ST-Segment Elevation Myocardial Infarction¶

Chapter 286 | Part 6: Disorders of the Cardiovascular System · Part 6 – Cardiovascular Disorders · Chapter 286

Key Clinical Points¶

STEMI occurs when coronary blood flow decreases abruptly after a thrombotic occlusion of a coronary artery previously affected by atherosclerosis.
Pain is deep, visceral, heavy, squeezing, and crushing; it commonly occurs at rest, is more severe, and lasts longer than angina pectoris.
Radiation of discomfort to the trapezius is not seen in patients with STEMI and suggests pericarditis.
Cardiac troponin T (cTnT) and cardiac-specific troponin I (cTnI) are the preferred biochemical markers for myocardial injury.
Aspirin (160–325 mg chewed) is essential initially, followed by daily oral administration of 75–162 mg.
Reperfusion therapy (PCI or fibrinolysis) should be initiated within 120 minutes of first medical contact (FMC).
Nitrates are contraindicated in patients with suspected right ventricular infarction or those who have taken a phosphodiesterase-5 inhibitor within the preceding 24 hours.
Morphine is effective for pain relief but may cause bradycardia or hypotension, particularly in inferior infarction.
Intravenous beta blockers reduce the risks of reinfarction and ventricular fibrillation in eligible patients.
Mortality is approximately fourfold higher in patients aged >75 years compared with younger patients.

DEFINITION & OVERVIEW¶

• Acute Myocardial Infarction (AMI): A common diagnosis in hospitalized patients; currently a major challenge in low- and middle-income countries due to lack of infrastructure, personnel, and drugs. • Acute Coronary Syndrome (ACS): The working clinical diagnosis for patients with prolonged ischemic discomfort at rest. • STEMI vs. NSTEMI: The 12-lead ECG is the pivotal tool to distinguish unstable angina (UA) from non-ST-segment elevation myocardial infarction (NSTEMI) and to estimate the magnitude of necrosis in ST-segment elevation myocardial infarction (STEMI). • Table 286-1: Definitions of Myocardial Injury and Infarction * Myocardial Injury: Evidence of elevated cardiac troponin (cTn) with at least one value above the 99th percentile upper reference limit (URL). It is considered acute if there is a rise and/or fall of cTn values. * Acute Myocardial Infarction (MI): Requires myocardial injury plus clinical evidence of acute myocardial ischemia, including: * Symptoms of myocardial ischemia * New ischemic electrocardiographic (ECG) changes * Development of pathologic Q waves * Imaging evidence of new loss of viable myocardium or new regional wall motion abnormality in a pattern consistent with an ischemic etiology * Identification of a coronary thrombus by angiography or autopsy (not for types 2 or 3 MIs). * Type 1 MI: Postmortem demonstration of acute atherothrombosis in the artery supplying the infarcted myocardium. * Type 2 MI: Evidence of an imbalance between myocardial oxygen supply and demand unrelated to acute atherothrombosis. * Type 3 MI: Cardiac death in patients with symptoms suggestive of myocardial ischemia and presumed new ischemic ECG changes before cTn values became available or are abnormal. * Procedure-Related (Types 4 & 5): * Type 4a: PCI-related; defined by cTn elevation >5 times the 99th percentile URL in patients with normal baseline values. * Type 5: CABG-related; defined by cTn elevation >10 times the 99th percentile URL in patients with normal baseline values. * Type 4b (Stent Thrombosis) & Type 4c (Restenosis): Both meet type 1 MI criteria. * Prior/Silent/Unrecognized MI: Identified by abnormal Q waves, imaging evidence of loss of viable myocardium, or pathoanatomical findings.

EPIDEMIOLOGY¶

• Incidence: In the US, ~605,000 patients experience a new AMI and 200,000 experience a recurrent AMI annually. • Mortality Statistics: * Approximately 50% of AMI-related deaths occur before reaching the hospital. * In-hospital mortality rate: ~5% (decreased from 10%). * 1-year mortality rate: ~15%. * Age Factor: Mortality is approximately fourfold higher in patients aged >75 years compared to younger patients. • Risk Factors: * Primary: Hypertension, cigarette smoking, obesity, diabetes mellitus, and elevated circulating LDL-C. * Secondary/Less Common: Hypercoagulability, collagen vascular disease, systemic inflammatory diseases, cocaine abuse, and coronary emboli.

