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Coronary Artery Disease (CAD) CAD, which involves the narrowing or blockage of coronary arteries due to plaque buildup, can reduce blood flow to the heart. Blood Clots: An enlarged heart is more prone to developing blood clots, which can lead to stroke or pulmonary embolism.
(Arteriosclerosis, Thrombosis and Vascular Biology) A role for hemoglobin in atherosclerosis is supported by a study that used serial coronary CT angiography to demonstrate an association between persistently low serum hemoglobin levels and greater changes in coronary plaque volume.
She had acute pulmonary edema on exam. On arrival, lung ultrasound confirmed pulmonary edema (B lines). Mild Plaque no angiographically significant obstructive coronary artery disease. A 49 year old woman with h/o COPD only presented with sudden dyspnea. This is proximal LAD Occlusion until proven otherwise.
Publication date: Available online 12 June 2024 Source: The American Journal of Cardiology Author(s): Michele Russo, Massimiliano Camilli, Giulia La Vecchia, Riccardo Rinaldi, Alice Bonanni, Matteo Pio Natale, Carmine Salzillo, Ilaria Torre, Carlo Trani, Filippo Crea, Rocco A.
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). Smith comment : Is the ACS (rupture plaque) with occlusion that is now reperfusing?
The CXR demonstrated no pulmonary edema. Sudden narrowing of a coronary artery due to ACS (plaque rupture with thrombosis and/or downstream showering of platelet-fibrin aggregates). There was equally no anemia, sepsis, or hypoxia—only transient hypotension in the field. The Trop I returned 0.051 ng/mL, and cardiology was requested.
PAD is a serious, progressive cardiovascular disease primarily caused by a buildup of fatty plaque in the blood vessels, or atherosclerosis. This plaque narrows the blood vessels and reduces blood flow to the legs and feet, which may significantly impair physical function, walking performance and quality of life.
The patient was slightly tachypneic and mildly hypoxic in the stabilization room and therefore the physicians obtained a CT pulmonary angiogram as well as aortogram to rule out dissection and PE. Angiogram Culprit Lesion: 90% mid LAD stenosis with evidence of plaque rupture, TIMI III flow on angiography.
If the arrest was caused by acute MI due to plaque rupture, then the diagnosis is MINOCA. Here is my comment on MINOCA: "Non-obstructive coronary disease" does not necessarily imply "no plaque rupture with thrombus." They often cannot even be recognized as culprits, as fissured or ulcerated plaque. myocarditis).
As in all ischemia interpretations with OMI findings, the findings can be due to type 1 AMI (example: acute coronary plaque rupture and thrombosis) or type 2 AMI (with or without fixed CAD, with severe regional supply/demand mismatch essentially equaling zero blood flow). CT angiogram showed extensive saddle pulmonary embolism.
From there, the right ventricle pumps the blood to the lungs via the pulmonary arteries for reoxygenation. Here are a few issues that can arise: Coronary Artery Disease (CAD) : This occurs when plaque builds up inside the coronary arteries, narrowing them and restricting blood flow to the heart.
LAD plaque with 0-25 percent stenosis. No signs for aortic dissection or pulmonary embolus. --"Results were discussed with the ordering physician. If there are T-wave inversions and elevated trops in the context of persistent pain, think of other pathologies such as pulmonary embolism. A CT Coronary angiogram was ordered.
CT angiogram chest: no aortic dissection or pulmonary embolism. Serial chest xrays: progressive bilateral pulmonary edema. Only after her troponin peaked at 500,000 ng/L did she get her angiogram, which showed a 100% left main occlusion due to ruptured plaque. No further troponins were measured.
He was seen at another hospital and found to have a slightly elevated troponin, then underwent a CT pulmonary angiogram (PE) protocol which revealed a right sided pneumonia. But young people do have MI, due to anomalous coronary arteries, coronary artery dissection, Kawasaki dz, even atherosclerotic plaque rupture, and other etiologies.
Bedside POCUS showed very poor LV function and a few pulmonary B lines. A Chest X-ray did not show pulmonary edema. This was attributed to a "Type 2 MI", which is acute MI that is not due to ruptured plaque, but rather due to "supply demand oxygen mismatch". He was put on BiPAP. See these posts: Dynamic OMI ECG.
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