Type 2 myocardial infarction and spontaneous coronary artery dissection

This page covers troponin rises from processes other than atherothrombosis, which commonly underlie acute chest pain with troponin elevation (ESC 2023).^[2] It starts with the vocabulary, because the definitions changed in 2026, then works through supply–demand (secondary) MI, MINOCA and spontaneous coronary artery dissection.

• Reperfusion when the ECG shows occlusion: STEMI: reperfusion strategy, timing and transfer decisions.
• NSTE-ACS diagnosis and invasive timing: NSTE-ACS: NSTEMI and unstable angina — diagnosis, risk and invasive timing.
• CMR technique and LGE patterns: Cardiac MRI: LGE patterns and clinical questions.
• Bleeding, switching and stopping DAPT: DAPT complications: bleeding, switching and surgery.

Injury, infarction and the 2026 reclassification

Start with troponin. The Fifth UDMI defines acute myocardial injury as a rise and/or fall in cardiac troponin I or T with at least one value above the sex-specific 99th percentile URL (Box 1).^[1] It uses sex-specific thresholds to avoid a systematic bias and the under-recognition of myocardial injury in female patients.^[1]

Chronic myocardial injury is considered if two or more troponin values are above the sex-specific 99th percentile URL when testing is performed in a stable clinical setting (Box 2).^[1] It is confirmed when a cardiac or non-cardiac condition associated with cardiac remodelling is identified, and excluded when the elevation is explained by analytical interference or reduced clearance.^[1]

In the Fifth UDMI, acute myocardial injury shown to be due to ischaemia is the hallmark of MI, and it should be classified as infarction when the diagnostic criteria for MI are met.^[1] Its clinical diagnosis of MI requires acute myocardial injury and one or more of three features.^[1] The first is symptoms or other evidence of acute myocardial ischaemia, including new ischaemic changes or pathological Q waves on the ECG.^[1] The other two are imaging evidence of an acute coronary pathology, or new loss of viable myocardium or a new regional wall motion abnormality in a pattern consistent with an ischaemic aetiology.^[1] Non-ischaemic mechanisms of acute injury include inflammation, physiological stress response, catecholamine stress, cardiotoxic agents and trauma.^[1]

ESC 2023, using the Fourth UDMI terms, describes myocardial injury as myocyte necrosis and troponin elevation due to mechanisms other than myocardial ischaemia, acute (e.g. sepsis, myocarditis, takotsubo) or chronic (e.g. HF, cardiomyopathies, severe valve heart disease).^[2] It adds that the diagnosis of myocardial injury can change if subsequent investigations show that the patient meets the criteria for MI.^[2]

Selected rows of Fifth UDMI Table 2: mechanisms of acute myocardial injury

^[1]

Mechanisms can overlap: in sepsis, both inflammation and the physiological stress response may contribute.^[1] Acute myocardial injury therefore requires clinical evaluation to determine its aetiology, assess functional impact and identify ischaemia; if ischaemia is present, coronary and cardiac imaging is required to confirm or exclude MI.^[1]

From type 2 MI to secondary MI

The Fifth UDMI is a joint ESC, ACC, AHA and WHF statement.^[1] It is a consensus statement and should be applied in conjunction with national and regional clinical practice guidelines.^[1] It replaced the previous numerical classification with three clinical types: primary MI (spontaneous presentation due to a primary acute coronary pathology), secondary MI (supply–demand imbalance due to another acute condition) and procedure-related MI.^[1]

Why change? Grouping non-atherosclerotic coronary causes (e.g. coronary dissection, embolism or vasospasm) with supply–demand imbalance as type 2 MI limited its adoption in practice, because these patients follow very different diagnostic pathways and require different treatments.^[1] Under the Fourth UDMI, type 2 MI was diagnosed two ways: retrospectively, when angiography in presumed type 1 MI found no acute coronary pathology, and prospectively, when supply–demand imbalance from another acute condition was evident at presentation.^[1]

Fifth UDMI Table 1: type 2 MI against secondary MI (selected rows)

^[1]

Primary MI, by contrast, prioritizes sensitivity to avoid missing any primary acute coronary pathology.^[1] The Fifth UDMI proposes ICD-11 codes that record the mechanism: a separate code for spontaneous coronary artery dissection within primary MI, and a secondary-MI code paired with the code for the alternative acute condition (Table 4).^[1]

The older terms persist in the guidelines you will be examined on.^[2][3] ESC 2023 uses the fourth universal definition of MI; it defines type 2 MI as an ischaemic myocardial injury in the context of a mismatch between oxygen supply and demand that is not related to acute coronary atherothrombosis.^[2] ACC/AHA 2025 Table 4, adapted from the 2018 definition, describes type 2 MI as caused by an imbalance between myocardial oxygen supply and demand unrelated to acute coronary atherothrombosis.^[3]

^[1]

How the guidelines position themselves

• ACC/AHA 2025 ACS focuses on the management of type 1 AMI and states that the management of type 2 MI, SCAD and MINOCA is covered in separate documents; in the text held for this topic it has no SCAD recommendation row.^[3]
• ACC/AHA 2025 ACS adds that it can be challenging to differentiate type 1 versus type 2 MI, and that in cases of uncertainty, depending on the benefits and risks of a specific intervention, it may be appropriate to err on the side of considering an event type 1 ACS until established to be otherwise.^[3]
• NHFA/CSANZ 2025 (MJA summary) primarily addresses MI caused by atherosclerotic plaque rupture, ulceration, fissure or erosion, but says some recommendations may also apply to non-atherosclerotic causes such as SCAD.^[10]
• NHFA/CSANZ 2025 classifies SCAD, coronary embolism and coronary spasm or microvascular dysfunction as MI with acute coronary occlusion, because they can present identically to atherosclerotic AMI and may require urgent angiography to diagnose and treat appropriately; its 2016 guideline had called these type 2 MI.^[10]

