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Myocardial Infarction (MI) - Comprehensive Review

Definition

• Robbins & Kumar Basic Pathology, p. 467

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Epidemiology & Risk Factors

• ~10% of MIs occur before age 40; 45% occur before age 65
• Risk rises progressively with age and atherosclerotic risk factors
• Males have higher relative risk through middle age
• Females are generally protected during reproductive years, but postmenopausal decline in estrogen (with rising cholesterol, BP, and inflammatory markers) erases this protection - IHD is the most common cause of death in older women
• Postmenopausal hormone replacement therapy has not been shown to be protective, and may be detrimental (prothrombotic effect)
• Robbins, Cotran & Kumar Pathologic Basis of Disease, p. 511

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Pathogenesis

The Typical Sequence (responsible for ~90% of MIs)

1. An atheromatous plaque is eroded or suddenly disrupted by endothelial injury, intraplaque hemorrhage, or mechanical forces - exposing subendothelial collagen and necrotic plaque contents
2. Platelets adhere, aggregate, and are activated, releasing thromboxane A₂, ADP, and serotonin - causing further platelet aggregation and vasospasm
3. Coagulation is activated by exposure of tissue factor, adding to the growing thrombus
4. Within minutes, the enlarging thrombus completely occludes the coronary artery lumen

• Robbins & Kumar Basic Pathology, p. 468-469

Causes When Typical Atherothrombosis is Absent (~10% of cases)

• Coronary vasospasm (with or without atherosclerosis; cocaine, ephedrine)
• Embolism - from left atrial mural thrombus (AF), infective endocarditis vegetations, prosthetic material, or paradoxical embolism via patent foramen ovale
• Small vessel disease - vasculitis, amyloid deposition, sickle cell disease
• Prolonged demand-supply mismatch (tachycardia/hypertension in setting of fixed stenosis) - causing subendocardial necrosis without thrombus

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Progression of Necrosis: The Wavefront Phenomenon

• The subendocardium is most vulnerable because it is furthest from epicardial vessels and has the highest intramural pressures impairing blood flow
• Cardiac muscle requires ~1.3 mL O₂/100 g/min just to remain alive; normal resting delivery is ~8 mL O₂/100 g/min
• Even 15-30% of normal collateral flow can prevent cell death in border zones; however, the central zone of a large infarct has almost zero flow and does die
• Guyton & Hall Textbook of Medical Physiology, p. 271

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Infarct Patterns by Coronary Artery

• Robbins & Kumar Basic Pathology, p. 537

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Morphological Changes Over Time

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Biochemistry of Ischemia

• Aerobic metabolism ceases
• ATP drops, lactic acid accumulates
• Contractility is lost within minutes (reversible at this stage)

• Irreversible damage begins
• Sarcolemmal integrity is lost - intracellular macromolecules (troponin, CK-MB) leak into bloodstream

• Robbins & Kumar Basic Pathology, p. 491-493

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Cardiac Biomarkers

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ECG Changes

• Acute (hours): Hyperacute T waves → ST elevation (STEMI) or ST depression (NSTEMI/subendocardial)
• Days-weeks: ST segment returns toward baseline; T wave inversions appear
• Weeks-months: Pathological Q waves develop in leads over the infarct area (dead tissue is electrically silent)

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Clinical Presentation

• Epigastric pain or heartburn-like discomfort
• Jaw or arm pain alone
• Dyspnea without chest pain
• Fatigue, syncope
• "Silent MI" (especially in diabetics with autonomic neuropathy)

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Causes of Death After MI

1. Decreased cardiac output - infarcted muscle fails to contract; systolic stretch (dyskinesis) worsens this, as normal myocardium pushes ischemic segments outward (paradoxical motion), wasting contractile energy
2. Pulmonary edema - from left ventricular failure and elevated filling pressures
3. Ventricular fibrillation - most common cause of death (80-90% of ischemic cardiac deaths)
4. Cardiac rupture - free wall rupture (days 3-7, peak risk), papillary muscle rupture (acute MR), ventricular septal rupture

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Complications

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Management

Immediate (STEMI)

