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Antiplatelet therapy
Q1. A 70-year-old female patient with ongoing and severe chest pain is admitted to the chest pain unit at 4 am with a deep (> 3.0 mm) ST depression in the anterior leads and apical akinesia on echocardiography. She received aspirin (250 mg intravenous [i.v.]) and parenteral anticoagulation (5000 I.U. unfractionated heparin [UFH]) in the ambulance. The resident from the emergency room calls to inform you that the patient is still not pain-free and ST depression is now 1 mm. He would like to pre-treat this patient with 180 mg of ticagrelor? What is your advice as the interventional cardiologist on call?
This female patient should be scheduled for immediate invasive treatment with coronary angiography and it is not recommended to administer routine pre-treatment with a P2Y12 receptor inhibitor in patients in whom coronary anatomy is not known and an immediate invasive management is planned. Thus, any further antiplatelet treatment including a loading dose of either prasugrel 60 mg or ticagrelor 180 mg can be given after diagnostic angiography and before percutaneous coronary intervention (PCI) (section 5.1.1.2, Figure 7).
Q2. Why should we not consider a routine pre-treatment for all biomarker positive patients with suspected non-ST-elevation acute coronary syndrome (NSTE-ACS) and a planned coronary angiography?
Because it may be deleterious for a relevant proportion of patients with diagnoses other than NSTE-ACS (e.g. aortic dissection, bleeding complications including intracranial bleeding), and may increase bleeding risk or delay procedures in patients scheduled for coronary artery bypass grafting (CABG) after diagnostic angiography. A randomized trial showed no benefit of a pre-treatment with prasugrel compared with administration of the drug at the time of PCI, and specific randomized data are lacking for ticagrelor in NSTE-ACS patients. A pre-treatment regimen with a P2Y12 receptor inhibitor may only be considered in patients with high-risk NSTE-ACS who are not planned to undergo an early invasive strategy and do not carry a high bleeding risk. Fortunately, treatment with potent P2Y12 receptor inhibitors (ticagrelor or prasugrel) exhibits a fast onset of action, thereby allowing loading dose administration after diagnostic coronary angiography and before PCI.
Q3. Should this patient receive a glycoprotein (GP) IIb/IIIa antagonist upstream or during the PCI procedure?
No. Treatment with GP IIb/IIIa antagonists in patients in whom coronary anatomy is not known is not recommended and GP IIb/IIIa antagonists should only be considered for bail-out reasons if there is, for example, evidence of no-reflow or a thrombotic complication during PCI (section 5.1.2).
Q4. A 56-year-old male patient with a history of recent intracranial haemorrhage and severe arterial hypertension (systolic blood pressure > 200 mmHg) is admitted to the emergency department. He suffers from typical chest pain and the initial high-sensitivity cardiac troponin (hs-cTn) is markedly elevated (> 5 upper limit of normal [ULN]). Coronary angiography reveals single vessel disease with a stenosis of the medial right coronary artery (RCA). PCI is performed successfully. What are the options for P2Y12 inhibitor treatment for this patient?
The only optional treatment is clopidogrel (600 mg loading dose, 75 mg daily dose) for this patient. Of note, both potent P2Y12 receptor inhibitors prasugrel and ticagrelor are contraindicated in patients with a history of intracranial haemorrhage (Figure 7, Table 7).
Q5. What is the recommended treatment duration for dual antiplatelet therapy (DAPT) with aspirin and clopidogrel in this patient?
The recommended treatment duration for DAPT is 12 months unless there are contraindications or an excessive risk of bleeding. Indeed, the bleeding risk is high in this patient (e.g. PRECISE-DAPT ≥25 or ARC-HBR [Academic Research Consortium High Bleeding Risk] criteria met) and discontinuation of P2Y12 inhibitor therapy after 3 months should be considered (Figure 7, Table 7).
Q6. A 42-year-old male patient with diabetes, multivessel coronary artery disease (CAD), and a history of myocardial infarction (MI) with PCI of the proximal left anterior descending (LAD) coronary artery 13 months ago presents at an outpatient clinic for a routine follow-up. He has been on aspirin monotherapy for 3 weeks after having stopped a DAPT regimen with aspirin and ticagrelor after 12 months post-MI. What antithrombotic treatment should be recommended?
