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STEMI: Which coronary artery is occluded?

Posted Dec 14 2012 10:33am
This middle aged male with chest pain had this recorded by the medics at t = 0ST elevation in I and aVL and reciprocal ST depression in III, but also with STE in V2, and subtle ST depression in V3 and V4

What artery do you think is occluded?  Answer below.


The medics activated the cath lab prehospital, and then recorded this at t = 8 minutes:
There is now more STE in I and aVL, but also new STE in V3

In the ED, this was recorded at t = 28 minutes:
Now there is STE throughout the precordial leads.


The pattern of ST elevation in I and aVL and V2 (also usually with some ST depression in V3-V5) has been described as a "Midanterolateral MI" (see article below) due to occlusion of the first diagonal (branch of the LAD, also known as D1, or LADD1) artery.  The D1 branches off from the LAD to the lateral wall and may also supply some of the anterior wall.

In this case, as time and ischemia progressed, this became a full anterolateral MI, but the infarct-related artery was indeed a very large LAD D1.  It was rapidly treated and the maximum troponin was low, but there was an anterolateral wall motion abnormality on Echo.

Literature:

Isolated mid-anterior myocardial infarction: a special electrocardiographic sub-type of acute myocardial infarction consisting of ST-elevation in non-consecutive leads and two different morphologic types of ST-depression

Sclarovsky S. International Journal of Cardiology. Volume 46, Issue 1, August 1994, Pages 37–47



Abstract


We describe eight patients with a distinct electrocardiographic pattern of anterior wall myocardial infarction characterized by three main features: (1) a pattern of ‘transmural ischemia’ (ST-elevation with positive T-wave) in nonconsecutive leads: aVL and V2, and two different types of ST-depression; (2) a pattern of ‘true reciprocal changes’ (ST-depression and negative T-wave) in III and aVF; (3) a pattern of ‘sub-endocardial ischemia’ (ST-depression with positive T-wave) in V4–5, while ST in V3 was either isoelectric or depressed. We characterize the electrocardiographic features and correlate them with the echocardiographic, radionuclide, and angiographic data. All patients admitted to the coronary care unit from January 1990 to April 1992 with evolving acute myocardial infarction were evaluated prospectively. Patients whose admission electrocardiogram met the description above were included. The electrocardiographic evolution, echocardiographic, Technetium MIBI tomography, and coronary angiography are described. Of 471 patients with acute anterior wall myocardial infarction, admitted to the coronary care unit during the study period, eight patients met the inclusion criteria (1.7% of acute anterior wall myocardial infarction). Echocardiographyic studies revealed mid-anterior hypokinesis in two patients, anterior and apical hypokinesis in one, and no wall motion abnormality in four patients. Technetium MIBI tomography, done in five patients, was consistent with mid-anterior or mid-anterolateral infarction without involvement of the septum or apex. Coronary angiography, performed in seven patients, demonstrated significant obstruction of the first diagonal branch in all of the patients. In four patients, the diagonal occlusion was the only significant coronary lesion in the left coronary artery. Conclusion: Most of the anterior myocardial infarctions also involve the septal and apical regions. Anterior wall myocardial infarctions limited to the mid-anterior or mid-anterolateral wall, without apical or septal wall involvement are relatively rare. This study describes a special electrocardiographic form of anterior wall acute myocardial infarction. This distinct electrocardiographic pattern represents true mid-anterior wall myocardial infarction, caused by occlusion of a first diagonal branch of the left anterior descending coronary artery. The septal and apical regions are not involved because the blood supply via the left anterior descending artery is not interrupted.





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