Complications after myocardial infarction

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

Post-MI complications are best organised as recurrent ischaemia, electrical instability, pump failure, mechanical rupture, inflammation and thrombosis. The key exam and clinical move is to link the deterioration pattern to urgent bedside echocardiography and definitive specialist treatment.

Mechanical complications often present after an apparent period of stability and can deteriorate within minutes. Revascularisation reduces but does not abolish this risk, particularly after a large or late-presenting infarct.

Management is simultaneous: resuscitate, search for a reversible cause, restore coronary flow when indicated and involve interventional cardiology, cardiac surgery and critical care early.

Key points

Electrical complications are most prominent early: ventricular tachycardia/fibrillation, bradyarrhythmia and atrioventricular block can all cause sudden deterioration.
A new harsh pansystolic murmur with shock suggests ventricular septal rupture; an apical systolic murmur with flash pulmonary oedema suggests acute severe mitral regurgitation from papillary-muscle rupture.
Sudden hypotension, raised JVP and pulseless electrical activity may be free-wall rupture with tamponade; absence of a loud murmur does not exclude a mechanical defect.
Recurrent ischaemic pain or fresh ST change raises reinfarction, acute stent thrombosis or extension of infarction and demands an urgent ACS/reperfusion review.
Heart failure may reflect extensive LV injury, right-ventricular infarction, acute mitral regurgitation or a ventricular septal defect: identify the phenotype before giving fluid or vasodilator.
Early post-infarction pericarditis causes pleuritic positional pain; a later immune-mediated syndrome may include fever, pericardial or pleural pain and effusions.
LV aneurysm and akinetic segments predispose to heart failure, ventricular arrhythmia and mural thrombus; confirm thrombus with imaging before selecting anticoagulation.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Large or late-treated infarction

Extensive transmural necrosis leaves less functioning myocardium and more structurally weakened tissue. Delayed or unsuccessful reperfusion therefore increases pump-failure, arrhythmic and mechanical-complication risk.

Recurrent coronary occlusion

Acute stent thrombosis, persistent culprit occlusion or a new plaque event can extend injury or cause reinfarction. Recurrent pain with fresh ischaemic change is a warning pattern.

Infarct location and structures involved

Anterior or apical injury favours severe left-ventricular dysfunction and mural thrombus; inferior infarction may involve the right ventricle, atrioventricular conduction or papillary muscle.

Healing and remodelling response

Inflammation, scar formation and altered loading can produce pericarditis, ventricular aneurysm, functional mitral regurgitation and chronic arrhythmic substrate after the acute necrotic phase.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Acute electrical and contractile failure
Ischaemia disrupts membrane potentials, conduction and myocyte contraction. Ventricular arrhythmia, atrioventricular block, regional akinesis or immediate pump failure may therefore accompany the infarct.
2
Necrotic tissue weakens
During early healing, enzymatic breakdown temporarily reduces tissue strength. The free wall, interventricular septum or papillary muscle may rupture before a mature scar forms.
3
Loading drives remodelling
Surviving myocardium bears greater wall stress, promoting dilatation and fibrosis. Ventricular geometry may worsen functional mitral regurgitation and progress towards chronic systolic heart failure or aneurysm.
4
Stasis promotes thrombus
Akinetic or aneurysmal ventricular segments permit blood stasis over injured endocardium. Mural thrombus can form and later embolise into the systemic circulation.
5
Pericardial inflammation develops
Inflammation extending to the adjacent pericardium can cause early pleuritic pain. A later immune-mediated response may produce recurrent pericardial or pleural inflammation and effusion.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Ventricular arrhythmiaRed flag

Palpitations, syncope, broad-complex tachycardia, VF or cardiac arrest; correct ischaemia, hypoxia and electrolyte disturbance while following the RCUK peri-arrest or ALS algorithm.

Papillary-muscle ruptureRed flag

Abrupt pulmonary oedema, hypotension and a new apical systolic murmur after MI; the murmur may be soft when cardiac output is very low.

Ventricular septal ruptureRed flag

Acute heart failure or shock with a new harsh pansystolic murmur, often with a palpable thrill and biventricular failure.

Free-wall rupture and tamponadeRed flag

Sudden collapse, hypotension, raised JVP, electromechanical dissociation or PEA; a contained rupture may present more subtly as a pseudoaneurysm.

