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At the hospital, left main coronary-artery stenosis was seen on angiography (shown in a video). In a 57-year-old man with chest pain, an ECG obtained by EMS showed widespread ST-segment depressions.
His confusion progressively dissipated enroute to the hospital. Many of the changes seen are reminiscent of LVH with “strain,” and downstream Echo may very well corroborate such a suspicion, but since the ECG isn’t the best tool for definitively establishing the presence of LVH, we must favor a subendocardial ischemia pattern, instead.
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?
He is a Professor of Radiology and prior to joining Cleerly full-time, served as Vice-Chairman of Radiology at George Washington University (GWU) Hospital in Washington, DC. High Diagnostic Accuracy Of AI-Ischemia in Comparison To PET, FFR-CT, SPECT, and Invasive FFR: A PACIFIC Sub-Study. In Press European Heart Journal CV Imag 2024.This
A transthoracic echocardiogram showed an LV EF of less than 15%, critically severe aortic stenosis , severe LVH , and a small LV cavity. The aortic valve in this example also had critical stenosis by Doppler The patient continued to be hemodynamically unstable with poor cardiac output and very high LV filling pressures.
The patient had a critical LAD stenosis. When flow is restored, wall motion may completely recover so that echocardiogram does not detect the previous ischemia. Tight proximal LAD stenosis explains STE in precordial leads and I and aVL. All troponins were u ndetectable (less than 0.04 He underwent CABG. Conclusions: 1.
Again, it is common to have an ECG that shows apparent subendocardial ischemia after resuscitation from cardiac arrest, after defibrillation, and after cardioversion. and repeat the ECG, to see if the apparent ischemia persists. A third ECG was done about 25 minutes after the first: This shows resolution of all apparent ischemia.
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.
This suggests further severe ischemia. Even in patients whose moderate stenosis undergoes thrombosis, most angiograms show greater than 50% stenosis after the event. However, one can certainly imagine that many thromboses of non-obstructive lesions completely lyse and do not leave a stenosis on same day or next day angiogram.
On hospital day 3, the patient had recurrence of symptoms and the following EKG was obtained. This proves effective treatment of the recurrent ischemia. The patient had no further symptoms of ischemia. EKG 3 is diagnostic for developing re-occlusion, and EKG 4 proves that the nitrates relieved the 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?
Transcatheter aortic valve replacement (TAVR) is increasing in popularity for symptomatic severe aortic stenosis. Trans brachiocephalic approach patients had shorter mean procedure time and lower blood loss and shorter duration of hospitalization. No calcifications in the artery causing vascular stenosis.
STE limited to aVR is due to diffuse subendocardial ischemia, but what of STE in both aVR and V1? The additional ST Elevation in V1 is not usually seen with diffuse subendocardial ischemia, and suggests that something else, like STEMI from LAD occlusion, could be present. Was this: 1) ACS with ischemia and spontaneous reperfusion?
He was admitted to the hospital for evaluation of these symptoms — but no ECG was done at that time. The patient’s angiogram should have been expedited, but the EKG change was not recognized as recurrence of transmural ischemia. The red arrow points to a 90% stenosis in the proximal segment of the LAD.
Down-up T-waves in inferior leads are almost always reciprocal to ischemia in the territory underlying aVL. This is not normal and is a tip off that there is posterior ischemia accompanying the ischemia in aVL. Data from stress testing proves that the ST depression of ischemia does not localize. Culprit, stented) 3.
Background:Myocardial infarction with nonobstructive coronary artery disease (MINOCA) is a special syndrome with clear evidence of myocardial ischemia, but no clear stenosis of coronary artery imaging sign. Circulation, Volume 150, Issue Suppl_1 , Page A4143007-A4143007, November 12, 2024.
Whether these EKGs show myocarditis, a normal variant, or something else, they are overall not typical of transmural ischemia of the anterior or high lateral walls. Angiography revealed a 30% nonobstructive stenosis of the mid LAD. Patient 1 remained in the hospital overnight. The patient had none of these conditions.
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.
Another ECG was recorded 5 minutes later just before arrival at the hospital: Similar The patient was transported to a nearby suburban hospital with PCI capabilities while my partner cared for her. These findings are diagnostic of an apical OMI as a result of LAD Occlusion. She was defibrillated and resuscitated. Learning Points: 1.
The culprit lesion was a complex calcified mid LAD stenosis involving the first and second diagonal branches. Smith : the profound persistent STE suggests either persistent occlusion or " no reflow " with persistent downstream ischemia. In the first year since discharge, he has been hospitalized 3 times with CHF.
Cath at approximately 0945: "The LAD had a 90% proximal stenosis with TIMI 3 flow which corresponds to his ECG although LV function remains preserved. With nitroglycerin there is improvement in the 90% stenosis but still persistent stenosis consistent with the dynamic nature of his presentation. Is this Acute Ischemia?
Low LV filling pressures are due to several etiologies, most commonly due to volume depletion (dehydration or hemorrhage), but also due to other etiologies including, but not limited to: mitral stenosis, pulmonary hypertension (chronic, or due to pulmonary embolism), or poor RV performance.