Supply–demand (secondary) MI

Picture the patient: a man with known coronary disease, in fast AF from pneumonia, whose troponin is rising.^[1][8] The presumed mechanism is not a plaque event but an oxygen budget in deficit, although acute illness, particularly sepsis or bleeding, can also trigger atherothrombosis (Fifth UDMI).^[1]

Triggers

The Fifth UDMI describes supply–demand imbalance from increased demand (e.g. tachycardia or severe hypertension) or reduced supply (e.g. hypotension, hypoxia or anaemia).^[1] Acute ischaemia can therefore arise in many acute conditions, the most common being tachyarrhythmia.^[1] Two or more triggers often coexist, so it is not possible to define thresholds for any trigger that could be reliably applied to all.^[1]

^[1]

• ESC 2023 lists non-coronary mechanisms of type 2 MI as supply–demand mismatch due to hypoxia, hypotension, anaemia, tachycardia or bradycardia, and coronary ones as e.g. coronary embolus, dissection, spasm or microvascular dysfunction.^[2]
• ESC 2023: in some cases, severe anaemia may precipitate type 2 MI.^[2]
• ESC 2024 AF: AF is a common precipitant for type 2 MI.^[8]
• The Fifth UDMI notes that the duration and severity of the trigger, and whether there is underlying obstructive coronary disease or structural cardiac disease, influence the extent and severity of ischaemia.^[1]

Diagnosis: Box 4 criteria

The Fifth UDMI builds secondary MI in three steps.^[1] It is considered when acute myocardial injury occurs with an alternative acute condition causing supply–demand mismatch and at least one clinical or ECG feature; it becomes likely with supporting features; and it is confirmed by imaging.^[1]

Fifth UDMI Box 4: diagnostic criteria for secondary MI

^[1]

If imaging shows an acute coronary pathology, the diagnosis becomes primary MI.^[1] The criteria prioritize specificity and encourage coronary angiography and cardiac imaging, increasing the likelihood that the diagnosis has treatment implications for the patient.^[1]

^[1]

Why the bedside clues mislead

• Symptoms: patients are less likely to report chest discomfort and more likely to have other symptoms due to the underlying acute condition.^[1]
• Presentation: secondary MI is less likely to present with chest pain and more likely to present with breathlessness or other symptoms of the primary diagnosis.^[1]
• ECG: ischaemia from supply–demand imbalance can show regional ST-segment depression or T-wave inversion, but these changes are often global.^[1]
• Troponin: current assays cannot differentiate ischaemic from non-ischaemic causes of injury.^[1]

Because symptoms, signs and troponin alone cannot reliably establish MI here, additional clinical assessment and cardiac imaging are needed, when feasible and appropriate for the clinical status, to confirm or exclude secondary MI.^[1] Most patients in this setting will not have obstructive coronary disease or imaging evidence of new loss of viable myocardium, and secondary MI can be excluded.^[1]

Imaging: what to do and when

• Timing: outside the persistent-ischaemia scenario, imaging is often deferred until after the acute condition has been treated, so that non-invasive approaches such as CCTA can be applied (Fifth UDMI).^[1]
• CCTA after recovery: if primary MI is an unlikely differential diagnosis, non-invasive CT coronary angiography following recovery from acute illness may be considered (Fifth UDMI pathway footnote).^[1]
• Echocardiography: in secondary MI, differentiating a global reduction in LV function from regional wall motion abnormalities is important and can inform the diagnosis (Fifth UDMI).^[1]
• Physiology: in possible secondary MI, particularly where stenosis severity is unclear, FFR or resting indices may be helpful in detecting functionally significant stenosis (Fifth UDMI).^[1]
• CCTA: may aid in differentiating primary from secondary MI through plaque phenotyping, and in secondary MI may detect obstructive or flow-limiting coronary disease (Fifth UDMI).^[1]
• ESC 2023: once patients with suspected type 2 MI and myocardial injury have been stabilized and any precipitating illness treated, targeted echocardiography and/or coronary angiography (invasive or CCTA) can identify contributory cardiac conditions and guide long-term treatment.^[2]

Additional cardiac imaging is sometimes not appropriate in patients with comorbidities, advanced frailty or limited life expectancy due to the underlying acute condition; then the diagnosis may not be confirmable and clinical judgment is required (Fifth UDMI).^[1] Secondary MI is more likely with known coronary disease or significant myocardial injury that affects cardiac function, and these features can support a clinical diagnosis when imaging is not feasible or appropriate.^[1]

Management principles

ESC 2023, citing the lack of robust scientific evidence and the wide range of precipitating causes, states that there are currently no specific recommended pharmacological interventions for patients with type 2 MI (no class or level given).^[2] Management should instead focus on identifying and treating any precipitating conditions (e.g. anaemia, hypoxia) alongside strict control of CV risk factors.^[2]

