Myocardial Infarction Complications

📋 Key Information Summary

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Cardiogenic shock complicates 5–8% of STEMI presentations and carries mortality of 40–50% even with early revascularisation; haemodynamic criteria include systolic BP <90 mmHg for >30 min, cardiac index <2.2 L/min/m², and PCWP >18 mmHg.
Noradrenaline is the first-line vasopressor in cardiogenic shock (SOAP II trial); dobutamine is the first-line inotrope for low-output states without severe hypotension.
Mechanical circulatory support (MCS) — IABP is available in most Australian tertiary centres; Impella and VA-ECMO require specialist/cardiothoracic referral and are available at selected quaternary centres only.
Ventricular fibrillation (VF) and sustained ventricular tachycardia (VT) in the first 48 hours post-MI are early arrhythmias (reperfusion-related) and do not independently mandate ICD; VT/VF beyond 48 hours warrants electrophysiology review and consideration of ICD.
Complete heart block complicating inferior MI is usually transient (AV node level) and may require temporary pacing; anterior MI with new bundle branch block or complete block (His-Purkinje level) carries high mortality and often requires permanent pacing.
LV remodelling begins within hours of large transmural infarction; ACE inhibitors (ramipril, perindopril), beta-blockers (carvedilol, bisoprolol), and mineralocorticoid receptor antagonists (eplerenone) are the cornerstone pharmacotherapy to prevent adverse remodelling.
LV mural thrombus occurs in 5–15% of anterior STEMI with apical akinesis/dyskinesis; anticoagulation with warfarin (INR 2.0–3.0) for 3–6 months is first-line; DOACs are emerging but not yet standard of care for LV thrombus.
Post-MI pericarditis (epistenocardiac pericarditis) occurs within 1–5 days and is treated with aspirin 650–1000 mg TDS; colchicine 0.5 mg BD is recommended as adjunctive therapy.
Dressler syndrome (autoimmune pericarditis) occurs 2–10 weeks post-MI and is differentiated from recurrent ischaemia by pleuritic pain, pericardial rub, ST elevation (diffuse, concave-up), and elevated inflammatory markers.
NSAIDs and corticosteroids should be avoided in post-MI pericarditis where possible due to risk of impaired myocardial healing and increased reinfarction risk; aspirin at high dose is preferred.
Aboriginal and Torres Strait Islander Australians experience AMI at 1.7× the rate of non-Indigenous Australians and present later, with higher rates of cardiogenic shock and mechanical complications — culturally safe care pathways are essential.
Transfer criteria — cardiogenic shock, refractory arrhythmias, need for MCS, and mechanical complications (VSD, papillary muscle rupture) require emergent transfer to a PCI-capable or cardiothoracic centre.

Introduction & Australian Epidemiology

Myocardial infarction (MI) remains a leading cause of morbidity and mortality in Australia. Despite significant advances in early reperfusion therapy — primary percutaneous coronary intervention (PCI) and fibrinolysis — complications of MI continue to impose a substantial clinical burden. Understanding the pathophysiology, early recognition, and evidence-based management of these complications is essential for optimising patient outcomes in Australian emergency departments, coronary care units, and cardiology wards.

In Australia, approximately 57,000 acute coronary syndrome (ACS) hospitalisations occur annually (AIHW 2023). ST-elevation myocardial infarction (STEMI) accounts for roughly 30% of ACS presentations. Complications of MI can be broadly categorised as:

Haemodynamic — cardiogenic shock, mechanical complications (ventricular septal defect, free wall rupture, papillary muscle rupture)
Arrhythmic — ventricular arrhythmias, conduction disturbances, atrial fibrillation
Structural — LV remodelling, aneurysm formation, mural thrombus
Inflammatory — pericarditis, Dressler syndrome

The in-hospital mortality for STEMI in Australia is approximately 5–7% with contemporary management (ACSQA data). However, cardiogenic shock carries mortality rates of 40–50%, and mechanical complications such as ventricular septal defect or free wall rupture remain lethal without emergent surgical intervention.

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Time-critical: All patients with suspected mechanical complications of MI (new systolic murmur, sudden haemodynamic deterioration, recurrent chest pain with new ECG changes) require emergent echocardiography and immediate referral to a cardiothoracic centre.

