What are the major complications after an acute myocardial infarction (MI) and their recommended management?

Post-Myocardial Infarction Complications: Recognition and Management

Post-MI complications are life-threatening and require immediate recognition through continuous monitoring, with mechanical complications (ventricular septal defect, papillary muscle rupture, free wall rupture) demanding urgent echocardiography and surgical consultation, while arrhythmias and heart failure necessitate aggressive medical therapy and early revascularization to reduce mortality. 1

Mechanical Complications

Ventricular Septal Defect (VSD)

• VSD typically presents within the first week post-MI with sudden hemodynamic deterioration, a new harsh systolic murmur, and left-to-right shunting detectable by elevated oxygen saturation in the pulmonary artery compared to the right atrium. 1
• Immediate echocardiography (transthoracic or transesophageal) establishes the diagnosis, while balloon flotation catheter placement confirms shunting and guides hemodynamic monitoring. 1
• Insert an intra-aortic balloon pump immediately to stabilize the patient, perform coronary angiography unless the patient is severely unstable, and obtain urgent surgical consultation for repair. 1
• Hospital mortality after surgical repair ranges from 25-60%, with predictors of poor outcome including cardiogenic shock, posterior location, right ventricular dysfunction, advanced age, and delayed surgery. 1

Acute Mitral Regurgitation

• Three mechanisms cause post-MI mitral regurgitation: annular dilatation from LV dysfunction, papillary muscle dysfunction (usually inferior MI), or papillary muscle rupture. 1
• Papillary muscle rupture presents as sudden hemodynamic collapse with a soft murmur (due to abrupt left atrial pressure elevation), most commonly affecting the posteromedial papillary muscle from small infarcts in the right or circumflex artery distribution. 1
• Color Doppler echocardiography assesses severity; transesophageal echocardiography may be necessary for definitive diagnosis. 1
• Cardiogenic shock with severe mitral regurgitation requires emergency surgery with intra-aortic balloon pump placement during preparation, coronary angiography, and valve replacement (repair can be attempted in selected cases without rupture). 1

Left Ventricular Free Wall Rupture

• Suspect rupture when sudden hypotension occurs with pericardial tamponade signs (equalization of diastolic pressures, jugular venous distension). 1
• Immediate echocardiography confirms the diagnosis, and emergency surgical repair is the only viable option, as medical management alone carries extremely high mortality (3.3-6.5% per hour). 1

Ventricular Aneurysm

• Perform transthoracic echocardiography within 48 hours to identify aneurysm formation and detect intracavitary thrombus. 2
• If mobile or protuberant thrombi are present, immediately initiate intravenous unfractionated heparin or low-molecular-weight heparin, followed by oral anticoagulation for at least 3-6 months. 1, 2
• Consider LV aneurysmectomy with CABG for patients with intractable ventricular tachyarrhythmias and/or pump failure unresponsive to medical therapy and catheter-based interventions. 2

Arrhythmic Complications

Ventricular Tachycardia and Fibrillation

• Non-sustained ventricular tachycardia may be well tolerated and does not require treatment; prolonged episodes causing hypotension or heart failure require beta-blockers as first-line therapy unless contraindicated. 1
• For high risk of recurrent ventricular fibrillation, administer lidocaine 1 mg/kg IV bolus, followed by half this dose every 8-10 minutes to maximum 4 mg/kg, or continuous infusion 1-3 mg/min. 1
• Intravenous amiodarone (5 mg/kg over first hour, then 900-1200 mg/24h) is superior for recurrent sustained ventricular tachycardia requiring cardioversion or ventricular fibrillation. 1
• Immediate defibrillation is mandatory for ventricular fibrillation; if no defibrillator is available, attempt a precordial thump. 1
• Differentiate true ventricular tachycardia from accelerated idioventricular rhythm (harmless reperfusion consequence with ventricular rate <120 beats/min). 1
• Routine prophylactic antiarrhythmic drugs should not be used. 1

Bradycardia and Atrioventricular Block

• Sinus bradycardia is common in inferior MI and requires no treatment unless accompanied by severe hypotension, in which case administer IV atropine. 1
• Second-degree type I (Mobitz I/Wenckebach) AV block usually associates with inferior MI and seldom causes hemodynamic compromise; use atropine first, then pacing if it fails. 1
• Second-degree type II (Mobitz II) AV block and complete AV block require pacing; AV sequential pacing should be used in patients with complete AV block, RV infarction, and hemodynamic compromise. 1
• AV block with inferior MI is usually supra-Hisian and resolves spontaneously or after reperfusion; AV block with anterior MI is usually infra-Hisian with high mortality due to extensive necrosis. 1
• Insert a transvenous pacing electrode for advanced AV block with low escape rhythm, and consider it for new bifascicular or trifascicular block. 1

