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Discussion Starter · #1 ·
A 68 year old female with a history of hypertension and diabetes presents with chest pains intermittently for 4 days and now significantly worse acute onset shortness of breath. Her temperature is 37.1, blood pressure 85/65, heart rate 110, respirations 24, and oxygen saturation 79% on room air. Physical examination reveals diffuse pulmonary rales, a II/VI holosystolic murmur at the cardiac apex radiating to the axilla, and elevated jugular venous pressure. A Swan-Ganz catheter is inserted and the pulmonary capillary wedge pressure tracing shows large V waves. Her ECG shows significant ST segment elevation. Which of the following coronary arteries is the most likely culprit?

A) Left main coronary artery
B) Left anterior descending coronary artery
C) Left circumflex coronary artery
D) Right coronary artery

Waiting for your answers people!!!
 

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Massive MI

This lady seems to have developed acute heart failure due to papillary muscle rupture due to massive myocardial infarction.
The papillary muscle rupture has caused mitral regurgitation (holosystolic murmur radiating to the axilla).

I'd pick the left main coronary artery as the culprit :notsure:
 

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It is important to note that there are five papillary muscles of which 3 are in the right ventricle and 2 in the left.

Since this pt has signs of mitral regurgitation we can assume that he has L pap muscles that are dysfunctioning (not ruptured in acute ischemia but only in endocarditis or late-phase ischemia).

We are lucky because the anterior muscles receives "dual" supply from LAD and CFX. However the posterior has only the PDA to get his oxygen - thus more susceptible to ischemic damage!

So, in this case I would pick PDA which is a branch of the right coronary artery (in 70% of people who happen to have a "right-dominant circulation) or the CFX in "left-dominant" (20%) or both in "co-dominant"(10%).
 

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Discussion Starter · #5 ·
correct answer and explanation!

Answer: D - Right coronary artery
This patient has acute mitral valve regurgitation resulting in pulmonary edema and cardiogenic shock. Remember that the posteromedial palpillary muscle receives its sole blood supply from the right coronary artery, thus thrombosis of this vessel can completely disrupt this papillary muscle's function resulting in severe mitral regurgitation and even palpillary muscle rupture (as in our case which occurs a few days after the infarction). Treatment is emergent surgical repair. The anteromedial palpillary muscle has dual blood supply from the left anterior descending and left circumflex coronary artery, thus thrombosus of those vessels do not result in mitral regurgitation. The large V waves on the pulmonary capillary wedge tracing (which represents left atrial pressure) indicates backflow of blood from the left ventricle to the atrium. The murmur that our patient has is also typical for mitral regurgitation.
 
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