Cardiogenic Shock

Definition & Haemodynamic Criteria

Cardiogenic shock is defined as a state of critical end-organ hypoperfusion resulting from severe impairment of cardiac pump function. It is the leading cause of in-hospital death following acute MI.

Parameter	Diagnostic Criterion
Systolic BP	<90 mmHg for >30 min, or vasopressors required to maintain ≥90 mmHg
Cardiac index (CI)	<2.2 L/min/m²
Pulmonary capillary wedge pressure (PCWP)	>18 mmHg
End-organ signs	Altered mental status, cold clammy extremities, urine output <30 mL/hr, lactate >2 mmol/L
Echocardiographic EF	Typically <30% (not mandatory for diagnosis)

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Society for Cardiovascular Angiography and Interventions (SCAI) Shock Classification: Stages A (at risk) through E (extremis) should be applied to guide escalation of therapy. Patients progressing from SCAI Stage C (classic shock) to Stage D (deteriorating) should be considered for mechanical circulatory support without delay.

Vasopressor & Inotrope Selection

Pharmacological haemodynamic support should be initiated early while arranging revascularisation. The choice of vasoactive agent depends on blood pressure, cardiac output, and systemic vascular resistance.

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Noradrenaline (Norepinephrine)

Levophed® · First-line vasopressor in cardiogenic shock

Adult dose 0.1–0.5 mcg/kg/min IV infusion, titrated to MAP ≥65 mmHg

Indication Cardiogenic shock with hypotension (SBP <90 mmHg); preferred over adrenaline based on SOAP II subgroup data

Renal adjustment None required

PBS status ✔ PBS General Benefit (hospital use)

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Dobutamine

Dobutrex® · First-line inotrope for low-output states

Adult dose 2.5–20 mcg/kg/min IV infusion; start at 2.5–5 mcg/kg/min

Indication Low cardiac output with adequate BP (SBP ≥90 mmHg); may be combined with noradrenaline if hypotension develops

Renal adjustment None required

PBS status ✔ PBS General Benefit (hospital use)

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Adrenaline (Epinephrine)

Second-line inotrope/vasopressor

Adult dose 0.01–0.5 mcg/kg/min IV infusion

Indication Refractory cardiogenic shock not responding to noradrenaline + dobutamine; increases myocardial oxygen demand — use with caution

Caution Increases lactate independent of tissue hypoperfusion; may cause tachyarrhythmias

PBS status ✔ PBS General Benefit (hospital use)

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Milrinone

Primacor® · Phosphodiesterase-III inhibitor (inodilator)

Adult dose Loading 50 mcg/kg IV over 10 min (often omitted in shock), then 0.125–0.75 mcg/kg/min IV infusion

Indication Low-output heart failure/cardiogenic shock with elevated SVR; caution — causes vasodilation and hypotension

Renal adjustment Reduce dose by 50% if eGFR <30 mL/min (renally cleared)

PBS status ⚠ Authority Required (hospital use)

Mechanical Circulatory Support (MCS)

When pharmacological therapy is insufficient, mechanical circulatory support should be considered. Availability of specific devices varies across Australian centres, and early consultation with a cardiothoracic/heart failure centre is essential.

Device	Mechanism	Support Level	Availability in Australia
IABP (Intra-Aortic Balloon Pump)	Counterpulsation — augments diastolic coronary perfusion, reduces afterload	Partial (↑CO 0.5–1.0 L/min)	Most tertiary cardiac centres (Royal Melbourne, RPAH, Alfred, Prince Charles, Flinders, Fiona Stanley)
Impella (CP/5.5)	Percutaneous axial flow pump across aortic valve; provides direct LV unloading	Moderate (↑CO 2.5–5.5 L/min depending on model)	Limited — selected quaternary centres; increasing availability
VA-ECMO (Veno-Arterial Extracorporeal Membrane Oxygenation)	Complete cardiopulmonary bypass; provides full circulatory and respiratory support	Full (↑CO up to 6–7 L/min)	ECMO retrieval services (e.g., Alfred ECMO, Royal Prince Alfred, Prince Charles, St Vincent's Melbourne); retrieval from regional centres via dedicated teams
LVAD (Left Ventricular Assist Device)	Surgically implanted chronic mechanical support	Full (bridge to transplant/recovery)	Heart transplant centres only (St Vincent's Sydney, Alfred Melbourne, Prince Charles Brisbane)

