Acute pericarditis and atrial arrhythmia

ECG: Sinus rhythm, diffuse PQ segment depression (maximum in leads I, II and inferior leads) with PQ elevation in aVR and V1, moderate lateral ST-segment elevation; possible alternating amplitude of the QRS visible in V1 and V2;

A cardiac ultrasound revealed a moderate pericardial effusion. The association between chest pain (increased by inspiration and lessened by leaning forward), the electrocardiogram (diffuse PQ segment depression), pericardial effusion and a biological inflammatory syndrome leads to the diagnosis of acute pericarditis. A few minutes after the first tracing, palpitations and recording of this second tracing.

ECG 2;

ECG 2: Atrial extrasystole bursts followed by initiation of an episode of atrial fibrillation (irregular tachycardia with narrow QRS with baseline tremor);

ECG 3:

ECG 3: Atrial fibrillation;

ECG 4:

ECG 4: Tracing recorded 3 days later; asymptomatic patient with normalization of the electrocardiogram;

Comments: This patient presented an acute pericarditis complicated by an episode of spontaneously resolving atrial fibrillation. The literature describes a number of cases of paroxysmal or persistent atrial arrhythmias occurring in a setting of acute or chronic pericarditis. Changes in the atrial myocardium observed in chronic constrictive pericarditis are extensive, due to the small thickness of the atrial myocardium; they are reflected by an anatomical remodeling, frequent dilatation of the atrial mass with electrocardiographic signs of atrial enlargement and unquestionable increased incidence of atrial fibrillation episodes (about one third of patients).

The causal relationship between acute pericarditis and atrial fibrillation appears less clear. The presence of a PQ segment depression (as in this patient) constitutes a marker of an inflammatory disease of the atrial pericardium. Different animal models of acute pericarditis have documented the release of potentially arrhythmogenic pro-inflammatory cytokines. Prospective studies enabling to measure the actual incidence of this complication in humans are few with conflicting results. It appears that in acute pericarditis, atrial fibrillation occurs preferentially in patients already presenting other contributory factors (particularly elderly, hypertensive patients, with previous atrial dilatation). Inflammation of the atrial pericardium could therefore be considered as a cofactor in the initiation of atrial arrhythmia in patients previously at risk, the incidence being only slightly increased compared to that observed in the general population, except for severe forms with abundant effusion altering hemodynamics or highly prominent inflammatory syndrome (tuberculous pericarditis).

The episodes of arrhythmia are most often transient and spontaneously resolving suggesting a good effectiveness of the anti-inflammatory component of therapeutic treatment. On the other hand, the risk of long-term recurrence appears to be significant with or without clinical and ultrasound signs of recurrence of pericarditis. The thromboembolic risk appears limited with a documented low rate of embolic ischemic attack (TIA, stroke, peripheral embolism). The need to anticoagulate these patients should therefore be balanced by the transient nature of the arrhythmias, the seemingly limited risk of thromboembolic complications described in small sample-sized studies to date, and the theoretical risk (albeit not observed in the studies) of intrapericardial bleeding. Given the elevated risk of recurrence, it would appear reasonable to apply the usual recommendations in this subgroup of patients.

 

Take-home message: Acute pericarditis is one of the recognized etiologies of atrial arrhythmia. It appears, however, that inflammation of the atrial pericardium can only be considered as a cofactor in the initiation of atrial arrhythmia in patients previously at risk.