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HealthConsider > Blog > Health > Myocardial Infarction Clinical Guide
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Myocardial Infarction Clinical Guide

Last updated: August 29, 2025 4:29 am
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Myocardial Infarction Clinical Guide

Introduction

Myocardial infarction (MI), commonly known as a heart attack, results from acute ischemic necrosis of myocardial tissue due to obstruction of a coronary artery. It remains a leading cause of mortality and morbidity worldwide. Rapid recognition, prompt reperfusion, and evidence-based medical therapy are critical to salvaging myocardium, preventing complications, and improving patient outcomes.

Contents
  • Myocardial Infarction Clinical Guide
    • Introduction
    • Epidemiology and Risk Factors
    • Pathophysiology
    • Classification
    • Clinical Presentation and Diagnosis
      • Presentation
      • Diagnostic Evaluation
    • Acute Management
      • Initial Stabilization (MONA-B)
      • Reperfusion Therapy
      • Adjunctive Pharmacotherapy
    • Secondary Prevention and Long-Term Management
    • Monitoring and Follow-Up
    • Patient Education and Self-Care
    • Conclusion

Epidemiology and Risk Factors

  • Incidence: Approximately 805,000 MIs occur annually in the United States; over 20 million worldwide.
  • Age and Sex: Risk increases with age; men present earlier (average age 66) than women (average age 72).
  • Modifiable Risks:
  • Hypertension, dyslipidemia, smoking, diabetes mellitus, obesity, physical inactivity, and diet high in saturated fats.
  • Psychosocial stress and poor adherence to preventive measures.
  • Nonmodifiable Risks: Family history, age, male sex (or postmenopausal status in women), and genetic predisposition.

Pathophysiology

  • Atherosclerotic Plaque Rupture: Inflammation destabilizes atheromatous plaques, exposing subendothelial collagen and lipids.
  • Thrombus Formation: Platelet aggregation and fibrin deposition occlude the vessel, causing ischemia.
  • Myocardial Necrosis: Prolonged ischemia leads to irreversible cardiomyocyte death, beginning subendocardially and extending transmurally if untreated.

Classification

  • STEMI (ST-elevation MI): Complete occlusion of a major coronary artery; diagnostic ECG shows new ST elevations in at least two contiguous leads.
  • NSTEMI (Non–ST-elevation MI): Partial or transient occlusion; ECG may show ST depression or T-wave inversion; cardiac biomarkers (troponin) are elevated.
  • Unstable Angina: Clinical syndrome of ischemia without biomarker elevation or persistent ECG changes; managed similarly to NSTEMI.

Clinical Presentation and Diagnosis

Presentation

  • Typical Symptoms: Central chest pain or pressure, radiating to left arm, neck, or jaw; diaphoresis; dyspnea; nausea.
  • Atypical Symptoms: Elderly, women, and diabetics may present with fatigue, syncope, or epigastric discomfort without chest pain.

Diagnostic Evaluation

  1. Electrocardiogram (ECG): Obtain within 10 minutes of presentation; differentiate STEMI from NSTEMI/unstable angina.
  2. Cardiac Biomarkers: Serial troponin measurements confirm myocardial injury; CK-MB may be adjunct.
  3. Imaging: Echocardiography assesses wall motion abnormalities and mechanical complications (ventricular septal rupture, pericardial effusion).
  4. Coronary Angiography: Gold standard for lesion localization and guides revascularization strategy.

Acute Management

Initial Stabilization (MONA-B)

  • Morphine: Analgesia and preload reduction.
  • Oxygen: If SpO₂ < 90%.
  • Nitrates: Sublingual or IV to relieve ischemia.
  • Aspirin: 162–325 mg chewable immediately.
  • Beta-Blockers: IV or oral within 24 hours unless contraindicated.

Reperfusion Therapy

  • STEMI: Primary percutaneous coronary intervention (PCI) within 90 minutes of first medical contact is preferred.
  • If PCI not available within guideline-recommended window, administer fibrinolysis (e.g., tenecteplase) within 30 minutes.
  • NSTEMI/Unstable Angina: Early invasive strategy (PCI or CABG) guided by risk stratification (TIMI, GRACE scores).

Adjunctive Pharmacotherapy

  • Antiplatelet Agents: P2Y₁₂ inhibitor (clopidogrel, prasugrel, or ticagrelor) in addition to aspirin.
  • Anticoagulation: Unfractionated heparin or bivalirudin during PCI; consider enoxaparin for medical management.
  • High-Intensity Statin: Initiate or continue high-dose statin regardless of baseline LDL.
  • ACE Inhibitors or ARBs: Start within 24 hours to reduce remodeling and improve survival.
  • Aldosterone Antagonists: Eplerenone or spironolactone in patients with reduced ejection fraction and heart failure or diabetes.

Secondary Prevention and Long-Term Management

  • Lifestyle Modification: Smoking cessation, dietary counseling (Mediterranean diet), weight management, and regular aerobic exercise.
  • Risk Factor Control: Tight blood pressure (<130/80 mm Hg) and glycemic control (HbA₁c <7%).
  • Medication Adherence: Dual antiplatelet therapy for at least 12 months post-PCI; statins, beta-blockers, ACE inhibitors continued indefinitely.
  • Cardiac Rehabilitation: Supervised, multidisciplinary program including exercise training, education, nutritional guidance, and psychological support.

Monitoring and Follow-Up

  • Serial Ejection Fraction Assessment: Echocardiography at 4–6 weeks post-MI to guide device therapy (ICD) in left ventricular dysfunction.
  • Surveillance for Complications: Monitor for arrhythmias, heart failure, mechanical complications, and depression.
  • Regular Clinic Visits: Evaluate functional status, adherence, and adjust therapy.

Patient Education and Self-Care

  • Teach recognition of angina symptoms and activation of emergency services.
  • Provide a written action plan (medications, contact information, lifestyle goals).
  • Encourage participation in peer support groups to enhance adherence and psychosocial well-being.

Conclusion

Effective management of myocardial infarction hinges on rapid identification, timely reperfusion, evidence-based pharmacotherapy, and comprehensive secondary prevention. Multidisciplinary collaboration among emergency medicine, cardiology, nursing, rehabilitation, and primary care teams is vital to optimize recovery and reduce recurrent events.

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