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Patient
57-year-old man, obese, smoker, hypercholesterolemic, with a family history of coronary heart disease, hospitalized for constrictive chest pain since 3 hours;
Trace
Sinus rhythm, normal PR interval; discrete elevation in the high lateral territory (leads I, aVL) with minimal reciprocal depression in lead III; in this patient with many risk factors and with typical chest pain, emergency coronary angiography was proposed in spite of limited electrocardiographic changes; this examination revealed an occlusion of a dominant circumflex artery;
Patient
78-year-old man with no prior history, hospitalized for chest pain at H + 5;
Trace
Sinus rhythm, normal PR interval; poor R wave progression from V1 to V4 with Q-wave in leads I, aVL; wide amplitude elevation in the anterior territory (V2 to V5) and lateral territory (leads I, aVL); anterolateral infarction corresponding to a proximal LAD thrombosis;
Exergue
The diagnosis of lateral infarction is straightforward when it is part of an extensive myocardial disease (anterolateral or posterolateral) but can be much more difficult when isolated with often an elevation of very low amplitude in leads I and aVL.
The left ventricular lateral wall is supplied by branches from the LAD and circumflex arteries. On the ECG, a lateral infarction can be analyzed from the high lateral (leads I, aVL) and low lateral leads (V5-V6). There are generally three types of lateral infarctions: