Complications of acute myocardial infarction

This page covers the structural complications of an acute MI: papillary muscle rupture with acute mitral regurgitation (MR), ventricular septal rupture, free-wall rupture, pseudoaneurysm and true LV aneurysm, LV thrombus and pericardial complications.^[2][7][1] Shock from pump failure, reperfusion choices and pericarditis outside MI have their own pages: Cardiogenic shock, STEMI: reperfusion, NSTEMI and NSTE-ACS management and Acute pericarditis.

Overview and definitions

Picture a patient on day 3 after a late-presenting inferior STEMI who suddenly becomes breathless and hypotensive.^[7] ESC 2023 says mechanical complications are life-threatening and therefore require prompt identification and management.^[1]

ACC/AHA 2025 says timely reperfusion therapy has reduced the incidence of mechanical complications (ventricular septal rupture, mitral valve insufficiency due to papillary muscle infarction or rupture, or free wall rupture) after acute MI.^[2] A 2021 American Heart Association (AHA) scientific statement lists the most commonly encountered ones as acute MR secondary to papillary muscle rupture, ventricular septal defect (VSD), pseudoaneurysm and free wall rupture.^[7] It says each is associated with a significant risk of morbidity, mortality and hospital resource use.^[7]

The words matter in a viva. ACC/AHA 2025 says "contained rupture" is the preferred term for the entity sometimes called pseudoaneurysm (footnote to its Figure 9, Clinical Characteristics of Mechanical Complications of Acute Myocardial Infarction).^[2] The AHA statement describes LV pseudoaneurysms as developing when cardiac rupture is contained by pericardial adhesions.^[7] A true LV aneurysm is different: its wall is thin, scarred or fibrotic myocardium.^[7]

Summary of major mechanical complications (AHA 2021 scientific statement, Table 1)

^[7]

A footnote to that table says percutaneous repair needs discussion by the multidisciplinary heart team, because only a few cases are reported.^[7] The statement is a scientific statement rather than a guideline, so its table carries no class or level.^[7]

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How often, and who is at risk

^[1]

ESC 2023 says the incidence of mechanical complications has fallen significantly in the primary percutaneous coronary intervention (PPCI) era.^[1] It reports a large epidemiological investigation of almost 9 million ACS patients with an overall prevalence of 0.27% in STEMI and 0.06% in NSTEMI, and in-hospital mortality of 42.4% and 18%, respectively.^[1]

Rare does not mean benign.^[7] The AHA statement says the incidence remains low but the associated mortality is high, especially among older patients.^[7] It says patients with large infarcts, or who do not receive timely revascularisation, remain at risk.^[7]

• Who (AHA 2021): contemporary patients with mechanical complications tend to be older and female, to have a history of HF or chronic kidney disease, and often present with their first acute MI.^[7]
• Papillary muscle rupture (AHA 2021): the incidence of acute severe MR from papillary muscle rupture has declined in the reperfusion era (range 0.05% to 0.26%), but reported hospital mortality remains high, between 10% and 40%.^[7]
• Ventricular septal defect (AHA 2021): incidence after acute MI is approximately 0.3% in contemporary practice; risk factors include older age, female sex and delayed reperfusion.^[7]
• Free-wall rupture (AHA 2021): the most commonly reported mechanical complication, but its true incidence is unknown, because it usually presents as out-of-hospital sudden cardiac death and routine autopsy is lacking.^[7]
• LV thrombus (ESC 2023): its incidence after acute MI has declined, but it remains relatively common, particularly after anterior STEMI, where it can be present in more than 9% of patients according to a large meta-analysis.^[1]
• LV thrombus (ACC/AHA 2025): in the era of PCI its incidence after ACS has decreased and is estimated to be under 5% to 10% in the post-MI population.^[2]
• Post-MI pericarditis (ACC/AHA 2025): 0.1%–0.5% in the era of early coronary reperfusion therapy.^[2]
• Dressler syndrome (ESC 2025): now appears in under 1% of cases, mainly in larger infarctions and/or late reperfusion, typically 1–2 weeks after acute MI.^[4]

Shock is the usual company these complications keep.^[7] The AHA statement says that in contemporary studies close to three-quarters of these patients presented with cardiogenic shock, and the majority required vasopressors, a balloon pump or a percutaneous LV support device.^[7] ESC 2023 lists ischaemia-related HF, acute severe MR and mechanical complications as the major precipitating causes of cardiogenic shock in ACS.^[1]