Ischemic ST-Segment Depression Maximal in V1-V4 (Versus V5-V6) of Any Amplitude Is Specific for Occlusion Myocardial Infarction (Versus Nonocclusive Ischemia). 90% stenosis of the proximal ramus intermedius, pre procedure TIMI II flow The ramus intermedius is a normal variant on coronary anatomy that arises between the LAD and LCX.
Case 4 Transient STEMI, serial ECGs prehospital to hospital, all troponins negative (less than 0.04 Angiogram showed a critical LAD thrombotic stenosis. The patient went to cath and had a distal LAD 99% stenosis with thrombus and TIMI-2 flow. This makes it almost certain that the ST elevation on the first one is due to ischemia.
The first task when assessing a wide complex QRS for ischemia is to identify the end of the QRS. The ST segment changes are compatible with severe subendocardial ischemia which can be caused by type I MI from ACS or potentially from type II MI (non-obstructive coronary artery disease with supply/demand mismatch). What do you think?
Angiography : LMCA — 90-99% osteal stenosis. LCx — 50-69% stenosis of the 1st marginal branch; with 100% distal LCx occlusion. The patient was extubated on Day-3 of the hospital stay. The patient improved, and on Day-11 of the hospital stay — he was off inotropes and on a small dose of a ß-blocker.
Part of the ST depression with deep T wave inversion in the lateral chest leads clearly reflects LV "strain" from the marked LVH — but despite the very large QRS amplitudes, this ST-T wave appearance looks disproportionate, suggesting at least a component of ischemia. Cardiac Cath showed patent coronary arteries!
Angiogram around 9am: Culprit lesion mid LAD 100% stenosis TIMI 0 TIMI 3 after PCI Severe apical dyskinesis, severe anteroapical akinesis. Instead, pain is numbed and thus ischemia is obscured with opioids, excuses like hypertension are blamed, and unnecessary CT pulmonary angiograms are focused on. None further were ordered.
We performed this analysis to identify the prevalence of atrial fibrillation and associated outcomes in symptomatic internal carotid artery stenosis patients undergoing CAS or CEA.Methods:We analyzed the data from the National inpatient sample (NIS) between January 2016 to December 2021. versus 8.7%, p=0.41) and discharge home (32.4%
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.
Written by Pendell Meyers, edits by Steve Smith A man in his 60s with history of hypertension and MI 10 years ago, with PCI, presented to an outside hospital complaining of chest pain that started while mowing the lawn. His chest pain was located in the central chest, non-radiating, and associated with diaphoresis, nausea, and vomiting.
RCA ischemia often results in sinus bradycardia from vagal reflex or ischemia of the sinus node. He was taken to the cath lab and underwent emergent intervention: Thrombotic stenosis of the proximal RCA (95% with evidence of plaque rupture) is the culprit for the patient's inferoposterior STEMI. He was successfully stented.
Marked differences can be seen in the prevalence of coronary artery stenosis at autopsy by age and gender. In 30-39 year old women the rate of coronary stenosis at autopsy was 5/1,545 (0.3%) while 60-69 year old men had a prevalence of 12%, almost 40 times higher. The results of this dataset by age and gender follow. This happens.
Meschia’s lecture, “Asymptomatic Carotid Stenosis: Current and Future Considerations,” will be presented Feb. and Phyllis Gough Huffington Distinguished Chair of Neurology at McGovern Medical School; chief of neurology at Memorial Hermann Hospital-Texas Medical Center and co-director of UTHealth Neurosciences , all in Houston.
We evaluated the primary outcome (cardiovascular death, myocardial infarction, or hospitalization for unstable angina, heart failure, or resuscitated cardiac arrest) and other end points, by sex, in 1168 (22.6%) women and 4011 (77.4%) men. of invasive‐assigned men, and no ≥50% stenosis in 12.3% of invasive‐assigned men;P<0.001).
Aortic Dissection, Valvular (especially Aortic Stenosis), Tamponade. Evidence of acute ischemia (may be subtle) vii. heart auscultation (aortic stenosis); c. Clinical predictors of cardiac syncope at initial evaluation in patients referred urgently to general hospital: the EGSYS score. Left BBB vi. LVH or RV d.
Cardiology services were consulted at a PCI capable hospital. The patient was started on heparin for possible NSTEMI vs demand ischemia. Smith : "decompensation" of aortic stenosis might have initiated this entire cascade. Smith : "decompensation" of aortic stenosis might have initiated this entire cascade.
He works in a small hospital in Northern Michigan. The patient was transferred to a hospital with PCI capability. Here is the angiogram: Very tight stenosis in circumflex, but with TIMI-3 flow, thanks to thrombolytics. This case was sent by an old residency friend, Kirk Lufkin. Case A 61 year old female. No cardiac past history.
August 2024 Approvals Minima Stent System (P240003) (Approval Date: August 28, 2024) The Minima Stent System is an expandable cobalt-chromium metal mesh tube to reopen blood vessels in neonates, infants, and children with Coarctation of the Aorta and Pulmonary Artery Stenosis, specifically designed to expand as younger patients grow.
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