This patient is at high risk for future ischaemic events including re-infarctions. Adding a second antithrombotic agent to aspirin for extended long-term secondary prevention should be considered, given the lack of increased risk of major or life-threatening bleeding. Treatment options include a dual antithrombotic therapy (DAT) regimen with aspirin and rivaroxaban (2.5 mg twice daily [BID]) or a DAPT regimen with aspirin and ticagrelor (60 mg BID), prasugrel (5 or 10 mg once daily [OD]) or clopidogrel (75 mg OD) (Figure 7, Table 10).
Q7. What is the recommended peri-interventional anticoagulant treatment for patients undergoing PCI?
Any peri-interventional treatment for NSTE-ACS patients consists of anticoagulation to inhibit thrombin generation. Anticoagulation, usually administered intravenously, is recommended for all patients during invasive management such as PCI for NSTE-ACS. UFH is the standard of care for NSTE-ACS due to its favourable risk-benefit profile. Alternative drugs include bivalirudin and enoxaparin (Figure 7, Table 8).
Q8. A NSTE-ACS patient with a known history of heparin-induced thrombocytopenia is scheduled for PCI. What is the anticoagulant of choice?
UFH is contraindicated and bivalirudin would be the anticoagulant of choice during PCI. Bivalirudin dosing is as follows: 0.75 mg/kg i.v. bolus followed by i.v. infusion of 1.75 mg/kg/h for up to 4 h after the procedure as clinically warranted (Table 8).
Q9. A 49-year-old male patient with a body mass index of 22 kg/m2 and arterial hypertension presents to the emergency department with typical chest pain. He has not suffered any previous ischaemic events. The electrocardiogram (ECG) indicates ST depression and hs-cTn is 51 ng/L and 151 ng/L (ULN 14 ng/L) at admission and 1 h time points. Coronary angiography reveals two-vessel disease with a culprit lesion in the mid LAD. He is then scheduled for ad-hoc PCI of the remaining diseased vessel. What P2Y12 inhibitor should be given to this patient along with the procedure and for the months thereafter?
A P2Y12 receptor inhibitor is recommended in addition to aspirin and maintained over 12 months unless there are contraindications or an excessive risk of bleeding. Among the available potent P2Y12 receptor inhibitors (ticagrelor and prasugrel), the third generation thienopyridine prasugrel should be preferred over ticagrelor for NSTE-ACS patients who proceed to PCI. This recommendation is based on the results of the randomized ISAR-REACT 5 (Intracoronary stenting and Antithrombotic regimen–Rapid Early Action for Coronary Treatment) trial where prasugrel vs. ticagrelor significantly reduced the composite rate of death, MI, or stroke without any increase in bleeding complications (section 5.1.1.2, Figure 7).
Q10. Are there any individualized antiplatelet treatment strategies for certain subsets of NSTE-ACS patients?
NSTE-ACS patients treated with prasugrel or ticagrelor may suffer major or repetitive minor bleeding complications which may negatively impact treatment adherence. Here, de-escalation of P2Y12 receptor inhibitor treatment (e.g. with a switch from prasugrel or ticagrelor to clopidogrel) may be considered as an alternative DAPT strategy, especially for ACS patients deemed unsuitable for potent platelet inhibition. De-escalation may be done unguided based on clinical judgment or guided by platelet function testing or CYP2C19 genotyping, depending on the patient’s risk profile and availability of respective assays. The latter options leave room for a more individualized approach for antiplatelet treatment in ACS patients. It must be emphasized that such strategies are optional and should be implemented on a case-by-case decision (section 5.1.4).
Q11. What are the high-risk criteria for long-term treatment with a second antithrombotic agent besides aspirin?
Criteria for a high thrombotic risk are the presence of a complex CAD based on clinical judgment and at least one further criterion among risk enhancers or technical aspects (Table 11). Risk enhancers include diabetes mellitus requiring medication, history of recurrent infarction, any multivessel CAD or polyvascular disease (CAD or peripheral artery disease), premature (< 45 years) or accelerated (new lesion within a 2-year time frame) CAD, concomitant systemic inflammatory disease (e.g. HIV, systemic lupus erythematosus, chronic arthritis), or chronic kidney disease with estimated glomerular filtration rate 15–59 mL/min/1.73 m2. Technical aspects include at least three stents implanted, at least three lesions treated, a total stent length > 60 mm, a history of complex revascularization (left main, bifurcation stenting with ≥ 2 stents implanted, chronic total occlusion, stenting of last patent vessel), or a history of stent thrombosis on antiplatelet treatment (Table 11).