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IABP-SHOCK II trial (2012): Routine IABP use in cardiogenic shock complicating MI did not reduce 30-day mortality compared to medical therapy alone (IABP group 39.7% vs control 41.3%, p=0.69). Current guidelines (ESC 2023) downgraded IABP to Class IIb; consider on a case-by-case basis. Impella and VA-ECMO evidence is evolving (DanGer Shock trial 2024 showed mortality benefit with Impella CP in selected STEMI-shock patients).

Emergency Revascularisation

Early revascularisation remains the most important intervention in cardiogenic shock complicating MI. The SHOCK trial demonstrated a significant 6-month mortality benefit with early PCI or CABG compared to initial medical stabilisation (50.3% vs 63.1%). In Australia, this mandates emergent transfer to a PCI-capable facility if the presenting hospital does not have catheterisation laboratory access.

1

Recognise & Resuscitate

Identify SCAI shock stage, obtain arterial access, commence noradrenaline ± dobutamine, secure airway if GCS declining

2

Emergent Echo & PCI

Bedside echocardiography to exclude mechanical complications; activate cath lab for emergent revascularisation

3

Escalate MCS

If refractory despite inotropes/vasopressors — insert IABP or Impella; contact ECMO retrieval service if progressive deterioration

4

Multi-disciplinary Review

Heart failure, cardiothoracic surgery, and intensive care involvement; define goals of care and transplant candidacy if appropriate

Arrhythmic Complications

Classification by Timing

Arrhythmias are the most common complication of acute MI and a leading cause of early mortality. They are classified by timing relative to the infarct event, which has important prognostic and therapeutic implications.

Timing	Window	Common Arrhythmias	Mechanism	Prognostic Implication
Ultra-early	<2 hours	VF, VT, sinus bradycardia (inferior MI)	Acute ischaemia, vagal activation, reperfusion injury	High in-hospital mortality; does NOT independently mandate ICD if reversible
Early	2–48 hours	VT, VF, AF, accelerated idioventricular rhythm (AIVR)	Reperfusion arrhythmias, electrolyte shifts, catecholamine surge	AIVR is benign (reperfusion marker); VF/VT in this window generally do not mandate ICD
Late (>48 hrs)	>48 hours to discharge	Sustained VT, VF, complete heart block	Peri-infarct scar, re-entrant circuits, progressive conduction system fibrosis	Poor prognosis marker; warrants EPS and ICD consideration per ESC/AHA guidelines

Ventricular Arrhythmias Post-MI

Ventricular Fibrillation (VF) & Pulseless VT

Management follows standard ALS protocols (Australian Resuscitation Council Guideline 11.2). Early defibrillation is the definitive treatment.

Immediate: Defibrillation (biphasic 150–200 J, then escalating). Commence CPR if not immediately successful.
Adrenaline 1 mg IV every 3–5 minutes during cardiac arrest (ALS protocol).
Amiodarone 300 mg IV bolus for refractory VF/pulseless VT, followed by 150 mg IV if recurrent.
Correct reversible causes: Hypokalaemia (target K⁺ >4.0 mmol/L), hypomagnesaemia (MgSO₄ 2 g IV), acidosis, hypoxia.

Sustained Monomorphic VT (Haemodynamically Stable)

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Amiodarone

Cordarone X® · First-line antiarrhythmic for post-MI VT

Adult dose 150 mg IV over 10 min, then 1 mg/min for 6 hours (360 mg), then 0.5 mg/min for 18 hours (540 mg); switch to 200 mg PO BD–TDS when stable

Key monitoring ECG for QTc prolongation; thyroid function, LFTs at baseline; avoid in torsades risk

Renal adjustment No dose adjustment required

PBS status ✔ PBS General Benefit

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Lidocaine (Lignocaine)

Second-line for recurrent VT (ischaemia-related)

Adult dose 1–1.5 mg/kg IV bolus, then 1–4 mg/min infusion

Indication Recurrent VT despite amiodarone, or if amiodarone contraindicated

Renal adjustment Reduce infusion rate if eGFR <30 mL/min; increased seizure risk in renal impairment

PBS status ✔ PBS General Benefit (hospital use)

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Accelerated idioventricular rhythm (AIVR) is common after successful reperfusion (PCI or fibrinolysis) and is generally benign. It does NOT require treatment with antiarrhythmics. Atropine to increase the sinus rate may suppress AIVR if haemodynamically significant, but this is rarely needed.

