Inferior infarction, reperfusion and AIVR

N° 35
69-year-old man, smoker, referred by emergency services for an inferior infarction at H+1; initiation of fibrinolysis in the ambulance; on arrival in the department there is cessation of chest pain;
Inferior infarction, reperfusion and AIVR
Inferior infarction, reperfusion and AIVR

This patient presented with coronary syndrome due to thrombosis of the second segment of the right coronary artery. A rapid reperfusion (thrombolysis initiated at H+1) subsequently followed by angioplasty prevented any significant myocardial necrosis (cardiac ultrasound revealed normal motion of the inferior territory). The AIVR corresponds to a focal ventricular rhythm with a ventricular depolarization rate between 60 and 110 bpm (never exceeding 120 bpm by definition) and wide QRS (>120 ms), most often regular. The term ventricular tachycardia is appropriate only if the rate exceeds 100 bpm; the term slow ventricular tachycardia should not be used for a rate below 100 bpm. An AIVR occurs preferentially in the setting of a sinus bradycardia, the slowing of the normal heart rate favoring expression of ventricular ectopy. The rate is slightly faster than that of the sinus rhythm, which explains the frequent occurrence of fusion complexes (intermediate morphology between the 2 complexes) or capture complexes. There may be competition between the 2 rhythms. For illustrative purposes, the AIVR corresponds to an "accelerated escape" occurring in a context of sinus node dysfunction. Onset does not require early ventricular extrasystole, but rather slowing of the sinus rhythm. This rhythm is most often unstable and of limited duration (a few seconds to a few minutes), termination potentially occurring on a ventricular extrasystole whose morphology is generally different. Episodes can be repetitive and brief (fewer than 100 consecutive complexes). Atrial activity can be dissociated or 1/1 retrograde.

AIVR is a typical reperfusion arrhythmia and does not have the same prognostic significance as a fast and sustained ventricular tachycardia. AIVR very rarely causes a change in hemodynamics, the increase in rate being modest and not requiring any particular treatment. An AIVR may occur, as in this patient, during an inferior or posterior infarction which promotes the occurrence of a sinus bradycardia. Cases of AIVR have been described in patients without reperfusion (total absence of flow confirmed by coronary angiography) limiting the specificity and relevance of this criterion in suggesting a reperfusion. The specificity increases however if the AIVR is associated with other signs of reperfusion (resolution of pain, regression of the elevation, appearance of a negative T-wave). Sensitivity is low (absent in more than 50% of cases of reperfusion) despite the fact that the earlier and closer the electrical monitoring, the greater the probability of recording this type of tracing. The putative mechanism involved in the emergence of these foci is an increase in the automation of His-Purkinje network cells occurring at the time of reperfusion. An AIVR may also occur within a few days of the coronary episode with an almost equal distribution between an anterior infarction and inferior infarction.

Nowadays, coronary angiography is widely available allowing to directly visualize the lumen of the vessel. The utility of electrocardiographic reperfusion signs is therefore of less clinical relevance. These criteria are used in a patient having undergone thrombolysis, with the absence of reperfusion criteria raising the possibility of performing a rescue angioplasty.

An AIVR can occur during reperfusion of an inferoposterior myocardial infarction in a setting of sinus bradycardia. While it has limited prognostic meaning, it is indicative of an effective reperfusion if it is accompanied by resolution of pain and a decrease in elevation.