1. Aspirin 160-325 mg chewed immediately (buccal absorption; inhibits COX-1/thromboxane A₂)
2. O₂ only if SpO₂ <90%; routine O₂ not recommended with normal saturations
3. Nitroglycerin sublingual 0.4 mg q5 min (up to 3 doses) - reduces preload and dilates coronary vessels
   • Avoid if: SBP <90 mmHg, RV infarction (inferior ECG changes + JVP elevated + clear lungs), or phosphodiesterase-5 inhibitor use within 24 hours
4. Morphine 2-4 mg IV q5 min for pain relief (vagotonic - watch for bradycardia/hypotension)
5. Beta-blockers (e.g., metoprolol 5 mg IV q2-5 min, 3 doses) - reduce O₂ demand, decrease VF risk, reduce reinfarction; avoid if HR <60, SBP <100, or >1st degree heart block
6. Primary PCI - preferred reperfusion if achievable within 120 min of first medical contact
7. Fibrinolysis - if PCI not available within 120 min
8. Anticoagulation - heparin, enoxaparin, or bivalirudin
9. Dual antiplatelet therapy - aspirin + P2Y₁₂ inhibitor (clopidogrel, ticagrelor, or prasugrel)

• Harrison's Principles of Internal Medicine 22E, p. 1201-1213

Long-term Secondary Prevention

• Beta-blocker (reduces mortality post-MI, though recent meta-analysis data (PMID: 39298680) questions benefit in patients with preserved EF without heart failure)
• ACE inhibitor/ARB (especially with reduced EF, anterior MI, or heart failure)
• Statin (high-intensity)
• Dual antiplatelet therapy for 12 months
• Aldosterone antagonist (eplerenone/spironolactone) in post-MI with EF ≤40% and heart failure or diabetes

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Recent Evidence (2024-2026)

• Beta-blockers post-MI with preserved EF: A 2025 meta-analysis in Eur J Prev Cardiol (PMID: 39298680) questions the long-held practice of universal beta-blocker use after MI in patients without reduced EF or heart failure - suggesting limited benefit in this subgroup.
• Sudden cardiac death post-MI: A 2024 pooled cohort meta-analysis in Eur Heart J (PMID: 39378245) updated risk stratification data for SCD after MI.

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Key Mnemonics

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Your Exam Rules - Confirmed ✅

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Myocardial Infarction - 5 Marks (Physiology)

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Definition

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Cause / Pathophysiology

Atherosclerotic plaque rupture
        ↓
Platelet aggregation + thrombus formation
        ↓
Complete occlusion of coronary artery
        ↓
No O₂ delivery to myocardium
        ↓
Aerobic metabolism stops → ATP falls → cell death
        ↓
MYOCARDIAL INFARCTION (necrosis)

• Cardiac muscle needs 1.3 mL O₂/100g/min just to survive
• If even 15-30% of normal collateral blood flow is present, cells at the border may survive
• The subendocardium is most vulnerable (compressed by systolic contraction + farthest from epicardial vessels)

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Zones of MI (Concentric Zones)

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ECG Changes in MI

STAGE 1 - ISCHEMIA (minutes to hours)
→ Tall, peaked HYPERACUTE T waves
        ↓
STAGE 2 - INJURY (hours to days)
→ ST SEGMENT ELEVATION (hallmark of acute MI)
        ↓
STAGE 3 - NECROSIS (days to weeks)
→ Deep PATHOLOGICAL Q WAVE appears
        ↓
STAGE 4 - RESOLUTION (weeks to months)
→ Q wave persists; ST returns to baseline; T wave inverts

• Infarcted cells depolarize faster and repolarize abnormally
• This causes current of injury flowing toward the electrode over the infarct
• Reciprocal ST depression is seen in leads on the opposite side of the heart

AK Jain Reference: Refer to the chapter on "Electrocardiogram" - section on ECG changes in myocardial ischemia and infarction (Table on current of injury)

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Causes of Death After MI

1. Decreased cardiac output - due to loss of contracting muscle + systolic stretch (ischemic area bulges outward instead of contracting)
2. Pulmonary edema - back pressure from failing LV
3. Ventricular fibrillation - most common cause of death (electrical instability of ischemic cells)
4. Cardiac rupture - occurs after a few days when dead muscle degenerates and wall becomes thin

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Recovery After MI

• Dead muscle is replaced by fibrous scar tissue (non-contractile) over weeks
• Collateral circulation enlarges gradually
• The nonfunctional zone may partially recover if blood flow is restored

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Clinical/Applied Aspect

• STEMI (ST-elevation MI) = complete occlusion → transmural infarct → emergency PCI needed
• NSTEMI (non-ST elevation MI) = partial occlusion → subendocardial infarct
• Cardiac biomarkers released from dead cells: Troponin I/T (most specific), CK-MB, LDH
• Pain is central crushing chest pain radiating to the left arm/jaw (referred pain via T1-T5 dermatomes)
• Silent MI can occur in diabetics (no pain due to autonomic neuropathy)

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Systolic Stretch - Simple Explanation 💡

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First, understand the normal situation

• ALL muscle walls squeeze inward together
• This squeeze pushes blood OUT into the aorta
• Cardiac output is good ✅

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Now, what happens in MI?

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What is Systolic Stretch?

In simple words: Instead of the whole heart squeezing blood out, the healthy part contracts BUT the dead part balloons outward. The energy generated by the normal muscle is wasted in pushing that dead wall out.

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Why Does It Worsen Cardiac Output?

Normal Heart:
All walls squeeze inward → pressure builds → blood pushed OUT → Good CO ✅

Heart with MI (Systolic Stretch):
Normal walls squeeze inward
         ↓
Dead wall BULGES OUTWARD (systolic stretch)
         ↓
Pressure generated is wasted on bulging the dead wall
         ↓
Less blood is actually pushed forward into aorta
         ↓
CARDIAC OUTPUT FALLS ❌

1. You lose the contribution of the dead muscle
2. PLUS the energy of normal muscle is also wasted on stretching the dead area outward

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When Does It Become Dangerous?

• If >40% of the left ventricle is infarcted → cardiac output falls so badly → Cardiogenic shock
• Mortality of cardiogenic shock = 40-50% even with treatment
• This is a medical emergency

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One Line Summary for Exam

Systolic stretch = During MI, the ischemic/dead ventricular wall cannot contract and instead bulges outward during systole due to high intraventricular pressure, wasting the pumping energy of the normal muscle and thereby reducing cardiac output more than expected.

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Femoral Triangle - 5 Marks (Anatomy)

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Definition

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Boundaries

Mnemonic for borders: "I SAL" - Inguinal ligament (base), Sartorius (lateral), Adductor longus (medial), pointing Low (apex)

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Roof (Covering)

1. Skin
2. Superficial fascia - contains superficial inguinal lymph nodes, great saphenous vein
3. Deep fascia (Fascia lata) - pierced by the saphenous opening (fossa ovalis) through which the great saphenous vein passes to join the femoral vein

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Floor

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Contents

Lateral ←————————————————→ Medial

  N          A          V          L
Nerve     Artery      Vein      Lymphatics
(Femoral) (Femoral) (Femoral)  (Deep inguinal
                               lymph nodes &
                               femoral canal)

Mnemonic: NAVL - Nerve, Artery, Vein, Lymphatics (lateral to medial)

Details of Contents:

• Branch of lumbar plexus (L2, L3, L4)
• Outside the femoral sheath
• Divides into anterior and posterior divisions inside the triangle
• Supplies: quadriceps femoris, sartorius, skin of anterior thigh

• Continuation of external iliac artery below the inguinal ligament
• Enters at the midinguinal point (midpoint between ASIS and pubic symphysis)
• Inside the femoral sheath
• Gives off profunda femoris (deep femoral artery) in the triangle

• Continuation of popliteal vein
• Inside the femoral sheath
• Great saphenous vein joins it through the saphenous opening

• The femoral canal is the medial-most compartment of the femoral sheath
• Contains lymphatics and loose areolar tissue
• Its upper opening = femoral ring (site of femoral hernia)

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Femoral Sheath

• A funnel-shaped sleeve of fascia enclosing the femoral artery, vein, and canal (but NOT the nerve)
• Has 3 compartments:

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Blood Supply of the Femoral Triangle

• Femoral artery is the main vessel, entering at the midinguinal point
• Gives branch: Profunda femoris artery (about 3.5 cm below the inguinal ligament) - supplies most of the thigh

• Femoral vein drains the region
• Great saphenous vein opens into the femoral vein at the saphenous opening in the roof

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Applied Anatomy / Clinical Importance

1. Femoral hernia - The femoral canal (weakest point) allows abdominal contents to push through the femoral ring into the femoral canal. More common in females (wider pelvis). Appears as a swelling below and lateral to the pubic tubercle.
2. Femoral pulse - Palpated just below the midinguinal point; used in clinical examination and in CPR.
3. Femoral artery catheterization - Used for cardiac catheterization and angiography; femoral artery is accessed here.
4. Femoral vein cannulation - Emergency central venous access via femoral vein.
5. Femoral nerve block - Used for pain relief in femur fractures and knee surgeries.
6. Lymph node enlargement - Deep inguinal lymph nodes in the femoral canal enlarge in infections/cancers of the lower limb and perineum.

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