Atrial infarction (ATI) is detected in about 0.7–42% of autopsy findings of acute myocardial infarction (AMI) depends on whether or not the atria are specifically examined.1–3 Electrocardiography (ECG) is the only means of which antemortem diagnosis of ATI can be made. PR-segment represents the period of atrial repolarization. Significant PR-segment depression in inferior leads with reciprocal PR-segment elevation in lead I is used as one of the diagnostic criteria for ATI.4 However, the sensitivity of these diagnostic criteria is low, in the range of 5.4–6.9% due to low voltage generated by the thin atrial wall.5 PR-segment elevation in inferior leads was previously reported in left tension pneumothorax6 as well as during retrosternal reconstruction of esophagus.7 It has not been described in association with AMI for nearly half of a century.8 Case Report. A 70-year-old man had a smoking habit and hypercholesterolemia as the cardiovascular risk factors. He had no prior history of angina pectoris. He presented to the Emergency Room with sudden onset of severe chest pain. An ECG was performed at 2 hours after the onset of symptom. Figure 1 (conventional lead) showed ST-segment elevation in inferior leads and V6 with ST-segment depression in leads I, a VL and V1–4. There was also 0.5 mm PR-segment elevation in inferior leads, but no reciprocal PR-segment depression in leads I or a VR could be seen. The second to fifth beats were sinus rhythm (SR) with constant P-P interval, followed by an abrupt sinoatrial exit block (SAEB) with atrial escape rhythm in the subsequent 3 beats (sixth to eighth beat) which had different P wave morphology and PR interval. Finally SR took over again in the ninth and tenth beat with the same P wave morphology, PR interval and P-P interval as the previous sinus beats. Figure 2 (right precordial leads) showed ST-segment elevation in leads VR4–6 compatible with right ventricular infarct. PR-segment elevation in inferior leads could also be detected. Note that although it showed SR with constant PR interval, there were slight variations in the P-P interval among each pair of beats. Posterior lead ECG showed ST-segment elevation in leads V8–9 (not shown). The overall clinical picture was consistent with acute inferoposterior MI with right ventricular involvement. There were also evidences suggestive of atrial infarction or ischemia. He was brought to the cardiac catheterization laboratory immediately for primary angioplasty. Coronary angiography revealed an acute cut-off in the mid part of the dominant right coronary artery (RCA) (Figure 3). However, the conus branch, sinus node artery (SNA) and the right ventricular branch which originated proximal to the occlusion, had normal blood flow. The left anterior descending artery and the non-dominant left circumflex artery (LCX) were normal. The proximal LCX gave rise to a small left atrial branch to supply the superior portion of the left atrium (LA). Rheolytic thrombectomy was performed using a 2.0 mm X-Sizer (Microvena, Minnesota). After removal of some of the fresh thrombus, blood flow was quickly re-established in the RCA. A few slender atrial branches were seen arising from the mid RCA (Figure 4). The posterolateral branch also supply a small atrial branch to nourish the inferior portion of the LA (Figure 5). The culprit lesion in the mid RCA was ultimately covered with a HepacoatBX Velocity 3.5/28 mm stent (Cordis, a Johnson & Johnson Company, Rodens, The Netherlands). The stent was then post-dilated with a 4.5 mm balloon at 10 atmospheres. Intravenous bolus injection and infusion of tirofiban was given during and after the procedure. He made a prompt and uneventful recovery. He was seen in the outpatient clinic at 4 weeks and 3 months afterwards with no major cardiovascular events. Discussion. The clinical significance of ATI is not fully studied. Whether the loss of atrial kick and atrial arrhythmias contribute to higher mortality on top of the AMI and right ventricular infarction is still uncertain. In autopsy series, the right atrium (RA) was involved in majority of cases (81–98%) and the right atrial appendage (RAA) was affected in 78% of right-sided infarct.2,9 Biatrial involvement was relatively common (19–24%). The ATI is always transmural, the infarct area is usually located near the atrioventricular groove. The RA usually gets its blood supply from the branches arose from the RCA. The RCA gives off its second branch as the SNA which runs posteriorly to supply the anterior surface of the RA as well as the RAA. The SNA then extends superiorly to the ostium of the superior vena cava to supply the sinus node (SN). Small and rather inconstant atrial branches may originate at the acute margin or at the diaphragmatic surface of the heart to supply the lateral and posterior wall of the RA. These branches are termed intermediate and posterior atrial branches.10 The complications of ATI are listed in Table 1. In this patient, the occurrence of transient SAEB and atrial escape rhythm (Figure 1) was a sign of atrial ischemia affecting the SN and its surrounding atrial muscle. The variations in P-P interval (Figure 2) was due to sinus arrhythmia, probably secondary to SN ischemia which was manifested as variable delay in transmission of the impulse through the SN to the atrium. In the context of AMI, these ECG features were strongly suggestive of concurrent ATI with ischemia affecting the atrium around the SN. The diagnostic criteria of ATI are summarized in Table 2.4 The magnitude of PR-segment deviation is small with considerable interobserver variations.11 Moreover, PR-segment depression can be a normal electrocardiographic finding during exercise. That is the underlying reason why reciprocal change is emphasized so much in the diagnostic criteria. The vector of the PR-segment is directed towards the area of ATI. It is analogous to the direction of the current of injury in ventricular infarction.12 Since the atria occupy the postero-superior position compared with the ventricles, PR-segment elevation in leads a VR and a VL with reciprocal PR-segment depression in inferior leads and V1–2 are found in majority of cases. In isolated left ATI, PR-segment elevation may extend to leads I and V5–6 (lateral shift) while in isolated right ATI, lead I may have PR-depression (posterior shift).4 Our patient presented with an atypical ECG finding of PR-segment elevation in inferior leads without any reciprocal change in the complementary leads (lead I or a VR). However, in the setting of AMI and atrial arrhythmia, the diagnosis of concurrent ATI was beyond any doubt. Unlike the more commonly encountered type of ATI, our patient might represent a more inferoposterior involvement of the atria. With reference to the coronary angiographic findings, the acute occlusion of the right atrial branches and the small left atrial branch from the posterolateral branch was able to account for the ECG manifestation. Conclusion. PR-segment elevation in inferior leads is a very rare ECG finding. In this patient although it does not meet the diagnostic criteria of ATI, it definitely represented ATI in the clinical setting. In fact, any PR-segment shift in the presence of atrial arrhythmia, especially in the context of AMI should arouse the clinical suspicion of ATI.
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