• Why confirm the diagnosis? A secondary MI confirmed by coronary and/or cardiac imaging would have treatment implications for those with coronary disease and/or LV systolic dysfunction (Fifth UDMI).^[1]
• Bonus findings: imaging may also identify non-obstructive but clinically relevant coronary disease or previously unrecognized conditions such as non-ischaemic cardiomyopathy or valvular heart disease (Fifth UDMI).^[1]
• Evidence: in a prospective cohort with systematic coronary and cardiac imaging (Bularga 2022; 93 patients with type 2 MI by the previous definition after imaging, frailty and renal or hepatic failure excluded), coronary artery disease was found in 68% (63 of 93) and LV systolic dysfunction in 34% (32 of 93), previously unrecognized in 60% (38 of 63) and 84% (27 of 32), respectively.^[13]
• If MI is excluded: the underlying aetiology of acute myocardial injury should be determined when possible (Fifth UDMI).^[1]
• Rehabilitation: cardiac rehabilitation is less often offered to those with secondary MI, where arguably the role for education is more important; criteria that include coronary disease may encourage their inclusion (Fifth UDMI).^[1]

Settings where secondary MI is common

Fifth UDMI special situations (selected)

^[1]

ESC 2023 states that type 2 MI is common and associated with a prognosis similar to type 1 MI.^[2] The Fifth UDMI cites one study suggesting that its secondary-MI criteria would reduce the frequency of the MI diagnosis in acute illness and identify those at highest risk.^[1]

MINOCA: a working diagnosis, not a destination

A troponin-positive patient goes to the catheter laboratory and the arteries look non-obstructive.^[2] The label you write next depends on the document.

MINOCA: the ESC 2023 and Fifth UDMI definitions

^{[2] [1]}

The Fifth UDMI changed "infarction" to "injury" because most patients are subsequently found to have a non-coronary cardiac cause (e.g. myocarditis, Takotsubo syndrome, cardiomyopathy) or a non-cardiac cause (e.g. pulmonary embolism).^[1] If MI is later confirmed, the final diagnosis is classified as primary, secondary or procedure-related MI.^[1]

^{[2] [4] [1]}

ESC 2023 calls MINOCA an umbrella term covering coronary and non-coronary causes, the latter both cardiac and extra-cardiac.^[2] When no diagnosis is established after angiography, MINOCA is a working diagnosis as opposed to a final one, and failure to identify the cause may result in inadequate or inappropriate therapy.^[2]

Working it up

^[2]

ESC 2023 notes that patients will not require all of these tests; the appropriate tests should be selected based on presentation and clinical course.^[2] The Fifth UDMI adds that intravascular imaging can find subtle primary-MI pathology such as plaque erosion/rupture, mural thrombus without plaque rupture or SCAD, and invasive functional testing may identify microvascular dysfunction and/or epicardial spasm.^[1] CMR yield is higher within 2 weeks of presentation, because after this time changes may resolve, particularly in Takotsubo syndrome or acute myocarditis.^[1]

ESC 2023 Recommendation Table 13: myocardial infarction with non-obstructive coronary arteries (all rows)

^[2]

• AHA/ACC 2021 chest pain: for high-risk patients with acute chest pain who are troponin positive in whom obstructive CAD has been excluded by CCTA or ICA, CMR or echocardiography can be effective in establishing alternative diagnoses (COR 2a, LOE B-NR).^[4]
• AHA/ACC 2021 chest pain: in acute chest pain and myocardial injury with nonobstructive coronary arteries on anatomic testing, CMR with gadolinium contrast is effective to distinguish myopericarditis from other causes, including MINOCA (COR 1, LOE B-NR).^[4]
• ESC 2023: secondary prevention therapies should be considered for those with evidence of coronary atherosclerotic disease and to control risk factors; MINOCA patients require follow-up review and may need repeat echocardiography and MRI depending on the initial findings.^[2]
• ESC 2026 cardiac rehabilitation: favourable results of cardiac rehabilitation have also been reported in patients with MINOCA.^[9]

Spontaneous coronary artery dissection: who and why

A 44-year-old woman with no risk factors presents with chest pain and a rising troponin.^[5] Her risk score is low, which is one reason SCAD is missed: patients with SCAD typically fall into the lowest risk groups on traditional risk scores, and some are not referred for coronary investigations (ESC ACCA 2018).^[6]

The AHA 2018 scientific statement defines SCAD as an epicardial coronary artery dissection that is not associated with atherosclerosis or trauma and not iatrogenic.^[5] The ESC ACCA 2018 position paper describes the acute development of a false lumen within the coronary artery wall, which may compromise flow by external compression of the true lumen.^[6] Both are consensus documents: the AHA statement says its medical-therapy approaches are based largely on expert opinion given the paucity of evidence, and the ESC paper is not intended to replace individualized decision-making.^[5][6]

^{[5] [6]}

• ESC 2023: SCAD is an infrequent cause of ACS in general but accounts for a significant proportion of ACS cases in young/middle-aged women.^[2]
• ESC ACCA 2018: contemporary series report SCAD in 0.07–0.2% of all angiograms and 2–4% of angiograms performed for ACS, although the study with the highest ACS prevalence did not exclude all atherosclerotic cases.^[6]
• Fifth UDMI (invasive coronary angiography section): the reported prevalence of acute coronary pathologies other than atherothrombosis varies widely, with SCAD at 0.1%–4.0%.^[1]
• Fifth UDMI: SCAD should be considered particularly in female patients under 50 years of age and in pregnancy or the post-partum period.^[1]
• AHA 2018: SCAD most commonly occurs in patients with few or no traditional cardiovascular risk factors; its true prevalence remains uncertain because it is underdiagnosed.^[5]
• ESC ACCA 2018: pregnancy-associated cases make up around 10% in most contemporary series, and SCAD should no longer be considered primarily a peripartum condition.^[6]

