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