for 1 yearAspirin and ticagrelor for 1 yearAspirin and prasugrel for 1 year17 Question 17. A 52-year-old woman presents with chest pain and is found to have 2-mm T inversion in the lateral leads and troponin I of 0.14 ng/ml. She is given clopidogrel 300 mg, aspirin 325 mg, heparin 4000 units and drip on admission. She undergoes coronary angiography next day and is found to have 95% mid RCA stenosis. What PCI pharmacotherapy is associated with the best outcomes during and after PCI?HeparinBivalirudinHeparin and GPIHeparin or bivalirudin and start ticagrelor instead of clopidogrelBivalirudin and start ticagrelor instead of clopidogrel
18 Question 18.Should the patient in Question 16 receive anticoagulation after coronary angiography? Yes/NoShould the patient in Question 17 receive anticoagulation after PCI? Yes/No
19 Question 19. Choose the correct answer(s) (multiple answers possible):Ticagrelor reduces mortality in invasively and non-invasively managed ACSTicagrelor may be administered before coronary angiographyTicagrelor is a reversible ADP receptor antagonist, but because of a 15-hour half-life, its effect lasts ~3–4 daysTicagrelor has a higher non-CABG bleeding risk than clopidogrel, but this bleeding hazard is not clearly accentuated in older patients or those with prior strokePrasugrel is only used in patients managed with PCI, and is loaded after coronary angiography (may be loaded before angiography in STEMI)Prasugrel reduces MI but does not reduce mortality, except in STEMI patients (also, a mortality reduction trend is seen in diabetics)Prasugrel showed excessive bleeding hazard in older patients or those with prior stroke
20 Question 20. Concerning prasugrel and ticagrelor:Ticagrelor and prasugrel are preferred over clopidogrel in all ACS patients (all ACS for ticagrelor, ACS managed with PCI for prasugrel) (class I recommendation in ESC)Prasugrel and ticagrelor are particularly beneficial in high-risk conditions (STEMI, diabetes, recurrent events, and complex PCI)Consider the bleeding risk, particularly age >75 and prior stroke with both agents, especially prasugrelEven in the absence of the high-risk conditions (STEMI, diabetes, recurrent events), prasugrel and ticagrelor are warranted in ACSA head-to-head trial of prasugrel vs ticagrelor showed superiority of prasugrel on ischemic outcomes, with a similar bleeding risk
21 Question 21. A 56-year-old man has NSTEMI and undergoes BMS placement in the mid-RCA. He does not have any prior bleeding history. His EF is normal. Beside lifelong aspirin, which antiplatelet and β-blocker therapies should he receive (multiple answers possible)?Clopidogrel for 1 monthClopidogrel or ticagrelor for 1 yearClopidogrel, prasugrel or ticagrelor for 1 year.Consider chronic clopidogrel therapy beyond 1 year if his bleeding risk is deemed lowLifelong metoprolol (medium or high doses)1 year of metoprolol (medium doses)
22 Question 22. A 42-year-old woman with a smoking history presents with a severe episode of resting angina. ECG shows diffuse T inversion. Troponin I peaks at 2 ng/ml. Coronary angiography shows a long (~35 mm), smooth, non-calcified 70% stenosis of the mid-RCA. Her coronary arteries are tortuous. What is the likely mechanism?VasospasmPlaque rupturePlaque erosionSpontaneous coronary artery dissection
23 Question 23. What is the next step for the patient of Question 22?Direct stentingNTG followed by direct stentingNTG followed by conservative managementNTG, followed by OCT then direct stenting
24 Question 24. A 55-year-old man has a history of untreated HTN. He presents with chest pain and dyspnea. He has severe HTN upon presentation, 220/120 mmHg. His pain and HTN do not improve with NTG and he requires a 24- hour intravenous drip of nicardipine and multiple agents to control HTN. ECG shows LVH with a strain pattern. Initial troponin I is 0.08 and it peaks at 0.6 ng/ml. Creatinine is 1.5 mg/dl. Echo shows LVH with mild LV systolic dysfunction and elevated LA pressure. What is the diagnosis and the next step?Type 1 MI from plaque rupture. Must perform early invasive strategyType 2 MI from severe HTN. HTN control is the initial measure. Perform stress testing once HTN is controlled and chest pain resolves
25 Question 25. A 55-year-old man has a history of untreated HTN. He presents with chest pain and dyspnea. He has severe HTN upon presentation, 190/110 mmHg. After the administration of two NTG tablets, chest pain resolves and BP declines to 145/85 mmHg. Troponin I is 0.04 ng/ml and peaks at 0.15 ng/ml. What is the diagnosis and the next step?Type 1 MI from plaque rupture. Must perform early invasive strategyType 2 MI from severe HTN. HTN control is the initial measure
26 Answer 1. C. He fulfills the MI definition as he has an elevated troponin with a rise and fall pattern, along with ST changes. The degree of troponin rise (> 1 ng/ml) as well as the ST changes are concerning for underlying CAD, whether type 1 MI (plaque rupture initiated by the infectious status) or severe ischemic imbalance on top of underlying CAD. In the absence of contraindication, coronary angiography may be performed after his infection and renal function stabilize.
