Myocardial Infarction

MI is ischemia and death of an area of myocardial tissue due to insufficient blood flow and oxygenation, usually from thrombus formation on a ruptured atherosclerotic plaque in the epicardial arteries. Clinical presentation is most commonly with chest pain, but women and patients with diabetes may have atypical symptoms. Diagnosis is by clinical history, ECG changes, an increase in cardiac enzymes, and evidence of wall motion abnormalities on imaging. Management depends on the timing of the presentation and local resources with regard to thrombolytic therapy versus percutaneous intervention. All patients receive nitrates, pain control, aspirin, anticoagulation, and beta-blockers (unless contraindicated).

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Myocardial infarction (MI), commonly known as a “heart attack,” is defined as acute myocardial injury and tissue death resulting from ischemia.


  • 1 of the leading causes of death in the United States
  • Prevalence: 3% in Americans > 20 years of age
  • Incidence in the United States:
    • 600 cases per 100,000 people
    • 1.5 million cases annually
  • More common in older patients:
    • Approximately 60%–65% of MIs occur in patients > 65 years of age.
    • Approximately 33% of MIs occur in patients > 75 years of age.
    • 80% of all MI-related deaths occur in patients > 65 years of age.
  • Men > women

Risk factors

The risks of MI increase proportionately with increases in risk factors for coronary atherosclerosis (coronary artery disease (CAD)).

  • Hypertension
  • Hyperlipidemia
  • Smoking
  • Age: elderly patients are more likely to:
    • Have STEMI than NSTEMI 
    • Have a silent or unrecognized MI
    • Present with atypical symptoms (e.g., weakness, confusion, syncope)
    • Have higher in-hospital mortality
    • Have heart failure associated with an MI
  • Family history of premature coronary heart disease (CHD), defined as:
    • A 1st-degree male relative < 45 years of age
    • A 1st-degree female relative < 55 years of age


Classification of MI according to the assumed cause:

  • Type 1: acute thrombus on a ruptured atherosclerotic plaque
  • Type 2: ↑ oxygen demand in the myocardium without adequate oxygen supply (whether or not there is underlying atherosclerotic CAD)
  • Type 3: clinical symptoms of MI with ECG changes, but with death of the patient occurring before lab tests are performed
  • Type 4a: MI associated with percutaneous coronary intervention (PCI) or from procedure-related complications associated with ↓ coronary blood flow.
  • Type 4b: intervention-related MI with stent/scaffold thrombosis
  • Type 5: MI related to coronary artery bypass graft (CABG) surgery

Classification of MI based on ECG findings and pathology:

  • STEMI: 
    • Due to a major occlusion of a coronary artery, causing transmural infarction (through the heart muscle wall)
    • Produces ECG changes with ST elevation and Q waves
    • Due to less severe occlusion of a coronary artery, causing a subendocardial MI (not through the entire heart muscle wall)
    • ECG does not show ST elevation


  • Characteristics of unstable versus stable plaque: 
    • Unstable plaque:
      • Thin fibrous cap
      • Massive inflammatory cell infiltrate
      • ↑ Activity of metalloproteinase enzymes (weakens the fibrous cap)
      • ↑ Lipid content
      • Angiogenesis
      • Rupture of unstable plaque in a coronary artery → thrombosis
    • Stable plaque: 
      • Thick fibrous cap
      • Narrowing of an artery → inability to meet oxygen demand with ↑ exertion 
      • May lead to stable angina (symptoms only with exertion)
  • Coronary artery occlusion → ischemia → death of the tissue (infarction) in the area of the heart supplied by that artery:
    • Partial occlusion of the coronary artery → affects the inner myocardium (subendocardium) → may cause: 
      • NSTEMI
      • Unstable angina (if the ischemia does not result in cell death)
    • Complete occlusion → transmural infarction → STEMI
Natural history of the vulnerable/unstable plaque

Natural history of the vulnerable/unstable plaque:
Unstable atherosclerotic plaques are thought to account for the majority of MIs and are characterized by macrophage inflammation, a thin fibrous cap, remodeling, microcalcification, and angiogenesis.