ETIOLOGY & PATHOPHYYSOLOGY¶

• Mechanism of STEMI: Occurs when coronary blood flow decreases abruptly due to a thrombus at a site of vascular injury (e.g., from smoking, hypertension, lipid accumulation, and inflammation). * Plaque Rupture: Most common cause; occurs when the surface of an atherosclerotic plaque is disrupted via erosion or rupture. * Vulnerable Plaque Characteristics: Rich lipid core, thin fibrous cap, expansive remodeling, neovascularization (angiogenesis), plaque hemorrhage, adventitial inflammation, and a "spotty" pattern of calcification. • Thrombogenesis Process: * Formation of platelet monolayer → Activation by agonists (collagen, ADP, epinephrine, serotonin) → Conformational change in GP IIb/IIIa receptor → Binding of fibrinogen → Platelet cross-linking. * Coagulation Cascade: Tissue factor exposure in damaged endothelial cells → Activation of Factors VII and X → Conversion of prothrombin to thrombin → Conversion of fibrinogen to fibrin. Thrombin participates in an autoamplification reaction. • Determinants of Myocardial Damage (7 factors): 1. Territory supplied by the affected vessel. 2. Whether the vessel is totally occluded. 3. Duration of coronary occlusion. 4. Quantity of blood from collateral vessels. 5. Demand for oxygen in the myocardium. 6. Endogenous factors allowing spontaneous lysis of the thrombus. 7. Adequacy of myocardial perfusion when flow is restored.

CLINICAL FEATURES¶

• Pain Characteristics: * Nature: Deep, visceral; described as heavy, squeezing, or crushing (occasionally stabbing or burning). * Location: Central chest and/or epigastrium; may radiate to arms, abdomen, back, lower jaw, and neck. * Duration: Typically longer than angina pectoris; does not subside with rest if started during exertion. • Associated Symptoms: Sweating, nausea, vomiting, anxiety, and a sense of impending doom. • Physical Findings: * General: Anxiety, restlessness, pallor, perspiration, and cool extremities. * Cardiac Signs: Fourth and third heart sounds; decreased intensity of the first heart sound; paradoxical splitting of the second heart sound; muffled apical impulse. * Specific Findings: * Midsystolic or late systolic apical murmur (mitral valve dysfunction). * Pericardial friction rub (in transmural STEMI). * Reduced carotid pulse volume. * Temperature elevation up to 38°C during the first week. • Atypical Presentations: * High Risk Groups: Patients with diabetes mellitus and elderly patients often present with painless STEMI or sudden-onset breathlessness. * Other Manifestations: Sudden loss of consciousness, confusional state, profound weakness, arrhythmia, peripheral embolism, or unexplained drop in arterial pressure.

DIFFERENTIAL DIAGNOSIS¶

• Common Mimics: Acute pericarditis, pulmonary embolism, acute aortic dissection, costochondritis, and gastrointestinal disorders. * Key Differentiator: Radiation of discomfort to the trapezius is NOT seen in STEMI; its presence suggests pericarditis.

DIAGNOSTIC APPROACH¶

Electrocardiogram (ECG):
Role: Primary tool for triage and distinguishing UA, NSTEMI, and STEMI.
Table 286-2: Electrocardiographic Criteria for ST-Elevation Myocardial Infarction
Non-V1–V4 leads: New ST-elevation at the J-point in ≥ 2 contiguous leads ≥ 0.1 mV (1 mm).
Leads V1–V4:
≥ 0.2 mV (2 mm) in men ≥ 40 years old.
≥ 0.25 mV (2.5 mm) in men < 40 years.
≥ 0.15 mV (1.5 mm) in women regardless of age.
Cardiac Biomarkers:
Preferred Markers: Cardiac troponin T (cTnT) and cardiac-specific troponin I (cTnI).
Clinical Utility: Troponin is more robust than CK-MB; it remains elevated for 7–10 days. CK-MB is useful only for detecting very recent injury.
Cardiac Imaging (Echocardiography):
Utility: Identifies wall motion abnormalities, RV infarction, pericardial effusion, and LV thrombus.
Complications: Detects ventricular septal defect (VSD) and mitral regurgitation.

