Widowmaker
We recently ran an early morning 911 call for chest pain. Upon arrival we encountered a 69 year-old male who stated that he had intense pressure-like pain rated 10 of 10 that began after minor exertion. His wife administered 325 mg of aspirin and called 911 as soon as the symptoms were reported. The patient reported no significant medical history.
The initial 12 lead EKG is seen here. There are ST elevations noted in V1, V2, V3, AVL, and Lead I. Notable ST depressions are seen in all the inferior leads (II, III, AVF) as well as the precordial lateral leads (V5 and V6).
This evidence indicates an acute infarction with widespread consequences. The involvement of V1-V3 indicates anteroseptal damage. The addition of AVL and Lead I indicate damage that extends to the lateral left ventricle. Anteroseptal STEMI’s are caused by an occlusion of the artery that supplies this part of the heart with perfusion, namely the left anterior descending artery (LAD). Lateral STEMI’s are caused by an occlusion of the circumflex artery that wraps around the left lateral wall of the left ventricle.
Since this patient shows evidence of simultaneous occlusion of two different arteries, the LAD and circumflex, we have to decide whether this is a poorly timed coincidence or if the two arteries are linked in some way. Looking at the anatomy of the cardiac arteries, you can see that the arteries are linked in that they both stem from the main stem of the left coronary artery (LCA).
Occlusions of the proximal LAD that interrupt blood flow to the intraventricular septal wall, anterior left ventricle and lateral left ventricle are devastating events. This type of MI is often called the widowmaker. Aside from the fact that the occlusion deprives a huge part of the myocardium from perfusion you have the complications associated with damage to the intraventricular septum.
If you get a chance one day to raise your hand and pick your heart attack, don’t pick the septal one. Within the wall of the ventricular septum lies the AV node, the Bundle of His and the proximal origins of both the right and left bundle branches. This is the core processing unit for your ventricles’ electrical stimulation center. Damage to these structures can cause profound and deadly disruptions to electrical stimulation of the ventricles.
With any MI involving the septum (V1, V2), closely monitor your patient’s EKG for dire signs such as sudden axis shift, widening of the QRS, or new onset of bundle branch blocks. Seeing these events in the context of a septal MI is seeing the patient electrical conduction system coming apart right before your eyes. These patients are statistically more likely to present with sudden cardiac arrest with their MI event. As a matter of fact, the first cardiac symptom for some patients with septal infarction is death!
Definitive treatment for anteroseptal, anterolateral, or combination infarctions includes recognition with assessment, 12 lead confirmation, labs to evaluate electrolyte levels and cardiac biomarkers and early involvement with cardiology consultation. The arterial occlusion is best addressed in the cardiac catheterization suite. Supportive therapy and early intervention should include consideration of aspirin, oxygen, nitrates, and morphine, but none of these treatments should delay access to percutaneous cardiac intervention (PCI).
This patient benefitted from the outstanding cardiac care between the local EMS and hospital organizations and received immediate access to the PCI lab where they opened his occlusion with 4 stents. The patient rolled to recovery laughing and joking with the PCI staff.