Associations and triggers

Selected rows of AHA 2018 Table 2: conditions and factors associated with SCAD

^[5]

• Fibromuscular dysplasia is a nonatherosclerotic, noninflammatory vascular disease that can affect nearly any arterial bed and can manifest as stenosis, aneurysm, tortuosity or dissection (AHA 2018).^[5]
• ESC ACCA 2018 reports extra-coronary FMD in 11–86% of patients with SCAD (41–86% after excluding three studies in which <50% of patients were screened), but cautions against equating SCAD with FMD.^[6]
• Precipitants listed by AHA 2018 include intense exercise (isometric or aerobic), intense Valsalva, retching, vomiting, bowel movement, coughing, lifting heavy objects, intense emotional stress, labor and delivery, recreational drugs (cocaine, methamphetamines) and exogenous hormones or hormone modulators.^[5]
• Sex differences: emotional stressors have more often been reported in women, whereas physical stressors such as intense isometric exercise and weight lifting have more often been reported in men (AHA 2018).^[5]
• Inheritance: outside known connective tissue disorders, SCAD does not appear to be strongly inherited; only 1.2% of 412 patients in one series described a family history (ESC ACCA 2018).^[6]
• Atherosclerosis: significant atherosclerosis is rare in typical SCAD (although this may partly reflect the criteria used to define cases), and patients have fewer traditional risk factors than patients with atherosclerotic coronary disease (ESC ACCA 2018).^[6]

Pathophysiology: a bleed inside the wall

In SCAD, a false lumen inside the coronary artery wall may compromise flow by compressing the true lumen.^[6] The AHA 2018 statement describes the predominant mechanism of myocardial injury as coronary obstruction caused by an intramural hematoma or intimal disruption rather than atherosclerotic plaque rupture or intraluminal thrombus.^[5] The ESC ACCA paper places the false lumen generally in the outer third of the tunica media.^[6]

^[6]

It remains unclear whether one mechanism dominates or both causal events are possible (ESC ACCA 2018).^[6]

^{[5] [6]}

SCAD: presentation and angiographic diagnosis

• Patients usually present with an ACS with positive biomarkers of myocardial necrosis; STEMI in 26–55% across the larger series, and ventricular arrhythmia in a minority (2.8–10%) (ESC ACCA 2018).^[6]
• AHA 2018 reports STEMI in 26% to 87%, NSTEMI in 13% to 69%, cardiogenic shock in as many as 2% to 5%, and ventricular arrhythmias or sudden cardiac death in 3% to 11% of reported series.^[5]
• Chest pain is the most frequently described symptom (reported in 60–90%); this may be because dissection per se is inherently painful, in addition to ischaemic pain (ESC ACCA 2018).^[6]
• Cardiac enzymes are almost invariably increased, although the initial troponin in the emergency department may be normal (AHA 2018).^[5]
• Wall motion abnormalities are common, but overall LV ejection fraction is often preserved (AHA 2018).^[5]

Getting the diagnosis

• AHA 2018: once SCAD is suspected, coronary angiography should be performed as early as feasible, especially in STEMI.^[5]
• ESC ACCA 2018: early coronary angiography should be considered to exclude SCAD in patients with clinical features of ACS but at low risk of atherosclerotic AMI, in particular young to middle-aged women.^[6]
• ESC ACCA 2018: intracoronary nitroglycerin should be given, where blood pressure allows, to ensure complete vasodilation and rule out associated coronary spasm.^[6]
• ESC ACCA 2018: CTCA sensitivity and specificity for SCAD are not known and false negatives are reported, so suspected SCAD is recommended to undergo coronary angiography as the primary diagnostic investigation of choice.^[6]
• AHA 2018: CCTA is not recommended as the first-line investigation for suspected acute SCAD, and normal CCTA results do not exclude SCAD.^[5]

Angiographic types

Most SCAD does not look like a textbook dissection flap.^[5] Relying only on multiple lumens or contrast staining would miss more than 70% of cases (AHA 2018).^[5]

Angiographic types of SCAD: the Saw classification as described by AHA 2018 and ESC ACCA 2018, with type 4 from ESC ACCA 2018

^{[5] [6]}

ESC ACCA 2018 also describes intermediate appearances between types 1 and 2: a type 2 pattern with a short segment of dual lumen or contrast hold-up, in keeping with a localized fenestration.^[6] Care must be taken not to misread SCAD as normal coronaries, atherosclerotic disease, coronary vasospasm, thromboembolism or takotsubo syndrome (AHA 2018).^[5]

^{[5] [6]}

• Distribution: the LAD is most commonly affected (32%–46% of cases); mid to distal segments are affected in the majority, and multivessel SCAD occurs in 9% to 23% (AHA 2018).^[5]
• Multivessel SCAD means simultaneous dissections in more than one artery without continuity, reported in 5–13% of the larger series; careful assessment of apparent non-culprit vessels is recommended (ESC ACCA 2018).^[6]
• Other features reported include increased coronary tortuosity, a false lumen starting or ending at a side branch, absence or reduced incidence of co-existent atherosclerosis (unaffected coronaries usually normal or near-normal), coronary FMD and association with myocardial bridging (ESC ACCA 2018).^[6]
• Differential diagnosis includes atherosclerotic ACS, coronary artery spasm, Takotsubo cardiomyopathy, coronary thromboembolism and MINOCA; there are no specific blood biomarkers for SCAD (ESC ACCA 2018).^[6]

