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Compensatory enlargement was defined as being present when the total coronary arterial cross-sectional area at the stenotic site was greater than that at the proximal nonstenotic site. Thus, the lumen observed may actually still be the same size as the original, normal lumen. Unfortunately, vascular remodeling is variable and inconsistent.
There is increased LV cavity dimensions with an increase in transient ischemic dilation, suggesting Left Main, or 3-vessel coronary artery disease. 2. Coronary angiography reveals significant and severe CAD involving all three epicardial vessels. He awoke earlier that morning in his usual state of health. Type I ischemia.
Jesse McLaren on when to consider Spontaneous Coronary Artery Dissection (SCAD), which patients are at risk for reocclusion, and the challenges of diagnosing SCAD in patients who have nonischemic ECGs despite silent occlusion, occlusions perfused by collaterals, or from non-occlusive MI on this ECG Cases.
Intermediate-risk patients may be further stratified based on recent stress testing or coronary angiogram findings plus a modified HEART or Emergency Department Assessment of Chest Pain (EDACS) score. Encourage your ED to set up an algorithm that you can follow based on your laboratory’s assay. She does not smoke.
Note that as many as 7% of patients with acute coronary syndrome have chest pain reproducible on palpation [Lee, Solomon]. which reduces the pre-test probability of acute coronary syndrome by less than 30% [McGee]. Chest pain reproducible on palpation does not rule out acute coronary syndrome. Guagliumi, G., Iwaoka, R.
The patient has no specific risk factors for acute coronary syndrome (ACS) or dissection. Case: You are working a busy shift in a rural emergency department (ED) and your excellent Family Medicine trainee presents a case of a 63-year-old woman with chest pain and some intermittent radiation into the inter-scapular region.
Major adverse cardiac event rates in moderate-risk patients: Does prior coronary disease matter? Major adverse cardiac event rates in moderate-risk patients: Does prior coronary disease matter? He has no history of coronary artery disease. If we thought about ACS, we brought them in. AEM June 2022. AEM June 2022.
What Your Gut Says: The patient has a tachydysrhythmia which may be the presentation of acute coronary syndrome (ACS) even though the patient has no ischemic symptoms. Essentially, we are using the troponin assay to find patients with ACO who may be benefited by coronary interventions or risk factor modification.
Date: January 16th, 2020 Reference: Troponin Testing and Coronary Syndrome in Geriatric Patients With Nonspecific Complaints: Are We Overtesting? Date: January 16th, 2020 Reference: Troponin Testing and Coronary Syndrome in Geriatric Patients With Nonspecific Complaints: Are We Overtesting? Reference: Wang et al.
But cardiac arrest is a period of near zero flow in the coronary arteries and causes SEVERE ischemia. Then assume there is ACS. Smith's ECG Blog ( See My Comment in the March 1, 2023 post) — DSI does not indicate acute coronary occlusion! It also does not uniformly indicate severe coronary disease.
Why Was Cardiac Cath Negative for Coronary Disease? As noted by Dr. Nossen — this patient qualified as MINOCA ( M yocardial I nfarction with N on- O bstructive C oronary A rteries ) — since troponin was positive on his 2nd admission, yet there was no evidence of obstructive coronary disease on cath.
Although the attending crews did not consider the ECG pathognomonic for occlusive thrombosis, they nonetheless considered the patient high-risk for ACS and implored him to reconsider. One cannot rely on this feature as a means of detecting changes – subtle, or dramatic – for volatile occlusive coronary thrombus.
Category 1 : Sudden narrowing of a coronary artery due to ACS (plaque rupture with thrombosis and/or downstream showering of platelet-fibrin aggregates. It’s judicious, then, to arrange for coronary angiogram. Supply-demand mismatch (non-occlusive coronary disease, or exacerbation of preexisting flow insufficiency) a.
