Electrocardiographic Localization of the Occlusion Site in Left  Anterior Descending Coronary Artery in Acute Anterior
Myocardial Infarction

Methods and Results: The study included 50 patients with a first acute anterior myocardial infarction. The electrocardiogram with the most pronounced ST segment deviation before the start of reperfusion therapy was evaluated and correlated with the left anterior descending occlusion site as determined by coronary angiography. ST segment elevation in lead aVR, ST segment depression in lead V₅ and ST segment elevation in V₁>2.5 mm strongly predicted left anterior descending occlusion proximal to first septal, whereas abnormal Q wave in V_4-6 was associated with occlusion distal to first septal. Abnormal Q wave in lead aVL was associated with occlusion proximal to first diagonal, whereas ST depression in lead aVL was suggestive of occlusion distal to first diagonal branch. For both first septal and first diagonal, ST segment depression ≥1 mm in inferior leads strongly predicted proximal left anterior descending artery occlusion, whereas absence of ST segment depression in inferior leads predicted occlusion distal to first septal and first diagonal. All the patients were followed during their in-hospital stay (median of 7 days), during which four patients in the proximal to first septal and first diagonal group and one patient in the distal to first septal and first diagonal group died (p ≤ 0.001).

Coronary angiography: All the patients underwent coronary angiogram within three days of acute MI. Four patients underwent coronary angiogram and primary angioplasty during the acute phase. The culprit lesion in LAD was defined as the one causing the most severe stenosis and its location in relation to S₁ and D₁ was noted. Flow over the culprit lesion was graded using the Thrombolysis in acute Myocardial Infarction (TIMI) criteria.

Electrocardiography: In the acute phase, the ECG with the most pronounced ST segment deviation before the start of reperfusion therapy was evaluated. TP segment was used as the isoelectric line. The PR segment was used when T and P waves merged. Using manual Vernier Calliper, ST segment deviation was measured at the ‘J’ point in all the leads. Besides ST segment deviation, the incidence of complete right bundle branch block (cRBBB) and abnormal Q waves were assessed.

Statistical analysis: Data were expressed as median plus minimum and maximum for continuous variables and as rates (%) for categorical variables. Sensitivity, specificity, positive predictive value and negative predictive value were determined for each variable. Statistical significance was assessed by students t test and a p value < 0.05 was taken as statistically significant.

Results

The first diagonal (D₁) may arise from LAD either proximal to first septal perforator (S₁) or distal to it. The culprit lesion was proximal to S₁ in 24 patients, distal to S₁ in 26 patients, proximal to D₁ in 28 patients and distal to D₁ in 22 patients.For correlation with ECG, patients were divided into those with LAD occlusion proximal (n=24) or distal to S₁ (n=26) and later in the same group of patients either proximal (n=28) or distal (n=22) to D₁(Table 2).
Demographic and clinical data: The baseline characteristics of the patients and the subgroups were comparable with respect to gender, mean age, time to ECG from the onset of chest pain (Table 2).
Coronary angiography: None of the patients had triple vessel disease. Between proximal and distal lesions, there was no difference regarding the presence of single or two-vessel disease. There were no cases of left main stenosis. There was no significant difference in TIMI flow. Angiographic signs of thrombus were present in four patients.

Electrocardiographic predictors (Table 3):
ECG predictors of LAD occlusion proximal to S₁: ST in aVR was present in 12 patients (50%) with occlusion proximal to S₁ and in none of the occlusion distal to S₁. It was 100% specific for occlusion proximal to S₁ and only 50% sensitive. The amount of ST in aVR was small, the median being 0.5 (0.5-1.0).

ST in inferior leads was predictive of LAD occlusion proximal to S₁ with a sensitivity of 85% and a specificity of 91%. Complete RBBB was not seen in any of our patients; 13 patients (53%) with occlusion proximal to S₁ had ST segment elevation in V₁ >2.5 mm versus 8 patients (30%) with occlusion distal to S₁. ST in V₁ >2.5 mm was 71% sensitive and 66% specific in predicting LAD lesion proximal to S₁. ST segment depression in lead V₅ was very specific (100%) for LAD occlusion proximal to S₁ but was not sensitive (8%). It was present in one patient (4%) with proximal to S₁ occlusion and in none with distal to S₁ occlusion.

ECG predictors of LAD occlusion proximal to D₁:ST segment depression in leads II, III and aVF was present in 21 patients (75%) with occlusion proximal to D₁ and in 2 patients (10%) with distal occlusion. Inferior leads ST≥1 mm was highly predictive of LAD occlusion proximal to D₁. An abnormal Q wave in lead aVL (Q aVL width ≥30 ms) was more frequent in LAD occlusion proximal to D₁ in comparison with distal to D₁ occlusion (21 v. 3 patients). It was 90% specific for LAD occlusion proximal to D₁, but was only 66% sensitive.