MANAGEMENT & TREATMENT¶

Prehospital/Initial Care:
Aspirin: 160–325 mg chewed immediately; followed by daily oral 75–162 mg.
Nitrates: Contraindicated in suspected RV infarction or if PDE-5 inhibitors were used within the last 24 hours.
Morphine: For pain relief; caution for bradycardia/hypotension (especially in inferior MI).
Pharmacologic Therapy:
Beta-blockers: Intravenous use reduces risk of reinfarction and ventricular fibrillation in eligible patients.
Reperfusion Therapy Decision Pathway:
Step 1: Initial Site Assessment
If at a PCI-capable hospital → Proceed to primary PCI if FMC-device time ≤ 120 min.
If at a non-PCI-capable hospital → Evaluate Door-in-Door (DIDO) time.
Step 2: DIDO Evaluation (Non-PCI-capable site)
If DIDO ≤ 30 min → Transfer for primary PCI if FMC-device time is as soon as possible and ≤ 120 min.
If DIDO > 30 min OR anticipated FMC-device > 120 min → Administer fibrinolytic agent within 30 min of arrival.
Step 3: Post-Fibrinolysis/Delayed Strategy
If evidence of failed reperfusion → Transfer for primary PCI.
If part of "urgent strategy" → Transfer for angiography/revascularization in 2–3 days.
Final Outcome (All Paths): Diagnostic angiogram results in Medical therapy, PCI, or CABG.
SCD Prevention Decision Pathway:
Decision Node 1: [Condition 1] → Yes → ICD (Class I).
Decision Node 2: [Condition 2] → Yes → ICD (Class I); No → GDMT.
Decision Node 3: [Condition 3] → Yes → ICD (Class IIa); No → ICD should not be implanted (Class III: No benefit).

COMPLICATIONS & PROGNOSIS¶

• Electrical Complications: Arrhythmias, ventricular fibrillation. * Mitigation: Intravenous beta-blockers reduce risk of reinfarction and VF in eligible patients. • Mechanical Complications: * Ventricular Septal Rupture (VSR): * Incidence: 0.2–3% without reperfusion; 0.2–0.34% with fibrinolysis; 3.9% in cardiogenic shock. * Timing: Bimodal peak (within 24h and 3–5 days); range 1–14 days. * Signs: Harsh holosystolic murmur, thrill, S3, pulmonary edema, RV/LV failure, cardiogenic shock. * Rupture of the Ventricular Free Wall: * Incidence: ~0.3–1%; fibrinolysis does not reduce risk; primary PCI seems to reduce risk. * Timing: Bimodal peak (within 24h and 3–5 days); range 1–14 days. * Signs: Anginal/pleuritic pain, syncope, hypotension, signs of tamponade. * Papillary Muscle Rupture: * Incidence: ~0.1–1% (posteromedial more frequent). * Clinical: Abrupt onset of shortness of breath and pulmonary edema; hypotension. * Echocardiography: Hypercontractile LV, flail leaflet, severe mitral regurgitation.

SPECIAL POPULATIONS¶

• Diabetes & Elderly: * Higher proportion of painless STEMI. * Increased risk of atypical presentations (e.g., sudden breathlessness). * Mortality significantly higher in patients >75 years.

KEY PEARLS & CLINICAL TRAPS¶

• Time is Muscle: Reperfusion goal is ≤ 120 min from first medical contact (FMC). * Troponin Utility: Preferred marker; remains elevated for 7–10 days. CK-MB only useful for very recent injury. * Nitrate Warning: Contraindicated in RV infarction or if PDE-5 inhibitors were used within the last 24 hours. * Atypical Presentation Alert: Patients with diabetes or advanced age may present without chest pain but with distress; consider STEMI. * Trapezius Rule: Pain radiating to the trapezius suggests pericarditis, not STEMI.

Reference Tables¶

TABLE 286-1 Definitions of Myocardial Injury and Infarction Criteria for Myocardial Injury The term myocardial injury…¶

