Improving the Diagnosis of Culprit Left Circumflex Occlusion With Acute Myocardial Infarction in Patients With a Nondiagnostic 12-Lead ECG at Presentation: A Retrospective Cohort Study

Abstract

Background Left circumflex culprit is often missed by the standard 12-lead ECG . Extended lead systems (body surface potential map [ BSPM ]) should improve the diagnosis of culprit left circumflex stenosis with myocardial infarction. Methods and Results Retrospective analysis of a hospital research registry (August 2000-August 2010) comprising consecutive patients with (1) ischemic-type chest pain at rest; (2) 12-lead ECG and 80-lead BSPM at first medical contact; and (3) cardiac troponin-T 12 hours after symptom onset and/or creatine kinase MB fraction, were undertaken. Enrolled in the cohort were patients with culprit left circumflex stenosis (thrombolysis in myocardial infarction flow grade 0/1) at angiography. Acute myocardial infarction AMI was defined as cardiac troponin-T ≥0.1 μg/L and/or creatine kinase MB fraction >2 upper limits of normal. Enrolled were 482 patients: 168 had exclusion criteria. Of the remaining 314 (age 64±11 years; 62% male), 254 (81%) had AMI : of these, 231 had BSPM STE -sensitivity 0.91, specificity 0.72, positive predictive value 0.93, negative predictive value 0.65, and c-statistic 0.803 for AMI ( P<0.001). Of those with BSPM STE and AMI (n=231), STE was most frequently detected in the posterior (n=111, 48%), lateral (n=53, 23%), inferior (n=39, 17%), and right ventricular (n=21, 9%) territories. Conclusions Among patients with 12-lead ECG non-ST-segment-elevation myocardial infarction and culprit left circumflex stenosis, initial BSPM identifies ST-segment elevation beyond the territory of the 12-lead ECG . Greater use of the BSPM may result in earlier identification of AMI , which may lead to more rapid reperfusion.

Keywords: acute coronary occlusion; acute myocardial infarction; body surface potential mapping; left circumflex artery.

Figure 1

Patient enrollment methodology. AMI indicates acute myocardial infarction; BSPM, body surface potential map; STEMI, ST‐segment–elevation myocardial infarction.

Figure 2

Schematic of the 80‐lead body surface potential map electrode positions.

Figure 3

Case example (A) 12‐lead ECG showing minimal lateral territory ST‐segment sagging (V₅–V₆) with T‐wave inversion in lead aVL; (B) ST0 isopotential BSPM showing high right anterior and posterior STE (red maxima 1.38 mm)13; and (C) coronary angiogram showing distal LCx stenosis (red arrow). BSPM indicates body surface potential map; LCx, left circumflex artery; STE, ST‐segment elevation.

Figure 4

Case example (A) 12‐lead ECG showing 0.05 mV STD in leads V₃ to V₅ and T‐wave inversion in lead III and V₁ to V₄; (B) ST0 isopotential BSPM showing (i) anterior territory minima (blue) (−1.68 mm) and (ii) right ventricular and posterior maxima (red) (1.07 mm); and (C) coronary angiogram showing culprit occlusion of the proximal LCx, with 60% to 70% stenoses in both the distal LMS and proximal LAD. BSPM indicates body surface potential map; LAD, left anterior descending artery; LCx, left circumflex artery; LMS, left main‐stem artery; STD, ST‐segment depression.