Background: Historically, we have treated acute coronary syndrome with supplemental oxygen regardless of the patient ’ s oxygen saturation. More recent evidence, however, demonstrates that too much oxygen could be harmful ( AVOID Trial ) by causing coronary vasoconstriction and increasing oxidative stress. Low O2 protocol: 3.1%
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). This patient is actively dying from a left main coronary artery OMI and cardiac arrest from VT/VF or PEA is imminent!
Acute coronary syndrome (ACS) is responsible for the majority (60%) of all OHCAs in patients. Emergency coronary angiography is reasonable for select (eg, electrically or hemodynamically unstable) adult patients who are comatose after OHCA of suspected cardiac origin but without ST elevation on ECG (Class IIa, LOE B-NR).
For the same reason, you should not delay coronary angiography because pain resolves with morphine. Smith : As Willy states, ACS with persistent symptoms is a guideline recommended indication for <2 hour angio (both ACC/AHA and ESC). So I would be worried about inferior OMI. A patient with OMI can have a totally normal ECG!"
ACS and STEMI generally do not cause tachycardia unless there is cardiogenic shock. Then ACS (STEMI) might be primary; this might be cardiogenic shock. One must clearly rule out these processes before jumping on the ACS diagnosis. An angiogram showed no acute coronary lesions. Are the lungs clear? The K returned at 6.9
Myth 1 Absence of Classic Chest Pain obviates the need for ACS work up The absence of chest pain in no way excludes the diagnosis of ACS. Around 33-50% of the patients with ACS present to the hospital without chest pain. Close to 20% of patients diagnosed with acute MI present with symptoms other than chest pain.
showed that among patients with either acute coronary syndrome or acute pulmonary embolism and negative T waves in the precordial leads (V1-V4), that inverted T waves in leads III and V1 were present in only 1% of patients with acute coronary syndrome and 88% of patients with pulmonary embolism. In fact, Kosuge et al. Stein et al.
It should be emphasized here that this is a presentation of high-pretest probability for Acute Coronary Syndrome (ACS). ACE inhibitors, or potassium-sparing diuretics), are particularly susceptible. In the case of ACS, the ECG can rapidly change from this. Past medical history included HTN, HLD, and MI 10 years prior.
The scan also showed “scattered coronary artery plaques”. __ Smith comment 1 : the appropriate management at this point is to lower the blood pressure (lower afterload, which increases myocardial oxygen demand). They too have dense white masses consistent with coronary atherosclerosis. The blue circle shows the LCx.
She was known to have a history of poorly controlled COPD, AFib, and multivessel coronary disease. This should prompt immediate investigation into supply-demand mismatching, or ACS. David Didlake, FF/EMT-P, AG-ACNP @DidlakeDW An elder female presented to the ED with worsening shortness of breath. A 12 Lead ECG was captured.
This was texted to me from a former resident, while working at a small rural hospital, with the statement: "I can’t convince myself of anything here, but he’s a 63-year-old guy with prior stents and a good story for ACS." We don't know if he had a stress test, a CT Coronary angiogram, or they just decided to do an angiogram.
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 coronary angiogram. Does the ECG normalize?
The ECG is just a test: a Bayesian approach to acute coronary occlusion If a patient with a recent femur fracture has sudden onset of pleuritic chest pain, shortness of breath, and hemoptysis, the D-dimer doesn’t matter: the patient’s pre-test likelihood for PE is so high that they need a CT. But does this matter?
Such findings would normally suggest primary ischemia with concomitant surveillance of coronary occlusion, but these ST/T changes might very well be secondary to the Escape mechanism at hand. Steve Smith [link] @SmithECGblog A 72 y/o Male experiences a syncopal episode while seated. Crew members note residual pallor and clammy skin.
ACS then becomes less likely. Before the lab values returned this patient had a n emergent coronary CT angiogram done that ruled out CAD. A false positive cath lab activation is also off course acceptable for this diagnosis if you cannot get an emergent coronary CT angiogram. There are no coronary stenoses.
The commonest causes of MINOCA include: atherosclerotic causes such as plaque rupture or erosion with spontaneous thrombolysis, and non-atherosclerotic causes such as coronary vasospasm (sometimes called variant angina or Prinzmetal's angina), coronary embolism or thrombosis, possibly microvascular dysfunction. This is not the case.