Image: “Natural history of the vulnerable plaque” by Ben Smith. License: CC BY 4.0

Clinical Presentation

The classic symptom of MI in most patients is acute chest pain. However, some patients may present with more vague symptoms.


  • Typical: 
    • Chest pain: 
      • Retrosternal
      • Dull, squeezing/pressure-like pain
      • May radiate to the left arm, shoulder, or jaw
      • Usually constant, lasting ≥ 20–30 minutes 
    • Diaphoresis
    • Dyspnea
    • Nausea
  • Associated symptoms:
    • Dizziness
    • “Indigestion” and/or vomiting
    • Syncope
    • Epigastric pain (with inferior-wall MI)
    • Palpitations
  • Atypical presentation more common in women, the elderly, or patients with diabetes:
    • Absence of chest pain or atypical locations/quality
    • May present with only the usual associated symptoms

Physical examination

  • Vitals: 
    • Tachycardia
    • Bradycardia with right coronary artery (RCA) occlusion (supplies the sinoatrial (SA) and atrioventricular (AV) nodes)
    • Hypotension
  • Cardiovascular:
    • S3 heart sound (early diastolic sound heard at the end of rapid ventricular filling)
    • S4 heart sound (late diastolic sound heard at the onset of atrial contraction)
    • Jugular venous distention: RCA occlusion → right-sided heart failure (HF)
    • Hepatic congestion: RCA occlusion → right-sided HF
  • Pulmonary edema: left coronary artery occlusion → left-sided HF
    • Crackles
    • Wheezing
  • Skin:
    • Cool
    • Pale or cyanotic
    • Diaphoretic


Patients presenting with a history of acute chest pain or suspicious atypical symptoms are evaluated with ECG. Cardiac troponin levels should be obtained within 10 minutes of the patient’s arrival in the ED. Abnormalities in both confirm the diagnosis of MI.


  • Findings in STEMI and their evolution: 
    • Tall, peaked (hyperacute) T waves may be seen early in the course.
    • ≥ 1-mm ST elevation in ≥ 2 contiguous leads
    • Reciprocal ST depression
    • New left bundle branch block (LBBB) and symptoms → STEMI until proven otherwise
    • Pathologic Q waves typically emerge between 6 and 16 hours after symptom onset
    • T-wave inversion follows
    • ST-segment normalization
    • T-wave normalization over several hours to days
  • Findings in NSTEMI:
    • ST depression (not elevations)
    • Nonspecific changes
    • Inverted T waves
Table: Localization of STEMI on ECG
Artery occludedLeads with ST elevationLocation of MI
Proximal LADV1–V2Septal
Distal LADV5–V6Apical
LCX or LADI, aVLLateral
RCA (more common) or LCXII, III, aVFInferior
RCA or LCXV7–V9 (ST depressions in V1–V3)Posterolateral
LAD: left anterior descending artery
LCX: left circumflex artery
RCA: right coronary artery

Laboratory evaluation

Cardiac enzymes: 

  • Structural proteins in the heart that are released as a result of myocardial injury
  • Troponin I:
    • Serum levels:
      • Start to ↑ within 2–3 hours after the onset of chest pain
      • Peak levels at 12–48 hours
      • Return to baseline over 4–10 days
    • Highest sensitivity and specificity (compared to other cardiac enzymes)
    • Serial lab draws are used to assess for a rise and fall in levels (recheck in 1–3 hours).
    • The degree of ↑ correlates with the size of the infarct.
    • Can be ↑ as the result of causes of coronary ischemia other than acute MI:
      • Arrhythmia
      • Cocaine
      • PCI
      • Coronary embolism
      • Aortic dissection
    • Can be ↑ with noncoronary ischemia or myocardial injury:
      • Electrical shock
      • Hypoxia
      • Myocarditis
      • Takotsubo cardiomyopathy: sudden, temporary weakening of the heart muscle (usually related to a stressor)
    • Patients with CKD:
      • May have stably ↑ levels in the absence of myocardial damage
      • A rise or fall in troponin I value > 20% over 6–9 hours is indicative of acute MI in patients with end-stage CKD.
  • CK-MB isoenzyme: 
    • Less sensitive and specific than troponin
      • ↑ within 3–6 hours after chest pain
      • Peaks within 12–24 hours
      • Normalizes 48–72 hours after MI
    • Continued ↑ after 72 hours is diagnostic of reinfarction.
    • The degree of ↑ in CK-MB correlates with the size of the infarct.