Why they happen: anatomy and mechanism

Each complication has its own anatomy. The most commonly encountered mechanical complications are acute MR from papillary muscle rupture, ventricular septal defect, pseudoaneurysm and free-wall rupture (AHA 2021).^[7] The AHA statement says a pseudoaneurysm develops when cardiac rupture is contained by pericardial adhesions, and that a true aneurysm is made of a thin, scarred or fibrotic myocardial wall; ACC/AHA 2025 says LV thrombus typically occurs in the setting of a large anterior STEMI.^[7][2]

Papillary muscles

The AHA statement explains the blood supply.^[7] The anterolateral papillary muscle has a dual supply from the LAD and from the diagonal or marginal branch of the circumflex coronary artery.^[7] The posteromedial muscle has a single supply from the circumflex or the right coronary artery, depending on dominance.^[7] So anterolateral rupture is extremely uncommon, and posteromedial rupture typically occurs with inferior or lateral STEMI.^[7] Rupture may be complete or partial, which may influence how severe the symptoms are.^[7]

The septum

Anterior and apical VSDs come from infarcts in the LAD territory; posterior VSDs come from inferior infarcts (AHA 2021).^[7] Right ventricular (RV) infarction or ischaemia with severe dysfunction is an important feature of VSDs caused by acute proximal right coronary occlusion.^[7] Posterior VSDs are often accompanied by MR, commonly from ischaemic tethering.^[7]

The free wall, pseudoaneurysm and true aneurysm

The AHA statement says early trials of fibrinolysis against placebo showed an early increased risk of free-wall rupture after 24 hours with fibrinolytic therapy, which supports a higher risk of rupture with delayed reperfusion.^[7] The statement attributes this to intramyocardial haemorrhage, myocardial dissection and subsequent rupture.^[7] When a cardiac rupture is contained by pericardial adhesions, a pseudoaneurysm forms.^[7] Compared with true aneurysms, pseudoaneurysms more often involve the inferior or lateral wall, perhaps because pericardial adhesions develop dependently in the recumbent, convalescing patient.^[7] A true LV aneurysm most commonly involves the anterior or apical walls; its most common cause is total thrombotic occlusion of the LAD, though inferior or basal involvement from right coronary occlusion can also be seen.^[7]

Thrombus and pericardium

ACC/AHA 2025 says LV thrombus typically occurs with a large anterior STEMI and can lead to thromboembolic complications, including stroke and systemic embolisation.^[2] Its highest-risk patients have anterior STEMI involving the LAD, LV ejection fraction (LVEF) under 30% (especially with an LV aneurysm), and longer times to reperfusion.^[2]

ACC/AHA 2025 says early post-MI pericarditis is presumed to be inflammatory, from adjacent myocardial necrosis.^[2] Dressler syndrome is believed to be immune-mediated, a response to pericardial irritation or damage such as any degree of haemopericardium.^[2]

^[7]

Recognising a mechanical complication

The trigger is a change in the patient after MI, and both ACS guidelines list the changes to look for.^[1][2] ESC 2023 says sudden hypotension, recurrence of chest pain, new cardiac murmurs suggestive of acute MR or a VSD, pulmonary congestion, or jugular vein distension should raise suspicion of a mechanical complication.^[1] ACC/AHA 2025 says that, although occasionally found incidentally, they commonly present with recurrent or refractory chest pain or a new murmur accompanied by disproportionate HF, cardiogenic shock or sudden cardiac death, within the first week after an acute MI.^[2]

Deterioration can be abrupt.^[2] ACC/AHA 2025 says haemodynamic deterioration is unpredictable and can be precipitous in previously stable patients.^[2] The AHA statement says mechanical complications usually present with haemodynamic instability, either initially or after admission for acute MI.^[7]

Bedside clues by complication

^[7]

Two traps catch candidates.^[7] In papillary muscle rupture the murmur may be absent, so the absence of a murmur does not exclude it (AHA 2021).^[7] Free-wall rupture is sometimes preceded by chest pain and nausea, and the ECG may show new ST elevation as blood irritates the pericardium (AHA 2021).^[7]

What else could it be

Shock after MI has a differential, and the AHA statement tabulates it (its Table 2, Differential diagnosis for mechanical complications of acute myocardial infarction).^[7] Selected rows are shown here.^[7]

Differential diagnosis of a suspected mechanical complication (AHA 2021, Table 2; selected rows)

^[7]

Investigations

Echocardiography is the test that answers the question.^[1] ESC 2023 says immediate echocardiographic assessment is indicated when mechanical complications are suspected.^[1] It says all patients presenting with cardiogenic shock or haemodynamic instability should undergo emergency TTE to identify the underlying cause, in particular to assess LV and RV function and look for evidence of mechanical complications.^[1] ACC/AHA 2025 text says urgent echocardiography, which may include an initial point-of-care ultrasound by trained clinicians, is indicated for cardiogenic shock, haemodynamic instability or suspected mechanical complications (no COR or LOE for this sentence).^[2]

