Differences in initial electrocardiographic findings between ST-elevation myocardial infarction due to left main trunk and left anterior descending artery lesions

Current prompt revascularization by primary percutaneous coronary intervention and optimized medical therapy for ST-elevation myocardial infarction (STEMI) have resulted in dramatic improvement of patient mortality [1]. This improvement provided by serial medical interventions, beginning with first medical contact, has increased in recent years. On the other hand, since short-term mortality in STEMI caused by left main trunk (LMT) lesions remains high, faster diagnosis and medical intervention is required to improve patient survival [2, 3].

Conventional electrocardiography remains the gold standard modality for early diagnosis of STEMI, even in the current advanced diagnostic modality era. The Electrocardiogram (ECG) plays an important role in diagnosis and identification of the location of the culprit infarct artery, and its diagnostic accuracy is reported to be high [4].

However, it is not always easy to confirm that the culprit lesion is an LMT lesion, based only on initial ECG findings; it is especially difficult to distinguish an LMT lesion from a left anterior descending artery (LAD) lesion (Fig. 1). Definition of differences in respective ECG findings of these two lesions may help choose a more appropriate medical intervention strategy and thus improve short term-mortality [5].

To investigate electrocardiographic differences in the initial ECG that may distinguish STEMI due to an LMT lesion from those due to an LAD lesion, electrocardiographic parameters were compared among the following three groups; LMT, proximal LAD, and distal LAD lesions.

To identify electrocardiographic differences allowing distinction of STEMI due to an LMT lesion from that due to an LAD lesion, electrocardiographic parameters were assessed quantitatively. Baseline characteristics among the LMT, pLAD, and dLAD groups are presented in Table 1. Patients in the LMT group were more likely to have hypertension, low hemoglobin, low LDL-cholesterol, low triglyceride, and impaired renal function. Patients in whom hemodynamic instability developed at onset, vital shock and heart failure, constituted a higher proportion in the LMT group than the pLAD and dLAD groups.

The present study investigated electrocardiographic differences in STEMI due to LMT lesions versus STEMI due to LAD lesions, with a view to identification of distinguishing findings between such ECGs. A deep ST-segment depression in the inferior leads with low ST-segment elevation in the precordial leads, and ST-segment depression in V5–6 were distinctive findings in the LMT group as opposed to the proximal and distal LAD groups. A larger magnitude of ST-segment depression in lead II than the magnitude of ST-segment elevation in lead V2, and ST-segment depression in lead V5, suggested low probability of an LAD lesion. These findings were proposed as identifiable distinctive criteria for STEMI due to LMT lesions, and the diagnostic accuracy was equivalent also in patients without concomitant coronary diseases.

Since ECG findings in acute coronary syndromes due to LMT lesions exhibit a number of variations, it is difficult to demonstrate clear characteristics for such findings [8]. The present study population was focused on STEMI to obtain a meaningful result. Moreover, this study demonstrated that approximately 50% of such patients exhibited either RBBB or LBBB, which reflects a broad ischemic area corresponding to the broad dominant area of the myocardium supplied by the LMT. It is well known that such types of block make it difficult to identify the culprit artery in myocardial infarction by ECG. In addition, it is impossible to assess quantitative ST-segment levels, since both types of block prevent definition of the site of the J-point. Some reports on electrocardiographic features in myocardial infarction due to LMT lesions have included patients with bundle branch block [9]. We believe that such patients must be analyzed separately. The identification of ECG criteria for distinguishing LMT lesions suggested by the present study was made possible by the above two points regarding the target population, focusing on STEMI except for the patients with bundle branch block. From this point of view, our new criteria can be regarded as a novel tool that can be used to make rapid determination of LMT lesions by ECG alone.

Hirano et al. suggested that ECGs in LMT infarction can be divided into two patterns: RBBB with left axis deviation or northwest axis, and anteroseptal and lateral infarction appearance (ST-segment elevation in leads V2–5, I, and aVL) [10]. However, the present study demonstrated a wider variety of ECG patterns than in their previously proposed two patterns. This difference may be due to differences in the study population that may have included non-STEMI patients.

The present study demonstrated significant differences in ST-segment deviation between the LMT and LAD groups: (1) ST-segment elevation in lead aVR, (2) magnitude of ST-segment elevation in precordial leads, (3) magnitude of ST-segment depression in inferior leads, and (4) ST-segment depression in leads V5–6. The presence or absence of ischemia in the left circumflex artery is thought to be the cause of these differences. Generally, electrocardiographic features in STEMI due to left circumflex artery lesions are characteristically observed as ST-segment elevation in leads I, aVL, and V5–6, and ST-segment depression in leads V2–5 [11‐16]. However, ST-segment deviation due to an LMT lesion does not consist of simple additions of ST-segment deviation of LAD and that of left circumflex artery; ischemia in the left and right ventricular outflow tract or the basal septum, among other factors, may influence the ECG finding.

ST-segment elevation in lead aVR is the best known ECG finding for assessment of the LMT lesion [17‐20]. Yamaji et al. reported that ST-segment elevation in lead aVR was present in 88% of LMT lesions, but only 43% of LAD lesions [21]. Hence it has been considered to have high sensitivity but low specificity. Although the proportion of ST-segment elevation in lead aVR in the present study cohort was lower in all three groups (64.7% in LMT group, 11.1% in pLAD group, and 4.4% in dLAD group) than that in this prior report, the diagnostic accuracy appeared to be adequate. On the other hand, the diagnostic accuracy of our novel suggested ECG criteria, namely larger magnitude of ST-segment depression in lead II than that of ST-segment elevation in lead V2 and ST-segment depression in lead V5, can be regarded as equivalent to, or more than that in lead aVR; these criteria are particularly excellent in negative predictive value.

The present study suggested that ST-segment depression in lead V5–6 was a distinctive finding in the LMT group. It is a finding associated with ischemia in the apical area. Apical ischemia is determined by several anatomical factors: length of LAD and supply from other arteries such as large obtuse marginal branch or diagonal branch [22]. On the other hand, the magnitude of ST-segment depression in the inferior lead exhibited a significant difference across the three groups, which became gradually smaller in the order LMT > pLAD > dLAD. Although this occurs as a reciprocal change of ST-segment elevation in precordial leads, the above anatomical factors have been reported to be associated with generation of the reciprocal change. Our data agree with prior reports that reciprocal change is rare in distal LAD lesions compared to proximal LAD lesions [23‐25].

The present study demonstrated other differences in findings across the three groups. The magnitude of ST-segment elevation in leads I and aVL has often been reported to exhibit differences in proximal and distal LAD lesions, and such differences are used for identifying these lesions [24]. The present study showed its frequency to be in the order of LMT > pLAD > dLAD (I, 47.1% in LMT, 26.1% in pLAD, 14.5% in dLAD; aVL, 58.8% in LMT, 40.6% in pLAD, 16.4% in dLAD). These findings may be useful in distinguishing between LMT, proximal, and distal LAD lesions.

This study has several limitations. Although the initial ECG was investigated at onset, the time from onset to recording of the ECG varied among patients. There was no comparison of a preceding ECG immediately before STEMI onset included in the analysis, since STEMI is not a scheduled event. Several baseline characteristics differed significantly between the LMT and LAD groups and this may possibly have had an impact on the ECG findings. In addition, the sample size was small.

A larger magnitude of ST-segment depression in lead II than that of ST-segment elevation in lead V2 and ST-segment depression in lead V5 are proposed as identifiable distinctive ECG criteria of STEMI due to LMT lesion.