Supporting labs: 

  • LDH and AST → may be ↑, but no longer used in the diagnosis of MI.
  • BNP → ↑ in heart failure
  • Potassium and magnesium levels should be optimized during management.
  • Drug screen to evaluate for cocaine or methamphetamine use.

Comparison within acute coronary syndrome

The following table compares unstable angina, NSTEMI, and STEMI on the basis of clinical features, ECG, and laboratory findings.

Table: Comparison within acute coronary syndrome
DiagnosisClinical featuresECG findingsLaboratory findings
Unstable anginaIschemic chest pain that occurs at rest or with previously tolerated levels of exertion
  • None
  • STD
  • TWI
Normal troponin
NSTEMIProlonged ischemic chest pain in any setting
  • None
  • STD
  • TWI
Elevated troponin
STEMIProlonged ischemic chest pain in any setting
  • STE
  • New LBBB
Elevated troponin
LBBB: left bundle branch block
STD: ST-segment depression
STE: ST-segment elevation
TWI: T-wave inversion


  • Chest X-ray: 
    • Should be done to evaluate for other causes of chest pain, such as:
      • Pneumonia
      • Pneumothorax
      • Mediastinal widening → aortic dissection
    • May show pulmonary edema → heart failure
  • Coronary angiography:
    • Gold standard test
    • Findings:
      • Localizes narrowed or occluded coronary arteries
      • New regional wall motion abnormalities consistent with an ischemic infarct
      • Left ventriculography can assess left ventricular function.
  • Determines the need for intervention with stenting or surgery
  • Transthoracic echocardiography:
    • Left ventricular ejection fraction (LVEF) is the best predictor of survival in STEMI.
    • New regional wall motion abnormalities can be visualized
    • Can evaluate for complications of MI:
      • Free-wall rupture
      • Ventricular septal rupture
      • Mitral regurgitation
      • Aneurysm formation
      • Presence of a thrombus


Initial therapy

Prompt recognition of the diagnosis of acute MI is imperative in order to realize the benefit from reperfusion therapy. 

  • Oxygen: previously used with every patient, currently used only if: 
    • O2 saturation < 90%
    • Respiratory distress present
    • Heart failure present
    • Other high-risk features of hypoxia
  • Treat ventricular arrhythmias (if present).
  • Aspirin:
    • Prevents thrombus formation/expansion 
    • ↓ Mortality
  • Nitroglycerin (sublingual):
    • Start if the patient still has chest pain, hypertension, or heart failure
    • Vasodilation → preload → ↓ oxygen demand → ↓ symptoms
    • Add IV nitrates if symptoms persist after 3 sublingual doses
    • Avoid in patients with:
      • Hypotension
      • Right ventricular infarction (inferior-wall MI) → ↓ preload to the right ventricle can ↓ cardiac output even further
  • Beta-blockers:
    • ↓ Heart rate and contractility → ↓ oxygen demand→ ↓ symptoms
    • ↓ Mortality
    • Contraindicated if the patient has:
      • Heart failure
      • Bradycardia
      • Severe reactive airway disease
      • Cocaine-induced MI
  • Morphine:
    • Provides relief of ischemic pain (↓ preload)
    • ↓ Anxiety and the adrenergic drive that causes further vasoconstriction
    • Can ↑ mortality
    • Can cause respiratory depression
  • Treat heart failure with diuretics (if present).
  • Start high-dose statin therapy (e.g., atorvastatin) as early as possible and before PCI.
  • IV saline to ↑ cardiac output and perfusion with right ventricular MI
  • Anticoagulation recommendations vary with the clinical situation and plan for PCI or thrombolytic therapy: 
    • Heparin
    • Low-molecular-weight heparin (LMWH)