Atrial Fibrillation

• Atrial fibrillation is common post-MI; exercise caution with acute rate control for rapid ventricular rate given possible compensation for decreased ventricular function. 3
• Cardioversion is indicated if the patient is hemodynamically unstable with persistent AF. 4
• Start anticoagulation based on CHA2DS2-VASc score. 4

Heart Failure and Cardiogenic Shock

Acute Heart Failure

• Administer intravenous furosemide and an afterload-reducing agent for patients developing heart failure. 1
• ACE inhibitors are mandatory within the first 24 hours for patients with heart failure, LV systolic dysfunction, diabetes, or anterior infarct. 1
• Beta-blockers are indicated in patients with heart failure and/or LVEF <40% after stabilization to reduce death, recurrent MI, and hospitalization. 1
• Mineralocorticoid receptor antagonists (MRAs) are required in patients with LVEF <40% and heart failure or diabetes who are already receiving an ACE inhibitor and beta-blocker, provided no renal failure or hyperkalemia exists. 1

Cardiogenic Shock

• Insert an intra-aortic balloon pump and perform emergency coronary angiography followed by PTCA or CABG. 1
• Immediate PCI is indicated for cardiogenic shock if coronary anatomy is suitable. 1
• Norepinephrine is the first-line vasopressor for cardiogenic shock with hypoperfusion. 3

Right Ventricular Infarction

• RV infarction presents with hypotension, clear lung fields, and elevated jugular venous pressure, occurring in up to 50% of inferior MIs. 5
• Treat vigorously with intravascular volume expansion using normal saline and inotropic agents if hypotension persists. 1
• Never administer nitrates to patients with RV infarction, as this causes catastrophic hypotension. 5

Thromboembolic Complications

Deep Vein Thrombosis and Pulmonary Embolism

• These complications are now relatively uncommon except in patients kept in bed due to heart failure. 1
• Prevent with prophylactic doses of low-molecular-weight heparin in bedridden patients; treat with therapeutic doses followed by oral anticoagulation for 3-6 months when they occur. 1

Intraventricular Thrombus and Systemic Emboli

• Echocardiography may reveal intraventricular thrombi, especially in large anterior infarctions. 1
• If thrombi are mobile or protuberant, treat initially with intravenous unfractionated heparin or low-molecular-weight heparin, then oral anticoagulants for at least 3-6 months. 1

Pericarditis

• Acute pericarditis complicates MI and associates with worse outcome, presenting with sharp chest pain related to posture and respiration, distinguished from recurrent infarction or angina. 1
• Confirm diagnosis with a pericardial rub on examination. 1
• Treat troublesome pain with high-dose aspirin (650 mg every 4-6 hours). 1
• Three major pericardial complications can occur: early infarct-associated pericarditis, late pericarditis (Dressler syndrome), and pericardial effusion. 1

Critical Monitoring and Surveillance

• Continuous cardiac telemetry is mandatory for arrhythmia detection, with serial ECGs to assess for recurrent ischemia and serial troponin measurements every 6-8 hours for 24 hours. 5
• Routine echocardiography during hospital stay is required to assess resting LV and RV function, detect early mechanical complications, and exclude LV thrombus. 1
• Emergency equipment including atropine, lidocaine, transcutaneous pacing patches, transvenous pacemaker, defibrillator, and epinephrine must be immediately available. 5

Critical Pitfalls to Avoid

• Do not delay echocardiography—early imaging within 48 hours is essential for detecting thrombus and guiding anticoagulation decisions. 2
• Do not withhold anticoagulation if mobile/protuberant thrombi are present—immediate heparinization is required to prevent systemic embolization. 2
• Avoid beta-blockers in patients with hypotension, acute heart failure, AV block, or severe bradycardia. 1
• Do not use calcium channel blockers, as they have not reduced mortality in acute MI and may be harmful. 1
• Ventricular ectopic beats are nearly universal on day one and require no specific therapy despite complex patterns. 1

Long-Term Management

• Continue ACE inhibitors, beta-blockers (if heart failure or LVEF <40%), and aspirin 75-100 mg indefinitely. 1, 2
• Dual antiplatelet therapy (aspirin plus ticagrelor or prasugrel) is required for 12 months after PCI unless excessive bleeding risk exists. 1
• Start high-intensity statin therapy as early as possible with LDL-C goal <1.8 mmol/L (70 mg/dL) or ≥50% reduction if baseline LDL-C is 1.8-3.5 mmol/L. 1
• Maintain anticoagulation for at least 3-6 months for intraventricular thrombus, potentially longer if thrombus persists on follow-up imaging. 2