Inferior infarction and Dressler’s syndrome

ECG 1A: Sinus rhythm with a normal PR interval; there is poor R wave progression in the precordium compatible with the history of a previous anterior infarction; there is also a Q-wave in the inferior territory with persistence of a slight elevation with negative T-wave pointing to a recent lower infarction;

The coronary angiography confirmed the presence of a recent inferior infarction; no action of revascularization could be achieved. After a pain-free interval of 6 weeks, the patient is again hospitalized in the setting of prolonged chest pain with fever and cough;

ECG 1B: The tracing reveals sequela of inferior and anterior necrosis; there is a significant modification of repolarization with presence of negative symmetrical T-waves in inferior leads and from V3 to V6; this tracing is consistent with a Dressler’s syndrome occurring as a result of non-reperfused inferior necrosis;

Comments: This patient presented an inferior infarction examined belatedly and without possible reperfusion followed by a Dressler’s syndrome a few weeks after the patient’s discharge with the presence of moderate left pleural effusion, pericardial effusion and hyperleukocytosis. Anti-inflammatory treatment allowed eliminating the symptomatology.

Dressler’s syndrome initially described in 1956 corresponds to a complication occurring in post-infarction. Since the introduction of fibrinolytic therapy and angioplasty in the acute phase, its incidence has considerably decreased. Indeed, a rapid reperfusion allows to limit the extension of the necrosis. Dressler’s syndrome is more frequent in instances of extensive infarction and late reperfusion. This complication usually occurs after a few weeks of latency (usually between 2 and 5 weeks) in the aftermath of a major infarction. Dressler’s syndrome is typically manifested by a resurgence of chest pain exacerbated at inspiration associated with: fever, cough, pericardial friction (less common), a biological inflammatory syndrome (hyperleukocytosis, increased SR and CRP), a pleural effusion most often left-sided, and a possible moderate pericardial effusion. The occurrence of tamponade in this setting is rare. The underlying pathophysiological mechanism is not clearly established although an autoimmune mechanism may explain the occurrence of symptomatology after a latency phase.

The electrocardiogram can reveal the usual signs of pericarditis even if the diagnosis can be rendered difficult by the concomitant changes in relation to the post-infarction. A widespread T-wave inversion is probably the most frequent sign.

Evolution is most often spontaneously favorable although with a possible risk of recurrence in the following weeks. Therapeutic management is largely empirical and is based on the introduction of non-steroidal anti-inflammatory drugs or large-dose aspirin. Corticosteroid therapy or colchicine therapy may be considered for resistant or recurrent forms.

Take-home message: Dressler’s syndrome corresponds to a pericarditis occurring a few weeks after an extensive infarction. Its incidence has considerably decreased since the development of reperfusion techniques. It should nevertheless be evoked in a non-reperfused or late-reperfused patient with typical symptomatology.