Slide 1: 83-year-old male presents to the ED with exertional chest pain. On exam he appears unwell, is volume overloaded, and you hear a murmur. Troponin-T is 0.04 ng/mL. What does the EKG show?

Slide 2: EKG with arrows pointing to inferior STDs, 1-2 mm STE in aVR, R in aVL (>11 mm = LVH), and lateral STDs with TWIs. What is you differential diagnosis?

Slide 3: STE in aVR plus diffuse STDs. Global ischemia. Coronary causes include left main occlusion, proximal LAD occlusion, and severe triple vessel disease. Non-coronary causes include hypoxia, hypotension, anemia, and severe aortic stenosis. Note non-coronary causes: diffuse sub-endocardial ischemia 2/2/ supply-demand mismatch.

Slide 4: Returning to our case…

STE in aVR and signs of global ischemia plus chest pain with evidence of heart failure suggests active ischemia. Cardiology consult for possible urgent angiography. Coronary angiography showed non-occlusive coronary arteries. What’s the likely diagnosis?

Slide 5: TTE confirms global ischemia from severe AS. Increasing LV afterload from severe AS causes LVH and diastolic dysfunction, raising intra-cardiac pressures.

Decreased CPP. Elevated intra-cardiac pressures reduce the pressure gradient for coronary perfusion, so perfusion decreases.

Any subsequent cardiac stress (eg. tachycardia, volume, catecholamines) precipitates supply-demand mismatch, angina, and ECG with global ischemia. Graph showing oxygen demand on the y-axis and heart rate/stress on the x-axis. Two lines on the graph showing that as mild diastolic dysfunction is worsened to severe diastolic dysfunction, the angina threshold is crossed at a lower heart rate/stress. The line for severe diastolic dysfunction has a steeper slope than the line for mild diastolic dysfunction.


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