ICD Indications Post-MI

Implantable cardioverter-defibrillator (ICD) placement for primary prevention should not be considered during the acute admission. Assessment occurs at 6–12 weeks post-MI once optimal medical therapy is established and LV function is reassessed.

Primary prevention: LVEF ≤35% at ≥6–12 weeks post-MI despite optimal medical therapy (ACEi/ARB + beta-blocker + MRA) — refer for ICD assessment (ESC Class I, NHFA/CSANZ consensus).
Secondary prevention: Survived cardiac arrest not due to reversible cause, sustained VT not within 48 hours of MI — ICD indicated.
EPS-guided: If LVEF 36–40% with NYHA II–III and additional risk factors (non-sustained VT, positive EPS) — consider ICD.

Conduction Disturbances & Temporary Pacing

Conduction Disturbance	MI Location	Level of Block	Prognosis	Pacing Indication
1st-degree AV block	Any	AV node	Benign (monitor)	None unless symptomatic
2nd-degree Type I (Wenckebach)	Inferior	AV node	Usually transient, benign	If HR <50 with symptoms (transcutaneous pacing standby)
2nd-degree Type II (Mobitz II)	Anterior	His-Purkinje	May progress to complete block; ominous	Temporary transvenous pacing — prophylactic
Complete heart block (CHB)	Inferior	AV node	Usually transient (1–2 weeks), narrow QRS escape	If HR <40, haemodynamic compromise, or ventricular escape >3 sec pause — temporary pacing
Complete heart block (CHB)	Anterior	His-Purkinje	High mortality (extensive septal necrosis); wide QRS escape	Immediate temporary transvenous pacing; likely permanent pacemaker required
New bundle branch block (RBBB ± LAFB/LPFB)	Anterior	His-Purkinje	High risk of progression to CHB; marker of large infarct	Prophylactic temporary pacing if alternating bundle branch block or associated with CHB

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Atropine (500 mcg IV, repeat every 3–5 min, max 3 mg) is effective for AV nodal block (inferior MI) but is ineffective for His-Purkinje block (anterior MI with CHB). Do not rely on atropine for infranodal complete heart block — proceed directly to temporary transcutaneous or transvenous pacing.

Temporary Pacing — Technical Considerations

Transcutaneous pacing (Zoll/defibrillator pads): Immediate, non-invasive; suitable for bridge to transvenous pacing or as sole therapy in transient bradycardia. Sedation/analgesia required (fentanyl 25–50 mcg IV + midazolam 1–2 mg IV).
Transvenous pacing (right internal jugular or left subclavian approach): Inserted under fluoroscopy or echocardiographic guidance in catheterisation laboratory or ICU. Required for prolonged (>5–7 days) AV block, His-Purkinje block, or haemodynamically unstable bradycardia unresponsive to transcutaneous pacing.
Permanent pacemaker: Considered if AV block persists >14 days post-inferior MI, or if His-Purkinje block persists beyond the acute phase.

Post-MI Ventricular Dysfunction

Left Ventricular Remodelling

LV remodelling is the structural and functional adaptation of the left ventricle following myocardial infarction. It begins within hours of the ischaemic event and may continue for months to years. Remodelling is initially adaptive (maintaining stroke volume) but becomes maladaptive, leading to progressive ventricular dilation, sphericity, and ultimately heart failure.

Pathophysiology

Infarct expansion: Thinning and stretching of the infarcted myocardial segment (first 72 hours); greatest risk with large transmural anterior MI.
Compensatory hypertrophy: Non-infarcted segments undergo eccentric hypertrophy to maintain cardiac output.
Ventricular dilation: Progressive increase in end-diastolic and end-systolic volumes; spherical geometry increases wall stress (Laplace law).
Neurohormonal activation: RAAS activation, sympathetic nervous system upregulation, and inflammatory cytokines drive ongoing remodelling and fibrosis.