Pump failure or cardiogenic shockRed flag

Cold peripheries, confusion, oliguria, narrow pulse pressure and pulmonary or systemic congestion; consider LV, RV and mechanical causes.

Pericarditis or LV thrombus

Pleuritic positional pain and diffuse ST/PR change suggest pericarditis; embolic symptoms or a large anterior apical infarct should prompt assessment for LV thrombus.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
12-lead ECG plus continuous rhythm monitoringFirst step
Why
Detect recurrent ischaemia, ventricular arrhythmia, bradycardia or AV block.
Interpretation and limitations
Compare serial tracings; instability drives immediate treatment rather than waiting for a perfect rhythm label.
02
Urgent transthoracic echocardiography
Why
Assess LV/RV function, acute MR, septal defect, pericardial effusion/tamponade and LV thrombus.
Interpretation and limitations
Use Doppler and contrast when needed; a technically limited scan must not delay TOE, surgery or catheter-laboratory escalation in shock.
03
Arterial blood gas with lactate
Why
Grade respiratory failure and tissue hypoperfusion.
Interpretation and limitations
A rising lactate or worsening acidosis despite initial treatment signals persistent shock and need for higher-level support.
04
FBC, U&E, magnesium, glucose, LFT and coagulation
Why
Find anaemia, bleeding, electrolyte triggers and end-organ injury and prepare for intervention.
Interpretation and limitations
Correct potassium and magnesium abnormalities; interpret creatinine and liver injury as dynamic perfusion markers.
05
Serial high-sensitivity troponin with clinical/ECG correlation
Why
Support suspected recurrent infarction when there is new pain or ST change.
Interpretation and limitations
Troponin remains elevated after MI; a fresh rise/fall alone is insufficient without new ischaemic evidence.
06
Urgent coronary angiography when recurrent occlusion is suspected
Why
Identify acute stent thrombosis, persistent culprit occlusion or new coronary compromise.
Interpretation and limitations
Proceed through the ACS pathway; haemodynamic instability may require simultaneous mechanical-complication assessment.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Recurrent ischaemia versus pericarditis

Recurrent pressure-like pain with territorial ECG change favours coronary re-occlusion. Pleuritic, positional pain with diffuse changes and a rub suggests post-infarction pericardial inflammation.

Pulmonary embolism

Pleuritic pain, unexplained hypoxaemia, tachycardia and right-heart strain can reflect PE rather than recurrent infarction or left-sided failure. Definitive evaluation follows clinical probability.

Uncomplicated pump failure versus rupture

New pulmonary oedema may reflect extensive ventricular injury, but abrupt shock or a new murmur raises acute mitral regurgitation or septal rupture. Urgent Doppler echocardiography discriminates.

Hypovolaemic or haemorrhagic shock

Procedure-related bleeding can cause hypotension, tachycardia and oliguria after MI. Low filling pressures, falling haemoglobin or an identified bleeding source favour volume loss over cardiogenic congestion.

Acute aortic syndrome

Abrupt severe chest or back pain, pulse disparity, neurological deficit or new aortic regurgitation suggests dissection. This can mimic coronary occlusion and changes antithrombotic decisions urgently.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01First-lineAny sudden deterioration after MIFirst stepFirst lineShock, hypoxaemia, chest pain, arrhythmia, syncope or a new murmur

1Start ABCDE, attach defibrillator pads, obtain a 12-lead ECG, IV access, blood gas/lactate and targeted oxygen only for hypoxaemia.
2Call senior cardiology and critical care immediately; obtain bedside echocardiography without delaying resuscitation.
3Treat the dominant reversible cause: recurrent coronary occlusion, arrhythmia, hypovolaemia/bleeding, pump failure or mechanical rupture.
4Move early to the catheter laboratory, theatre or critical care according to the identified cause.

02Second-lineNew murmur, pulmonary oedema or shockSecond lineSuspected VSD, acute MR or free-wall rupture

1Perform urgent expert echo; use TOE if transthoracic views are inadequate and the patient can tolerate it.
2DefinitiveStabilise airway, ventilation and perfusion with invasive monitoring and specialist vasoactive support; avoid treatment that delays definitive repair.
3Contact cardiac surgery and interventional cardiology at diagnosis, not after medical therapy fails.
4Use temporary circulatory support only after multidisciplinary assessment as a bridge to repair, recovery or decision.