Here is the post shock ECG: Cardiology was called stat for ischemic VT, query SCAD vs thrombotic occlusion vs coronary vasospasm. Cath lab was activated: There was no coronary artery disease, but there was spontaneous coronary artery dissection (SCAD) of the distal LAD, which was narrowed by 95%, and treated medically.
These have all been small studies, studying very few patients with ACS, and often used final cardiology interpretation rather than patient outcome. Smith : This study had such low risk patients that not a single patient was ultimately diagnosed with ACS. It is well known that NOMI usually has a normal ECG or nonspecific ECG.
I was there and said, "No, I think this is all due to severe chronic cardiomyopathy and cardiac arrest due to primary ventricular fibrillation, not due to ACS." _ Why did I say that? For this reason we did not believe this was an acute coronary event and did not activate the cath lab. Here is the initial ED ECG. What do you think?
ACS would be highly unusual in a young athlete, and given the information on his race bib, one must first suspect that the abnormal ST elevation is due to demand ischemia, not ACS. The next day, and angiogram showed normal coronary arteries. His initial ECG is shown here. He awoke and did well.
RBBB + LAFB in the setting of ACS is very bad. Some patients have baseline RBBB with LAFB, but in patients with likely ACS, these are associated with severe infarction with cardiac arrest, cardiogenic shock or impending shock. Patients with ACS and RBBB/LAFB usually have a left main vs. proximal LAD. There is STE in aVR.
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?" Smith and Meyers answer: First , LM occlusion is uncommon in the ED because most of these die before they can get a 12-lead recorded.
More past history: hypertension, tobacco use, coronary artery disease with two vessel PCI to the right coronary artery and circumflex artery several years prior. This is diagnostic of ACS; it appears to be a reperfused acute inferior OMI. He reports feeling nauseated with emesis. There is ischemic ST depression in V4-V6.
Emergent coronary angiography is not recommended over a delayed or selective strategy in patients with ROSC after cardiac arrest in the absence of ST-segment elevation, shock, electrical instability, signs of significant myocardial damage, and ongoing ischemia (Level 3: no benefit). COR 2a, LOE B-R. COR 2a, LOE C-LD. COR 2b, LOE B-R.
Now, it is true that shortly after a non-ACS cardiac arrest, there can be transient diffuse ST depression, but not ST elevation in a coronary distribution, and there should not be a wall motion abnormality. There was faint filling of the distal branches of the RCA by collaterals from the left coronary system.
There were zero patients in this study with a "normal" ECG who had any kind of ACS! Old ‘NSTEMI’ A history of coronary artery disease and a stent to the same territory further increases pre-test likelihood of acute coronary occlusion, including in-stent thrombosis. So this study is actually worthless. Deutch et al.
Cardiology admitted him for observation with plans for next-day coronary angiogram. Smith and Meyers found that patients presenting with high-risk ACS and any ST-depression, even less than 1 mm, maximal in leads V1-V4 to be 97% specific for OMI and 96% specific for OMI requiring emergent PCI. [5] He left AMA and is lost to follow-up.
The patient was thought to have low likelihood of ACS, and cardiology recommended repeat troponin, urine drug testing, and echocardiogram. At that point, cardiology elected to treat for ACS. Another option would be to use Optical Coherence Tomography for Coronary Imaging ). Initial hscTnI was 10 ng/L (ref. <14).
Despite many ECG signs of OMI being missed the door-to-cath time was still fast, because all the healthcare providers were focused on the pathology of acute coronary occlusion and not were distracted by the lack of STEMI criteria. Start using the terms acute coronary occlusion and occlusion MI.
Ischemia from ACS causing the chest discomfort, with VT another consequence (or coincidence)? Cardioversion will address the rhythm problem immediately, also if the chest discomfort subsides when SR is restored, ischemia from ACS becomes much less likely. In either case, prompt cardioversion is indicated.
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