion, cardiac tamponade, acute trauma, immunosuppressed state, concurrent anticoagulant use, failed NSAID therapy, elevated troponin, and recurrent symptoms.

C. Laboratory Tests to Monitor Response To, and Adjustments in, Management.

CRP/ESR can be used as a marker to help monitor response to therapy.

D. Long-term management.

At the present time, there is no recommendation for long-term therapy in patients with recurrent symptoms.

E. Common Pitfalls and Side-Effects of Management

A common pitfall is the misdiagnosis of acute pericarditis. An acute MI can present with similar symptoms, similar EKG findings, and elevated cardiac biomarkers.

IV. Management with Co-Morbidities

A. Renal Insufficiency.

NSAIDS and colchicine should be used with caution in patients with renal insufficiency.

The use of certain diagnostic studies including CCT and CMR should also be used with caution in patients with renal insufficiency due to the risk of contrast induced nephropathy and nephrogenic systemic fibrosis, respectively.

B. Liver Insufficiency.

Colchicine should be used with caution in patients with liver disease due to the risk of hepatotoxicity. NSAIDS have also been shown to cause hepatotoxic reactions in disease-specific states.

C. Systolic and Diastolic Heart Failure

NSAIDS should be used with caution in patients with pre-existing heart failure due to the risk of exacerbation.

D. Coronary Artery Disease or Peripheral Vascular Disease

NSAIDS may potentially inhibit the cardioprotective effects of aspirin. The lowest possible dose in the shortest possible duration should be used.

E. Diabetes or other Endocrine issues

Steroids can exacerbate hyperglycemia and should be used with caution in patients with diabetes mellitus.

F. Malignancy

No change in standard management.

G. Immunosuppression (HIV, chronic steroids, etc).

No change in standard management.

H. Primary Lung Disease (COPD, Asthma, ILD)

No change in standard management.

I. Gastrointestinal or Nutrition Issues

The major adverse effect prompting the discontinuation of colchicine is diarrhea so should be used with caution in patients with motility disorders.

J. Hematologic or Coagulation Issues

NSAIDS and aspirin should be used with caution in patients with bleeding disorders due to their anti-platelet effects and increased risk of bleeding. Colchicine should also be avoided in patients with blood dyscrasias.

K. Dementia or Psychiatric Illness/Treatment

No change in standard management.

V. Transitions of Care

C. When is the Patient Ready for Discharge.

The patient is ready for discharge when high-risk features have been addressed and clinical symptoms are resolving.

1. When should clinic follow up be arranged and with whom.

Routine follow-up with a primary care physician is adequate to monitor for resolution of symptoms and any side effects of medications.

2. What tests should be conducted prior to discharge to enable best clinic first visit.

There is no consensus on tests that should be done prior to discharge; however, it may be useful to obtain a CRP level as this could be used as a surrogate marker for active inflammation in the setting of pericarditis.

3. What tests should be ordered as an outpatient prior to, or on the day of, the clinic visit.

A CRP level may be checked and used to compare to CRP levels prior to treatment to help determine the efficacy of treatment.

E. Placement Considerations.

No special placement considerations are needed.

F. Prognosis and Patient Counseling.

The prognosis is usually good. The patient should be warned of the risk of recurrence of symptoms with discontinuation of therapy as well as possible failure of therapy.

What's the evidence?

Bendjelid, K, Pugin, J. “Is Dressler Syndrome Dead”. Chest. vol. 126. 2004. pp. 1680-1682.

Boushahri, A, Katz, R. “Post-myocardial infarction (Dressler’s) syndrome following early reperfusion”. Br J Cardiol. vol. 19. 2012. pp. 95-6.

Imazio, M, Negro, A, Belli, R, Beqaraj, F, Forno, D, Giammaria, M, Trinchero, R, Adler, Y, Spodick, D. “Frequency and Prognostic Significance of Pericarditis Following Acute Myocardial Infarction Treated by Primary Percutaneous Coronary Intervention”. Am J Cardiol. vol. 103. 2009. pp. 1525-1529.

Welin, L, Vedin, A, Wilhelmsson, C. “Characteristics, prevalence, and prognosis of postmyocardial infarction syndrome”. Br Heart J. vol. 50. 1983. pp. 140

Shahar, A, Hod, H, Barabash, GM. “Disappearance of a Syndrome: Dressler's Syndrome in the Era of Thrombolysis”. Cardiology. vol. 85. 1990. pp. 255

Spodick, D. “Decreased Recognition of the Post-Myocardial Infarction (Dressler) Syndrome in the Postinfarct Setting: Does It Masquerade as "Idiopathic Pericarditis" Following Silent Infarcts”. Chest. vol. 126. 2004. pp. 1410-1411.

Tralhao, A. “The Return of a Disappearing Entity: Dressler’s syndrome after transvenous pacemaker implantation”. BMJ Case Report. 2014 Mar 20. pp. 2014

Khandaker, MH, Espinosa, RE, Nishimura, RA, Sinake, LJ, Hayes, SN, Melduni, RM, Oh, JK. “Pericardial Disease: Diagnosis and Management”. Mayo Clin Proc. vol. 85. 2010. pp. 572-593.

Yared, K, Baggish, AL, Picard, MH, Hoffmann, U, Hung, J. “Multimodality Imaging of Pericardial Diseases”. JACC: Cardiovascular Imaging. vol. 3. 2010. pp. 650-660.

Maisch, B, Seferovic, PM, Ristic, AD, Erbel, R, Rienmuller, R, Adler, Y, Tomkowski, WT, Thiene, G, Yacoub, MH. “Guidelines on the Diagnosis and Management of Pericardial Diseases Executive Summary”. European Heart Journal. vol. 25. 2004. pp. 587-610.

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