Pharmacological Prevention of Remodelling

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Perindopril

Coversyl® · ACE inhibitor — cornerstone of anti-remodelling therapy

Adult dose Start 2 mg daily, titrate to 8 mg daily over 2–4 weeks as tolerated

Evidence SAVE, AIRE, TRACE trials — 20–25% relative risk reduction in mortality when started within 24–72 hours of MI

Renal adjustment Start at 2 mg every 2 days if eGFR <30 mL/min

PBS status ✔ PBS General Benefit

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Ramipril

Tritace® · ACE inhibitor

Adult dose Start 2.5 mg BD, titrate to 5–10 mg daily

Evidence AIRE trial — significant mortality reduction post-MI with clinical/radiographic heart failure

PBS status ✔ PBS General Benefit

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Carvedilol

Dilatrend® · Beta-blocker (non-selective β + α1 blocker)

Adult dose Start 3.125 mg BD, titrate every 2 weeks to target 25 mg BD (≤85 kg) or 50 mg BD (>85 kg)

Evidence CAPRICORN trial — significant reduction in mortality and recurrent MI post-MI with LV dysfunction

PBS status ✔ PBS General Benefit

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Eplerenone

Inspra® · Mineralocorticoid receptor antagonist

Adult dose Start 25 mg daily, increase to 50 mg daily after 4 weeks

Indication Post-MI with LVEF ≤40% and either heart failure or diabetes; EPHESUS trial — 15% relative mortality reduction

Renal adjustment Contraindicated if eGFR <30 mL/min (hyperkalaemia risk)

PBS status ⚠ Authority Required

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Sacubitril/Valsartan

Entresto® · ARNI — consider if HFrEF develops post-MI

Adult dose Start 24/26 mg BD (or 49/51 mg BD if prior ACEi/ARB tolerated), titrate to 97/103 mg BD

Indication HFrEF (LVEF ≤40%) — switch from ACEi after 36-hour washout; PARADIGM-HF trial

Renal adjustment Start at 24/26 mg BD if eGFR <30 mL/min

PBS status ⚠ Authority Required

LV Aneurysm Formation

A true LV aneurysm is a localised area of thinned, scarred myocardium that bulges during systole and diastole. It typically develops 4–8 weeks post-large transmural anterior MI.

Incidence: 5–10% of anterior STEMI in the primary PCI era (lower than historical rates of 10–35%).
Diagnosis: Echocardiography (parasternal and apical views); cardiac MRI with late gadolinium enhancement is gold standard for characterising scar and aneurysm extent.
ECG findings: Persistent ST elevation in anterior leads beyond 2 weeks post-MI (differentiate from acute ischaemia).
Complications: Heart failure, ventricular arrhythmias (re-entrant circuits within scar), mural thrombus, systemic thromboembolism.
Management: Pharmacological (ACEi, beta-blockers, diuretics); surgical ventricular restoration (Dor procedure) for refractory heart failure or recurrent VT; ICD for VT not amenable to ablation.

LV Mural Thrombus

Left ventricular mural thrombus is a common complication of anterior STEMI, particularly when there is apical akinesis or dyskinesis. The incidence has decreased with contemporary anticoagulation and early reperfusion but remains clinically important.

Feature	Detail
Incidence	5–15% of anterior STEMI (higher with large infarcts, apical akinesis/dyskinesis)
Diagnostic modality	Transthoracic echo (sensitivity 60%); contrast echo or cardiac MRI (sensitivity >90%) if suboptimal acoustic windows
Thromboembolic risk	Up to 10% risk of stroke/peripheral embolisation if untreated
First-line anticoagulation	Warfarin (INR 2.0–3.0) for 3–6 months; repeat echo at 3 months to assess thrombus resolution
DOACs	Emerging evidence (WATCHMAN-like data, case series); not yet standard of care for LV thrombus in Australian guidelines; may be considered if warfarin contraindicated (Haematology/EP consult)
Triple therapy	If concurrent PCI with stent: aspirin + clopidogrel + warfarin (shortest duration possible, typically 1–3 months), then dual therapy (clopidogrel + warfarin) for remainder, then warfarin alone. Bleeding risk is high — PPI co-prescribe.

