Dressler syndrome: post-infarction complications

Dressler syndrome is an immune-mediated pericarditis that develops days to weeks after myocardial or pericardial injury, such as myocardial infarction, cardiac surgery, catheter interventions, or trauma. It is classically described as "late post-infarction pericarditis" with fever, pleuritic chest pain, and pericardial effusion. Today, it is considered part of the broader concept of post-cardiac injury syndrome (PCIS), which includes post-pericardiotomy syndrome and pericarditis following ablation/implantation. [1]

The incidence of the classic post-MI variant has declined with the era of early reperfusion and statins, but PCIS remains relevant after surgery and invasive procedures. Symptoms typically begin within 1-6 weeks; however, the time window varies, so in a patient with a "recent" MI/surgery, the development of chest pain and fever always requires the exclusion of pericarditis. [2]

The pathogenesis is predominantly autoimmune: exposure to myocardial/pericardial antigens triggers sterile inflammation in the serous membranes (pericardium, pleura). This explains the frequent association with pleurisy and elevated inflammatory markers in the absence of infection. A small proportion of patients develop significant effusion with the risk of tamponade. [3]

It is important to distinguish Dressler syndrome from early post-infarction pericarditis (in the first 24 to 30 days, due to necrosis), ischemia/restenosis, pulmonary embolism, and pneumonia: these are different causes of chest pain, and treatment options vary. Correct classification determines the choice of anti-inflammatory therapy and anticoagulant restrictions. [4]

How does this manifest itself?

Typical complaints include stabbing/burning chest pain that intensifies with inspiration and in the supine position and decreases with leaning forward; subfebrile/fever, weakness, and sweating. Pericardial friction on auscultation, pericardial effusion on echocardiography, and pleural pain/effusion are often present. Blood tests reveal elevated CRP/ESR; leukocytosis is variable. [5]

An ECG often reveals classic signs of pericarditis—diffuse ST elevation and PR depression—but interpretation is difficult in the setting of a recent infarction. Therefore, echocardiography plays a key role: even a small effusion supports the diagnosis, while a large one or one with signs of hemodynamic influence requires urgent management. Cardiac magnetic resonance imaging can confirm pericardial inflammation in cases of questionable findings. [6]

The post-cardiac surgery variant (postpericardiotomy syndrome) is often accompanied by a higher incidence of pleurisy and fever and may have a later onset. Prophylactic use of colchicine in the large COPPS/COPPS-2 studies reduced the risk of this syndrome, although due to gastrointestinal side effects, the benefit must be weighed against tolerability. [7]

Danger signals: progressive dyspnea, tachycardia, falling blood pressure, jugular vein distension, and pulsus paradoxus are possible signs of cardiac tamponade. In these cases, urgent evaluation and, if confirmed, pericardiocentesis are indicated. [8]

Diagnostics: what and in what sequence

The diagnosis of pericarditis is based on ≥2 of 4 criteria: typical pain, pericardial friction rub, ECG changes, echocardiographic effusion; plus supportive features (CRP, pleural effusion, MRI signs). Dressler syndrome/PCIS is suggested by an association with recent cardiac/pericardial injury and the absence of alternatives (ischemia, PE, infection). [9]

Basic examinations: complete blood count, CRP/ESR, troponin (differential with recurrent ischemia/myocarditis is important), ECG, echocardiography. In case of fever/local symptoms, infectious causes are excluded. In case of atypical course or relapses, MRI (pericardial edema/contrast) is useful. [10]

After surgery/invasive procedures, it is important to rule out mechanical and thromboembolic complications (pericardial hemorrhage, pulmonary embolism), especially during therapeutic anticoagulation. In patients in the early post-infarction period, NSAIDs, other than aspirin, may interfere with myocardial healing—this is taken into account when prescribing. [11]

In cases of moderate to large effusion, signs of tamponade are assessed and a decision is made regarding pericardiocentesis. Puncture is also indicated if a purulent/malignant process is suspected (not typical for Dressler, but important to remember). [12]

Treatment: anti-inflammatory base and the role of colchicine

The first-line treatment for post-MI is acetylsalicylic acid (ASA) at anti-inflammatory doses (e.g., 750-1000 mg every 8 hours with gradual reduction), as it is compatible with antithrombotic therapy after MI. Ibuprofen/other NSAIDs are used if MI is not relevant or ASA is not suitable, but in recent MI they are avoided due to the potential impact on healing and antithrombotic therapy. [13]

