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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".)
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.
A pathological classification of no-reflow was proposed: structural no-reflow—microvessels within the necrotic myocardium exhibit loss of capillary integrity (it is usually irreversible)—and functional no reflow—patency of microvasculature is compromised due to distal embolization, spasm, ischemic injury, reperfusion injury.
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).
We have developed a Proximal balloon Occlusion With forcEd aspiRation (POWER) technique to prevent distal embolization in CAS with the filter protection device. Purpose:Since the balloon protection device became unavailable in Japan three years ago, the DWI-positive rate after carotid artery stenting (CAS) has increased.
24: Joint American College of Cardiology/Journal of the American College of Cardiology Late-Breaking Clinical Trials (Session 402) Saturday, April 6 9:30 – 10:30 a.m.
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.
Then, part of the thrombus embolized into the LCx causing an inferoposterolateral OMI. (As As an aside, the LCx OMI is a type 2 event, since it is due to supply-demand mismatch from thrombus, and not due to atherosclerotic plaque rupture or erosion). The November 10, 2020 post — for PTA. The March 17, 2023 post — for PTA.
CT angiogram chest: no aortic dissection or pulmonary embolism. 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. Serial chest xrays: progressive bilateral pulmonary edema. Diagnostic of Massive OMI.
BACKGROUND:Many ischemic strokes are diagnosed as embolic strokes of undetermined source (ESUS). Recent evidence suggests that nonstenotic carotid plaque (nsCP) may be a substantial contributor to the risk for ESUS. Stroke, Ahead of Print.
Angiogram: --"Suspected culprit for the patient's non-ST elevation myocardial infarction with refractory chest discomfort (although it had resolved prior to arrival to the cardiac catheterization lab), is a ruptured plaque in the distal circumflex with local embolic occlusion of the distal OM 3."
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