Introduction
Pathological Q waves may appear on the 12-lead electrocardiogram (ECG) during acute ST-segment elevation myocardial infarction (STEMI) and signify loss of electrical excitation. Anterior wall STEMI often results in loss of R waves in the precordial leads and subsequent appearance of pathological Q waves. Not infrequently, very early loss of R waves may be visible in patients presenting with anterior STEMI and occasionally, these R waves reappear in the first months following the index event. Despite reports in the literature [
1‐
9], the prognostic significance of R-wave reappearance (RWR) in the setting of primary percutaneous coronary intervention (pPCI) remains uncertain. In this report we present two patients with anterior STEMI who underwent uncomplicated pPCI. The follow-up ECGs were indicative of the amount of myocardial recovery after the acute event as shown by cardiovascular magnetic resonance (CMR) imaging.
Discussion
This case report describes two anterior wall STEMI patients with early R-wave loss in the precordial leads. Both patients had a proximal LAD occlusion, and uncomplicated PCI with stenting was performed within 5 h after symptom onset. Follow-up ECGs in case 1 showed complete RWR, while follow-up ECGs in case 2 showed persistent loss of R waves. In both cases CMR, performed within 1 year after the index event, showed that the occurrence of RWR was indicative of the amount of myocardial recovery.
RWR is not an uncommon phenomenon in anterior STEMI patients undergoing successful reperfusion therapy. The incidence rates reported in the literature are 39% and 77% during 6 and 6–60 month follow-up periods, respectively [
5,
7].
The appearance of pathological Q waves in the chronic phase of STEMI has been classically associated with myocardial necrosis, whereas Q waves in the early stages of STEMI may result from a transient loss of electrical function due to intense ischaemia [
10]. The exact mechanism of RWR has not been clarified, but the time course may give insight into the mechanism involved in this phenomenon. After the acute phase of STEMI, the infarcted myocardium may gradually shrink as part of the remodelling process. If myocardial fibres are then able to cover the infarcted area, this may result in RWR [
11]. However, this process may take several months to years while the RWR in case 1 occurred within 1 month. Bateman et al. [
1] explained early RWR by the existence of an ‘electrically silent’ area in context of myocardial stunning with transient loss of potential in cellular membrane. Finally, the exact position of precordial electrodes could vary during recording of the ECGs influencing R-wave voltage. This seems of minor influence in case 1 as all follow-up ECGs consistently showed complete RWR.
The prognostic significance of RWR remains unclear. Several studies [
2,
4,
6,
7,
9] reported that patients with RWR had a smaller infarct size and better left ventricular function whereas Iwasaki et al. [
5] showed no such association. The CMR in case 1 showed a smaller infarct size and peri-infarct border zone as compared with case 2. The peri-infarct border zone is postulated to represent a mix of viable and scarred myocardium. This heterogeneous region may act as a substrate for ventricular arrhythmic events which is an indicator of prognosis [
12]. In this case, the occurrence of RWR corresponded with a better myocardial recovery revealed by CMR and therefore may provide important prognostic information. By reporting these cases, we would like to create awareness of this phenomenon and encourage future research to enlighten its significance.