Intracoronary imaging: useful, but it can extend the dissection

The catheter is part of the risk: AHA 2018 says underlying arterial fragility in SCAD is believed to accentuate the risk of iatrogenic dissection.^[5] AHA 2018 reports iatrogenic catheter-induced dissection in 3.4% overall in SCAD against <0.2% for standard angiography; a single study cited by ESC ACCA 2018 reported 2% during angiography against 0.2% in non-SCAD angiography, and 14.3% during PCI.^[5][6] ESC ACCA 2018 therefore advises a meticulous co-axial catheter technique and avoidance of aggressive or deeply engaging guiding catheters.^[6]

Intracoronary imaging in SCAD

^{[2] [5] [6]}

The Fifth UDMI notes that intravascular imaging can identify the intramural haematoma of SCAD as an alternative acute coronary pathology.^[1] ESC 2023 states that there are no RCTs to guide SCAD management and that the use of intravascular imaging rests on cohort studies and expert opinion.^[2]

SCAD: conservative care or revascularisation

The default is to leave the artery alone.^[2][5] The ESC 2023 narrative says conservative medical management, as opposed to PCI, is generally recommended for patients with SCAD.^[2] The reason is twofold: the majority of conservatively managed SCAD first stabilizes and then heals completely over time (ESC ACCA 2018), and observational studies consistently associate PCI in SCAD with an increased risk of complications and suboptimal outcomes (AHA 2018).^[6][5]

Formal rows on revascularisation in SCAD (guidelines checked for this topic)

^{[2] [10] [3]}

The NHFA/CSANZ narrative explains its rows: in ACOMI or NSTEACS due to SCAD with haemodynamic stability, routine revascularisation is not recommended because of PCI-related complications and limited evidence of benefit, but haemodynamic compromise or significant ongoing ischaemia may require urgent PCI or CABG.^[10] ACOMI, the NHFA/CSANZ term, means acute coronary occlusion myocardial infarction.^[10]

^{[2] [5] [10] [6]}

Why PCI is hazardous

• ESC 2023: in an international case series, coronary complications following PCI occurred in >30% of patients.^[2]
• ESC 2023 reports a pooled analysis of three SCAD-PCI cohorts including 215 patients (94% female) from Dutch, Spanish and UK registries, with a matched conservatively managed cohort, in which PCI was associated with complications in ≈40% of cases (including 13% with serious complications).^[2]
• AHA 2018: guidewires may enter the false lumen and occlude the true lumen, and balloons and stents can propagate the intramural haematoma upstream and downstream, worsening obstruction.^[5]
• AHA 2018: the intramural haematoma naturally resorbs, which can cause subacute and late stent strut malapposition, potentially predisposing to future stent thrombosis.^[5]
• ESC ACCA 2018: in the Canadian series (168 cases), revascularization procedural success was only achieved in 64%, and only 30% maintained durable results at long-term follow-up.^[6]

The study's own abstract (Kotecha 2021) gives PCI complications in 38.6% (83/215), serious in 13.0% (28/215), in patients who were high risk at presentation, and concludes that while a conservative approach is favoured, higher-risk presentations may require PCI.^[12]

If you must intervene

• PCI techniques (ESC 2023): useful strategies may include minimal plain balloon angioplasty to restore flow followed by a conservative strategy, targeted stenting to seal the proximal and distal ends of the dissection, and/or extended stent lengths to prevent haematoma propagation.^[2]
• Stent type (ESC ACCA 2018): where stents are deployed, second-generation drug-eluting stents are advised; in the absence of randomized data, no specific alternative PCI strategy can be recommended.^[6]
• CABG (ESC 2023 narrative): CABG is recommended when dissection affects the left main or two proximal vessels, if PCI is not feasible or unsuccessful, and if there are symptoms and signs of ongoing ischaemia (no class or level given).^[2]
• Grafts (ESC 2023): ESC 2023 reports that, in a small observational study, patients with SCAD treated with CABG had favourable early clinical outcomes, with an event rate up to 5 years similar to that of patients treated conservatively, despite a 68% rate of graft occlusion at 5 years; it says the rate of graft occlusion over time can be explained by the fact that CABG in these patients may be technically challenging, as the dissected coronary artery is more prone to anastomosis failure, and because spontaneous healing over time may restore the flow in the anastomosed vessel, and for this reason vein grafts should be considered in these patients to preserve arterial conduits for future use.^[2]
• AHA 2018 consensus: conservative therapy may not be appropriate with ongoing ischemia, left main dissection or hemodynamic instability; there, urgent PCI or CABG should be considered, individualized to anatomy and local expertise.^[5]
• Thrombolysis (ESC ACCA 2018): contraindicated for acute SCAD, given reports of dissection extension and even coronary rupture with tamponade after lytic therapy.^[6]

Watching the conservative patient

• Observational data indicate angiographic healing in the majority (70%–97%) of conservatively managed patients who were selectively restudied weeks to months later (AHA 2018).^[5]
• Early recurrent MI may develop in 5% to 10% of conservatively managed patients, mostly from extension of dissection within the first 7 days (AHA 2018).^[5]
• AHA 2018: patients are typically admitted for a minimum of 48 hours, and a prolonged period of in-hospital monitoring (3–5 days) is justified as part of a conservative strategy; ESC ACCA 2018 suggests prolonged inpatient monitoring (∼5 days).^[5][6]
• In a recent prospective series, 9 of 272 (3.3%) conservatively managed patients required in-hospital revascularization (ESC ACCA 2018).^[6]
• Chest pain does not necessarily imply active ischemia and may come from the dissection itself; chest pain alone should not prompt emergency revascularization, especially without evidence of ischemia or with normal flow (AHA 2018).^[5]

SCAD: antithrombotic therapy and β-blockers

ESC ACCA 2018 noted that there were, to date, no randomized controlled trials comparing pharmacological treatment strategies for SCAD.^[6] ESC 2023 lists the optimal antiplatelet strategy, including the optimal combination and duration in the acute and post-ACS periods, as a gap in evidence.^[2] So the statements below differ, and you should quote each with its source.^[6]

Antithrombotic therapy in SCAD: what each document says (no class or level given in any of them)

^{[2] [7] [5] [6]}

AHA 2018 points to bleeding risk, especially menorrhagia in premenopausal women, and uncertain benefit when it calls for individual selection of DAPT and aspirin in conservatively managed survivors.^[5] For DAPT bleeding, switching and stopping in general, see the DAPT topic linked above.

