1. Arrhythmic Complications in Acute ACS

Life-threatening arrhythmias—including ventricular tachycardia/fibrillation (VT/VF), new-onset atrial fibrillation (AF), and bradyarrhythmias—peak in the first 48 hours after myocardial infarction (MI). Early detection, Advanced Cardiovascular Life Support (ACLS)-based stabilization, and targeted antiarrhythmic therapy are essential to salvage myocardium and prevent end-organ injury.

A. Ventricular Tachycardia/Fibrillation (VT/VF)

1. Pathophysiology & Risk Factors

Acute ischemia leads to electrical heterogeneity and reentry circuits within the myocardium. The risk of VT/VF is amplified by large infarct size, delayed reperfusion, electrolyte disturbances (particularly Potassium levels below 4.0 mEq/L or Magnesium levels below 2.0 mg/dL), left ventricular dysfunction, and a prior history of VT/VF.

2. Recognition & Monitoring

• Continuous telemetry monitoring is recommended for the first 48 hours post-MI.
• Sudden hypotension, pulselessness, or loss of consciousness should prompt immediate assumption of VT/VF.
• A post-resuscitation electrocardiogram (ECG) is crucial to assess for ongoing ischemia or other arrhythmic substrates.

3. ACLS Algorithm & Initial Management

• Immediate high-energy defibrillation (≥200 Joules biphasic) is the cornerstone of treatment for VF or pulseless VT.
• High-quality cardiopulmonary resuscitation (CPR) should be performed with a compression-to-ventilation ratio of 30:2, minimizing pauses in chest compressions.
• Identify and correct reversible causes (the “Hs and Ts”): Hypoxia, Hypovolemia, Hydrogen ion (acidosis), Hypo/Hyperkalemia, Hypothermia; Tension pneumothorax, Tamponade (cardiac), Toxins, Thrombosis (pulmonary or coronary).

4. Pharmacotherapy of Refractory VT/VF

B. Atrial Fibrillation (AF)

New-onset AF in the setting of ACS can worsen ischemia, precipitate heart failure (HF), and substantially increase the risk of stroke. Management involves a careful balance between rate versus rhythm control strategies and mitigating bleeding versus thromboembolic risks.

1. Rate vs. Rhythm Control

• Rate control is generally the initial approach in hemodynamically stable patients; the target heart rate is typically <110 bpm.
• Rhythm control (e.g., IV amiodarone or electrical cardioversion) should be considered if the patient exhibits hypotension, ongoing ischemia, or signs of HF attributable to the AF.

2. Pharmacotherapy

• Beta-blockers: First-line agents for rate control. Use with caution or avoid in patients with cardiogenic shock or severe decompensated HF.
• Non-dihydropyridine calcium channel blockers (diltiazem/verapamil): An option for rate control if there is no significant left ventricular dysfunction.
• Amiodarone: Useful for both rate and rhythm control, particularly in patients with left ventricular dysfunction or hypotension.
• Anticoagulation: Assess thromboembolic risk (e.g., CHA₂DS₂-VASc score) and bleeding risk (e.g., HAS-BLED score). In patients with recent ACS and/or percutaneous coronary intervention (PCI), efforts should be made to minimize the duration of triple therapy (aspirin + P2Y₁₂ inhibitor + oral anticoagulant).

C. Bradyarrhythmias

Bradycardia and atrioventricular (AV) block, especially in the context of inferior MI, often result from increased vagal tone or ischemia affecting the conduction tissues. High-degree AV block may necessitate temporary or permanent pacing.

1. Recognition

• Sinus bradycardia (heart rate <50 bpm), Mobitz type II second-degree AV block, or third-degree (complete) AV block identified on ECG.

2. Initial Management

• Atropine: 0.5 mg IV every 3–5 minutes as needed, up to a maximum total dose of 3 mg.
• If refractory to atropine: Dopamine infusion (2–10 µg/kg/min) or Epinephrine infusion (2–10 µg/min).

3. Pacing

• Transcutaneous pacing can serve as a bridge to transvenous pacing for patients with persistent, symptomatic high-degree AV block.
• A permanent pacemaker is indicated if high-degree AV block (Mobitz II or complete AV block) persists post-MI, particularly if associated with anterior MI.

2. Mechanical Complications after Myocardial Infarction

Mechanical complications such as free wall rupture, ventricular septal defect (VSD), and papillary muscle rupture typically present acutely (often days 3–7 post-MI) with sudden hemodynamic collapse. Rapid diagnostic imaging (primarily echocardiography), aggressive hemodynamic support, and prompt surgical consultation are lifesaving.

A. Free Wall Rupture

• Timing: Usually occurs 3–7 days post-MI. Risk factors include transmural anterior MI, advanced age, and hypertension.
• Presentation: Sudden profound hypotension, signs of cardiac tamponade (Beck’s triad: hypotension, jugular venous distension, muffled heart sounds), and often pulseless electrical activity (PEA) arrest.
• Diagnosis: Bedside echocardiography revealing pericardial effusion, potentially with signs of diastolic right ventricular collapse.
• Management:
  • Emergent pericardiocentesis for temporizing relief of tamponade.
  • Intravenous fluids and vasopressors to maintain systemic perfusion.
  • Mechanical circulatory support (MCS), such as Veno-Arterial Extracorporeal Membrane Oxygenation (VA-ECMO), may serve as a bridge to definitive surgical repair.

