Читать книгу Practical Cardiovascular Medicine - Elias B. Hanna - Страница 60

1 Question 1. A 72-year-old man is admitted with fever, severe bilateral pneumonia, and sepsis. His exam does not suggest volume overload. During his first hospitalization day, his ECG shows transient deep ST depression in the lateral leads. His troponin I peaks at 1.2 ng/ml, with a rise and fall pattern; BNP = 65. He has acute renal failure with creatinine of 1.7 mg/dl. He does not complain of chest pain. His echo shows a hyperdynamic LV. What is the next step?His troponin rise is due to ischemic imbalance. He does not fulfill the definition of MI. No need for further cardiac workupHis troponin is partly due to ischemic imbalance. He fulfills the definition of MI. Perform stress testing before dischargeHis troponin is partly due to ischemic imbalance. He fulfills the definition of MI. Perform coronary angiography after stabilization of infectious state and renal function

2 Question 2. A 72-year-old man is admitted with fever, severe bilateral pneumonia, and sepsis. His exam does not suggest volume overload. His ECG shows mild lateral T inversion. His troponin I peaks at 0.8 ng/ml, with a rise and fall pattern; BNP = 65. He has acute renal failure with creatinine of 1.7 mg/dl. He does not complain of chest pain. His echo shows a hyperdynamic LV. What is the next step?His troponin rise is due to ischemic imbalance. He does not fulfill the definition of MI. No need for further cardiac workup at this pointHis troponin is partly due to ischemic imbalance. He fulfills the definition of MI. Perform stress testing before discharge His troponin is partly due to ischemic imbalance. He fulfills the definition of MI. Perform coronary angiography after stabilization of his infectious state and renal function

3 Question 3. A 72-year-old man is admitted with melena and severe anemia (hemoglobin 6.5 g/dl). He is tachycardic but not in shock. His ECG shows diffuse 1.5 mm ST depression that has resolved after transfusion. His troponin I peaks at 3 ng/ml, with a rise and fall pattern. He does not complain of chest pain. His echo shows severe anterior hypokinesis. What is the next step?Transfuse and treat with proton pump inhibitors (PPI). No need for coronary angiography. Perform outpatient stress testingTransfuse and treat with PPI. No need for any cardiac workup unless angina occurs despite hemoglobin stabilizationTransfuse, treat with PPI, and perform gastroscopy. Perform coronary angiography once bleeding has stabilized for 1–2 weeksTransfuse, treat with PPI, and perform gastroscopy. Administer β-blockers and nitrates. Perform coronary angiography once bleeding has stabilized for 1–2 weeks

4 Question 4. A 62-year-old man has a history of heart failure with LVEF of 25%. Coronary angiography performed a year previously showed mild, non-obstructive plaques. He presents with acutely decompensated HF, volume overload, and chest tightness. His troponin I peaks at 1 ng/ml with a rise and fall pattern (his baseline troponin is 0.05 ng/ml). His ECG shows LVH with a strain pattern; no Q waves are seen. What is the next step?Diuresis and vasodilator therapy. Initiate antithrombotic therapy. Once proper diuresis is achieved, perform coronary angiographyDiuresis and vasodilator therapy. No need to repeat coronary angiography

5 Question 5. A 62-year-old man presents with progressive dyspnea and chest tightness for the last week. Exam and X-ray are diagnostic of pulmonary edema and severe HF. Echo shows LVEF 25% with global hypokinesis. Troponin I peaks at 0.5 ng/ml with a rise and fall pattern. ECG shows LVH with strain. Creatinine is 1.7 mg/dl. What is the next step?Diuresis, vasodilator therapy, and antithrombotic therapy. Once proper diuresis is achieved, perform coronary angiography during this hospitalizationDiuresis and vasodilator therapy. Once proper diuresis is achieved, perform coronary angiography during this hospitalizationDiuresis and vasodilator therapy. Once proper diuresis is achieved, perform stress testing for ischemic evaluationDiuresis and vasodilator therapy. Perform elective coronary angiography in the outpatient setting

6 Question 6. A 62-year-old man presents with progressive dyspnea and chest tightness for the last week. Exam and X-ray are diagnostic of pulmonary edema and severe HF. Echo shows LVEF 25% with global hypokinesis and inferior akinesis. Troponin I peaks at 0.5 ng/ml with a rise and fall pattern. ECG shows diffuse ST depression and inferior Q waves. Creatinine is 1.7 mg/dl. What is the next step?Diuresis, vasodilator therapy, and antithrombotic therapy. Once proper diuresis is achieved, perform coronary angiography during this hospitalizationDiuresis and vasodilator therapy. Once proper diuresis is achieved, perform coronary angiography during this hospitalizationDiuresis and vasodilator therapy. Once proper diuresis is achieved, perform stress testing for ischemic evaluationDiuresis and vasodilator therapy. Perform elective coronary angiography in the outpatient setting