Q12. Does it make sense to continue parenteral anticoagulation therapy after PCI?
No, there is no supportive compelling evidence. A prolonged parenteral anticoagulation after PCI has never been shown to reduce periprocedural ischaemic events while it may increase the risk of bleeding. Thus, all the respective drugs should be discontinued immediately after PCI except for specific clinical settings such as the confirmed presence of left ventricular aneurysm with thrombus formation, the presence of a mechanical valve, or atrial fibrillation requiring anticoagulation, which is usually done with UFH in (per)-acute settings.
Q13. Is there any evidence for dropping aspirin in the early months after PCI in NSTE-ACS patients?
Yes, there is now evidence. The randomized TWILIGHT (Ticagrelor With Aspirin or Alone in High-Risk Patients After Coronary Intervention) trial examined the effect of ticagrelor alone after a period of 3 months DAPT vs. ticagrelor plus aspirin with regard to clinically relevant bleeding among patients at high risk for bleeding or ischaemic event who had undergone PCI. The primary bleeding endpoint was significantly reduced by omitting aspirin with a significant interaction according to ACS at presentation. The trial was not powered for the composite endpoint of death from any cause, non-fatal MI, or non-fatal stroke.
Anticoagulation and antiplatelet therapy
Q14. A patient with atrial fibrillation and a mechanical prosthetic heart valve, treated with a vitamin K antagonist (VKA), is admitted with suspected NSTE-ACS. Coronary angiography is planned. How do you manage anticoagulation?
Coronary angiography can be performed on VKA since interruption and bridging with parenteral anticoagulation is associated with increased thromboembolic episodes and bleedings. The radial artery is the default vascular access. In the case of PCI, additional low-dose parenteral anticoagulation (e.g. UFH 60 IU/kg i.v. [Class 1 recommendation] or enoxaparin 0.5 mg/kg i.v. [Class IIa recommendation]) should be considered if the international normalized ratio is < 2.5 (section 5.3.1).
Q15. What about if the patient is on non-VKA oral anticoagulant (NOAC)?
Coronary angiography can be performed without interruption of NOAC using the radial artery as the default vascular access. In the case of PCI, additional low-dose parenteral anticoagulation (e.g. UFH 60 IU/kg i.v. [Class 1 recommendation] or enoxaparin 0.5 mg/kg i.v. [Class IIa recommendation]) should always be considered, regardless of the timing of the last NOAC administration (section 5.3.1).
Q16. A 72-year-old male with non-ST-elevation MI (NSTEMI) underwent PCI with a drug-eluting stent (DES) in the first obtuse marginal branch. He has permanent ‘non-valvular atrial fibrillation’ with a CHA2DS2-VASc score ≥1 and is on VKA. How would you optimize the patient’s anticoagulation?
NOAC should be used instead of VKA at the recommended dose for stroke prevention because of its superior safety profile (e.g. lower bleeding risk). Given the implantation of a single DES into a vessel with limited myocardium at risk, DAPT should be administered up to 1 week in addition to NOAC. Thereafter, DAT with NOAC and single antiplatelet therapy (by preference clopidogrel) should be administered up to 12 months (Figure 8, section 5.3.1).
Q17. A 64-year-old female patient with non-insulin dependent diabetes mellitus and permanent atrial fibrillation (CHA2DS2-VASc score ≥ 2) is admitted for a NSTEMI. She underwent an early invasive coronary angiography with PCI of the distal left main coronary artery with two DES. How would you manage triple antithrombotic therapy (TAT)?
This patient is at high thrombotic risk given the presence of diabetes and the complex coronary anatomy (section 5.1.4, Table 11). The theoretical bleeding risk is low according to the HAS-BLED score of 1. TAT consisting of a NOAC at the dose recommended for stroke prevention associated with DAPT (aspirin and clopidogrel) should be administered up to 1 month. Thereafter, DAT with NOAC and single antiplatelet therapy (SAPT) (preferably clopidogrel) should be administered up to 12 months (section 5.3.1, Figure 8).
