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Post cath ECG: Now there are hyperacute T-waves again, and recurrent ST depression in V2 This ECG would normally diagnostic of OMI until proven otherwise No further troponins were measured, but it looks like there is recurrent OMI Next day: A CT CoronaryAngiogram was done (CTCA) CARDIAC MORPHOLOGY AND FUNCTION: 1. IMPRESSION: 1.
This EKG is diagnostic of transmural ischemia of the inferior wall. If it is angina, lowering the BP with IV Nitroglycerine may completely alleviate the pain and the (unseen) ECG ischemia. Or is it a very tight stenosis that does not allow enough flow to perfuse myocardium that has a high oxygen demand from severely elevated BP?
The diagnostic coronaryangiogram identified only minimal coronary artery disease, but there was a severely calcified, ‘immobile’ aortic valve. Aortic angiogram did not reveal aortic dissection. The patient was brought directly to the cardiac catheterization lab for PCI, bypassing the ED.
It should be known that each category can easily manifest the generic subendocardial ischemia pattern. In general, subendocardial ischemia is a consequence of global supply-demand mismatch that usually ameliorates upon addressing, and mitigating, the underlying cause. What’s interesting is that the ECG can only detect ischemia.
His response: “subendocardial ischemia. History sounds concerning for ACS (could be critical stenosis, triple vessel), but differential also includes dissection, GI bleed, etc. Smith : It should be noted that, in subendocardial ischemia, in contrast to OMI, absence of wall motion abnormality is common. Anything more on history?
There is ventricular hypertrophy in the absence of abnormal loading conditions, such as aortic stenosis, or hypertension, for example – of which the most common variant is Asymmetric Septal Hypertrophy. There is LBBB-like morphology with persistent patterns of subendocardial ischemia.
There is appreciable STE aVR with near-global STD that appropriately maximizes in Leads II and V5, and thus suggesting a circumstance of generic, diffusely populated, circumferential subendocardial ischemia versus occlusive coronary thrombus. [1] It’s judicious, then, to arrange for coronaryangiogram.
The patient has also developed sinus bradycardia, which may result from right coronary artery ischemia to the SA node. During angiogram in the cath lab, the patient suffered two episodes of ventricular fibrillation for which he was successfully defibrillated. Two stents were placed with resultant TIMI 3 flow.
Diamond and Forrester accomplished this by first establishing the prevalence of coronary artery disease based on how clinically likely patients with chest pain symptoms were found to have coronary disease based on a coronaryangiogram. The results of this dataset by age and gender follow. This happens. But its rare!
The patient was started on heparin for possible NSTEMI vs demand ischemia. Smith : "decompensation" of aortic stenosis might have initiated this entire cascade. What "initiates" the aortic stenosis cascade? increasing stenosis, ischemia, volume changes, increased blood pressure, atrial fibrillation, etc.)
It is not clear by her note what she meant by this (whether or not she recognized this EKG as diagnostic of transmural ischemia, and if so, of what territory) but emergent reperfusion therapy was not pursued. Subendocardial ischemia does not localize. At 1022, a troponin I (ref range <0.034 ng/mL) resulted at 4.437 ng/mL.
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