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Routine screening echo: An echocardiogram at 3–5 days post-anterior STEMI is recommended to assess for mural thrombus (even in asymptomatic patients). Repeat at 3 months if thrombus detected to guide duration of anticoagulation. If thrombus has resolved and EF improved, anticoagulation may be ceased.

Newer Therapies for LV Dysfunction — SGLT2 Inhibitors

SGLT2 inhibitors (dapagliflozin, empagliflozin) are now established in HFrEF management and are increasingly used in the post-MI setting where LV dysfunction develops.

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Dapagliflozin

Forxiga® · SGLT2 inhibitor

Adult dose 10 mg PO daily

Indication HFrEF (LVEF ≤40%) — DAPA-HF trial; reduces CV death and HF hospitalisation

Renal adjustment Initiate if eGFR ≥20 mL/min; no dose adjustment

PBS status ⚠ Authority Required

Pericarditis & Dressler Syndrome

Classification

Pericardial inflammation following MI is classified into two distinct entities based on timing and pathophysiology:

Feature	Post-MI (Epistenocardiac) Pericarditis	Dressler Syndrome
Timing	1–5 days post-MI	2–10 weeks post-MI (weeks to months)
Mechanism	Direct inflammation of pericardium adjacent to infarcted myocardium	Autoimmune (anti-myocardial antibodies); systemic inflammatory response
Incidence	10–20% (decreased with early reperfusion)	1–5% (rare in the primary PCI era)
Pericardial rub	Present in ~30–85%	Common
Effusion risk	Small–moderate effusion common; tamponade rare	Moderate–large effusion; tamponade possible

Diagnostic Criteria

Diagnosis of post-MI pericarditis requires at least 2 of the following 4 criteria:

Pleuritic chest pain — sharp, positional (worse supine, better leaning forward), distinct from ischaemic pain
Pericardial friction rub — high-pitched, scratchy, best heard at left sternal border with diaphragm during end-expiration
ECG changes — diffuse concave-upward ST elevation (not in a single coronary territory), PR depression (most specific in lead II), or new/worsening pericardial effusion on echo
Inflammatory markers — elevated CRP and/or ESR; WBC may be elevated

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Differentiating post-MI pericarditis from recurrent ischaemia/reinfarction is critical. Post-MI pericarditis causes diffuse ST elevation (not territorial), PR depression, and pleuritic pain. Recurrent ischaemia causes territorial ST changes, troponin rise pattern typical of acute MI, and crushing/pressure-type chest pain. When in doubt, treat as recurrent ischaemia and obtain urgent angiography — do not delay reperfusion for pericarditis workup.

Feature	Post-MI Pericarditis	Recurrent Ischaemia / Reinfarction
Pain character	Sharp, pleuritic, positional	Crushing, pressure, retrosternal
ECG	Diffuse concave ST elevation, PR depression	Territorial ST elevation/depression, reciprocal changes
Troponin	Mildly elevated (from index MI or myopericarditis) — no re-elevation pattern	Rise and fall pattern consistent with acute MI
CRP	Elevated	Usually normal early
Friction rub	Present	Absent
Echo	Pericardial effusion; preserved regional wall motion	New or worsening wall motion abnormality

Treatment Protocols

First-Line Therapy

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Aspirin (high dose)

Preferred anti-inflammatory for post-MI pericarditis

Adult dose 650–1000 mg PO TDS (1950–3000 mg/day) for 1–2 weeks, then taper over 2–4 weeks (reduce by 250–500 mg every 1–2 weeks)

Rationale Aspirin is preferred over NSAIDs post-MI as it does not impair myocardial healing, does not increase reinfarction risk, and has antiplatelet benefit

Caution GI side effects — co-prescribe PPI (pantoprazole 40 mg daily); avoid in active GI bleeding