Q18. A 72-year-old female patient with hypertension, non-insulin dependent diabetes mellitus, and atrial fibrillation treated with NOAC (last dose taken 6 hours before hospital admission) is admitted at 12 am for NSTEMI. She is free of angina at admission. Your resident asks whether we should postpone invasive coronary angiography to the next morning. What is your answer?
This patient should receive aspirin at the initial oral loading dose of 150–300 mg (or 75–250 mg i.v.) and a proton-pump inhibitor, additional low-dose parenteral anticoagulation (e.g. UFH 60 IU/kg i.v. [Class 1 recommendation] or enoxaparin 0.5 mg/kg i.v. [Class IIa recommendation]), and sent to the catheterization laboratory for an early invasive coronary angiography within 24 h, which in this case may be best during the afternoon. We may consider postponing to the next morning if the catheterization laboratory is not available and transfer is needed to a hub hospital (Figure 9).
Q19. PCI with DES implantation of the mid LAD coronary artery is performed in the afternoon. Your resident comes back to you and asks how to manage antithrombotic therapy thereafter?
Your answer is that a loading dose of clopidogrel (600 mg orally) should be administered as soon as the decision for PCI is made. Then comes the decision of TAT duration. The high bleeding risk of the patient (HAS-BLED score ≥ 3) seems to outweigh a moderately increased thrombotic risk (section 5.1.4). You explain that TAT is recommended for up to 1 week post-PCI, followed by DAT (NOAC with SAPT, preferably clopidogrel) for up to 6 months (section 5.3.1, Figure 8 ).
Q20. Your junior doctor keeps asking questions and whether ARC-HBR is better than any ‘usual score’ for bleeding risk assessment. What is your answer?
The ARC-HBR is an alternative tool to assess the bleeding risk (Table 7) in patients undergoing PCI. It represents a pragmatic approach that includes the most recent trials performed in HBR patients who were previously excluded from clinical trials on DAPT duration or intensity. In the presence of high bleeding risk criteria (i.e. when one major or two minor ARC-HBR criteria are met), an NSTE-ACS patient treated with stent implantation should discontinue P2Y12 receptor inhibitors after 1 week. In NSTE-ACS patients treated with VKA, clopidogrel alone should be considered up to 12 months (class of recommendation IIa, level of evidence B). ARC-HBR criteria may be difficult to apply in clinical practice as several of the criteria are quite detailed. However, this score is comprehensive, robust, and has been validated.
Q21. A 58-year-old smoker male, is admitted for NSTEMI. He is on NOAC for intermittent episodes of atrial fibrillation but currently he presents in sinus rhythm. PCI with multiple DES implantation is performed after a loading dose of 600 mg clopidogrel. Transthoracic echocardiography shows a normal left ventricular function, no valve disease, and a normal-sized left atrium. Your resident is sceptical and asks whether clopidogrel may be switched to ticagrelor or prasugrel with concomitant aspirin administration and interruption of the NOAC for the next coming weeks.
The CHA2DS2-VASc score is 1 suggesting a low-to-moderate risk of stroke. On the other hand, the coronary thrombotic burden is high. NOAC may be withdrawn and DAPT with aspirin and ticagrelor or prasugrel may be administered for the first few weeks assuming that the risk of stent thrombosis is prevailing (section 5.3.1). However, supportive data are lacking, and this can only be a case-by-case decision. Oral anticoagulation should be resumed as soon as possible.
Q22. A 62-year-old female patient, hypertensive, treated with apixaban 5 mg b.i.d. for permanent atrial fibrillation, presents with acute chest pain, ischaemic ECG changes, and significantly elevated hs-cTn T of 350 ng/L (ULN 14 ng/L). She had a prior cardioembolic stroke. She undergoes coronary angiography with PCI and double DES implantation of the bifurcation LAD with the first diagonal branch. How would you manage the antithrombotic therapy?
