A Case of Acute Coronary Syndrome Featuring a Forgotten and Disguised Intruder

Abstract

An infrequently diagnosed case of atrial infarction (AI) which occurred in conjunction with left ventricular myocardial infarction is presented. Atrial infarction was recognized by the presence of PR-segment depression in conjunction with premature atrial complexes. Spatial vector analysis of premature atrial complexes, is highlighted as a means to localize AI.

Case presentation

A 52-year-old male patient, a cigarette smoker with a history of type II diabetes mellitus and dyslipidemia but no history of cardiovascular disease, presented to hospital due to sudden onset, constrictive retrosternal chest pain of thirty-minute duration. A twelve lead-electrocardiogram (Figure 1) recorded on admission showed a basic sinus rhythm, a heart rate of 94 beats per minute, coving and subtle elevation of the ST-segment in leads II, aVF and III, subtle ST-segment elevation in lead V6 and at least 0.1 mV ST-segment depression (STD) in leads V2 through V5; STD in lead V2 was horizontal and associated with a negative T wave whereas in leads V3 through V5 STD was upsloping and associated with a positive T wave.

What other ECG abnormalities do you observe? What do they suggest? What would be your next course of action?

Discussion

This ECG is notable for two additional abnormalities. First, each sinus P wave, is associated with an atrial depolarization (P′) wave (arrowheads in Figure 2) that is superimposed upon and deforms the ST-segment. Each P′ wave shows a very short coupling interval (approximately 240 msec) thereby raising suspicion that it may be a manifestation of atrial reciprocal activation. Yet, this was precluded by the absence of lengthening of the preceding PR interval, that is a prerequisite of its development. Consequently, P′ waves were interpreted as a manifestation of premature atrial depolarization, and because of a fixed coupling interval they were ascribed to reentry in the atrial myocardium. None of the premature P′ waves is followed by a pause, suggesting, failure to penetrate the sinus node, that is, sinus nodal entrance block. The PR interval is stable at approximately 160 msec and does not prolong after a premature P′ wave suggesting that the latter fails to penetrate a significant part of the atrioventricular node, that is atrioventricular nodal entrance block. Premature P′ waves are inverted in leads II, aVF, and III, and upright in leads aVR and aVL, indicating a P′ wave vector directed superiorly in the frontal plane, thus suggesting an ectopic focus in the posteroinferior atrial wall [1,2]. Furthermore, premature P′ waves are upright in lead V1 and inverted in leads V5 and V6 indicating a P′ wave vector directed anteriorly and rightward in the horizontal plane, thus suggesting a left atrial ectopic rhythm. The second abnormality detected in this ECG, is PR segment depression with respect to the TP segment in leads II, aVF, V3 and V4 (arrows in Figure 2), which, together with the non-conducted premature atrial complexes (P′ waves) were ascribed to posteroinferior left atrial infarction (AI) [3]. Scrutiny of the presenting ECG (Figure 1) also shows that the ST-segment deviation vector is better seen in the horizontal than in the frontal plane and more in leads V3 to V4 than in leads V1 to V2. It is, therefore, inferred that early in an ischemic process affecting the inferior and inferior-lateral left ventricular walls, the basal (formerly posterior) and mid inferior segments which likely bend upwards, were the segments affected the most [4]. Indeed, this was confirmed in a posterior leads ECG which disclosed at least 0.05 mV ST-segment elevation in leads V7-V9. The patient underwent emergency coronary angiography which showed a total occlusion in the proximal segment of a co-dominant left circumflex artery (arrow in Figure 3) tackled successfully with stenting achieving a good clinical outcome. Discharge ECG (Figure 4) showed signs of an evolved inferior wall myocardial infarction with extension to the lateral wall.

Atrial infarction, still remains underdiagnosed primarily because its ECG manifestations are subtle and non-specific [3]. According to Liu et al. [5] whose ECG criteria for AI are the most widely accepted, depression of the PR segment of small magnitude and without accompanying PR segment elevation is not enough by itself to suggest AI. However, Burch, reported that PR segment depression as small as a fraction of a millimeter or more was always associated with AI detected at autopsy [6]. In another series of histologically confirmed AI, none of the patients showed PR segment elevation and all showed PR segment depression [7]. Conclusively, the presence of PR segment deviation of any magnitude in a clinical context of acute myocardial ischemia and its resolution upon amelioration of ischemia or establishment of a healed infarct favors the diagnosis of AI [8]. Furthermore, any form of supraventricular arrhythmia occurring in the context of ventricular myocardial infarction should be considered highly suggestive of an accompanying AI [5,9].

Herein, the ECG pattern of AI comprised approximately 0.05 mV PR segment depression in leads II and aVF, and slightly less than 0.1 mV PR segment depression in leads V3 and V4 without accompanying PR segment elevation and non-conducted premature atrial depolarizations. Both, PR segment depression and premature atrial depolarizations disappeared after recanalization of the occluded left circumflex artery and such a temporal association and evolution with acute and resolving myocardial ischemia favored their ischemic origin, specifically AI. Furthermore, the PR segment deviation vector observed in our case would appear to partly fulfill criteria for right AI but also criteria for left AI [3,5]. Nevertheless, the inverted P′ waves in leads II, aVF, III and V6 and the upright P′ waves in lead V1 indicated a spatial P′ wave vector pointing superiorly, to the right and anteriorly, thus suggesting an ectopic focus in the posteroinferior aspect of the left atrium [1,2]. If the ectopic focus had been located in the posteroinferior aspect of the right atrium, the vector of atrial premature depolarization would have been directed superiorly but also posteriorly thereby yielding inverted P′ waves in lead V1 [1]. Knowledge of the site of AI is still clinically useful even in the absence of complications like in the present case. For example, given the reported association of left AI with left inferobasal (formerly posterior) myocardial infarction, the diagnosis of the former may raise suspicion of the latter [10]. Indeed, this association is corroborated in the present case. Furthermore, atrial ischemia/infarction, promotes reentry, by causing significant local conduction delay, thereby facilitating induction and maintenance of atrial fibrillation [11]. Herein, the exceptionally short coupling interval of the premature atrial depolarizations ascribed to reentry indicated that the refractory period of the atrial myocardium is very short. Accordingly, our patient was at high risk of developing atrial fibrillation precipitated by the atrial premature depolarizations; yet, such an arrhythmia did not occur apparently, because the atrial myocardium was completely repolarized at the crucial time.

Conclusions

The case of AI presented herein, remind us of the particular scrutiny required to identify ECG signs favoring its diagnosis; it manifested as PR segment depression and premature P′ waves. This case highlights spatial vector analysis of premature atrial complexes, as a means to localize AI. The diagnosis of AI entails important short- and long-term clinical implications and should be sought in cases of left ventricular myocardial infarction.