Introduction
Post-myocardial infarction syndrome, also known as Dressler syndrome, post-traumatic pericarditis, post-cardiac injury syndrome, or post-pericardiotomy syndrome, is the secondary inflammation of the pericardium (sac around the heart) with or without pericardial effusion (fluid build-up within the pericardium). It may be due to an immune reaction set off by any trauma to the heart or pericardium. First described by William Dressler in 1956, it is not to be confused with Dressler’s syndrome, which is a syndrome of hemoglobinuria named after Lucas Dressler, who described it in 1854.
Who Is Susceptible to Post-Myocardial Infarction Syndrome?
Dressler syndrome has been reported to occur in around three to four percent of individuals with a history of myocardial infarction, but the incidence is in a rapid decline owing to the advancements in acute myocardial infarction care. The advancements in a reduction in the size of the infarcts and subsequent myocardium damage prevent secondary immune-mediated damage. The risk of Dressler increases with the size of the myocardial infarct, and the risk of recurrence increases with a previous history of Dressler.
The predisposing factors of Dressler are as follows:
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Viral infection.
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Myocardial damage from surgical interventions.
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Young age.
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History of pericarditis.
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History of Prednisone therapy.
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B negative blood group.
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Halothane anesthesia usage.
There has been no clear evidence of the association of Dressler syndrome with the degree of myocardial trauma. Young patients undergoing cardiac surgeries having a B negative blood group and a history of pericarditis and Prednisone therapy must caution surgeons to be mindful of early signs of Dressler.
What Is the Cause of Post-Myocardial Infarction Syndrome?
Post-myocardial infarction syndrome is caused as a result of post-traumatic pericarditis from blunt or penetrating trauma. It may also be caused due to iatrogenic reasons like percutaneous coronary, intracardiac interventions, pacemaker lead insertion, and radiofrequency ablation.
An initial injury to the pericardium is believed to be the trigger for Dressler, due to which mesothelial pericardial cells combine with blood in the pericardial space and instigate an immune response. This results in an immune complex deposition in the pericardium, pleura, and lungs. This reaction and deposition occur anywhere between a few days to a few weeks (two days to six weeks).
It is observed that there is an increase of antimyocardial antibodies targeting the exposed antigens over the pericardium in the blood of patients with Dressler. The syndrome can be precipitated by viral infections from coxsackie B, adenovirus, and cytomegalovirus.
What Are the Clinical Features of Post-Myocardial Infarction Syndrome?
The clinical features of Dressler develop about one to six weeks post-initial trauma to the pericardium. The symptoms are:
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Fever.
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Malaise or generalized weakness.
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Pleuritic chest pain.
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Irritability.
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Palpitations or tachycardia (rapid heart rate).
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Dyspnea (with or without hypoxia).
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Pericardial effusion.
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Painful joints (arthralgia).
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Loss of appetite.
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Pulsus paradoxus.
The reported fever can be as high as 104 degrees Fahrenheit or 40 degrees Celsius and last for about two weeks. The chest pain increases while breathing in or when lying down. Pulsus paradoxus may be observed in some cases where there is a more than 10 mmHg fall in blood pressure during inspiration, and a decrease in pulse amplitude is palpable on the radial artery. Some patients may present with pneumonitis (inflammation of lung tissue) and large pulmonary effusions (fluid accumulation between chest and lung lining).
How to Diagnose Post-Myocardial Infarction Syndrome?
The gold standard diagnostic procedure for Dressler is done using an echocardiogram which evaluates the presence and quantity of pericardial effusion and the degree of cardiac output. Echocardiograms can also determine congestive cardiac failure and measure ventricular contractility and cardiac tamponade. Echo interpretation becomes easier with the increasing pericardial effusion. Along with echo, ultrasonography can also be performed, especially in acute emergencies. At times, the posterior pericardium may be difficult to visualize with an echo; cardiac MRI (magnetic resonance imaging) may be employed to determine any effusion, which may also become loculated. This loculation and posterior pericardial effusion are better visualized with a cardiac MRI than with an echo. In the absence of gold standard tests, a simple chest X-ray may sometimes be beneficial in detecting any pleural and pericardial effusions by showing flattening or enlargement of different segments. Laboratory studies might reveal elevated WBCs (white blood cells), increased ESR (erythrocyte sedimentation rate), increased CRP (C-reactive protein), and a high title of anti-heart antibodies.
The characteristics of Dressler ECG (electrocardiograph) include:
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Initially, ST-segment elevation.
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T-wave inversion.
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Later, electrical alternans (amplitude and direction change with each beat).
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Low voltage QRS.
Additionally, pericardial fluid may be drained and examined for cell count, differential count, cultures, gram stain, cytology, total protein, and triglyceride levels.
How to Treat Post-Myocardial Infarction Syndrome?
Most patients with a confirmed Dressler diagnosis can be treated with NSAIDs (non-steroidal anti-inflammatory drugs)) like Aspirin, Ibuprofen, or Naproxen, which are tapered over four to six years as the pericardial effusion gradually reduces. A few patients may not respond to the NSAID therapy; for them, corticosteroids like Prednisone may be prescribed and tapered over four weeks. Colchicine has also been prescribed as a treatment option, while this can also be prescribed as a prophylaxis prior to cardiac procedures, but no significant effect is observed after Dressler development.
Severe cases might be precautionary to future cardiac events (like tamponade and constrictive pericarditis and require hospitalization for pericardial drainage). Pericardiocentesis drainage is done over a period of two to three days.
What Is the Prognosis of Post-Myocardial Infarction Syndrome?
Successful management of Dressler usually shows a good prognosis, even in patients requiring peri-cardiac drainage. Such patients carry an additional risk of recurring effusion and hemodynamic compromise. Persistent, recurrent pericarditis may be indicative of pericardial stripping.
What Is the Differential Diagnosis of Post-Myocardial Infarction Syndrome?
Differential diagnoses of post-myocardial infarction syndrome include:
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Pulmonary embolism (artery within the lung gets blocked by a clot).
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Sepsis (extreme reaction to infections).
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Pneumonia (infectious inflammation of the air sacs of the lungs).
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Congestive heart failure (heart does not pump sufficient blood).
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Influenza (or flu, a viral infection).
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Recurrent cardiac injury.
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Acute anemia (sudden rapid drop in blood count).
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Endocarditis (infection of the endocardium).
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Uremia (high urinary waste levels in the blood).
What Are the Complications of Post-Myocardial Infarction Syndrome?
Complications of post-myocardial infarction syndrome include:
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Pericardial tamponade.
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Complete cardiovascular collapse.
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Constrictive pericarditis.
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Insufficient diastolic filling and systolic squeeze.
Conclusion
Owing to the rarity of incidence, there is no specific need for adopting prevention means against Dressler syndrome. But patients with risk can be prophylactically treated with Colchicine. The risk of pericardiocentesis-associated complications has been reported in 4 to 30 percent of cases, with major compilations accounting for not more than two percent. The total treatment of non-complicated cases should not last beyond six weeks. Although widely non preventable, Dressler needs to be accurately diagnosed with nascent symptoms so that the patient does not even have to spend a single night of hospitalization.