Imaging rows during the ACS admission

^{[1] [2]}

ACC/AHA 2025 says TTE is generally the preferred modality because it is non-invasive and can assess ventricular and valvular function, as well as possibly detect LV thrombus or mechanical complications.^[2] It says TTE is therefore strongly preferred for all patients hospitalised with STEMI, because complications may be more likely.^[2]

Diagnostic findings (AHA 2021 scientific statement)

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The first hours: stabilise, call the surgeon, choose support

Three things need doing: image the heart, involve a surgical Heart Team and, if the patient is haemodynamically unstable, consider temporary circulatory support while repair is planned.^[1][2][3] ACC/AHA 2025 says a Heart Team approach to guide the feasibility, timing and nature of corrective intervention, and the need for and selection of MCS, is recommended as soon as a mechanical complication is diagnosed (supportive text; no COR or LOE given).^[2]

Repair and circulatory support rows

^{[1] [3] [2]}

The ESC 2026 row carries two footnotes that decide device choice.^[3] The choice of passive IABP or active percutaneous MCS should be based on the severity of cardiogenic shock as assessed by the Shock Team.^[3] In a large VSD, temporary MCS should be used with caution because of a potential increase in left-to-right shunt with veno-arterial extracorporeal life support (VA-ECLS), or shunt inversion with a microaxial flow pump.^[3] In ventricular free-wall rupture, temporary MCS should be avoided; however, VA-ECLS can be considered to allow emergent cardiac surgery in profound cardiogenic shock and/or cardiac arrest if there is no sign of irreversible brain injury.^[3]

ESC 2026 also recommends a multidisciplinary Shock Team for potential candidates for temporary MCS, to guide device selection (modality and type) based on patient and HF characteristics (Class I, Level C).^[3]

Why the balloon pump still has a place here

ESC 2023, ESC 2026 and ACC/AHA 2025 each have a row against the IABP in cardiogenic shock, but the ESC 2023 row itself is limited to ACS with cardiogenic shock and without mechanical complications.^[1][3][2] ESC 2023 says the routine use of an IABP in ACS patients with cardiogenic shock and without mechanical complications is not recommended (Class III, Level B).^[1] ESC 2026 says an IABP is not recommended in unselected patients with cardiogenic shock, due to the lack of effect (Class III, Level B1).^[3] ACC/AHA 2025 says that in acute MI with cardiogenic shock the routine use of an IABP or VA-ECMO is not recommended, due to a lack of survival benefit (COR 3: No benefit, LOE B-R).^[2] ESC 2023 narrative adds that patients with ACS-related mechanical complications should be considered for an IABP while awaiting surgery.^[1]

ACC/AHA 2025 gives the physiology: in ventricular septal rupture an IABP has been shown to reduce left-to-right shunting and improve haemodynamics in patients with and without shock, and favourable haemodynamic effects are also noted in acute ischaemic MR.^[2] It says various devices have been used when the IABP fails or when haemodynamic instability remains profound.^[2] The AHA statement says the IABP-SHOCK II trial did not show a mortality benefit from an IABP in patients with acute MI complicated by cardiogenic shock, and that the trial excluded patients with mechanical complications.^[7]

What the device evidence actually shows

No randomised trial has tested MCS for mechanical complications (ACC/AHA 2025).^[2] ACC/AHA 2025 says no randomised controlled trials (RCTs) have evaluated the role of MCS in improving clinical outcomes with mechanical complications, and that the choice of MCS should be individualised to patient characteristics, the nature of the complication and the haemodynamic profile.^[2] ESC 2023 calls temporary MCS for mechanical complications, either to improve pre-operative status or prophylactically, a new trend in management that needs more data to show whether it provides clinical benefit.^[1]

• Systematic review (reported by ACC/AHA 2025): of patients bridged with MCS to surgery for ventricular septal rupture, 111 studies (n = 2,440), almost all patients received initial IABP support (n = 2,263); among 129 given an additional device (77.5% on VA-ECMO), in-hospital mortality was lowest with VA-ECMO (29.2%) and 52.0% with an IABP alone.^[2]
• Two database analyses outside that review (reported by ACC/AHA 2025): higher in-hospital death with VA-ECMO in post-MI mechanical complications.^[2]
• ECLS (Extracorporeal Life Support) Organizations Registry (reported by ACC/AHA 2025): 158 patients with post-MI mechanical complications on VA-ECMO; survival to discharge 37.3%, and VA-ECMO complications in 75.3%.^[2]
• National Inpatient Sample (reported by ACC/AHA 2025): 10,726 patients with post-STEMI mechanical complications; VA-ECMO was associated with increased in-hospital mortality (OR 2.80, 95% CI 1.92–4.04), while IABP use was not associated with lower mortality.^[2]
• The caveat ACC/AHA 2025 attaches: both data sources counted VA-ECMO used at any time in the admission, including after surgery, a cohort at highest risk of in-hospital death.^[2]