Risk stratification

  • Important for prognosis: 
    • Patients at the highest risk for further cardiac events may benefit from a more aggressive therapeutic approach:
      • Risk scores such as TIMI (Thrombolysis in Myocardial Infarction), Global Registry of Acute Coronary Events (GRACE), or Platelet Glycoprotein IIb/IIIa in Unstable Angina: Receptor Suppression Using Integrilin Therapy (PURSUIT) have good predictive ability.
      • These scoring systems take into account markers of predictive outcome for prognosis.
    • End points for predictive outcome:
      • Death
      • Future MI
      • Need for urgent revascularization
  • TIMI risk scores help in decision-making for urgent revascularization:
    • Based on:
      • ECG features
      • Elevated cardiac enzymes
      • Evidence of hemodynamic instability
      • Persistent chest pain despite appropriate medical therapy
      • Age
      • Comorbidities (other CHD risk factors)
      • Recent aspirin use
    • For TIMI score > 3 with NSTEMI or unstable angina, revascularization with PCI is recommended:
      • Low risk: score of 0–2
      • Intermediate risk: score of 3–4
      • High risk: score of 5–7 


  • PCI:
    • Indications:
      • STEMI
      • NSTEMI with TIMI score > 3
    • ↓ Amount of myocardial damage
    • ↓ Mortality 
    • For patients who present ≤ 2 hours after the onset of symptoms → PCI with drug-eluting stent to prevent restenosis, if available:
      • Improves survival
      • ↓ Rate of intracranial hemorrhage and recurrent MI as compared with fibrinolysis
  • If PCI is not readily available, then thrombolytic agents are recommended for reperfusion:
    • Tenecteplase and reteplase (fibrin-specific) are preferred.
    • Streptokinase and alteplase are other options.
    • Consider fibrinolytic therapy in patients with ≤ 12 hours of symptoms.
    • All are contraindicated with active bleeding, recent stroke, or suspected aortic dissection.
  • For patients with symptoms > 2–3 hours:
    • Transfer for primary PCI if available within 120 minutes (including transfer time).
    • Start dual antiplatelet therapy: aspirin plus P2Y12 inhibitors (clopidogrel, prasugrel, ticagrelor).
    • Glycoprotein IIb/IIIa inhibitors (e.g., abciximab) 
  • Indications for CABG surgery after MI:
    • Failure of thrombolytics or PCI to reperfuse damaged myocardium
    • Hemodynamically important mechanical complications (e.g., rupture)
    • Anatomy not amenable to PCI

Post-MI care

Improved long-term prognosis is seen with:

  • Antiplatelet therapy to ↓ the risk of recurrent coronary artery thrombosis or, with PCI, coronary artery stent thrombosis
  • ACEi therapy to prevent remodeling of the left ventricle
  • Statin therapy
  • Anticoagulation in the presence of left ventricular thrombus or chronic atrial fibrillation to prevent embolization


After MI, different risks develop as time passes after the acute event. Patients with type 2 MI have a higher prevalence of heart failure, kidney disease as a complication of MI, and atrial fibrillation.

  • Death: 1 of 3 patients do not survive their initial MI.
  • Potential complications in the first 1–3 days post-MI:
    • Ventricular arrhythmia (most common cause of death)
    • Acute heart failure
    • Cardiogenic shock
    • Pericarditis:
      • Pleuritic chest pain that increases with lying supine
      • Pericardial rub on auscultation
      • Fever
      • Dry cough
      • ECG showing diffuse ST elevations
      • Pericardial effusion seen on echocardiogram
  • 3–14 days post-MI:
    • Free-wall rupture: 
      • Can result in cardiac tamponade or pseudoaneurysm formation
      • Incidence is highest during macrophage-mediated removal of necrotic myocardium.
    • Papillary muscle rupture:
      • Posteromedial papillary muscle rupture due to posterior descending artery occlusion
      • Posteromedial-wall rupture → acute mitral regurgitation
      • Holosystolic murmur over the 5th intercostal space at the midclavicular line
      • May present with signs of left-sided heart failure (pulmonary edema, crackles, dyspnea)
    • Ventricular septal rupture:
      • Caused by left anterior descending artery occlusion
      • Coincides with macrophage infiltration of the wall
      • May present as a holosystolic murmur over the left sternal border 
      • May present with signs of right-sided heart failure (e.g., jugular venous distention, peripheral edema) or biventricular failure
      • May progress to cardiogenic shock due to a ↓ in cardiac output
    • Mural thrombus formation with potential embolization of the clot can lead to:
      • Limb ischemia
      • Stroke
      • Mesenteric ischemia
      • Renal infarction
  • > 14 days post-MI:
    • Dressler syndrome:
      • Autoimmune sensitization to antigens released during cardiomyocyte death 
      • Presents with signs of pericarditis (pleuritic pain, friction rub, fever) 
      • May result in elevation of troponins and leukocytosis
      • ECG shows diffuse ST elevations
      • Pericardial effusion: abnormal amount of fluid in the pericardial cavity of the heart 
      • Can be complicated by cardiac tamponade/hemopericardium
    • Ventricular aneurysm presenting with: 
      • Persistent ST elevations and T-wave inversions > 3 weeks post-MI
      • Signs of angina (e.g., dyspnea on exertion)
      • Systolic murmur and/or S3/S4 sounds

