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Myocardial Infarction (MI) - Comprehensive Review

Definition

• Robbins, Cotran & Kumar Pathologic Basis of Disease, p. 511

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Epidemiology & Risk Factors

• 10% of MIs occur in people under 40 years; 45% occur under 65 years
• Male sex increases relative risk through middle age
• Postmenopausal women lose estrogen protection, with rising CAD risk; IHD is the most common cause of death in older females
• Postmenopausal hormonal replacement therapy has not been shown to be protective and may be detrimental (pro-thrombotic effect)
• Classic risk factors: hypertension, dyslipidemia, diabetes, smoking, obesity, family history

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Classification

Type 1 MI

• STEMI - ST-segment elevation on ECG + elevated cardiac biomarkers
• NSTEMI - Same biomarker elevation but without ST-elevation

Type 2 MI

• Sabiston Textbook of Surgery, p. 2928

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Pathogenesis

1. Plaque disruption - An atheromatous plaque is eroded or suddenly ruptured by endothelial injury, intraplaque hemorrhage, or mechanical forces, exposing subendothelial collagen and necrotic plaque contents
2. Platelet activation - Platelets adhere, aggregate, and release thromboxane A2, ADP, and serotonin - causing further platelet aggregation and vasospasm
3. Coagulation cascade - Tissue factor activates the coagulation cascade, adding to the thrombus
4. Complete occlusion - Within minutes, the thrombus can completely occlude the coronary lumen

Atypical causes (~10% of cases):

• Vasospasm (cocaine, ephedrine, Prinzmetal angina)
• Embolism (from LA thrombus in AF, endocarditis vegetations, prosthetic material, paradoxical embolism via PFO)
• Vasculitis
• Hematologic abnormalities (e.g., sickle cell disease, hypercoagulable states)
• Amyloid deposition in vascular walls
• Robbins, Cotran & Kumar Pathologic Basis of Disease, pp. 511-512

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Coronary Artery Territories

• Right ventricular infarction complicates 15-30% of RCA occlusions
• Isolated RV infarction: only 1-3% of cases

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Morphologic Evolution (Table 12.5 from Robbins)

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ECG Changes in MI (Ganong's Physiology)

• Acute phase: ST-segment elevation in leads over the infarct; reciprocal ST depression in opposite leads
• Days to weeks later: ST abnormalities subside; dead muscle becomes electrically silent
• Chronic changes: New Q waves appear; loss of R-wave progression in anterior leads
• Non-Q-wave infarcts: less severe but higher rate of subsequent reinfarction
• Ganong's Review of Medical Physiology, p. 534

ECG Localization

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Diagnosis

Biomarkers

• Present at very low concentrations in normal serum
• High-sensitivity (hs) assays: detection threshold ~1-2 ng/L; upper 99th percentile ~10-30 ng/L (varies by age, sex, assay)
• Rise detectable within 3-6 hours of infarction onset
• Elevations are not exclusive to MI - also seen in myocarditis, pericarditis, pulmonary embolism, renal failure, sepsis, critical illness, and after intense exercise
• Serial troponins with rising/falling pattern are key to diagnosing AMI vs. chronic elevation

• Henry's Clinical Diagnosis and Management by Laboratory Methods, p. 313

Diagnostic Triad

1. Clinical symptoms (chest pain, diaphoresis, radiation to arm/jaw, dyspnea)
2. ECG changes
3. Rise and/or fall of cardiac biomarkers (troponin)

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Management

Immediate Goals

• Restore perfusion as fast as possible ("time is muscle")
• Limit infarct size
• Prevent and treat complications

STEMI

• Primary PCI (percutaneous coronary intervention): preferred reperfusion strategy - goal door-to-balloon time <90 min
• Thrombolysis: if timely PCI unavailable

NSTEMI/UA

• Antiplatelet therapy, anticoagulation
• Intervention can be delayed up to 72 hours in some cases (risk-stratify with TIMI/GRACE score)

Drug Therapy

Critical distinction: In a suspected right-sided MI (inferior STEMI + right-sided leads), nitroglycerin can precipitate fatal hypotension by reducing preload to a preload-dependent right ventricle. Always check right-sided ECG (V4R) in inferior MI.

• Sabiston Textbook of Surgery, pp. 2934-2936

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Complications (~75% of patients experience at least one)

1. Contractile Dysfunction

• LV failure proportional to volume of damage
• Cardiogenic shock: ~10% of transmural MIs; typically when ≥40% of the LV is damaged; high mortality

2. Arrhythmias

• Most common cause of early out-of-hospital death
• Ventricular fibrillation is the most dangerous
• A defibrillator must be immediately available for all MI patients
• AF, heart block (especially in inferior MI with AV node involvement) also common

3. Papillary Muscle Dysfunction/Rupture

• Papillary muscles often ischemic - causes mitral regurgitation
• Papillary muscle rupture (day 3-7): catastrophic acute MR - medical emergency

4. Myocardial Rupture (1-3% of MIs, frequently fatal)

• Free wall rupture → hemopericardium → cardiac tamponade (most common)
• Ventricular septal rupture → VSD with left-to-right shunt
• Papillary muscle rupture → severe acute mitral regurgitation

5. Right Ventricular Infarction

• Usually from RCA occlusion extending into RV
• Results in right-sided heart failure: JVD, hypotension, clear lungs (no pulmonary edema)
• Treatment: IV fluids to maintain preload; avoid preload-reducing agents (nitrates, diuretics)

6. Infarct Expansion and Ventricular Aneurysm

• Infarct expansion: thinning and dilation of infarcted zone (days-weeks)
• True aneurysm: late complication; dyskinetic wall segment; risk of mural thrombus and systemic embolism; anticoagulation recommended
• Risk of VT from re-entry around the aneurysm

7. Mural Thrombus

• Forms on dyskinetic endocardium, especially anterior MI
• Risk of systemic arterial embolism (stroke, limb ischemia)

8. Pericarditis

• Early (1-3 days): fibrinous pericarditis over the infarcted zone
• Dressler syndrome (weeks later): immune-mediated; pleuropericarditis, fever

9. Sudden Cardiac Death (SCD)

• 325,000 deaths/year in the US
• Mechanism: ventricular fibrillation or asystole
• One-third of out-of-hospital STEMI patients die within 1 hour of onset before reaching care
• ICD implantation markedly improves prognosis in at-risk survivors
• Robbins, Cotran & Kumar Pathologic Basis of Disease, pp. 516-518

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Post-MI Management (Long-term)

• Dual antiplatelet therapy (duration depends on stent type)
• Statin (high-intensity)
• Beta-blocker (especially if reduced EF)
• ACE inhibitor/ARB (if EF ≤40%)
• Cardiac rehabilitation
• Risk factor modification (smoking cessation, BP control, glucose control, weight loss)
• ICD implantation if EF ≤35% persists after 3 months of optimal therapy

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Key Summary Points

The overall in-hospital death rate for MI is less than 7%. Out-of-hospital STEMI mortality is far worse - one-third of patients die before reaching the hospital, usually from arrhythmia within 1 hour of onset.