Drugs and ventilation

Medical therapy alone carries a high risk.^[2] ACC/AHA 2025 says medical therapy alone carries a high risk of early death, and definitive surgical correction is frequently the treatment of choice.^[2] For papillary muscle rupture, the AHA statement says positive pressure ventilation can improve gas exchange and haemodynamics by reducing LV preload and afterload and MR, and augment cardiac output.^[7] In haemodynamically stable patients, intravenous nitroglycerin or nitroprusside can be given in critical care to reduce LV afterload.^[7] It notes that vasopressors and inotropes for mechanical complications have not been tested in clinical trials.^[7]

^{[2] [3] [6] [1]}

Definitive repair and its timing

Surgery is the default answer.^[1][2] ESC 2023 says surgery is currently regarded as the treatment of choice for ACS with mechanical complications, although percutaneous strategies are occasionally used in selected candidates with a prohibitive risk profile or contraindications to surgery.^[1] ACC/AHA 2025 says overall surgical mortality is approximately 40%, but surgery remains the treatment strategy of choice.^[2]

Timing is the hard part.^[2] ACC/AHA 2025 says that, although the exact timing remains uncertain, early corrective surgery is the treatment of choice.^[2] Surgical risk is highest in cardiogenic shock and appears lower when surgery is delayed; the early hazard is attributed to patient acuity, end-organ injury and a lack of tissue integrity for a lasting repair.^[2] Observed mortality after delayed surgery (more than 7 days) is lower, but patient selection and survivor bias contribute to this observation.^[2]

Temporary MCS has changed the calculus.^[2] ACC/AHA 2025 says the availability of temporary MCS has led to increasing trends for delayed surgery, because of concern about the initial extent of tissue destruction.^[2] Delayed intervention may enable haemodynamic stabilisation, recovery of end-organ injury, and infarct healing and maturation that could facilitate definitive repair.^[2]

• Revascularisation at repair (ESC 2023 narrative): in patients with MI-related mechanical complications who require coronary revascularisation, coronary artery bypass grafting (CABG) is recommended at the time of surgical repair (no class or level given).^[1]
• Very high-risk NSTE-ACS needing immediate revascularisation (ESC 2023 narrative): PCI is usually preferred for timeliness, unless concomitant mechanical complications dictate a preference for surgery.^[1]
• Percutaneous repair (ACC/AHA 2025): used in patients with prohibitive surgical risk or contraindications to surgery, as a primary or temporising option in acute MR and ventricular septal rupture, and still an evolving area of investigation.^[2]
• Bridge to surgery (ACC/AHA 2025): selected patients may be candidates for definitive or temporising percutaneous structural intervention as a bridge to definitive surgery.^[2]
• Replacement therapy (ACC/AHA 2025): select patients may be considered for cardiac transplantation or a durable LV assist device as a primary or bailout strategy to improve survival.^[2]
• Team and palliative care (ESC 2023): a multidisciplinary approach is of paramount importance at all stages of care, from initial stabilisation to the therapeutic strategy, including palliative care.^[1]

Papillary muscle rupture and acute mitral regurgitation

Think of it in a patient with an inferior or lateral STEMI who develops pulmonary oedema, with or without a murmur.^[7] The 2025 ESC/EACTS valve guideline lists acute MR as a complication of MI through papillary muscle rupture, and says that, except for papillary muscle rupture, acute primary MR rarely leads to cardiogenic shock.^[5]

• Timing (AHA 2021, Table 1): 3–5 days after a transmural inferior or lateral infarct, with acute pulmonary oedema and/or shock.^[7]
• Course (AHA 2021): patients who do not present in shock commonly deteriorate rapidly.^[7]
• Echo (AHA 2021, Table 1): a severe and often eccentric MR jet and a mobile mass in the LV, sometimes prolapsing into the left atrium.^[7]
• Urgency (AHA 2021): acute papillary muscle rupture is a surgical emergency requiring immediate evaluation by a surgical team.^[7]
• Operation (AHA 2021): emergency mitral valve replacement is the treatment of choice; repair, typically for partial rupture with stable haemodynamics, can be considered by surgeons with expertise in mitral repair.^[7]
• Prohibitive surgical risk (AHA 2021): transcatheter edge-to-edge mitral repair can be considered in select patients as part of a Heart Team approach.^[7]
• Concomitant CABG (AHA 2021): can be performed for optimal revascularisation, with operative mortality similar to mitral surgery alone.^[7]

