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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.
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.
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.
ET Main Tent (Hall B1) Coronary Sinus Reducer for the Treatment of Refractory Angina: A Randomised, Placebo-controlled Trial (ORBITA-COSMIC) Transcatheter Aortic Valve Implantation Versus Surgical Aortic Valve Replacement in Patients at Low to Intermediate Risk: One Year Outcomes of the Randomized DEDICATE-DZHK6 Trial Effect of Alcohol-mediated Renal (..)
Once stabilized, intravascular ultrasound showed significant thrombus and plaque in the LAD. Due to ongoing shock despite initial mechanical support, the patient was escalated to an Impella CP device after a transthoracic echo confirmed no left ventricle thrombus.
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).
This case was provided by Spencer Schwartz, an outstanding paramedic at Hennepin EMS who is on Hennepin EMS's specialized "P3" team, a team that receives extra training in advanced procedures such as RSI, thoracostomy, vasopressors, and prehospital ultrasound. An angiogram is a "lumenogram;" most plaque is EXTRALUMINAL!!
She had some very minor plaque but certainly nothing that could explain the heart attack and therefore she was discharged with a diagnosis of MINOCA i.e Then I think it is important that patient has an assessment of the function of the heart by means of an ultrasound to look for cardiomyopathies, Takotsubo etc.
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. Beware a negative Bedside ultrasound. No further troponins were measured. She died before she could get a heart transplant.
A bedside ultrasound should be done to assess volume and other etiologies of tachycardia, but if no cause of type 2 MI is found, the cath lab should be activated NOW. Then, part of the thrombus embolized into the LCx causing an inferoposterolateral OMI. (As Smith comment: this is diagnostic of OMI until proven otherwise.
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