7 Question 7. A 56-year-old man, with no cardiac history, presents with one severe episode of chest pain that started after pushing some furniture. The pain lasted 20 minutes and did not recur. His admission BP is 160/95 mmHg, and no murmur or rub is heard. His ECG is normal. His initial troponin I is 0.02 ng/ml, and peaks at 0.05 ng/ml (99th percentile < 0.04 ng/ml). Renal function is normal. What is the next step?Initiate antithrombotic therapy. Coronary angiography within 24 hours.Initiate antithrombotic therapy. Coronary angiography within 72 hours.Stress testing before discharge for risk stratification.

8 Question 8. A 47-year-old man, smoker, diabetic, presents to the emergency department with sharp chest pain that has been occurring intermittently at rest for the last 2 days. It does not prevent him from performing his daily activities. On exam, his BP is 145/92 mmHg, heart rate 85 bpm. He has no HF or murmur. ECG shows inferior T-wave inversion of 1 mm, and the admission hs-troponin I is undetectable (< 0.005 ng/ml). What is the next step?Perform inpatient stress testing. Home discharge followed by outpatient stress testing is not acceptablePerform inpatient stress testing. Home discharge followed by outpatient stress testing (within 72 hours) is acceptablePerform coronary angiographyDischarge home and arrange for clinic follow-up within a week. Further workup depends on progression of symptoms

9 Question 9. A 56-year-old woman has a history of RCA PCI 8 months previously. She presents with one episode of chest pain that felt similar to her prior angina. It occurred once at rest, 2 days ago, lasted 20 minutes and did not recur. ECG shows LVH with strain and inferior Q waves. Serial troponin levels are < 0.04 ng/ml. Creatinine is normal. What is the next step?Coronary angiography within 72 hoursCoronary angiography within 24 hoursStress testing 3–6 hours after presentation

10 Question 10. In comparison with men, women with ACS (multiple answers)Have a higher in-hospital mortalityAre less likely to benefit from an early invasive strategyHave fewer underlying comorbiditiesHave a higher proportion of non-obstructive CAD and less extensive CAD Have a higher bleeding riskHave a higher ischemic burden despite a lower prevalence and extent of CAD

11 Question 11. A 56-year-old woman presents with severe chest pressure that lasted 2 hours. Her ECG shows deep T-wave inversion across the precordial leads. BP was 190/105 mmHg on presentation. Troponin rises to 2.5 ng/ml. A coronary angiography is performed and only shows minimal plaques < 25%. What is the differential diagnosis at this point (multiple answers)?Stabilized plaque ruptureCoronary vasospasmTakotsubo cardiomyopathyMyopericarditisPulmonary embolismHypertensive crisis with elevated LVEDP and ischemic imbalanceDemand/supply mismatch from anemia or tachyarrhythmia

12 Question 12. For the patient in Question 11, what additional testing best helps establish a diagnosis?Cardiac MRIIVUSEcho

13 Question 13. A 62-year-old man presents with angina and a troponin of 0.12 ng/ml. ECG shows 1 mm dynamic lateral ST depression. He is started on antithrombotic therapy. Coronary angiography is performed and reveals a 40% hazy lesion in the mid RCA with TIMI grade 3 flow. It is eccentric with overhanging edges (Figure 1.9, Appendix 1). There is minimal disease otherwise. What is the next step?PCI of the hazy lesionFFR of the RCAIVUS of the RCAMedical therapy since lesion is < 50%

14 Question 14. A 66-year-old woman presents with severe chest pain that started 2 hours ago. The pain is ongoing, unrelieved with NTG, with severe distress, diaphoresis, and severe nausea. BP = 165/90, heart rate 90 bpm, O2 saturation 100% on ambient air. Exam does not reveal signs of HF. No rub is heard, and BP is equal in both arms. The abdomen is soft and non-tender. ECG is normal. Initial troponin is detectable but below MI cutoff. What is the next step?The pain is unlikely cardiac, as ECG is normal during ongoing pain. ACS likelihood is low. Obtain serial troponin levels then perform stress testingThe pain is likely cardiac by clinical features. Give morphine, metoprolol, and anticoagulation, then perform coronary angiography within 24 hoursThe pain is likely cardiac. Perform chest X-ray. Perform urgent coronary angiography

