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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. MINOCA I do not have the bandwidth here to write a review of MINOCA.
ET Main Tent (Hall B1) - A Double-blind, Randomized Placebo Procedure-controlled Trial of an Interatrial Shunt in Patients with HFrEF and HFpEF: Principal Results From the RELIEVE-HF Trial - Empagliflozin After Acute MyocardialInfarction: Results of the EMPACT-MI Trial - CSL112 (Apolipoprotein A-I) Infusions and Cardiovascular Outcomes in Patients (..)
Background:The no-reflow has been reported to be associated with larger infarct size and mortality after acute myocardialinfarction (AMI). The incidence of no-reflow was higher in patients with attenuated plaque ≥5 mm in length as evaluated by intravascular ultrasound (IVUS).Objective:The vs. 8.6%, p < 0.001).
If the arrest was caused by acute MI due to plaque rupture, then the diagnosis is MINOCA. MINOCA: MyocardialInfarction in the Absence of Obstructive Coronary Artery Disease). Here is my comment on MINOCA: "Non-obstructive coronary disease" does not necessarily imply "no plaque rupture with thrombus." myocarditis).
To prove there is no plaque rupture, you need to do intravascular ultrasound (IVUS). An angiogram is a "lumenogram;" most plaque is EXTRALUMINAL!! Such cases are classified as MINOCA (MyocardialInfarction with Non-Obstructed Coronary Arteries). It can only be seen by IVUS. MINOCA has many etiologies. Learning Points: 1.
The term MINOCA stands for Myocardialinfarction with non-obstructive coronary arteries. 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 I’ll try and explain this a bit better by using a case study.
Today, they viewed the angiogram and concluded that the thrombus at the mid RCA must have extended proximally from the culprit ruptured plaque, extending proximal to the RV marginal branch and temporarily occluding it. However, by the time of the angiogram it had embolized distally, and had only done so after the right sided ECG was recorded.
ng/mL This single initial troponin at this level, in the context of chest pain, is high enough to be diagnostic of acute myocardialinfarction. LAD plaque with 0-25 percent stenosis. If there are T-wave inversions and elevated trops in the context of persistent pain, think of other pathologies such as pulmonary embolism.
BACKGROUND:Aortic arch plaques are associated with an increased risk of ischemic stroke in patients with cryptogenic stroke or prior embolic events. Arch plaques were assessed by suprasternal transthoracic echocardiography; plaques ≥4 mm in thickness were classified as large plaques. Stroke, Ahead of Print.
Here it is annotated in red: Our extremely smart radiologist, Gopal Punjabi , assures me that this finding can only be due to myocardialinfarction, not myocarditis. The patient was found to have an embolic source. MyocardialInfarction with Non-Obstructive Coronary Arteries. Embolism with lysis.
Angiogram: --"Suspected culprit for the patient's non-ST elevation myocardialinfarction 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."
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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