Keep rupture apart from acute ventricular secondary MR after MI.^[5] ESC/EACTS 2025 says increasing evidence supports mitral transcatheter edge-to-edge repair (M-TEER) in acute ventricular secondary MR, particularly after acute MI, because of lower mortality than surgery or medical treatment in propensity-matched analyses, and that this might help weaning from MCS.^[5]

Ventricular septal rupture

Think of it when examination shows a new pansystolic murmur, commonly at the lower left sternal edge, often with hypotension and signs of low cardiac output (AHA 2021).^[7] The AHA statement says it typically occurs 3 to 5 days after infarction, with presentations ranging from an incidental murmur to circulatory collapse.^[7]

• Untreated course (AHA 2021): mortality of uncorrected defects approaches 80% at 30 days, so conservative medical therapy alone is limited to haemodynamically insignificant defects or prohibitive surgical risk.^[7]
• Afterload reduction (AHA 2021): effective afterload reduction to decrease the left-to-right shunt is essential; IABPs with drug therapy are used in over 80% of emergency and 65% of urgent repairs.^[7]
• Shunt run (AHA 2021): right heart catheterisation shows a diagnostic step-up in oxygenation between the right atrium and pulmonary artery.^[7]
• Emergency surgery (AHA 2021): indicated for cardiogenic shock and/or pulmonary oedema refractory to MCS.^[7]
• Delay when stable (AHA 2021): lower mortality is reported when surgery is delayed for a week after diagnosis, although selection and survival bias may explain this; the statement suggests delaying surgery when feasible in a haemodynamically stable patient without respiratory failure.^[7]
• Why delay (AHA 2021): to avoid bleeding from antiplatelet drugs and allow better patient selection; in patients without symptoms or end-organ failure, delay may allow scar to form around the defect, giving a better anchor for sutures and less patch dehiscence.^[7]
• Operative mortality (AHA 2021): remains at 40% and has not changed significantly in decades.^[7]
• Percutaneous closure (AHA 2021): can be considered when surgical risk is excessive; procedural success approaches 89% (range 80–100) in centres of excellence, but hospital mortality remains excessively high and complications are common, including device embolisation, arrhythmia, haemolysis and incomplete closure needing surgery.^[7]

Device choice needs care here.^[3] ESC 2026 says temporary MCS should be used with caution in a large VSD, because VA-ECLS may increase the left-to-right shunt and a microaxial flow pump may invert it.^[3]

Free-wall rupture

Free-wall rupture usually presents as out-of-hospital sudden cardiac death (AHA 2021).^[7] The AHA 2021 Table 1 presentation cell for rupture of the ventricular free wall reads: commonly 3–5 days post transmural infarct; tamponade and shock.^[7]

• Diagnosis (AHA 2021): high clinical suspicion, prompt diagnosis confirmed by echocardiography and immediate surgery are needed; extracorporeal membrane oxygenation (ECMO) may be needed for pre-operative stabilisation.^[7]
• ECMO caveat (AHA 2021): in circulatory collapse, immediate ECMO may allow stabilisation and definitive repair, but poor venous return with tamponade may limit ECMO flow.^[7]
• ESC 2026 footnote: temporary MCS should be avoided in free-wall rupture; VA-ECLS can be considered to allow emergent surgery in profound cardiogenic shock and/or cardiac arrest if there is no sign of irreversible brain injury.^[3]
• Outcome (AHA 2021): surgery can be lifesaving, but hospital mortality after surgical repair exceeds 35%.^[7]
• Subacute rupture (ESC 2025): a post-MI pericardial effusion over 10 mm at end-diastole should be investigated for possible subacute heart rupture.^[4]

Pseudoaneurysm and true LV aneurysm

^[7]

Pseudoaneurysms are most commonly associated with prior acute MI, though they may follow cardiovascular surgery, blunt or penetrating chest trauma, or infective endocarditis (AHA 2021).^[7] Acute anterior wall rupture is thought to cause massive haemopericardium, catastrophic tamponade and immediate death, but other pseudoaneurysms can stay undiagnosed for several months or longer.^[7] The AHA statement advises urgent surgical intervention for all operative candidates, although little is known about the natural history of medically managed patients.^[7] After a remote MI, an incidentally found pseudoaneurysm may be planned for closure on an urgent rather than emergent basis.^[7]

A true aneurysm brings its own problems.^[7] The AHA statement links it to an increased risk of angina, partly from raised LV end-diastolic pressure, and to thrombus formation, worsening HF and haemodynamically significant ventricular tachyarrhythmia.^[7] ACC/AHA 2025 names LVEF under 30%, especially with an LV aneurysm, among the highest-risk features for LV thrombus.^[2]