15 Question 15. A 70-year-old man who has insulin-dependent diabetes presents with chest pain and inferior ST-segment depression (dynamic). His troponin I is 0.55 ng/ml. He is currently chest pain free. He is tachycardic (sinus tachycardia 105 bpm) with BP of 110/75 mmHg. What is the appropriate therapy?Aspirin, clopidogrel load, GPI, and UFH. Perform coronary angiography within 24 hours.Aspirin and UFH. Perform coronary angiography within 72 hoursAspirin and UFH. Perform coronary angiography within 24 hoursAspirin, clopidogrel load, and UFH. Perform coronary angiography within 24 hoursAspirin, clopidogrel load, metoprolol, and UFH. Perform coronary angiography within 24 hours

16 Question 16. A 70-year-old woman presents with NSTEMI. Her coronary angiogram shows multiple moderate lesions in the LAD and RCA. The physician decides to treat her medically. What is the best long-term antiplatelet regimen?Aspirin only, as no PCI was performedAspirin and clopidogrel for 1 yearAspirin and ticagrelor for 1 yearAspirin and prasugrel for 1 year

17 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 therapy and he should undergo coronary angiography once he has received proper diuresis. In acute HF, in the absence of acute ST elevation, angiography and PCI are not warranted urgently, as supine positioning, sedation, and contrast loading are likely to aggravate HF and myocardial ischemia. His Q-wave MI is > 24 hours old (by history), without persistent ST elevation.

32 Answer 7. A. Any increase in troponin above the 99th percentile with a rise and fall pattern, in the context of angina presentation, and in the absence of severe non-cardiac illness (sepsis, anemia, HF, tachyarrhythmia) is diagnostic of primary NSTEMI (ACS). This patient is managed with antithrombotic therapy and an initial invasive strategy rather than stress testing. His GRACE risk score is < 140 (age < 70, no ST depression, HF, hypotension, tachycardia); thus, coronary angiography may be performed at 24–72 hours per TIMACS and VERDICT trials. However, ESC and ACC guidelines favor early invasive strategy <24 hours in all NSTEMIs.

33 Answer 8. D. Traditional risk factors, like smoking and diabetes, increase the general probability of CAD but only weakly increase the likelihood of ACS in a patient with acute chest pain syndrome. Other factors, such as pain timing/duration, troponin, and ECG should be taken into account: (1) the undetectable troponin makes ACS very unlikely; (2) T-wave inversion < 3 mm is non-diagnostic and does not significantly increase the likelihood of ACS or worsen its prognosis; (3) chest pain occurrence and timing are atypical. In this patient with undetectable hs-troponin, early discharge is appropriate. Early stress testing at 6–12 hours after admission or post-discharge stress testing are appropriate (A or B), but not necessary in the setting of undetectable troponin and atypical symptoms.

34 Answer 9. C. A history of PCI dictates an initial invasive strategy in case of recurrence of typical pain within 6–12 months of PCI. While the pain is concerning, it does not have a typical exertional pattern, and it is resting pain with negative troponin. Considering her troponin and non-specific ECG, the ACS likelihood is not high. In women with negative troponin, no ST changes, and low TIMI risk score, an initial invasive strategy is associated with increased risk of death/MI, and thus initial stress testing is preferably performed.Answer 10.

35 Answer 10. A, B, D, E, F.

36 Answer 11. A, B, C, D (see explication under Answer 12).

37 Answer 12. A. About 10% of patients with NSTEMI, particularly women, are not found to have any significant CAD. In those cases, reasons A through G can explain the troponin rise. Demand/supply mismatch without underlying CAD usually causes a troponin rise < 1 ng/ml, and thus is not likely to explain the patient’s troponin (causes F and G). Similarly, in pulmonary embolism, troponin does not usually rise beyond 1 ng/ml.In the absence of obstructive CAD, a myocardial process, such as myocarditis or takotsubo cardiomyopathy, must be considered. Transient severe myocardial ischemia is also possible (vasospasm or stabilized plaque rupture). The deep T inversion is consistent with takotsubo cardiomyopathy, but also myocarditis and a post-ischemic state. In all those cases, the distribution of the echocardiographic wall motion abnormality helps establish a diagnosis. MRI is most helpful: late gadolinium enhancement rules out takotsubo cardiomyopathy and is only seen with infarction or myocarditis. The distribution of late gadolinium enhancement distinguishes myocarditis from an ischemic pattern:⁵²Distribution not consistent with an arterial territory + subepicardial 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.