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Thus, it has recently become generally accepted that most plaque ruptures resulting in myocardial infarction occur in plaques that narrow the lumen diameter by 40% of the arterial cross section may be involved by plaque. The pathologist may see a plaque that constitutes, for example, 50% of the cross-sectional area.
MINOCA may be due to: coronary spasm, coronary microvascular dysfunction, plaque disruption, spontaneous coronary thrombosis/emboli , and coronary dissection; myocardial disorders, including myocarditis, takotsubo cardiomyopathy, and other cardiomyopathies. See "Mechanisms of acute coronary syndromes related to atherosclerosis".)
Atherosclerosis is an insidious and progressive inflammatory disease characterized by the formation of lipid-laden plaques within the intima of arterial walls with potentially devastating consequences. However, despite a heterogenous substrate underlying coronary thrombosis, treatment remains identical.
The mechanisms by which ICAD causes stroke include plaque rupture with in situ thrombosis and occlusion or artery-to-artery embolization, hemodynamic injury, and branch occlusive disease.
Anaphylaxis leads to plaque rupture or erosion leading to acute myocardial infarction (type II) and acute coronary stent thrombosis (type III). Here we share a case of Kounis syndrome type I caused by an allergy caused by a Cryptopteran bite.
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.
Thrombosis is the main pathological process of stroke and is therefore an important therapeutic target in stroke prevention. Additionally, the formation of thromboinflammation leads to increased instability of atherosclerotic plaques. Stroke, Ahead of Print.
Sudden narrowing of a coronary artery due to ACS (plaque rupture with thrombosis and/or downstream showering of platelet-fibrin aggregates). The underlying etiology is either Type 1 or Type II ischemia, although sometimes there’s overlap of both. Type I ischemia. Type II ischemia.
To prove there is no plaque rupture, you need to do intravascular ultrasound (IVUS). An angiogram is a "lumenogram;" most plaque is EXTRALUMINAL!! One of the most common is rupture of a non-obstructive plaque, with thrombus formation and OMI that spontaneously lyses and leaves a wide open artery. It can only be seen by IVUS.
How common is thrombosis in the culprit artery of Wellen syndrome ? It is generally believed it is more of a mechanical plaque lesion. However by no means, we can say thrombosis do not occur. RCA and LCX Wellens do occur, making this entity’s perceived unique importance less certain 3.
Smith comment : a very high proportion of MINOCA are ruptured plaque with lysed thrombus. That plaque is at risk of thrombosing again. It is worthwhile remembering that the majority of plaques which rupture are non-obstructive before they ulcerate and thrombose. Most plaque is outside the lumen!!
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.
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. FFR can be useful.
Atherosclerotic cardiovascular disease (ASCVD), caused by plaque buildup in arterial walls, is one of the leading causes of disability and death worldwide.1,2 7 Research has shown inflammation plays a significant role in the development of atherosclerosis and ASCVD,8-10 and even the formation of plaque.11 4 In the U.S.
Category 1 : Sudden narrowing of a coronary artery due to ACS (plaque rupture with thrombosis and/or downstream showering of platelet-fibrin aggregates. elevated BP), but rather directly correlated with coronary obstruction (due to plaque rupture and thrombosis) and, potentially, stymied TIMI flow. Severe Hypoxia b.
The primary non-inferiority endpoint was MACCE (a composite of cardiac death, MI, ischaemic stroke, stent thrombosis, or target vessel revascularisation). These patients were identified to have non-flow-limiting vulnerable coronary plaques through intracoronary imaging.
IHC revealed beta‐amyloid plaques in the parenchyma and vessel walls, confirming a diagnosis of CAA.ConclusionApparently cryptogenic lobar hemorrhage may be caused by both occult micro‐AVM/fistula and CAA. A repeat 6‐vessel DSA was again unremarkable as was repeat brain MRI.
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. Young people can suffer acute coronary occlusion, whether by typical atherosclerotic plaque rupture, or by coronary anomalies, coronary aneurysms, dissections, spasm, etc. Diagnostic of Massive OMI.
Therefore it means acute type 1 ACS plaque rupture with impeded flow and impending full occlusion until proven otherwise. The reappearance of de Winter's pattern caused by acute stent thrombosis: A case report. Then, the patients third ECG showed a very rare combination of de Winter T waves happening during LBBB. Am J Emerg Med.
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).
BACKGROUND:Sex-specific differences in plaque composition and instability underscore the need to explore circulating markers for better prediction of high-risk plaques. Plaque stability was determined by gold-standard histological classifications. Adipokine, lipid, and immune profiling was conducted.
Angiography was technically challenging as the patient was receiving CPR, but the cardiologist suspected acute stent thrombosis and initiated cangrelor, although no repeat angiography was able to be obtained. Mechanisms of plaque formation and rupture. Coronary plaque disruption. She was defibrillated perhaps 25 times.
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". Most MINOCA is due to ruptured plaque with thrombus that lyses and does not leave behind a visible culprit. So there is a new inferior severe wall motion abnormality. The dye don't lie".except
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