Left ventricular thrombus

Think of it after a large anterior STEMI.^[2][1] ESC 2023 says echocardiography remains the first-line test, and that CMR is the gold standard for diagnosis and assessment.^[1] It reports contemporary CMR data with LV thrombi in up to 6.3% of all STEMI patients and 12.2% of those with anterior STEMI, suggesting that echocardiography may underestimate the incidence.^[1] Patients whose thrombi were seen only on CMR appear to have outcomes similar to those whose thrombi were evident on echo.^[1]

LV thrombus rows (ESC 2023, Recommendation Table 14)

^[1]

• Timing of imaging (ESC 2023): identification of LV thrombus has been reported to increase in the first 2 weeks after MI; these data suggest that a high proportion may develop after discharge, so delayed imaging at 2 weeks in high-risk patients may be of value.^[1]
• Imaging (ACC/AHA 2025 synopsis): echocardiography is the recommended modality for diagnosis, given wide access and low cost; cardiac MRI is more sensitive and may be considered when clinical suspicion is high and echo is inconclusive; repeat imaging can sometimes detect thrombus forming later in high-risk patients.^[2]
• Duration (ESC 2023 text): once diagnosed, OAC (warfarin or NOAC) should be considered for 3–6 months, guided by repeated echo or CMR, weighing bleeding risk and the need for concomitant antiplatelet therapy.^[1]
• Duration (ACC/AHA 2025 synopsis): most patients will warrant anticoagulation for 3 months, when repeat imaging can assess residual thrombus to help decide whether a longer course is warranted (no COR or LOE given).^[2]
• Bleeding balance (ACC/AHA 2025): because dual antiplatelet therapy (DAPT) is recommended for most patients early after ACS, adding an anticoagulant needs to be considered in the context of the overall bleeding risk versus the risk of an embolic event.^[2]
• Which anticoagulant (ACC/AHA 2025): DOACs are routinely used, but data comparing them with vitamin K antagonists are limited; observational studies and small RCTs have suggested DOACs may be non-inferior for mortality, stroke or thrombus resolution, and may offer a better bleeding profile.^[2]

The evidence base is thin.^[1][2] ESC 2023 says prospective randomised data are lacking on the optimal regimen, duration and combination with antiplatelet agents, and that therapy should be tailored to clinical status and follow-up results.^[1] ACC/AHA 2025 says current management rests mostly on retrospective and observational data and expert consensus.^[2]

^{[2] [1]}

Pericardial complications after MI

ESC 2023 says the pericardial complications that may develop after an acute MI include early infarct-associated pericarditis (from a few hours to 4 days after acute MI, mostly transient), late pericarditis or post-cardiac injury (Dressler) syndrome (typically 1–2 weeks after acute MI), and pericardial effusion.^[1] ACC/AHA 2025 says early pericarditis typically arises 1 to 3 days after a transmural event, and that a second form may occur weeks after MI (Dressler syndrome).^[2]

Post-MI pericarditis by guideline

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ACC/AHA 2025 Table 19 gives high-dose aspirin 500–1,000 mg every 6–8 h until symptoms improve, and colchicine 0.5–0.6 mg once or twice daily for 3 months, for persistent or late pericarditis symptoms.^[2] Its footnote says daily dosing should be used below 70 kg, with further adjustment in stage 4–5 kidney disease, severe hepatic impairment, or with concomitant P-glycoprotein and/or moderate and severe CYP3A4 inhibitors.^[2]

ESC 2025 says both early post-MI pericarditis and Dressler syndrome are markers of larger infarct size, but without independent prognostic significance.^[4] Diagnosis and first-line drugs for pericarditis outside MI are covered in Acute pericarditis.

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

Complications and pitfalls

• Fibrinolysis in shock: ESC 2023 says fibrinolysis should be considered in STEMI with cardiogenic shock if a PPCI strategy is not available within 120 min of STEMI diagnosis and mechanical complications have been ruled out (Class IIa, Level C).^[1]
• The absent murmur: in papillary muscle rupture a murmur may be absent, due to rapid equalisation of left atrial and left ventricular pressures (AHA 2021).^[7]
• Routine IABP: not recommended in ACS with cardiogenic shock without mechanical complications (ESC 2023, Class III, Level B); the mechanical-complication rows are the exception.^[1]
• MCS in rupture: ESC 2026 says temporary MCS should be used with caution in a large VSD and avoided in free-wall rupture, although in free-wall rupture VA-ECLS can be considered to allow emergent cardiac surgery in profound cardiogenic shock and/or cardiac arrest if there is no sign of irreversible brain injury.^[3]
• NSAIDs and steroids in post-MI pericarditis: ACC/AHA 2025 calls glucocorticoids and NSAIDs other than aspirin potentially harmful, because of a possible increase in the risk of recurrent MI or impaired myocardial healing and risk of rupture.^[2]
• Late thrombus: ESC 2023 says a high proportion of LV thrombi may develop after discharge, and that delayed imaging at 2 weeks in high-risk patients may be of value.^[1]
• Bleeding: OAC for LV thrombus is weighed against bleeding risk and the need for concomitant antiplatelet therapy (ESC 2023; ACC/AHA 2025).^[1][2]