Colchicine is added to anti-inflammatory therapy to reduce the risk of protracted pericarditis and relapses; dosage is based on body weight (usually 0.5 mg 1-2 times a day without a loading dose) for 3 months at the first episode. The efficacy of colchicine in acute and recurrent pericarditis has been proven in ICAP RCTs; in postpericardiotomy syndrome, a prophylactic effect has been demonstrated in COPPS/COPPS-2. The decision on duration and tolerability is made individually. [14]

Glucocorticosteroids are reserved for use in cases of ineffectiveness/intolerance to ASA/NSAIDs+colchicine or for special indications (autoimmune diseases, pregnancy with restrictions on NSAIDs, etc.). They are generally avoided as first-line therapy due to the increased risk of relapse and the need for slow withdrawal. When prescribed, low-moderate doses should be used with a very gradual reduction based on symptomatic monitoring and CRP. [15]

In cases of large effusion/tamponade, pericardiocentesis is performed; in cases of "malignant" recurrent pericarditis, pericardiectomy is considered in exceptional cases. In severe recurrences outside the post-infarction context, some guidelines allow anti-IL-1 drugs, but for post-infarction pericarditis, their role is still limited and requires individual consideration. [16]

Special issues and security

Antithrombotic therapy. In cases of large pericardial effusion, anticoagulants increase the risk of hemopericardium; the question of their continuation is decided on an individual basis, weighing the risks of thrombosis (post-MI/stenting/AF) and tamponade. In each case, a joint decision by the cardiologist and cardiac surgeon and frequent echo monitoring are critical. [17]

The role of antibiotics. Dressler's syndrome is a sterile inflammation; empirical antibiotics are not indicated in typical cases and without a focal infection. Their use delays diagnosis and carries excessive risks. The exception is clear signs of an infectious process. [18]

Physical activity. During active inflammation, activity restriction is recommended (at least until symptoms and CRP return to normal, usually 2-4 weeks), followed by a gradual return to the post-MI rehabilitation program. Early overexertion is associated with relapses. [19]

Side effects. The most common side effects of colchicine are dyspepsia/diarrhea (usually resolved by reducing the dose); NSAIDs have gastrotoxicity (covered by PPIs), renal effects, and effects on blood pressure. These should be discussed before starting therapy and monitored over time. [20]

Prognosis and risk of relapse

With timely treatment, Dressler syndrome usually has a benign course, and patients fully return to rehabilitation after myocardial infarction/surgery. Relapses are possible, but less common with the use of colchicine and the "correct" gradual withdrawal of anti-inflammatory drugs. Tamponade develops infrequently, but requires readiness for immediate evacuation of the effusion. [21]

The incidence of postpericardiotomy syndrome and recurrences is reduced with prophylactic colchicine administration in selected groups (taking into account tolerability). This is important for cardiac surgery centers and ERAS-cardiology programs: standardized protocols reduce hospitalizations and re-visits. [22]

Long-term survival is determined not so much by the pericarditis itself as by the underlying cardiovascular risk (infarction size and location, LV function, and the presence of complications). Therefore, the management of Dressler syndrome is always integrated into the secondary prevention of coronary heart disease. [23]

Patients with recurrent episodes of pericarditis benefit from follow-up in specialist centres (pericarditis clinics) and access to expert-level MRI/Echo as this speeds up diagnosis, allows for the sparing use of steroids and reduces anxiety. [24]

Differential Diagnosis (What Not to Miss)

Recurrent ischemia/stent thrombosis. Chest pain in a "recent" infarction patient is always ischemic until proven otherwise; troponins/EKG dynamics/echo-regional contractility help differentiate. Pericarditis usually produces diffuse, rather than regional, ECG changes. [25]

Pulmonary embolism and pneumonia can mimic pleuritic pain and fever. Assessment of the likelihood of PE, D-dimer/CT angiography, and pleural X-ray/ultrasound, as indicated, are included in the exclusion algorithm. [26]

Residual pericardial friction in the early post-infarction period does not always indicate Dressler syndrome. The dynamics of symptoms, the time interval since the event, and inflammatory markers are important. MRI is helpful when the picture is unclear. [27]

Infectious pericarditis (including postoperative pericarditis) is rare, but should be considered in the presence of high fever, neutrophilia, purulent sputum/foci of infection, and immunosuppression. In doubtful cases, pericardial puncture with fluid analysis is recommended. [28]