or mid-wall predominance → myocarditisDistribution consistent with an arterial territory + subendocardial or transmural predominance → infarctionIn all three cases (myocarditis, infarction, takotsubo), edema may be seen on T2-weighed images if the process is acute. The distribution of edema also distinguishes myocarditis from infarction. IVUS and OCT may be done and may detect plaque disruption, even in some cases where MRI is unrevealing; they may obviate the need for MRI.
38 Answer 13. C. In ACS, it is important to ascertain that a seemingly non-obstructive plaque is truly non-obstructive. For example, a 40–50% hazy stenosis with irregular or overhanging borders is possibly unstable and may be anatomically significant by IVUS (more obstructive and ulcerated than the angiography suggests).
39 Answer 14. C. About 40–45% of acute LCx occlusions do not show any significant ST-T abnormality. In fact, ~20% of NSTEMIs have acute coronary occlusion, mostly LCx or RCA, and may be STEMI-equivalents that lack ST elevation and sometimes ST depression. LCx and RCA occlusions represent 2/3 of these “occluded” NSTEMIs. Beside the unremarkable ECG, the first troponin may be negative in these patients, which explains the diagnostic delay. Hints to a true ACS: (i) ongoing, unexplained severe distress/pain (rule out clinically and by X-ray aortic dissection, perforated peptic ulcer, and abdominal catastrophe); (ii) posterior-lead ECG; (iii) ECG abnormality may emerge when ECG is repeated every 10 min. Even if the posterior-lead ECG is normal, treat the patient as acute coronary occlusion and perform urgent catheterization. Perform chest X-ray to rule out pneumothorax and any suggestion of aortic dissection or perforated peptic ulcer (subdiaphragmatic air). Morphine should not be used, as it masks an ongoing angina and provides false reassurance.
40 Answer 15. C. Upstream GPI (before PCI) is not justified, whether upstream clopidogrel is administered or not. On admission, the patient may receive dual antiplatelet therapy with aspirin and clopidogrel or ticagrelor. However, in 2 trials using potent ADP-receptor antagonists (prasugrel in ACCOAST, and prasugrel and ticagrelor in ISAR-REACT 5), and in the large SCAAR registry, their upstream administration pre-catheterization did not improve outcomes; if PCI is to be performed, the ADP-receptor antagonist is administered during PCI. Upstream administration may particularly delay the care of patients who eventually need CABG, such as, potentially, this insulin-dependent diabetic man. The patient has a very high-risk NSTEMI, with a high GRACE score > 140 (in light of the age ≥ 70, tachycardia, SBP < 120, and both troponin rise and ST changes). An early invasive strategy < 24 hours is preferred. Since coronary angiography will be performed in less than 12–24 hours, heparin is preferred over enoxaparin. He has tachycardia and SBP < 120 mmHg, hence he is in a pre-shock state and should not receive metoprolol in the first 24 hours.
41 Answer 16. C (B is an acceptable option). The patient likely had plaque rupture of one of her moderate lesions, leading to thrombus and microembolization. Her plaques stabilized with antithrombotic therapy. Clopidogrel (CURE trial) and ticagrelor (PLATO) are therapies that have shown benefit in medically treated ACS patients, ticagrelor being the superior agent (ticagrelor showed mortality and MI reductions in this subgroup of medically treated patients). Prasugrel is only studied in ACS patients treated with PCI; it failed to show superiority in medically treated ACS (TRILOGY ACS trial).
42 Answer 17. D. The downstream use of GPI (during PCI) is not clearly beneficial, except in bail-out situations. Ticagrelor reduces ischemic events and mortality more than clopidogrel after ACS. Heparin has been shown to be as safe and efficacious as bivalirudin in a large study with balanced GPI use and radial access.173
43 Answer 18. (i) yes, (ii) no. Anticoagulation for at least 48 hours is warranted in NSTEMI patients managed without PCI. Low-dose UFH, with no bolus, may be started 8–12 hours after coronary angiography and continued for a total of 48 hours. Fondaparinux may be used for 2–8 days. Enoxaparin may also be used but is associated with a higher bleeding risk after catheterization.In patients who undergo PCI, the anticoagulant is stopped after PCI. Only bivalirudin may be infused for 1–4 hours after PCI. In patients who receive GPI during PCI, GPI may be continued for up to 24 hours.
44 Answer 19. All are correct.
45 Answer 20. All are correct.
46 Answer 21. C, D, and F. Regardless of the stent type, NSTEMI patients should receive 1 year of ADP-receptor antagonist. Beyond one year, DAPT trial suggests a benefit of dual antiplatelet therapy in patients who have not bled in the first year, especially the MI subset. If EF is normal, β-blocker does not have a clear benefit beyond 1 year after MI.
47 Answer 22.D. The smooth angiographic appearance and the age and sex of the patient suggest vasospasm, plaque erosion, or spontaneous coronary dissection. The latter is the most likely diagnosis here: (i)the length of the stenosis is concerning for dissection; (ii) a tortuous or corkscrew coronary artery further supports spontaneous coronary dissection.
48 Answer 23. C. OCT helps show features of plaque erosion and SCAD. Plaque erosion is characterized by thrombus with an intact intimal cap or a fibrointimal plaque. However, when SCAD is suspected, it is best to avoid any coronary manipulation, including OCT, as each manipulation increases the risk of intramural hematoma propagation. When the flow is preserved and the disease is not critical, SCAD is best treated conservatively with no PCI. The majority of SCADs (70-97%) will heal by 1-2 months.
49 Answer 24. B. Patients with true ACS/type 1 MI may have HTN secondary to the distress of angina. However, in the case presented here, the persistence of HTN and its requirement for multiple agents implies that malignant HTN is the primary process responsible for the patient’s pain and troponin rise. The severe LVH, seen on echo, accentuates ischemic demands and is a marker of uncontrolled HTN. The degree of troponin rise (< 1 ng/ml) is consistent with ischemic imbalance. Ischemic workup, possibly stress testing, may be performed once HTN is controlled and chest pain resolves.
50 Answer 25. A. Compare this case to Question 24. The quick resolution of HTN with NTG implies that HTN was secondary to myocardial ischemia (catecholamine surge), rather than a cause of ischemia. Even the milder troponin rise, in context, is worrisome for true ACS and plaque rupture.
References
Definition of MI, type 1 and type 2 MI
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