Prognosis and disposition

Outcome varies by lesion, and surgery carries its highest risk in shock.^[7][2] ACC/AHA 2025 says mortality with surgery is highest in cardiogenic shock and in patients needing early emergency or urgent intervention after acute MI.^[2] The AHA statement gives mortality of 10–40% for papillary muscle rupture, 30–40% for VSD, over 50% for free-wall rupture and under 10% for pseudoaneurysm (its Table 1).^[7]

• Where the patient goes (ACC/AHA 2025): transfer to a Level 1 cardiac intensive care unit (CICU) with temporary MCS and experienced surgical, interventional, HF and palliative care teams is recommended (supportive text); no RCTs have evaluated transfer to dedicated centres.^[2]
• Surgeon early (AHA 2021): most mechanical complications of acute MI are surgical emergencies, and early involvement of the cardiac surgeon to discuss timing is of paramount importance.^[7]
• Shock team (AHA 2021): in patients with mechanical complications and Society for Cardiovascular Angiography and Interventions (SCAI) stage B through E shock, the statement suggests that multidisciplinary shock team assessment and management has the potential to improve clinical outcomes.^[7]
• Palliative care (AHA 2021): consultation should be considered early in the course of acute MI, especially if risk factors for morbidity and mortality are high; its role includes symptom control and eliciting patient and family values and care preferences.^[7]
• Before discharge (ACC/AHA 2025): in patients with ACS, an LVEF assessment is recommended to guide therapy and for risk stratification (COR 1, LOE C-LD).^[2]

Special populations

• Older patients: mortality from mechanical complications is high, especially among older patients, and contemporary patients with mechanical complications tend to be older (AHA 2021).^[7]
• Women: female sex is a risk factor for VSD, and contemporary patients with mechanical complications tend to be female (AHA 2021).^[7]
• Chronic kidney disease: a history of chronic kidney disease is among the features of contemporary patients with mechanical complications (AHA 2021); colchicine for persistent or late post-MI pericarditis symptoms needs further dose adjustment in stage 4–5 kidney disease (ACC/AHA 2025, Table 19 footnote).^[7][2]
• Body weight under 70 kg: daily colchicine dosing for persistent or late post-MI pericarditis symptoms (ACC/AHA 2025, Table 19 footnote).^[2]
• Patients on DAPT: anticoagulation for LV thrombus is weighed against overall bleeding risk (ACC/AHA 2025), and the ESC 2025 high-dose aspirin row for post-MI pericarditis, in its post-cardiac injury syndrome recommendations, explicitly covers patients already on antiplatelet therapy.^[2][4]
• NSTEMI: ESC 2023 reports a large epidemiological investigation of almost 9 million ACS patients in which mechanical complications occurred in 0.06% of NSTEMI cases versus 0.27% of STEMI cases, with in-hospital mortality of 18% after NSTEMI (42.4% after STEMI).^[1]
• Pregnancy and children: no separate rows for these complications were found in the guidelines checked for this topic, so none are stated here.

Evidence, guidelines and regional differences

Randomised evidence is lacking for several key decisions.^[2][1] ACC/AHA 2025 says no RCTs evaluate transfer to centres with cardiac surgical expertise or the role of MCS in mechanical complications.^[2] ESC 2023 notes a lack of prospective randomised data on the optimal anticoagulation regimen, its duration and its combination with antiplatelet agents for LV thrombus after MI.^[1] The ESC rows written for mechanical complications and for LV thrombus are all Level C; the two ACC/AHA mechanical-complication rows are LOE C-EO and B-NR.^[1][3][2]

^{[1] [3] [4] [2]}

How the ESC rows fit together

The ESC 2023 IABP row and the ESC 2026 HF MCS row are both in force among the guidelines checked for this topic.^[1][3] The newer ESC 2026 row sits in its table on temporary MCS in cardiogenic shock and covers temporary MCS in mechanical complications related to MI as a bridge to definitive treatment.^[3] Its footnote leaves the choice between a passive IABP and active percutaneous MCS to the Shock Team, by shock severity.^[3]