Harrison's 22e, p.2118

Criteria for Myocardial Injury
The term myocardial injury should be used when there is evidence of elevated
cardiac troponin (cTn) levels with at least one value above the 99th percentile
upper reference limit (URL). The myocardial injury is considered acute if there is
a rise and/or fall of cTn values.
Criteria for Acute Myocardial Infarction (types 1, 2, and 3 MI)
The term acute myocardial infarction (MI) should be used when there is acute
myocardial injury with clinical evidence of acute myocardial ischemia and with
detection of a rise and/or fall of cTn values with at least one value above the
99th percentile URL and at least one of the following:
• Symptoms of myocardial ischemia
• New ischemic electrocardiographic (ECG) changes
• Development of pathologic Q waves
• Imaging evidence of new loss of viable myocardium or new regional wall
motion abnormality in a pattern consistent with an ischemic etiology
• Identification of a coronary thrombus by angiography or autopsy (not for
types 2 or 3 MIs)
Postmortem demonstration of acute atherothrombosis in the artery supplying
the infarcted myocardium meets criteria for type 1 MI. Evidence of an
imbalance between myocardial oxygen supply and demand unrelated to acute
atherothrombosis meets criteria for type 2 MI. Cardiac death in patients with
symptoms suggestive of myocardial ischemia and presumed new ischemic
ECG changes before cTn values became available or abnormal meets criteria
for type 3 MI.
Criteria for Coronary Procedure–Related MI (types 4 and 5 MI)
Percutaneous coronary intervention (PCI)–related MI is termed type 4a MI.
Coronary artery bypass grafting (CABG)–related MI is termed type 5 MI.
Coronary procedure–related MI <48 h after the index procedure is arbitrarily
defined by an elevation of cTn values >5 times for type 4a MI and >10 times for
type 5 MI of the 99th percentile URL in patients with normal baseline values.
Patients with elevated preprocedural cTn values, in whom the preprocedural
cTn levels are stable (<20% variation) or falling, must meet the criteria for a
>5- or >10-fold increase and manifest a change from the baseline value of
>20%. In addition, they must have at least one of the following:
• New ischemic ECG changes (this criterion is related to type 4a MI only)
• Development of new pathologic Q waves
• Imaging evidence of loss of viable myocardium that is presumed to be new
and in a pattern consistent with an ischemic etiology
• Angiographic findings consistent with a procedural flow-limiting complication
such as coronary dissection, occlusion of a major epicardial artery or graft,
side-branch occlusion-thrombus, disruption of collateral flow, or distal
embolization
Isolated development of new pathologic Q waves meets the type 4a MI or type 5
MI criteria with either revascularization procedure if cTn levels are elevated and
rising, but less than the prespecified thresholds for PCI and CABG.
Other types of type 4 MI include type 4B MI stent thrombosis and type 4C MI
restenosis that both meet type 1 MI criteria.
Postmortem demonstration of a procedure-related thrombus meets the type 4a
MI and type 5 MI criteria if associated with a stent.
Criteria for Prior or Silent/Unrecognized MI
Any one of the following criteria meets the diagnosis for prior or silent/
unrecognized MI:
• Abnormal Q waves with or without symptoms in the absence of nonischemic
causes
• Imaging evidence of loss of viable myocardium in a pattern consistent with
ischemic etiology
• Pathoanatomical findings of a prior MI

TABLE 286-2 Electrocardiographic Criteria for ST-Elevation Myocardial Infarction New ST-elevation at the J-point in 2…¶

Harrison's 22e, p.2119

New ST-elevation at the J-point in 2 contiguous leads with the cut-point:
• In all leads other than leads V–V: ≥0.1 mV (1 mm on standard scale)
2 3
• In leads V–V:
2 3
• ≥0.2 mV (2 mm) in men ≥40 years old
• ≥0.25 mV (2.5 mm) in men <40 years
• ≥0.15 mV (1.5 mm) in women regardless of age

TABLE 286-3 Mechanical Complications of ST-Elevation Myocardial Infarction CHARACTERISTIC Incidence¶

Harrison's 22e, p.2122

CHARACTERISTIC	VENTRICULAR SEPTAL RUPTURE	RUPTURE OF THE VENTRICULAR FREE WALL	PAPILLARY MUSCLE RUPTURE
Incidence	0.2–3% without reperfusion therapy, 0.2–0.34% with fibrinolytic therapy, 3.9% in patients with cardiogenic shock	Approximately 0.3–1%; fibrinolytic therapy does not reduce risk; primary PCI seems to reduce risk	Approximately 0.1–1% (posteromedial more frequent than anterolateral papillary muscle rupture)
	Bimodal peak; within 24 h and 3–5 days; range, 1–14 days	Bimodal peak; within 24 h and 3–5 days; range, 1–14 days
Clinical manifestations	Chest pain, shortness of breath, hypotension	Anginal, pleuritic, or pericardial chest pain; syncope; hypotension; restlessness; sudden death	Abrupt onset of shortness of breath and pulmonary edema; hypotension
	Harsh holosystolic murmur, thrill, S, 3 accentuated S, pulmonary edema, RV and LV 2 failure, cardiogenic shock	Jugular venous distention (29% of patients), pulsus paradoxus (47%), electromechanical dissociation, cardiogenic shock
Echocardiographic findings	Ventricular septal rupture, left-to-right shunt on color flow Doppler echocardiography through the ventricular septum, pattern of RV overload	>5 mm pericardial effusion not visualized in all cases; layered, high-acoustic echoes within the pericardium (blood clot); direct visualization of tear; signs of tamponade	Hypercontractile LV, torn papillary muscle or chordae tendineae, flail leaflet, severe mitral regurgitation on color flow Doppler echocardiography
	Increase in oxygen saturation from the RA to RV, large v waves	Ventriculography insensitive, classic signs of tamponade not always present (equalization of diastolic pressures in the cardiac chambers)