Differential Diagnosis

  • Unstable angina: presents with chest pain due to transient myocardial ischemia and may be a warning sign for the risk of heart attack (MI) in the future. Diagnosis is by history and examination, ECG, and stress testing, with possible additional nuclear medicine imaging, echocardiography, or coronary angiography. Troponin will be normal. Treatment includes antiplatelet medications, nitrates, statins, beta-blockers, and PCI.
  • Vasospastic angina: uncommon cause of chest pain due to transient coronary artery spasms. The clinical presentation of vasospastic angina is characterized by spontaneous episodes of chest pain due to a transient decrease in blood flow to the epicardial arteries. Diagnosis is made by clinical history, normal exam, and ECG. Cardiac enzymes and PCI are usually normal. Management includes the prevention of vasospasm with calcium channel blockers and the relief of angina with nitrates. 
  • Aortic dissection: due to shearing stress from pulsatile pressure causing a tear in the tunica intima of the aortic wall, often associated with hypertension. Patients with aortic dissection often present with acute, tearing chest or back pain. Diagnosis is made by CT imaging. Type A dissections (in the ascending aorta) are a surgical emergency because of the risk of imminent rupture. Type B dissections (in the descending aorta) can often be managed medically with beta-blockers and calcium channel blockers. 
  • Pulmonary embolism: presents with pleuritic pain, dyspnea, tachycardia, and occasionally chest pain. Risk factors for pulmonary embolism are prolonged immobilization, oral contraceptives or estrogen therapy, smoking, and obesity. Diagnosis of venous thromboembolism is made by CT. ECG may be normal or may show ST-segment changes. Management is urgent, with anticoagulation to prevent further propagation of the clot.
  • Pericarditis: inflammatory disorder of the pericardium resulting in chest pain that is usually constant and may manifest with diffuse ST-segment elevation on ECG. Etiologies can be infectious (usually viral), post-MI, due to medications, or due to malignancy. Treatment is supportive if viral or with management of the underlying cause.
  • Costochondritis: due to inflammation of the cartilage in the rib cage. Costochondritis presents with chest pain that is reproducible on palpation. It may be due to trauma, strain, or viral infection. Diagnosis is made clinically and by the exclusion of coronary disease with appropriate testing. Treatment is with local measures and NSAIDs.
  • Esophageal spasm: painful contraction of the esophagus that can present with severe, intermittent chest pain. Diagnosis is by ruling out cardiac causes of chest pain, esophageal manometry, and a barium swallow study. Management may include antispasmodic medications and, in some cases, surgery.
  • Takotsubo cardiomyopathy: type of nonischemic cardiomyopathy in which there is transient regional systolic dysfunction of the left ventricle. Patients present with symptoms of acute coronary syndrome, including chest pressure and shortness of breath. ECG may show ST-segment elevations. Coronary angiography will not show obstructed arteries. Echocardiography will demonstrate characteristic apical wall motion abnormalities. Treatment includes beta-blockers and the removal of inciting stressors.
  • Myocarditis: inflammatory disease of the myocardium that can mimic an acute MI, especially in younger patients (< 45 years). It may occur alone or in association with a systemic process. There are numerous etiologies, but all lead to inflammation and myocyte injury. The diagnosis is supported by clinical findings, laboratory evaluation, and cardiac imaging. Management is supportive and aimed at addressing complications.


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