03Third-lineElectrical instabilityThird lineVT/VF, unstable tachycardia or symptomatic bradycardia/AV block

1Follow the RCUK 2025 ALS/peri-arrest algorithm, using immediate defibrillation or synchronised cardioversion when indicated.
2Correct ongoing ischaemia, hypoxia, acidosis, potassium and magnesium disturbance; assess for acute coronary re-occlusion.
3Use pacing and antiarrhythmic therapy according to rhythm and haemodynamic state with expert help.
4EscalationEscalate recurrent VT/VF despite optimal therapy to an electrophysiology, interventional and critical-care discussion, including selected temporary support.

04EscalationLater complication reviewEscalationPersistent heart failure, embolic event, pleuritic pain or aneurysmal ECG/imaging pattern

1Repeat ECG and echocardiography, adding CMR or contrast echo when anatomy or thrombus remains uncertain.
2Treat heart failure and secondary prevention through NICE pathways; anticoagulate confirmed LV thrombus only after balancing bleeding and antiplatelet therapy.
3Manage pericarditis with cardiology input because NSAIDs and antithrombotic therapy require careful post-MI risk assessment.
4Arrange specialist follow-up for aneurysm, arrhythmia risk, ventricular function and device eligibility.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Electrical instability

Ventricular tachycardia or fibrillation can cause sudden arrest, while bradycardia and atrioventricular block may produce syncope or shock. Ongoing ischaemia and electrolyte disturbance can perpetuate either pattern.

Pump failure and cardiogenic shock

Extensive left-ventricular injury causes pulmonary congestion and low output; right-ventricular infarction causes a different preload-sensitive phenotype. Both can progress to renal, hepatic and cerebral hypoperfusion.

Mechanical rupture

Papillary-muscle rupture causes acute severe mitral regurgitation, septal rupture creates a left-to-right shunt, and free-wall rupture can cause haemopericardium and tamponade. Each can deteriorate rapidly and requires immediate specialist escalation.

Ventricular thrombus and embolism

Large anterior or apical akinesis can support mural thrombus. Systemic embolisation may cause stroke or limb and visceral infarction, while combined antithrombotic treatment increases management complexity.

Chronic structural and inflammatory sequelae

Adverse remodelling can lead to chronic heart failure, ventricular aneurysm and scar-related arrhythmia. Early or immune-mediated pericarditis may cause recurrent pain and effusion.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

Continuous ECG and repeated 12-lead ECGs for new pain, syncope or haemodynamic change.
Frequent BP, respiratory status, urine output, peripheral perfusion and mental state; use invasive monitoring in shock.
Serial lactate, pH, potassium, magnesium, creatinine and liver tests during instability.
Repeat echocardiography when the murmur, congestion or perfusion changes, and before/after definitive intervention.
Before discharge, document LVEF, rhythm burden, residual ischaemia, secondary-prevention plan and cardiac-rehabilitation referral.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

Murmur intensity can mislead

A small pressure gradient in profound shock can make severe acute MR or a septal rupture surprisingly quiet.

Inferior MI has a distinct pattern

Right-ventricular infarction and AV block are important causes of hypotension; bedside echo and right-sided ECG leads help distinguish them from LV congestion.

PEA is a diagnosis prompt

After MI, PEA should trigger immediate consideration of tamponade from free-wall rupture as well as the standard reversible causes.

Troponin is not the reinfarction diagnosis

Because it remains raised, reinfarction requires a new clinical/ECG pattern plus a convincing biomarker change or angiographic evidence.

Thrombus changes antithrombotic complexity

Adding anticoagulation to antiplatelets raises bleeding risk; confirm the indication and agree the shortest safe combined plan with cardiology.

11Common pitfallsFrequent interpretation and management errors.

01
Attributing new pulmonary oedema to uncomplicated LV failure without listening for a murmur and obtaining urgent echo.
02
Waiting for a loud murmur before considering papillary-muscle or septal rupture.
03
Giving repeated fluid boluses to undifferentiated post-MI shock despite pulmonary congestion or a mechanical lesion.
04
Calling persistent troponin elevation reinfarction without new ischaemic evidence.
05
Delaying surgical or catheter-laboratory contact until vasoactive treatment has failed.