This patient has a moderate-high risk of stroke with a CHA2DS2-VASc score of 4. In addition, she has a high coronary thrombotic risk given the bifurcation PCI. NOAC should be maintained and DAPT with aspirin and clopidogrel should be initiated for at least 1 week and up to 1 month, followed by DAT with SAPT (preferably clopidogrel up to 12 months) (section 5.3.1, Figure 8).
Q23. The general practitioner is seeking guidance at the 6-month follow-up. He asks: how long should DAT be administered?
Your answer is that if there is no bleeding complication, DAT is recommended for up to 1 year and then stop antiplatelet therapy if there is no additional argument for CAD progression. With respect to NOAC, 12 months with continuation of oral anticoagulation only is recommended (section 5.3.1, Figure 8). There are data from a randomized clinical trial supporting NOAC alone over DAT beyond 1 year.
Q24. He also asks whether there is a specific NOAC to be used in this setting.
The answer is no. All randomized clinical trials gathered data in favour of the four NOACs available including half of patients (50–60%) with NSTE-ACS. Considerations on a specific NOAC in NSTE-ACS patients could take place on a case-by-case basis: in patients at high bleeding risk, preference should go to NOACs showing the lowest incidence of bleeding; in patients with previous or at high risk of ischaemic stroke, preference could go to NOACs with the largest burden of data and showing the greatest risk reduction in stroke; in patients with previous MI or at high risk for ACS, preference could go to NOACs largely investigated in this setting; in patients with impaired renal function, preference could go to NOACs with the lowest dependency on renal excretion; finally, in patients medically managed, preference should go to apixaban, the only NOAC tested in that setting.
Q25. A 55-year-old hypertensive male patient with NSTE-ACS undergoes multivessel PCI with DES implantation of the left main bifurcation and of the proximal RCA. A treatment with aspirin 100 mg OD and prasugrel 10 mg OD is initiated. However, during the hospital admission the patient develops atrial fibrillation lasting more than 24 hours. Transthoracic echocardiography shows a normal left ventricular function, mild mitral regurgitation, and an enlarged left atrium. How do you manage the antithrombotic regimen?
The patient has a moderate stroke risk (CHA2DS2-VASc score ≥ 2) and a high likelihood that atrial fibrillation becomes recurrent or permanent. Therefore, a NOAC should be started at the dose of stroke prevention. In consideration of the high coronary thrombotic risk derived from multivessel stenting, this patient should continue with additional DAPT up to 1 month. However, prasugrel should be switched to clopidogrel with no need of a loading dose (section 5.3.1 and Figure 8).
Q26. A 68-year-old female patient with permanent atrial fibrillation received aspirin, clopidogrel, and apixaban 5 mg BID following NSTE-ACS. No significant CAD was evidenced. Considering that no revascularization was performed, how do you best manage the antithrombotic therapy?
The only evidence available thus far in this kind of patient is the one derived from the AUGUSTUS (Antithrombotic Therapy After Acute Coronary Syndrome or PCI in Atrial Fibrillation) trial. The patient can be discharged with apixaban 5 mg BID plus clopidogrel for at least 6 months (section 5.3.1).
Revascularization strategies
Q27. A 69-year-old patient with a history of CABG surgery presents to the emergency department in a hospital without PCI service for recurrent chest pain of increasing frequency during the last month. The chest pain at admission lasted about 20 minutes. He is haemodynamically stable with an unremarkable ECG, hs-cTn is within the normal range, and the calculated GRACE (Global Registry of Acute Coronary Events) risk score is < 140. The internal medicine resident asks you whether a transfer of this patient to a PCI centre is necessary.
Patients with no recurrence of symptoms and none of the very high or high-risk criteria are to be considered at low risk for short-term acute ischaemic events. Furthermore, patients previously regarded to be at intermediate risk (history of revascularization or diabetes mellitus), but ruled-out according to hs-cTn-based diagnostic algorithm, should also be regarded at low risk and follow a selective invasive strategy pathway (sections 6.1.2.3 and 6.7).
Q28. A 60-year-old patient with a body mass index of 30 kg/m2 and a family history of cardiovascular disease presents due to recurrent episodes of chest pain during the previous 2 weeks. At admission the 12-lead ECG indicates an iso-electric ST-segment. Serial hs-cTn testing (ULN 14 ng/L) reveals 25 ng/L and 27 ng/L at admission and 1 h and no further change. Should the patient be referred for invasive coronary angiography during index hospitalization?