PBS status ✔ PBS General Benefit

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Colchicine

Colgout® · Adjunctive anti-inflammatory

Adult dose 0.5 mg PO BD for 3 months (COPE trial, COlchicine for PErICarditis); OR 0.5 mg BD for 1 week then 0.5 mg daily for 3 months

Evidence CORE, COPE, CORP trials — reduces recurrence of pericarditis by ~50%

Renal adjustment Reduce dose by 50% if eGFR <30 mL/min; avoid if eGFR <10 mL/min

PBS status ✔ PBS General Benefit

Medications to AVOID

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NSAIDs (ibuprofen, naproxen, indomethacin) — impair myocardial scar formation, increase risk of myocardial rupture in the early post-MI period, and may increase reinfarction risk (with the exception of aspirin at anti-inflammatory doses).
Corticosteroids (prednisolone, dexamethasone) — impair myocardial healing, increase risk of ventricular wall thinning and aneurysm formation; should only be used as last resort for refractory pericarditis not responsive to aspirin + colchicine.
Anticoagulants in the setting of pericarditis — increased risk of haemopericardium and tamponade. If anticoagulation is required (e.g., LV thrombus, AF), use with caution and monitor closely for pericardial effusion development.

Second-Line / Refractory Therapy

Ibuprofen 600 mg TDS + colchicine 0.5 mg BD — reserved for patients without LV dysfunction and not at risk of myocardial rupture (generally >4 weeks post-MI).
IL-1 receptor antagonist (anakinra) — for recurrent, corticosteroid-dependent pericarditis; requires specialist (cardiology/rheumatology) initiation; not PBS-listed for this indication.
Pericardiocentesis — for large effusion with haemodynamic compromise (tamponade) or diagnostic uncertainty (rule out purulent pericarditis).

Cardiac Rehabilitation Considerations

Exercise should be restricted during the acute phase of post-MI pericarditis. Patients may participate in Phase II cardiac rehabilitation once symptoms have resolved, inflammatory markers have normalised, and there is no significant pericardial effusion on repeat echocardiography. Typically this means a delay of 2–4 weeks from symptom resolution.

Special Populations

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Pregnancy

ACE inhibitors / ARBs / ARNI

Contraindicated in all trimesters (teratogenic — renal agenesis, oligohydramnios). Use hydralazine + nitrates as alternative afterload reduction for LV dysfunction.

Warfarin

Teratogenic (first trimester — nasal hypoplasia, stippled epiphyses). Use LMWH for mural thrombus anticoagulation in pregnancy; consult Haematology.

Eplerenone / Spironolactone

Contraindicated — anti-androgenic effects. Avoid in pregnancy and breastfeeding.

Colchicine

Avoid in pregnancy (teratogenicity data limited; teratogenic in animal studies). Consider NSAIDs only in second trimester if essential, and under specialist guidance.

Amiodarone

Contraindicated — foetal thyroid toxicity (contains 37% iodine). Consider sotalol or flecainide for recurrent VT in pregnancy (consult Electrophysiology).

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Paediatrics

MI in children

Rare — consider Kawasaki disease (coronary aneurysms), anomalous coronary origin, myocarditis, or cardiomyopathy. Management guided by paediatric cardiology at tertiary centres (RCH Melbourne, Children's Hospital Westmead, QCH Brisbane).

Inotropic dosing

Dobutamine 2–20 mcg/kg/min; noradrenaline 0.05–1 mcg/kg/min — weight-based dosing; paediatric intensive care management essential.

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Elderly (≥75 years)

Cardiogenic shock

Higher incidence and mortality; MCS decisions require careful goals-of-care discussion. Frailty assessment should inform escalation planning.

Conduction disturbances

Higher baseline prevalence of conduction disease; threshold for temporary/permanent pacing should be lower. Pre-existing RBBB/LBBB may mask acute ischaemic ECG changes.

Bleeding risk

Triple therapy for LV thrombus carries high bleeding risk in elderly; prefer shorter durations (1 month triple → dual → warfarin alone). DOACs may be considered for AF with HAS-BLED assessment.

Renal function

Dose-adjust milrinone, colchicine, eplerenone per eGFR; higher risk of hyperkalaemia with ACEi + MRA combination — monitor K⁺ at 1 week, 2 weeks, monthly.

