CBS - The 17th Left Main & Coronary Bifurcation Summit, CBS2025

二尖瓣/三尖瓣瓣膜

Mitral Valve Remodeling and Strain in Secondary Mitral Regurgitation: Comparison With Primary Regurgitation and Normal Valves Surgery Does Not Improve Survival in Patients With Isolated Severe Tricuspid Regurgitation Combined Tricuspid and Mitral Versus Isolated Mitral Valve Repair for Severe MR and TR: An Analysis From the TriValve and TRAMI Registries 1-Year Outcomes After Edge-to-Edge Valve Repair for Symptomatic Tricuspid Regurgitation: Results From the TriValve Registry Transcatheter Mitral Valve Replacement in Patients with Heart Failure and Secondary Mitral Regurgitation: From COAPT Trial Regurgitant Volume/Left Ventricular End-Diastolic Volume Ratio: Prognostic Value in Patients With Secondary Mitral Regurgitation Association of Effective Regurgitation Orifice Area to Left Ventricular End-Diastolic Volume Ratio With Transcatheter Mitral Valve Repair OutcomesA Secondary Analysis of the COAPT Trial New Evidence Supporting a Novel Conceptual Framework for Distinguishing Proportionate and Disproportionate Functional Mitral Regurgitation

Sort by hits |<< 1 2 3 4 5 >>|

Original Research

JOURNAL：ACC Article Link

What's new in the “Fourth Universal Definition of Myocardial Infarction”

Salim Hayek, MD, FACC Keywords: Acute Coronary Syndrome; Angiography; Atrial Fibrillation; Autopsy; Biological Markers; Coronary Angiography; Coronary Artery Bypass; Coronary Artery Disease; Depression; Diabetes Mellitus; Type 2; Electrocardiography; Heart Failure; Kidney Diseases; Magnetic Resonance Imaging; Myocardial Infarction; Myocardial Ischemia; Percutaneous Coronary Intervention; Stents; Thrombosis; Tomography; X-Ray Computed; Transcatheter Aortic Valve Replacement; Troponin

Pre-reading

The following are key points to remember from the 2018 Fourth Universal Definition of Myocardial Infarction Consensus Document:

1. Major changes include the differentiation of myocardial infarction from injury, and delineation of roles for cardiac magnetic resonance imaging (MRI) and computed tomography (CT) angiography in the evaluation of acute coronary syndromes.
2. Cardiac troponin levels should be drawn on initial assessment and 3-6 hours later, possibly earlier (1-3 hours) with high-sensitivity assays. Defining a universal interval for serial sampling is challenging given the impact of the variation in time of symptom onset on the rise and fall of troponin measured by both conventional and high-sensitivity assays. Incorporation of a sound clinical assessment is essential in guiding sampling frequency and interpretation.
3. Myocardial injury is defined by only one criterion: the elevation of cardiac troponin, with at least one value above the 99th percentile upper reference limit, and thus represents an all-encompassing term for elevated troponins of ischemic and nonischemic etiologies.
4. A myocardial infarction is a myocardial injury attributed specifically to ischemia, i.e., with clinical evidence of a rise in troponin and at least one of the following: ischemic symptoms or electrocardiographic changes, development of pathologic Q waves, imaging evidence of new loss of viable myocardial or regional wall motion abnormalities consistent with ischemia, and last, identification of a coronary thrombus by angiography or autopsy.
5. Type 1 acute myocardial infarctions refers to those secondary to acute atherothrombosis. Type 2 is secondary to ischemia due to oxygen supply and demand mismatch unrelated to acute thrombosis. Type 3 refers to myocardial infarctions diagnosed post-mortem in patients who had presented with signs and symptoms suggestive of myocardial ischemia and passed before biomarkers were measured.
6. Type 4a and 5 events are post-percutaneous coronary intervention (PCI) and post-coronary artery bypass grafting (CABG), respectively, occurring <48 hours after the index procedure, and are defined by elevations in troponin beyond a prior stable baseline value and with electrocardiographic, angiographic, or imaging evidence of ischemia. Type 4b defines stent thrombosis (acute <24 hours, subacute 1-30 days, late 30 days-1 year, very late >1 year post-PCI), while type 4c indicates restenosis following PCI in the infarct territory.
7. Myocardial injury can occur during nonrevascularization cardiac procedures such as transcatheter aortic valve replacement by direct trauma or coronary obstruction/embolization, and are not classified as infarctions unless they meet biomarker and ischemia criteria for type 5 infarctions.
8. There are no specific categories for elevation in troponin in the setting of acute heart failure, kidney disease, critical illness, or noncardiac procedures. The diagnosis should be based on the presence or absence of ischemia and acute thrombosis, given type I and type II myocardial infarctions, or acute myocardial injury nonrelated to ischemia can occur in all these clinical scenarios.
9. Elevation in troponin in the setting of atrial fibrillation with rapid ventricular rate and accompanying ST depression should not be classified as type 2 myocardial infarction unless signs of overt ischemia are present. Otherwise, the rise in troponin should be attributed to myocardial injury.
10. Myocardial infarction in nonobstructive coronary artery disease (MINOCA) should be classified as either type 1 (thrombosis with recanalization) or type 2 (coronary spasm, coronary dissection) depending on the clinical presentation and angiogram findings.

Abstract

Recommended Article

What's new in the “Fourth Universal Definition of Myocardial Infarction”

Pre-reading