The lack of a significant increase of hs-cTn levels up to 3 h after admission suggests a low probability for NSTEMI (sections 3.3.3. and 3.3.4). Furthermore, the lack of recurrent angina or ECG changes during the hospital stay and the low GRACE score further confirms that invasive coronary angiography during index hospitalization is not required. However, it may be indicated after appropriate non-invasive ischaemia testing or detection of obstructive CAD by coronary computed tomography angiography (CCTA) (sections 6.1.2. and 6.7).
In case of an unclear NSTE-ACS diagnosis, non-invasive imaging during index hospitalization in addition to hs-cTn does not improve patient flow but might reduce the need for invasive coronary angiography (sections 3.3.5.2, 3.4 and 6.7); it is therefore recommended.
Q29. A 65-year-old patient with a history of hypertension is admitted to the coronary care unit with the working diagnosis of NSTE-ACS due to ongoing chest pain and acute heart failure. Clinical examination indicates bilateral pulmonary rales and arterial blood pressure of 150/90 mmHg. The 12-lead ECG is shown in Figure 1. The internal medicine resident asks you whether immediate invasive coronary angiography should be performed.
This patient fulfils two very high-risk criteria including acute heart failure clearly related to NSTE-ACS and ST-segment depression > 1mm in six leads plus ST-segment elevation aVR and V1 (highly suggestive for significant left main CAD). Due to a poor short- and long-term prognosis if left untreated, an immediate invasive diagnostic strategy (< 2 h from hospital admission) similar to STEMI with intent to perform revascularization is recommended (sections 6.1.2.1 and 6.7, and Figure 9). Admission hs-cTn measurement and echocardiography in the catheterization laboratory are also recommended but without delaying invasive coronary angiography.
Q30. An 80-year-old patient presents with typical chest pain during the last 2 months, which has been getting worse the last week before admission. Serial laboratory measurements show a rise in hs-cTn T from 35 ng/L to 505 ng/L (ULN 14 ng/L). A 12-lead ECG on admission reveals signs of transmural Q-wave inferior wall MI (Figure 2 upper part) with hypokinetic inferior wall motion with slightly reduced systolic left ventricular function (45%). Invasive coronary angiography performed 3 h after admission reveals a three-vessel CAD (Figure 2 lower part). How do you identify the culprit lesion? Is intracoronary imaging helpful?
More than half of NSTE-ACS patients with obstructive CAD have multivessel CAD. One-quarter present with an acute occluded coronary artery. Since nearly two-thirds of the occlusions are already collateralized, differentiation between an acute/subacute and chronic occlusion may be challenging (section 6.1.5). ECG and echocardiography or left ventricular angiogram may help to identify the culprit lesion corresponding to a regional wall motion abnormality (section 6.4). On the other hand, intracoronary imaging (intravascular ultrasound or optical coherence tomography [OCT]) is of limited value to identify culprit lesions, with the exception of MI with non-obstructed coronary arteries (MINOCA; section 7). Thus, the most probable culprit lesion in this patient is the occluded and partially collateralized RCA.
Q31. A 53-year-old women presents with NSTE-ACS. She is on hormone-replacement therapy due to premature menopause. The 12-lead ECG is shown in Figure 3 (left panel), while echocardiography was normal. Coronary angiography shows a three-vessel CAD with total occluded extended posterolateral branch of the left circumflex artery (LCx) (Rentrop I class collaterals), significant stenosis of the mid LAD, and critical stenosis of the proximal RCA (Figure 3 right panel). The anatomical SYNTAX (Synergy Between Percutaneous Coronary Intervention With Taxus and Cardiac Surgery) score is 14.5. The interventional fellow asks you whether to perform complete revascularization during the index PCI or just treat the culprit lesion.