β-blockers and recurrence

ESC ACCA 2018 notes that, apart from the potential benefit of β-blockers and control of hypertension, no current treatment strategy had to date been shown to reduce recurrence.^[6] Saw et al. prospectively followed 327 nonatherosclerotic SCAD patients at Vancouver General Hospital (90.5% women), with a median follow-up of 3.1 years.^[11] In multivariate modelling, only hypertension increased (hazard ratio 2.46) and β-blocker use diminished (hazard ratio 0.36) recurrent SCAD.^[11] The design was a prospective observational cohort, so the β-blocker finding is an association.^[11][6]

• AHA 2018: β-blockers should be considered in SCAD with LV dysfunction or arrhythmias and for management of hypertension; some experts advocate routine use, whereas others use them selectively out of concern for exacerbating vasospasm or symptomatic hypotension.^[5]
• AHA 2018 reports the Vancouver β-blocker association (hazard ratio 0.36 for recurrent SCAD) as strengthening the practice of β-blocker administration after SCAD.^[5]
• ESC ACCA 2018: the association of hypertension with recurrence and of β-blockers with less recurrence is not from a randomized study and awaits validation in other cohorts.^[6]
• ESC 2025 pregnancy (section on pregnancy-associated SCAD): limited observational data suggest that β-blockers (e.g. labetalol) and avoiding hypertension may be associated with a lower risk of recurrent SCAD.^[7]

Other drugs

• Significant LV systolic impairment: follow current guidelines, maximizing ACE inhibitor or ARB and β-blocker doses and adding an MRA as indicated, although hypotension frequently limits dose escalation in this younger population (ESC ACCA 2018).^[6]
• ACE inhibitors or ARBs should be used when MI is complicated by LV systolic dysfunction; women of reproductive age must be warned of the teratogenicity of renin-angiotensin system antagonists (AHA 2018).^[5]
• Statins: not recommended routinely after SCAD; reserved for guideline-based primary prevention indications or established concomitant atherosclerotic disease or diabetes (AHA 2018), or, in general, conventional indications independent of the SCAD event (ESC ACCA 2018).^[5][6]
• Antianginal drugs: for chest discomfort after SCAD in patients who are not candidates for revascularization or with suspected vasospasm or microvascular dysfunction, nitrates, calcium channel blockers or ranolazine may relieve symptoms (AHA 2018).^[5]
• ICDs: AHA 2018 finds insufficient evidence to alter ICD decisions on the basis of SCAD as the cause of the ischemic event.^[5]

SCAD after discharge: imaging, screening and recurrence

Follow-up imaging

• An assessment of LV systolic function is mandatory after SCAD, as after MI of other causes, to guide medical and potentially device therapy (ESC ACCA 2018).^[6]
• CCTA may be useful for non-invasive follow-up, particularly with proximal or large-calibre dissections, but distal, side-branch or <2.5 mm vessel involvement is generally not well seen (AHA 2018).^[5]
• ESC ACCA 2018 cites complete resolution in 83% of the largest multi-slice CT follow-up series (24 cases) but says further data are required before CTCA can be recommended for follow-up imaging.^[6]
• Repeat invasive angiography should be performed only when benefits may outweigh the risks, such as recurrent symptoms, abnormal functional tests, an unclear cause of stenosis, or high-risk anatomy (AHA 2018).^[5]
• For recurrent chest pain, ESC ACCA 2018 calls for careful assessment with serial ECG and high-sensitivity troponin, and reserves invasive angiography for hard evidence of ischaemia or myocardial necrosis.^[6]

Screening for associated arteriopathy

• AHA 2018: all patients who have had SCAD should undergo a complete vascular physical examination, and vascular imaging from the brain to pelvis should be considered in all patients.^[5]
• ESC ACCA 2018: imaging of extra-coronary vascular beds in patients with SCAD is advised.^[6]
• AHA 2018: imaging series have reported intracranial aneurysm in 14% to 23% of patients with SCAD.^[5]
• AHA 2018: without a suggestive history or examination, routine genetic testing after SCAD is not currently advised.^[5]

Recurrence and prognosis

Define recurrence carefully. AHA 2018 separates extension of the index dissection in the acute phase from de novo dissection affecting different segments later (>30 days), and limits "recurrent SCAD" to de novo SCAD.^[5]

^{[5] [11] [6]}

• Long-term mortality in survivors is low (ESC ACCA 2018), but MACE at 2 to 3 years were reported in 10% to 30%, mostly recurrent MI from recurrent SCAD (AHA 2018).^[6][5]
• De novo recurrence affects previously unaffected arteries 77% to 100% of the time (AHA 2018), and stenting at the first event does not appear to be protective (ESC ACCA 2018).^[5][6]
• To date, only severe coronary tortuosity has been identified as a recurrence risk factor, with recurrence most likely in a segment of tortuosity; FMD itself has not been identified as a predictor (AHA 2018).^[5]
• Apart from a potential β-blocker benefit and control of hypertension, no treatment strategy has been shown to reduce recurrence (ESC ACCA 2018).^[6]

