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Flashcards cover definitions of MI types (Type 1 vs Type 2), MINOCA, NSTEMI/STEMI thrombus differences, troponin interpretation, role of angiography, and management implications based on the provided notes.
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What criteria indicate evidence of overt ischemia in acute myocardial infarction (AMI) assessment?
Symptoms, ECG changes, or echocardiography showing ischemia.
What does MINOCA stand for and what is its defining feature?
MINOCA stands for Myocardial Infarction with Non-Obstructed Coronary Arteries; there is no obstructive CAD (typically <50% stenosis) on angiography despite an MI presentation.
How do NSTEMI and STEMI differ in thrombus composition and typical occlusion?
NSTEMI usually has a platelet-rich, non-occlusive thrombus; STEMI usually has a thrombus rich in platelets and fibrin and is typically occlusive.
What is the significance of multiple plaque ruptures in MI?
Multiple ruptures occur in 30–80% of MIs; usually only one plaque is the culprit; highlights the need for therapies to stabilize plaques and prevent recurrence.
Define Type 1 MI and Type 2 MI.
Type 1 MI is due to a primary coronary event (e.g., plaque rupture/erosion with thrombosis) often with CAD; Type 2 MI is due to ischemia from demand-supply mismatch from non-coronary factors, may have underlying CAD or not.
What proportion of Type 2 MI patients have underlying CAD?
About half of Type 2 MI patients have underlying CAD.
What is the clinical significance of a troponin I level > 1 ng/mL?
Strongly suggests obstructive CAD; high positive predictive value for CAD (about 90%), though reduced in the presence of renal dysfunction.
What troponin pattern is typical for Type 2 MI without CAD?
Troponin I is usually <0.6 ng/mL in Type 2 MI without underlying CAD.
How is Type 1 MI distinguished from Type 2 MI in clinical practice?
Type 1 MI is a primary coronary event with no acute noncardiac illness; Type 2 MI occurs in the setting of acute noncardiac illness causing ischemia.
What is the preferred acute management for Type 2 MI?
Treat the primary insult (e.g., sepsis, anemia, severe HTN, tachyarrhythmia); acute antithrombotic therapy and coronary angiography are not routinely indicated; ischemic work-up is elective.
What is the prognosis difference for Type 2 MI with vs without underlying CAD?
Type 2 MI without CAD has a very favorable prognosis with low cardiac mortality at 3 months; Type 2 MI with CAD has cardiac mortality similar to Type 1 MI and higher overall mortality.
In heart failure with troponin elevation, why is troponin elevation not automatically ACS?
Troponin elevation in HF can reflect microcirculatory compression and direct myocyte injury; many elevations are non-MI troponin elevations; CAD work-up may still be needed if CAD has not been addressed.
What is the role of coronary angiography in suspected Type 2 MI when CAD is not addressed?
Angiography is used selectively after stabilization/diuresis; acute antithrombotic therapy is not routinely used; ischemic work-up is elective based on ECG/echo and clinical context.
How does severe hypertension relate to MI type classification?
Hypertension can trigger Type 2 MI; in Type 1 MI, angina relief and nitroglycerin typically reduce BP, whereas malignant HTN may sustain high BP with limited response to nitro.
What is the management priority for suspected Type 2 MI with bleeding or anemia?
Address the primary insult (transfusion and treatment of GI bleeding, etc.); avoid antithrombotics for days to weeks if possible; coronary angiography may not be required unless CAD is suspected by ECG/echo.
What is the role of provocative testing in diagnosing coronary vasospasm?
Vasospasm is diagnosed when provocative testing during angiography reproduces vasospasm along with clinical symptoms and ST changes.
What underlying issues can cause coronary vasospasm or microvascular dysfunction without obstructive CAD?
Endothelial dysfunction leading to diffuse microvascular constriction or impaired microvascular dilation during stress.
What does MINOCA stand for, and who is more commonly affected?
MINOCA stands for MI with Non-Obstructed Coronary Arteries; it is more common in women and younger patients and is usually NSTEMI, with some STEMI presentations and many cases with completely normal arteries on angiography.
What are common non-ischemic conditions that can elevate troponin and mimic MI?
Myocarditis and Takotsubo cardiomyopathy can mimic MI; troponin can rise in these conditions even without obstructive CAD.
What is the recommended long-term approach after Type 2 MI with CAD?
CAD work-up and long-term management that resemble Type 1 MI, addressing CAD risk and considering revascularization if appropriate.