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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 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.
Sudden narrowing of a coronary artery due to ACS (plaque rupture with thrombosis and/or downstream showering of platelet-fibrin aggregates). This latter part has been implicated in embolic CVA. The underlying etiology is either Type 1 or Type II ischemia, although sometimes there’s overlap of both. Type I ischemia.
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.
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.
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.
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.
Third, a slow motion segment showing delayed, brisk filling of the PDA due to dislodgment of a thrombus from contrast injection and distal embolization. A distal RCA lesion ( blue arrow ), Delayed brisk filling of an initially occluded PDA due to a thrombus dislodged during injection which embolized distally.
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