Rehabilitation, activity and hormones

• AHA 2018: all patients with MI caused by SCAD should be referred for cardiac rehabilitation, tailored to cardiopulmonary factors such as ejection fraction and to age, pre-SCAD physical activity level and recovery goals.^[5]
• ESC ACCA 2018: cardiac rehabilitation should be considered, with a return to full activity and avoidance of extreme or isometric exercise.^[6]
• AHA 2018: patients should generally be advised to avoid prolonged high-intensity activities, highly competitive or contact sports, exercise to exhaustion, abrupt increases without a warm-up, extremes of temperature or terrain, and Valsalva during lifting or exercise.^[5]
• ESC 2026 cardiac rehabilitation (Recommendation Table 30): tailoring cardiac rehabilitation to women should be considered for women with ACS and CCS, spontaneous coronary artery dissection and HF to improve enrolment and adherence (Class IIa, Level B1).^[9]
• ESC 2026 cardiac rehabilitation: this is particularly important for younger women (<55 years) with causes of MI that are not typical, for example SCAD, although evidence on sex-specific effects of rehabilitation remains limited for conditions that predominantly affect women, such as SCAD.^[9]
• Hormones: systemic oestrogen and progesterone are usually avoided if possible (AHA 2018); avoiding hormonal contraception where possible may be a reasonable strategy (ESC ACCA 2018).^[5][6]
• Heavy menstrual bleeding: NSAIDs and tranexamic acid should generally be avoided in women with SCAD given their association with MI and thrombosis (AHA 2018).^[5]
• Mental health: anxiety and depression are common among survivors, especially after peripartum SCAD (AHA 2018).^[5]

Pregnancy-associated SCAD

In a pregnant or recently delivered woman with chest pain and a troponin rise, SCAD belongs near the top of the list.^[7][2] ESC 2023: SCAD is the most common cause of AMI in pregnancy, tending to occur mainly in late pregnancy or the early post-partum period.^[2] ESC 2025 pregnancy: it is the single most frequent cause of ACS during pregnancy and post-partum (43%), followed by atherosclerotic lesion (27%), coronary embolism (17%) and vasospasm (2%).^[7]

• Incidence 1.81 per 100 000 pregnancies; it may occur at any time during or after pregnancy, although >70% occur early post-partum, most commonly within the first week (ESC 2025 pregnancy).^[7]
• Pregnant women with SCAD tend to have a more severe clinical presentation than women with non-SCAD ACS (ESC 2025 pregnancy).^[7]
• A conservative approach to revascularization is advised in clinically stable women without active or ongoing ischaemia; CABG may be considered for left main or proximal involvement depending on technical considerations and local expertise, and a multidisciplinary team decides between PCI and CABG (ESC 2025 pregnancy narrative).^[7]
• AHA 2018: clopidogrel lacks clear safety data in pregnancy and breastfeeding and is generally not recommended when breastfeeding; low-dose aspirin is safe; labetalol is the preferred β-blocker, especially in early pregnancy.^[5]

Selected rows of ESC 2025 Recommendation Table 12: coronary artery disease and pregnancy

^[7]

After SCAD, women should be carefully counselled about recurrence in a subsequent pregnancy (ESC 2025 pregnancy).^[7] ESC ACCA 2018 regards any planned or unplanned pregnancy as high risk, while AHA 2018 notes that many clinicians recommend against pregnancy although few data support this.^[6][5]

ANZ practice

The 2025 NHFA/CSANZ ACS guideline is quoted here only through its Medical Journal of Australia summary.^[10] It reclassifies SCAD with other non-atherosclerotic occlusions as MI with acute coronary occlusion, and gives two SCAD rows in its Table 3 (hospital care and reperfusion strategies).^[10] The full guideline (Heart Lung Circ 2025) is not held as text for this topic in its version of record, so nothing on this page is taken from it directly.

• In people with ACOMI due to SCAD who are otherwise stable, routine revascularisation is not recommended (NHFA/CSANZ 2025, consensus recommendation).^[10]
• In people with SCAD and haemodynamic instability and/or ongoing ischaemia, consider selective revascularisation (NHFA/CSANZ 2025, weak recommendation, very low certainty of evidence).^[10]
• NHFA/CSANZ consensus recommendations are informed by expert opinion when there is indirect supporting evidence and the GRADE approach is not applicable.^[10]

Evidence, guidelines and controversies

• Terminology: ESC 2023 and the ACC/AHA 2025 Table 4 use the Fourth UDMI type 2 MI; the Fifth UDMI (2026) replaces it with secondary MI and moves SCAD into primary MI.^[2][3][1]
• Coding consequences: fewer than 20% of patients meeting Fourth UDMI type 2 criteria in two European countries received an ICD-10 code for MI (Fifth UDMI).^[1]
• Type 1 against type 2: ESC 2023 lists better differentiation of type 2 from type 1 MI before invasive assessment as a gap in evidence.^[2]
• SCAD evidence base: no RCTs guide SCAD management (ESC 2023); there have been no randomized comparisons of acute revascularization strategies (AHA 2018).^[2][5]
• Antiplatelet therapy in conservatively managed SCAD: ESC 2023 (same therapy as other ACS until evidence from ongoing prospective trials becomes available), ESC 2025 pregnancy in its section on pregnancy-associated SCAD (evidence favouring single antiplatelet therapy with aspirin) and the 2018 statements (divergent practice) differ.^[2][7][6][5]

