Discussion

DS, also known as post-myocardial infarction syndrome and first characterized by William Dressler in 1956, is a delayed complication of acute myocardial infarction occurring within 1 to 8 weeks after cardiac acute events. In the pre-thrombolysis era, its prevalence was 7–23%, then decreasing to <5% after the introduction of reperfusion therapies [2]. Typical symptoms of DS include pleuritic chest pain, pericardial and pleural effusion, low-grade fever, increase of inflammatory laboratory tests, enlargement of the cardiac silhouette, ST-elevation and T-wave changes. Diagnosis is typically made by clinical conditions, chest x-ray, EKG, echocardiography, or by chest computed tomography (CT), although cardiac nuclear magnetic resonance (NMR) would represent the gold standard [3].

Figure 1.

Computer tomography (CT) showing evident pleuritic and pericarditic effusions.

Etiology of DS is not clearly established, but an immunologic pathogenesis has been suggested, secondary to the release of cardiac antigens during cardiovascular events. This could stimulate antibodies formation, with further formation of immune complexes in pericardium, pleura and lungs, followed by an inflammatory response [4]. A recent French study evaluated 193 patients with a first episode of ST-elevation myocardial infarction, 58.5% of whom complicated by the presence of pericardial effusion [5]. All patients, symptomatic or not, were investigated with cardiac NMR. The authors showed that presence and volume of pericardial effusion were related to infarct size, microvascular obstruction, and systolic wall stress, and early reperfusion and optimal medical therapy resolved the condition. Treatment of DS remains largely empiric due to the absence of evidence based data. In agreement with the European Society of Cardiology guidelines, non-steroidal anti-inflammatory drugs (NSAIDs), such as ibuprofen, represent the first pharmacological choice in early post-infarction pericarditis [6]. On the one hand, such therapy was found to be related with a risk of scar thinning, infarct expansion and myocardial free wall rupture but, on the other, the same complications have also been issued to corticosteroid therapy [7].

High acetyl-salicylic acid dose (500 mg every 8 – 12 hours for 7 days), provides an efficacious anti-inflammatory effect and is generally well tolerated [8]. In particular, however, in patients who received a percutaneous coronary intervention, corticosteroids should be avoided for at least 4 weeks after the procedure, due to their potential impact on cardiac tissues [9]. By means of a PubMed search, we performed a review of the case reports available in literature. We found 19 cases (Table 1). DS occurred more frequently in the middle age (mean age 61±13 years) and in men (13 vs 6 case), on average 26 days after (range 1-120) from the acute event. Even though the clinical manifestations and pharmacological therapies were different, mortality appears to be low (1 fatal case only in our series). Interestingly, despite the above mentioned suggestions by Imazio et al [9], near 50% of DS cases reported received corticosteroid therapy, with positive response.

DS is part of the so-called post cardiac injury syndrome (PCIS), an inflammatory process that occurs in the setting of injury to the pericardium, epicardium or myocardium, following cardiac surgery, myocardial infarction, trauma, intra-cardiac ablation, percutaneous coronary intervention or implantation of a pacemaker or cardioverter-defibrillator. Moreover, DS can represent either a triggering factor of or a consequence of Takotsubo cardiomyopathy [10]. Even if male gender was more represented in our series, the risk of developing pericarditis is similar in men and women, also because women are more likely to present autoimmune diseases [11]. The peculiarity of the present case is given by its acute onset and a slightly anticipated time from infarction (15 vs 26 days), even if quite fitting into the observed range, probably secondary to a high inflammatory trigger. Although in the present case the presentation symptoms resembled that of a recurrence of acute cardiac ischemia, more often DS shows a subclinical evolution, so that some cases may be missed and the low incidence reported may be explained. However, the outcome is generally favorable, and the fatal case reported in this series makes reference to a sudden cardiac death, with autopsy findings of acute myocardial infarction and fibrinous pericarditis. However, in the actual era of aggressive treatment of myocardial infarction and given its the delayed onset, the possible occurrence of a Dressler’s syndrome should always kept in mind, and not only by cardiologists.