B. Ventricular Septal Defect (VSD)

• Pathophysiology: Necrosis of the interventricular septum leads to a defect, causing a left-to-right shunt and acute volume overload on the right ventricle and pulmonary circulation, precipitating acute HF.
• Signs: New, harsh, holosystolic murmur (often best heard at the left sternal border), hypotension, and signs of biventricular failure.
• Diagnosis: Echocardiography with color Doppler is diagnostic, allowing visualization and quantification of the shunt.
• Management:
  • Pharmacologic afterload reduction (e.g., sodium nitroprusside, ACE inhibitors if tolerated) to reduce the shunt fraction.
  • Intra-aortic balloon pump (IABP) counterpulsation can decrease afterload and improve forward cardiac output.
  • MCS (e.g., Impella, VA-ECMO) if hemodynamically unstable.
  • Urgent surgical repair is generally indicated. If the patient can be stabilized, delaying surgery for ≥7 days may allow for tissue consolidation and reduce suture friability, but this must be balanced against ongoing hemodynamic compromise.

C. Papillary Muscle Rupture

• Pathophysiology: Most often involves the posteromedial papillary muscle due to its single blood supply (typically from the right coronary artery or circumflex artery). Rupture leads to acute, severe mitral regurgitation (MR).
• Presentation: Sudden onset of severe dyspnea, pulmonary edema, cardiogenic shock, and a new systolic murmur of mitral regurgitation.
• Diagnosis: Transthoracic or transesophageal echocardiography (TTE/TEE) demonstrating a flail mitral leaflet and a severe regurgitant jet.
• Management:
  • Afterload reduction (e.g., nitroprusside) and diuretics to manage pulmonary congestion.
  • IABP to reduce afterload and improve forward cardiac output.
  • Urgent surgical mitral valve repair or replacement is definitive. MCS may be used as a bridge to surgery.

3. Secondary Prevention Pharmacotherapy

Long-term comprehensive medical therapy, including beta-blockers, ACE inhibitors/ARBs, high-intensity statins, and potentially mineralocorticoid receptor antagonists (MRAs), is crucial for reducing adverse cardiac remodeling, recurrent ischemic events, and mortality after ACS. Agent selection and timing should be individualized based on patient characteristics and comorbidities.

A. Beta-Blockers

• Mechanism of Action: Decrease heart rate, myocardial contractility, and myocardial oxygen demand; also possess antiarrhythmic properties.
• Indication: All patients post-ACS should be initiated on a beta-blocker within 24 hours if there are no contraindications (e.g., signs of shock, acute decompensated heart failure, significant bradycardia, or reactive airway disease).
• Agents: Cardioselective agents like metoprolol or bisoprolol are often preferred.
• Dosing Example: Metoprolol tartrate 25 mg orally every 6–12 hours, titrated to a target resting heart rate of 50–60 bpm as tolerated.
• Monitoring: Heart rate, blood pressure, signs of heart failure, and bronchospasm.
• Pitfalls: Avoid intravenous beta-blockers in patients with acute hemodynamic instability or decompensation.

B. ACE Inhibitors/ARBs

• Mechanism of Action: Reduce angiotensin II and aldosterone levels, leading to decreased adverse remodeling, afterload reduction, and neurohormonal modulation.
• Indication: Strongly indicated for patients with LVEF ≤40%, anterior MI, clinical heart failure, or diabetes mellitus; ideally initiated within 24 hours post-ACS if hemodynamically stable. Consider for all ACS patients.
• Agents: Lisinopril, ramipril are common ACE inhibitors. Angiotensin Receptor Blockers (ARBs) like valsartan or candesartan are alternatives for patients intolerant to ACE inhibitors (e.g., due to cough).
• Dosing Example: Lisinopril 2.5–5 mg orally daily, titrated upwards to target or maximally tolerated doses.
• Monitoring: Serum creatinine and potassium levels at baseline, after initiation/dose changes, and periodically. A transient rise in creatinine <30% from baseline is generally acceptable.
• Pitfalls: Avoid in patients with known bilateral renal artery stenosis or baseline hyperkalemia (Potassium >5.5 mEq/L).

C. Statins

• Mechanism of Action: HMG-CoA reductase inhibition, leading to a significant reduction in LDL-Cholesterol. Also possess pleiotropic effects including anti-inflammatory actions and plaque stabilization.
• Indication: All patients post-ACS, regardless of baseline LDL-C levels; initiate high-intensity statin therapy in-hospital or at discharge.
• Agents & Dosing: Atorvastatin 40–80 mg daily or Rosuvastatin 20–40 mg daily.
• Monitoring: Lipid panel 4–12 weeks after initiation or dose change to assess efficacy (target LDL-C <55-70 mg/dL depending on guidelines). Monitor creatine kinase (CK) if myopathy symptoms occur, and liver function tests (LFTs) if hepatic injury is suspected.
• Controversies/Considerations: Early addition of non-statin therapies (e.g., ezetimibe, PCSK9 inhibitors) may be considered if LDL-C remains ≥70 mg/dL despite maximally tolerated statin therapy.

D. Mineralocorticoid Receptor Antagonists (MRAs)

• Mechanism of Action: Blockade of aldosterone receptors, which reduces myocardial fibrosis, adverse remodeling, and sodium/water retention.
• Indication: Patients post-MI with LVEF ≤40% and either symptomatic heart failure or diabetes mellitus. Typically initiated 3–14 days post-MI, once stabilized.
• Agents & Dosing: Eplerenone (25 mg daily, titrated to 50 mg daily as tolerated) is preferred due to higher selectivity and fewer gynecomastia side effects. Spironolactone (12.5–25 mg daily) is an alternative.
• Monitoring: Serum potassium and renal function (eGFR) at baseline, within 3–7 days of initiation/dose change, monthly for the first 3 months, and periodically thereafter.
• Pitfalls: Discontinue or reduce dose if serum potassium rises >5.5 mEq/L or eGFR falls <30 mL/min/1.73m².