This site uses cookies to improve your experience. To help us insure we adhere to various privacy regulations, please select your country/region of residence. If you do not select a country, we will assume you are from the United States. Select your Cookie Settings or view our Privacy Policy and Terms of Use.
Cookie Settings
Cookies and similar technologies are used on this website for proper function of the website, for tracking performance analytics and for marketing purposes. We and some of our third-party providers may use cookie data for various purposes. Please review the cookie settings below and choose your preference.
Used for the proper function of the website
Used for monitoring website traffic and interactions
Cookie Settings
Cookies and similar technologies are used on this website for proper function of the website, for tracking performance analytics and for marketing purposes. We and some of our third-party providers may use cookie data for various purposes. Please review the cookie settings below and choose your preference.
Strictly Necessary: Used for the proper function of the website
Performance/Analytics: Used for monitoring website traffic and interactions
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.
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.
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.
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.
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.
The patient was found to have an embolic source. Provocative testing is very helpful for this Coronary Thrombus with lysis (one must do optical coherence tomography or at least intravascular ultrasound to find thes non-obstructive plaques that ruptured. Embolism with lysis. Need to find an embolic source.
We organize all of the trending information in your field so you don't have to. Join thousands of users and stay up to date on the latest articles your peers are reading.
You know about us, now we want to get to know you!
Let's personalize your content
Let's get even more personalized
We recognize your account from another site in our network, please click 'Send Email' below to continue with verifying your account and setting a password.
40 
Let's personalize your content