Rows on this page come from ESC 2023 ACS (Recommendation Tables 11 and 13), ESC 2025 pregnancy (Recommendation Table 12), ESC 2026 cardiac rehabilitation (Recommendation Table 30), the 2021 AHA/ACC chest pain guideline and NHFA/CSANZ 2025 (Table 3).^{[2][7][9][4][10]} The guidelines checked for this topic, with the date of the census, are listed in the evidence pack; ESC 2023, ESC 2025 pregnancy, the 2021 chest pain guideline and NHFA/CSANZ 2025 are the newest of their bodies on these questions among the guidelines checked. The AHA 2018 SCAD scientific statement and the ESC ACCA 2018 position paper are consensus documents; no class on this page is taken from them.^[5][6] ACC/AHA 2025 cites separate documents for these conditions, including the AHA 2018 SCAD statement used here.^[3] It also cites a 2019 AHA scientific statement on MI in the absence of obstructive coronary artery disease and a 2019 Circulation paper on type 2 MI and acute nonischemic myocardial injury.^[3] The last two, and the 2026 AHA/ACC perioperative guideline, are not held as text for this topic and were not checked.

Pitfalls

Exam pearls

• Fifth UDMI Box 4: once secondary MI is considered, and where coronary and/or cardiac imaging is feasible and appropriate, it is confirmed by ≥70% epicardial stenosis by angiography (or ≥50% epicardial stenosis that is flow-limiting on physiological assessment) without an acute coronary pathology, or by a new or presumed new regional wall motion abnormality or absent viable myocardium in a pattern consistent with an ischaemic aetiology.^[1]
• Most common trigger of secondary MI: tachyarrhythmia (Fifth UDMI).^[1]
• ESC 2023 MINOCA threshold: stenosis <50% in any major epicardial vessel; Fifth UDMI: no stenosis ≥50%.^[2][1]
• Saw type 2 is the commonest SCAD pattern; type 3 mimics atherosclerosis and needs intracoronary imaging (AHA 2018).^[5]
• AHA 2018 limits "recurrent SCAD" to de novo dissection; extension of the index dissection in the acute phase is a separate event.^[5]
• In the prospective Vancouver cohort of 327 patients with nonatherosclerotic SCAD (median follow-up 3.1 years), β-blocker use was associated with less recurrent SCAD in multivariate modelling (hazard ratio 0.36) (Saw 2017).^[11]

References13ShowHide

1. [1]Mills NL, et al. Fifth Universal Definition of Myocardial Infarction (2026): On behalf of the Joint European Society of Cardiology (ESC)/American College of Cardiology (ACC)/American Heart Association (AHA)/World Heart Federation (WHF) Task Force for the Universal Definition of Myocardial Infarction Endorsed by the European Association for Cardio-Thoracic Surgery (EACTS) and the Society of Thoracic Surgeons (STS) Affirmation of Value by the Society for Cardiovascular Angiography and Interventions (SCAI). Glob Heart, 2026.PMID 42666939
2. [2]Byrne RA, et al. 2023 ESC Guidelines for the management of acute coronary syndromes. Eur Heart J, 2023.PMID 37622654
3. [3]Rao SV, et al. 2025 ACC/AHA/ACEP/NAEMSP/SCAI Guideline for the Management of Patients With Acute Coronary Syndromes: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. J Am Coll Cardiol, 2025.PMID 40013746
4. [4]Gulati M, et al. 2021 AHA/ACC/ASE/CHEST/SAEM/SCCT/SCMR Guideline for the Evaluation and Diagnosis of Chest Pain: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. J Am Coll Cardiol, 2021.PMID 34756653
5. [5]Hayes SN, et al. Spontaneous Coronary Artery Dissection: Current State of the Science: A Scientific Statement From the American Heart Association. Circulation, 2018.PMID 29472380
6. [6]Adlam D, et al. European Society of Cardiology, acute cardiovascular care association, SCAD study group: a position paper on spontaneous coronary artery dissection. Eur Heart J, 2018.PMID 29481627
7. [7]De Backer J, et al. 2025 ESC Guidelines for the management of cardiovascular disease and pregnancy. Eur Heart J, 2025.PMID 40878294
8. [8]Van Gelder IC, et al. 2024 ESC Guidelines for the management of atrial fibrillation developed in collaboration with the European Association for Cardio-Thoracic Surgery (EACTS). Eur Heart J, 2024.PMID 39210723
9. [9]Bäck M, et al. 2026 ESC Guidelines on cardiac rehabilitation. Eur Heart J, 2026.PMID 42661418
10. [10]Brieger DB, et al. National Heart Foundation of Australia and Cardiac Society of Australia and New Zealand: Australian Clinical Guideline for Diagnosing and Managing Acute Coronary Syndromes 2025. Med J Aust, 2026.PMID 41693087
11. [11]Saw J, et al. Spontaneous Coronary Artery Dissection: Clinical Outcomes and Risk of Recurrence. J Am Coll Cardiol, 2017.PMID 28838364
12. [12]Kotecha D, et al. Risks and benefits of percutaneous coronary intervention in spontaneous coronary artery dissection. Heart, 2021.PMID 34006503
13. [13]Bularga A, et al. Coronary Artery and Cardiac Disease in Patients With Type 2 Myocardial Infarction: A Prospective Cohort Study. Circulation, 2022.PMID 35341327