Registry data suggest increased in-hospital mortality with a single-stage complete revascularization strategy compared to culprit-lesion-only PCI. The only randomized trial demonstrated less major adverse cardiac and cerebrovascular events at 1 year with single-stage PCI, largely driven by the lower rate of repeat revascularization with single-stage vs. staged multivessel PCI. Completeness of revascularization in some patients with complex anatomy might increase the PCI risk or require CABG surgery. It is reasonable in the absence of robust clinical data to tailor the need for and timing of complete revascularization to functional relevance of all stenoses, left ventricular function, age, general patient condition, and comorbidities (section 6.3.3 and 6.7). For the aforementioned patient, culprit-only PCI (revascularization of the posterolateral branch of the LCx) during index PCI followed by later staged complete revascularization may be the right strategy.
Q32. A 56-year-old man presents with NSTEMI with sinus tachycardia and non-significant Q-waves in the inferior ECG leads. Bedside echocardiography shows normal systolic left ventricular function and a moderate mitral regurgitation. A loading dose of aspirin (300 mg) and UFH intravenously is administered with sublingual glyceryl trinitrate leading to temporary pain relief. Urgent invasive coronary angiography was performed after recurrent chest pain demonstrating three-vessel CAD with subtotal occlusion of the distal RCA (culprit lesion), chronic total occlusion of the LCx, and a significant long lesion of the LAD (Figure 4). Your interventional resident asks whether a heart team discussion is necessary to treat the culprit lesion and what the best revascularization strategy is for this patient.
Considering the young age of the patient, the absence of comorbidities, an anatomical SYNTAX score > 22 and a stable haemodynamic presentation, CABG surgery should be considered despite scant supportive data in the specific setting of NSTE-ACS (section 6.5). Therefore, a heart team discussion should be considered. However, given the unstable clinical presentation and the reduced coronary flow at the culprit lesion, the treating physicians decided to perform PCI of the RCA. While the decision on immediate PCI of the culprit lesion does not require heart team consultation, the decision about the optimal strategy to complete revascularization in case of severe CAD is based on clinical status, comorbidities, and SYNTAX score (sections 6.5 and 6.7).
Q33. A 51-year-old man presents with typical chest pain, shortness of breath (26 breaths/min), room air O2 saturation of 88%, heart rate of 120 bpm, and non-invasive blood pressure of 90/55 mmHg. The 12-lead ECG showed ST-segment depression in leads II, III, and aVF. Bedside echocardiography revealed reduced left ventricular systolic function (30%) with global hypokinesia. An urgent coronary angiogram revealed three-vessel CAD with the culprit lesion located at mid RCA (Figure 5 left panel). Is there a need for percutaneous mechanical circulatory support devices during PCI?
This is a very high-risk NSTE-ACS presentation with cardiogenic shock. Urgent echocardiography without delay to assess left ventricular and valvular function, as well as to exclude mechanical complications, is recommended. The benefit of percutaneous mechanical circulatory support devices (MCS) and/or venoarterial extracorporeal membrane oxygenation (VA-ECMO) in cardiogenic shock is currently being investigated in several randomized clinical trials (Table S7, online supplement). In several small randomized clinical trials, and also in several large registries, there was no benefit of MCS compared to intra-aortic balloon pump (IABP). The use of IABP in cardiogenic shock patients without mechanical complications did not reduce mortality in the large-scale randomized IABP-SHOCK II trial (section 8.1). However, depending on age, comorbidities, neurological function, and severity of cardiogenic shock, MCS or VA-ECMO support might be considered after heart team discussion.
Q34. Should single-stage complete revascularization be performed in patients with NSTE-ACS and cardiogenic shock?
Nearly 80% of NSTE-ACS patients with cardiogenic shock have multivessel CAD. In the CULPRIT-SHOCK trial, the culprit-lesion-only PCI strategy led to a significant reduction of mortality and renal replacement therapy at 30 days, which was consistently shown at 1- year follow-up after PCI compared to immediate multivessel PCI. Thus, immediate treatment of the culprit lesion (in this case RCA) with staged PCI of the non-culprit lesion(s) is the recommended strategy (sections 6.7 and 8.1).
Q35. A 55-year-old woman is admitted to the emergency department for resuscitated out-of-hospital cardiac arrest due to ventricular fibrillation. The 12-lead ECG obtained at admission is shown in Figure 6. Haemodynamic status is stable and echocardiography revealed no abnormalities. Admission hs-cTn level is 250 ng/L (14 ng/L ULN). The internal medicine resident asks you whether this patient should undergo urgent invasive coronary angiography.
