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Myocardial ischemia may induce myocardial fibrosis, a condition that progressively leads to ventricular remodeling, heightening the risk of heart failure. 68 Ga-FAPI-04 PET/CT shows promise in assessing fibroblast activation in patients with early myocardial infarction characterized by prolonged myocardial ischemia.
A middle aged male with no h/o CAD presented with one week of crescendo exertional angina, and had chest pain at the time of the first ECG: Here is the patient's previous ECG: Here is the patient's presenting ED ECG: There is isolated ST depression in precordial leads, deeper in V2 - V4 than in V5 or V6. There is no ST elevation.
The ECG in the chart was read as "no obvious ST changes," (even though no previous ECG was available) and the formal read by the emergency physicians was: "ST deviation and moderated T-wave abnormality, consider lateral ischemia." When the ischemia is resolved, the wall motion may completely recover, or there may be persistent stunning.
Non-STEMI guidelines call for “urgent/immediate invasive strategy is indicated in patients with NSTE-ACS who have refractory angina or hemodynamic or electrical instability,” regardless of ECG findings.[1] 1] European guidelines add "regardless of biomarkers". But only 6.4% Clin Cardiol 2022 4. Herman, Meyers, Smith et al. McLaren and Smith.
Post by Smith and Meyers Sam Ghali ( [link] ) just asked me (Smith): "Steve, do left main coronary artery *occlusions* (actual ones with transmural ischemia) have ST Depression or ST Elevation in aVR?" That said, complete LM occlusion would be expected to have subepicardial ischemia (STE) in these myocardial territories: STE vector 1.
ST segment elevation in aVR in proximal LAD occlusion before first septal is thought to be due to transmural ischemia of the basal part of the septum. This patient had reported with recent onset angina. Injury current of basal part of septum is directed towards right shoulder and aVR. ST elevation was 2 mm in aVR and 1 mm in V1.
She requires maximal medical management per all current guidelines (including heparin and P2Y12 inhibitor per cardiology), as well as consideration for emergent cath in the case of persistent ischemia. So what will you do for this patient? They found an acute, total, thrombotic occlusion of the proximal LAD. They opened it. Patel et al.,
A middle-aged woman had intermittent angina for 48 hours, then onset of constant, crushing chest pain for 1.5 More likely, the patient had crescendo angina, with REVERSIBLE ischemia for 48 hours that only became potentially irreversible (STEMI) at that point in time. hours when she called 911. 0 0 1 41 238 MMRF 1 1 278 14.0
The stress electrocardiogram is non-diagnostic. The patient did not report angina with stress. This ST-T wave appearance in the lateral chest leads of ECG #2 is consistent with L V “ S train” vs ischemia. No wall motion abnormality at rest. No wall motion abnormality with stress. The ST-T wave picture in lead V 3 is interesting.
BackgroundPainful left bundle branch block (LBBB) syndrome is an uncommon disease that is defined as intermittent episodes of angina associated with simultaneous LBBB changes on an electrocardiogram (ECG) with the absence of flow-limiting coronary artery disease or ischemia on functional testing.
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