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Renal Impairment

Milrinone

Reduce dose by 50% if eGFR <30 mL/min; monitor for hypotension.

Eplerenone

Contraindicated if eGFR <30 mL/min; monitor K⁺ closely if eGFR 30–60 mL/min.

Colchicine

Reduce dose by 50% if eGFR <30 mL/min; avoid if eGFR <10 mL/min.

Dabigatran

Avoid if eGFR <30 mL/min; if DOAC considered for LV thrombus, prefer apixaban (least renal-dependent).

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Hepatic Impairment

Amiodarone

Hepatotoxic — avoid in severe hepatic impairment (Child-Pugh C); monitor LFTs at baseline and every 6 months.

Warfarin

Increased sensitivity in liver disease (impaired synthesis of clotting factors); lower doses required; INR monitoring essential.

Colchicine

Use with caution in hepatic impairment; dose reduction may be required.

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Immunocompromised

Dressler syndrome

May be attenuated or absent in immunosuppressed patients; high index of suspicion required for atypical presentations. Consider infectious pericarditis (TB, fungal) in differential.

Colchicine

Caution with concurrent immunosuppressant therapy; increased risk of myelosuppression with tacrolimus/ ciclosporin co-administration.

Aboriginal and Torres Strait Islander Health

Aboriginal and Torres Strait Islander Health Considerations

Aboriginal and Torres Strait Islander Australians experience acute myocardial infarction at approximately 1.7 times the rate of non-Indigenous Australians (AIHW 2023). The burden is disproportionately high in remote and very remote communities, where access to PCI-capable centres, mechanical circulatory support, and cardiothoracic surgery is limited. The median age of first AMI in Indigenous Australians is approximately 10 years younger than in non-Indigenous Australians, and in-hospital mortality is significantly higher.

Geographic remoteness

Remote communities (MM 5–7) have limited access to coronary care units, echocardiography, and PCI. Retrieval times to tertiary centres may exceed 6–12 hours, which is critical for cardiogenic shock and mechanical complications. Retrieval services (Royal Flying Doctor Service, state aeromedical services) must be activated early.

Delayed presentation

Indigenous Australians present later with MI, often at more advanced stages with greater LV dysfunction and higher rates of cardiogenic shock. Community education on recognising chest pain symptoms in culturally appropriate language and formats is essential.

Comorbidity burden

Higher rates of diabetes, chronic kidney disease, rheumatic heart disease, and smoking compound post-MI complications. Diabetes increases risk of atypical presentations (silent MI), LV dysfunction, and renal impairment requiring dose adjustments for key medications.

Medication access & adherence

PBS medications may be available through Closing the Gap PBS co-payment (reduced co-payment for eligible patients). Remote pharmacies may have limited stock. Long-acting formulations and Home Medicines Reviews should be facilitated. Medication adherence programs through Aboriginal Community Controlled Health Organisations (ACCHOs) improve outcomes.

Cultural safety

Involve Aboriginal Health Workers and Aboriginal Liaison Officers in all stages of care. Ensure culturally safe communication about serious complications and goals of care. Respect family and community decision-making processes. Recognise the role of sorry business (bereavement) and its potential impact on follow-up attendance.

Cardiac rehabilitation

Indigenous Australians have lower rates of cardiac rehabilitation participation. Adapted programs delivered through ACCHOs, incorporating physical activity, yarning circles, and bush medicine discussions, have shown improved engagement. Telehealth cardiac rehabilitation (e.g., via the Royal Flying Doctor Service) extends reach to remote areas.

Rheumatic heart disease overlap

Indigenous Australians have higher rates of RHD, which may complicate post-MI management (valvular disease, anticoagulation requirements, endocarditis risk). Aortic and mitral valve pathology may mimic or mask MI complications on echocardiography.

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Closing the Gap PBS co-payment: Eligible Aboriginal and Torres Strait Islander patients can access PBS medicines at a reduced co-payment (.70 general / free for concessional). Ensure Closing the Gap status is documented to facilitate access to essential post-MI medications (ACEi, beta-blockers, antiplatelets, anticoagulants, colchicine). Contact the nearest ACCHO for patient support and medication continuity.

📚 References

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