ECG predictors of LAD occlusion distal to S₁:Absence of ST segment depression in inferior leads was strongly predictive of LAD disease distal to S₁. Q wave in lead V₄ (width ≥20 msec), V₅ and V₆ (width ≥30 msec)⁵ was specific for LAD occlusion distal to S₁; in 22 patients it was found with occlusion distal to S₁ and only in 4 patients with proximal to S₁ occlusions. It was 88% specific and 25% sensitive for LAD occlusion distal to S₁.

ECG predictors of LAD occlusion distal to D₁:Absence of ST segment depression in inferior leads was also strongly related to LAD disease distal to D₁. ST segment depression in aVL was seen in one patient with occlusion distal to D₁ but none in proximal to D₁ occlusion. It was very specific (100%) for occlusion distal to D₁, but was not very sensitive (10%).

In-hospital outcome: All patients were followed up during their in-hospital stay. The median duration of stay in the hospital was 7 days (range 5-10 days). Among these 50 patients, 4 patients with lesion proximal to S₁ and D₁ died and one patient with lesion distal to S₁ and D₁ died (p<0.001).

Discussion

Several ECG findings help to localize the occlusion site of the LAD coronary artery with respect to its major branches.

ST segment elevation in lead aVR was found to be very useful to identify LAD occlusion proximal to S₁. Besides ST in aVR, ST in V₁>2.5mm and ST in V₅ were also strongly predictive of occlusion proximal to S₁. However cRBBB, which was earlier reported to be a marker of occlusion proximal to S₁,⁴ was not seen in the present study. Abnormal Q waves in V₄ through V₆ were indicative of occlusion distal to S₁.

The abnormal Q waves in lead aVL were predictive of occlusion proximal to D₁, whereas ST segment depression in the same lead was indicative of occlusion distal to D₁. For both S₁ and D₁, marked ST segment depression in inferior leads predicted proximal occlusion, whereas absence of inferior ST segment depression predicted distal occlusion.

ST elevation in lead aVR: STin aVR in left main lesion has been previously reported.⁶ Kataoka et al.⁷ found that in anterior acute MI, ST in the right precordial leads was associated with LAD occlusion proximal to S₁. Any ST in aVR is associated with LAD occlusion proximal to S₁ and is probably the result of transmural ischemia of the basal part of the septum.⁴ Engelen et al.⁴ have observed a similar pattern in 43% of patients in their series. In our series it was seen in 50% of the patients, which is comparable.

ST deviation in lead II, III and/or aVF: ST≥1 mm was highly suggestive of proximal LAD lesion. This finding is consistent with previous studies on inferior lead ST in anterior MI.^8,9 Inferior ST was not associated with disease in right coronary artery. This supports the theory that the inferior ST in anterior MI represents reciprocal changes.^10,11

ST deviation in lead aVL: ST in the lateral leads did not discriminate between occlusions proximal and distal to D₁. ST aVL was very specific (100%) for LAD occlusion distal to D₁. Its sensitivity was very low (10%).

ST deviation in leads V₁-V₆: Analyzing ST deviation in lead V₁ through V₆, ST in V₁>2.5 mm was the only ECG parameter that could be defined to discriminate between proximal and distal LAD occlusion in the individual patient. ST V₅ appeared to be very specific for LAD occlusions proximal to S₁.

Complete right bundle branch block: cRBBB has been reported to represent LAD occlusion proximal to S₁.⁴ As S₁ is the main source of blood supply to distal part of His bundle and the proximal bundle branches, the cRBBB is most likely to occur in the setting of acute MI. However we did not find any cRBBB in our study and this may be due to the small sample size.

Abnormal Q waves: In lead V₄-V₆, Q waves were specific (88%) for LAD disease distal to S₁. In case of myocardial necrosis beneath the anteroseptal leads, the septal vector in V₅ and V₆ will facilitate Q wave formation in those electrodes. In contrast, in proximal to S₁ occlusion the septal vector will decrease or even disappear and thereby hinder Q wave formation.

⁴ In-hospital outcome: All five patients who died had single vessel disease. Four patients had proximal LAD occlusion before S₁ and severe LV dysfunction. One patient in the distal group had occlusion distal to S₁ with mild LV dysfunction, and died due to intractable ventricular tachycardia.

Study limitations: One limitation of our study is a small number of patients included non-consecutively; hence specific conclusions cannot be drawn. Sample size of patients with multivessel disease is too small to draw any definite conclusions regarding its impact on ECG findings. Larger prospective studies are therefore required to clarify the impact of multivessel disease and interventions.

Conclusions: In acute anterior MI, ECG is useful to predict the LAD occlusion site in relation to its major side branches. Such localization may help to adopt a more aggressive approach to revascularization in the proximal LAD occlusion, to prevent extensive myocardial damage resulting in pump failure

Correspondence:
Dr CN Manjunath,
Professor of Cardiology,
Sri Jayadeva Institute of Cardiology,
Bannerghatta Road,
Jayanagar,
9th Block,
Bangalore 560069.
e-mail: karthik_vasudevan@yahoo.com

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