ANZ practice

The NHFA/CSANZ 2025 Australian ACS guideline is quoted here through its Medical Journal of Australia 2026 summary.^[6] It grades recommendations by GRADE strength and certainty, with consensus recommendations and practice points alongside.^[6]

• CABG at surgery (NHFA/CSANZ 2025, Table 3): in people with STEMI or acute coronary occlusion MI (ACOMI), mechanical complications and mitral valve disease (for example ventricular septal rupture, mitral valve insufficiency from papillary muscle infarction or rupture, or free wall rupture), perform CABG at the time of surgery (strong recommendation; low certainty of evidence).^[6]
• Balloon pump (NHFA/CSANZ 2025, Table 3): in people with ACS and cardiogenic shock, routine IABP insertion is not recommended (strong; high certainty).^[6]

Guidelines checked

A row called the newer one, or said to be in force, is so among the guidelines checked for this topic:

• Sources of the rows and statements used: ESC acute coronary syndromes (2023); ACC/AHA acute coronary syndromes (2025, JACC co-publication); ESC heart failure (2026); ESC myocarditis and pericarditis (2025); ESC/EACTS valvular heart disease (2025); NHFA/CSANZ ACS (2025, via its Med J Aust 2026 summary); and the AHA 2021 scientific statement on mechanical complications, which is not a guideline and gives no classes.^{[1][2][3][4][5][6][7]}
• Also swept for same-month or newer rows: ESC/EAS 2025 dyslipidaemia; ESC 2025 pregnancy; AHA/ACC 2025 blood pressure and 2026 pulmonary embolism; ACC/AHA 2026 dyslipidaemia; ESC 2026 cardiac rehabilitation; Fifth Universal Definition of MI 2026.

Exam pearls

• Mechanical complications may occur in the first days after MI, most commonly with STEMI (ESC 2023), and commonly present within the first week (ACC/AHA 2025); papillary muscle rupture occurs 3–5 days, and VSD and free-wall rupture commonly 3–5 days, after a transmural infarct (AHA 2021, Table 1).^[1][2][7]
• Posteromedial papillary muscle: single blood supply, and its rupture typically occurs with inferior or lateral STEMI (AHA 2021).^[7]
• VSD: oxygen step-up between right atrium and pulmonary artery on right heart catheterisation (AHA 2021).^[7]
• Contained rupture is the ACC/AHA 2025 preferred term for pseudoaneurysm.^[2]
• IABP: routine use is not recommended in ACS with cardiogenic shock and without mechanical complications (ESC 2023, Class III, Level B), but should be considered with haemodynamic instability or cardiogenic shock due to ACS-related mechanical complications (ESC 2023, Class IIa, Level C).^[1]
• Free-wall rupture: avoid temporary MCS; VA-ECLS can be considered to allow emergent cardiac surgery in profound cardiogenic shock and/or cardiac arrest if there is no sign of irreversible brain injury (ESC 2026 footnote to its temporary MCS in cardiogenic shock recommendations).^[3]
• LV thrombus: OAC (VKA or NOAC) should be considered for 3–6 months when thrombus is confirmed (ESC 2023, Class IIa, Level C); CMR is the gold standard for diagnosis (ESC 2023).^[1]
• Post-MI pericarditis: in its post-cardiac injury syndrome recommendations, ESC 2025 recommends high-dose aspirin as the first-choice anti-inflammatory therapy for post-MI pericarditis and in patients already on antiplatelet therapy (Class I, Level C).^[4]
• For early post-AMI pericarditis, ESC 2025 text says a 5–7-day course of aspirin, with colchicine, seems the most reasonable option; ACC/AHA 2025 says glucocorticoids and NSAIDs other than aspirin are potentially harmful.^[4][2]

References7ShowHide

1. [1]Byrne RA, et al. 2023 ESC Guidelines for the management of acute coronary syndromes. Eur Heart J, 2023.PMID 37622654
2. [2]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
3. [3]Køber L, et al. 2026 ESC Guidelines for the management of heart failure. Eur Heart J, 2026.PMID 42661420
4. [4]Schulz-Menger J, et al. 2025 ESC Guidelines for the management of myocarditis and pericarditis. Eur Heart J, 2025.PMID 40878297
5. [5]Praz F, et al. 2025 ESC/EACTS Guidelines for the management of valvular heart disease. Eur Heart J, 2025.PMID 40878295
6. [6]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
7. [7]Damluji AA, et al. Mechanical Complications of Acute Myocardial Infarction: A Scientific Statement From the American Heart Association. Circulation, 2021.PMID 34126755