According to the recently published COACT (Coronary Angiography After Cardiac Arrest) trial, an unselected immediate invasive strategy is not superior over a delayed invasive strategy in out-of-hospital cardiac arrest and haemodynamically stable NSTE-ACS (sections 6.6.2 and 6.7). Invasive coronary angiography performed 6 h after admission (Figure 6) showed a tight stenosis of the proximal LAD, which was successfully stented.
Q36. A 43-year-old woman presents to the emergency department of a tertiary hospital after a 30-minute episode of centrally located chest pain, radiating to the left arm following vigorous-intensity physical activity. She has no known cardiovascular risk factors. A 12-lead ECG showed normal sinus rhythm with T-wave inversion in V2–V4. Symptom intensity was partially improved following i.v. 300 mg aspirin and sublingual 400 µg glyceryl trinitrate and then became worse 30 minutes later. What is the optimal management strategy for this patient?
This patient fulfils the very high-risk criteria (recurrent chest pain despite medication) mandating an immediate invasive strategy (< 2 h, sections 6.1.2. and 6.7, Figure 9). In the coronary angiogram a filling defect suggesting intracoronary thrombus was observed in the posterolateral branch of the RCA. OCT of the lesion visualized spontaneous coronary artery dissection (SCAD) as the cause of NSTE-ACS (Figure 7). Medical management was chosen due to the distal location of SCAD. Complete healing with restoration of normal coronary flow was observed at one-month follow-up angiogram.
Q37 A 48-year-old man with a history of hyperlipidaemia and active smoking reports an episode of chest pain of 30 minutes’ duration after an episode of chest discomfort 6 hours previously. The physical examination and 12-lead ECG are unremarkable. Admission hs-cTn is 620 ng/L (14 ng/L ULN). Invasive coronary assessment performed during the same day shows diffuse atherosclerosis with intraluminal coronary haziness in the proximal LAD (Figure 8). Is intracoronary imaging of any help to identify the type of underlying disease within the culprit lesion?
In patients with MINOCA, OCT is the diagnostic tool for evaluating SCAD or erosion of plaque rupture. In this case, OCT revealed plaque rupture as the culprit lesion with subsequent thrombus formation and distal embolization (sections 3.2, 3.3, 6.1.2 and 6.1.7).
Q38. A 55-year-old woman without cardiovascular risk factors or prior cardiovascular event is admitted to the emergency department with epigastric pain which started suddenly 2 h before admission. The 12-lead ECG demonstrates ST-segment depression of 1 mm in the precordial leads. Admission hs-cTn level is 350 ng/L (14 ng/L ULN), ruling-in NSTE-ACS. Invasive coronary angiography reveals non-obstructive disease of the mid LAD (Figure 9). Your interventional fellow asks whether additional intracoronary imaging is necessary to evaluate the underlying disease.
This woman is presenting with MINOCA. Vascular spasm, endothelial erosions, or non-obstructive SCAD type 3 are frequent findings of MINOCA. Intracoronary imaging, and particularly OCT, is an accurate option for ruling-in SCAD-related intramural haematoma (sections 6.1.5 and 7). OCT imaging in this case revealed a large intramural haematoma.
Q39. What is the treatment strategy in case of SCAD type 3?
Type 3 refers to focal or tubular stenosis that mimics atherosclerosis. The benefit of revascularization in this case is not established and a conservative approach is usually the preferred strategy, at the exception of very high-risk profile patients (section 6.1.5). Aggressive antihypertensive therapy is preferred, while the benefit of antithrombotic therapy (in case of no PCI) is not well validated.
Q40. Is repeat invasive coronary angiography necessary to follow-up SCAD healing?
Among SCAD patients treated medically without any recurrent or persistent symptoms, no repeat invasive coronary angiography is necessary. Although CCTA may lack accuracy for an early diagnosis of SCAD, it is useful for the healing follow-up in case of documented SCAD with recurrent or persistent symptoms, even in the absence of recurrent MI or ischaemia (section 6.1.5.)
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† The Full Text Guidelines are available at:www.escardio.org/guidelines and https://dbpia.nl.go.kr/eurheartj
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