27 Answer 2. A. He does not fulfill the MI definition as he has an elevated troponin with a rise and fall pattern, but without associated chest pain, ST changes, or wall motion abnormality. The severe non-cardiac illness along with the mild degree of troponin rise (< 1 ng/ml) is consistent with ischemic imbalance and does not necessarily imply underlying CAD. There is no definite need for antithrombotic therapy, and a later, elective evaluation with stress testing may be performed.
28 Answer 3. C. The patient has a rise and fall in troponin along with ST changes and wall motion abnormality. This is a type 2 MI, related to ischemic imbalance in the context of severe, acute anemia. However, the extensive ST changes, the severity of troponin rise (> 0.5–1 ng/ml), and the wall motion abnormality are concerning for severe underlying CAD, which was probably stable and was unveiled by the stress of anemia/tachycardia. CAD needs to be addressed. Stress testing is unlikely to provide additional information, as the patient already shows severe myocardial ischemia and ST depression with the stress of anemia. Coronary angiography, followed by possible revascularization (PCI or CABG), is warranted. However, in a patient with active or recent bleeding, PCI or CABG is not advised, as peri-PCI or peri-CABG anticoagulation and dual antiplatelet therapy may not be tolerated. Wait 1–2 weeks (at least) after hemoglobin has stabilized and proper gastrointestinal therapy is performed (PPI, endoscopic cauterization). This allows a safer performance of revascularization if needed. β-Blockers should not be administered acutely, as the patient is in a pre-shock state and tachycardia is compensatory; they may be administered 24–48 hours later.
29 Answer 4. B. The mild rise in troponin is secondary to the ischemic imbalance of HF (LV dilatation increases wall stress/afterload; LVEDP elevation reduces coronary flow). Similarly, the chest tightness that occurs in decompensated HF is commonly secondary to ischemic imbalance. In fact, troponin rise in HF is a prognostic marker that correlates more with the severity of HF decompensation than the coronary status and does not necessarily imply ACS. The fact that a coronary angiography performed in the last 2–3 years did not reveal obstructive CAD strongly argues against ACS.
30 Answer 5. B. The mild troponin rise is at least partly secondary to the ischemic imbalance of HF. Yet, any HF, particularly acute or systolic HF, warrants evaluation for an underlying ischemic etiology (chronic CAD) using coronary angiography. Antithrombotic therapy does not appear warranted, as the ECG does not suggest acute ischemia. Elevated troponin alone does not establish the diagnosis of ACS in a patient presenting with HF. While the underlying CAD is often stable, ischemic evaluation is preferably performed before discharge. CAD, if present, is likely extensive with an increased risk of recurrent HF or MI. In one analysis, patients with acute HF and CAD who did not undergo revascularization before discharge had a significantly increased mortality in the ensuing 60–90 days; this excess in mortality was attenuated with revascularization (chapter 4, reference 204).
31 Answer 6. A. The Q waves suggest an ischemic etiology of HF. The Q-wave infarct may be recent, coinciding with his onset of symptoms. Moreover, global ischemia is suggested by the extensive ST depression and the wall motion abnormality that extends beyond the infarcted territory. Thus, unlike Question 5, ECG implies that HF is secondary to a recent infarction and acute ischemia. He should be treated as type 1 MI with antithrombotic
