Myocardial Infarction (MI) - "Heart Attack"

Definition

"The presence of acute myocardial injury detected by abnormal cardiac biomarkers in the setting of evidence of acute myocardial ischemia."

• Robbins & Kumar Basic Pathology, p. 354

Causes & Pathogenesis

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

• Coronary artery vasospasm
• Embolization from mural thrombi (e.g., atrial fibrillation) or valve vegetations
• Small vessel disease: vasculitis, amyloid deposition, sickle cell stasis
• Robbins & Kumar Basic Pathology, p. 354

Classification: Types of MI

By ECG Pattern (Clinical Subtypes)

• STEMI criteria: new ST elevation ≥0.1 mV at J-point in ≥2 contiguous leads (≥0.2 mV in V2-V3 in men ≥40 yrs)
• Frameworks for Internal Medicine; Robbins Pathology

Myocardial Response to Ischemia

• The subendocardium is most vulnerable - it has the highest oxygen demand and its blood vessels are compressed by systolic contraction.
• Necrosis starts in the subendocardium and expands outward in a "wavefront" pattern.
• A full transmural infarct achieves maximum extent in 3-6 hours without intervention.
• Cardiac muscle needs ~1.3 mL O2/100g/min to survive; normal delivery is ~8 mL O2/100g/min. Even 15-30% of normal flow can prevent death.
• Guyton and Hall Textbook of Medical Physiology, p. 271

Locations of MI (by Vessel)

• Robbins & Kumar Basic Pathology, p. 355

Patterns of Infarction

• Transmural infarction: Full-thickness necrosis; caused by epicardial vessel occlusion with thrombosis. Produces Q waves on ECG (STEMI).
• Subendocardial infarction: Restricted to the inner <1/2 of ventricular wall; corresponds to NSTEMI. More common when there is diffuse severe atherosclerosis without complete occlusion.

Causes of Death After MI

1. Decreased cardiac output and cardiogenic shock (systolic stretch - ischemic muscle bulges outward instead of contracting)
2. Pulmonary edema from damming of blood in pulmonary vessels
3. Ventricular fibrillation - the most common cause of death (80-90% of cardiac deaths post-MI)
4. Cardiac rupture (less common)

• Guyton and Hall Textbook of Medical Physiology, p. 271

Epidemiology (2025 ACC/AHA Data)

• ~805,000 MIs per year in the U.S. (605,000 first-time; 200,000 recurrent)
• Economic burden: ~$84.9 billion annually
• ~10% of MIs occur before age 40; ~45% before age 65
• Men are at greater risk, but the gap narrows with age (women are relatively protected pre-menopause)
• Mortality has declined thanks to early reperfusion and evidence-based prevention

Key Biomarker: Troponin

Summary

• Most are caused by plaque rupture + thrombus
• Time is muscle - intervention within 3-6 hours limits infarct size
• Classified as STEMI (transmural, needs immediate reperfusion) vs. NSTEMI (subendocardial)
• Diagnosed by troponin rise + ECG changes + symptoms
• The #1 cause of death post-MI is ventricular fibrillation

Hair Loss: Stages, Medications & Hair Transplant

Part 1 - The Hair Cycle (Biology of Hair Loss)

• Dermatology 2-Volume Set 5e, p. 3158

Part 2 - Stages of Hair Loss

In Men: The Norwood (Hamilton-Norwood) Scale

• Dermatology 2-Volume Set 5e, Fig. 157.2

In Women: The Ludwig Scale

• Dermatology 2-Volume Set 5e, Fig. 157.3

Part 3 - Medications for Hair Loss

1. Minoxidil (Topical / Oral)

• Mechanism: Vasodilation + angiogenic properties; prolongs anagen phase; increases dermal papilla cell proliferation; acts on potassium channels
• FDA-approved forms:
  • 5% solution/foam - men and women
  • 2% solution - women
• Oral low-dose minoxidil: 0.25-2.5 mg/day (women); up to 5 mg/day (men) - effective and usually well tolerated
• Important: Stopping minoxidil causes an acute telogen efflux 3-4 months after discontinuation
• Must be used continuously - effects reverse on stopping

2. Finasteride (Oral) - Men

• Mechanism: Inhibits 5α-reductase, blocking conversion of testosterone to DHT
• Dose: 1 mg/day orally
• FDA-approved for men
• Stopping finasteride causes gradual hair loss, returning to pretreatment state within ~1 year
• Topical finasteride spray is equally effective with less systemic DHT suppression
• Side effect: "Post-finasteride syndrome" - persistent sexual dysfunction and depression (reported in some men)

3. Dutasteride (Oral)

• Inhibits both isoforms of 5α-reductase (vs. finasteride which inhibits only type II)
• Dose: 0.5 mg/day
• More effective than finasteride with a similar safety profile
• Approved in some countries (not FDA-approved in the US for hair loss)

4. Other Medical Options

Treatment should be continued for at least 6 months before assessing efficacy. - Goldman-Cecil Medicine

Part 4 - Hair Transplant: Procedure

Who Is a Good Candidate?

• Age >25 years preferred (younger patients have unpredictable future hair loss)
• Donor hair density >80 follicular units/cm² = excellent; <40 = poor candidate
• Hair shaft caliber >70 microns gives denser coverage
• Norwood Stages 3-6 (frontal baldness) show the most dramatic results

The Two Main Techniques

1. FUT - Follicular Unit Transplantation (Strip Method)

1. A thin strip of scalp is surgically excised from the mid-occipital (back) donor area
2. The strip is divided by technicians into slivers, then further cut into individual follicular units (1-4 hairs each)
3. Grafts are stored in chilled saline
4. The surgeon creates small recipient sites (0.5-1 mm) using a blade or needle in balding areas at 35-40 follicular units/cm²
5. Technicians insert the grafts into recipient sites
6. Donor wound is sutured - leaves a linear scar (concealed by surrounding hair)

2. FUE - Follicular Unit Extraction

1. Individual follicular units are punched out directly from the donor scalp using a small (0.8-1 mm) circular punch
2. Each follicular unit is extracted one by one
3. Grafts are implanted into recipient sites (same as FUT)
4. No strip removed = no linear scar - leaves small "white dot" scars instead

• Dermatology 2-Volume Set 5e, pp. 3162-3165

Important Surgical Principles

• Frontal scalp is prioritized over vertex (crown): frontal transplants give maximum cosmetic impact and are more stable long-term
• Crown transplants carry risk: progressive 360° hair loss can create a peripheral ring of bald scalp around grafts that looks unnatural over time
• A typical session takes 4+ hours; 2-4 sessions may be needed months apart
• Conservative hairline design is essential - must look natural over decades

Post-Transplant Medications

• Anti-inflammatory steroids | Reduce swelling | | Minoxidil | Enhances and hastens growth of transplanted hairs during recovery | | Finasteride | Minimizes ongoing native hair loss; improves long-term transplant results |

The transplanted hair falls out 2-3 weeks after the procedure (shock loss) - this is normal. New hair growth begins at 3-6 months, with full results at 12-18 months.

Key Points to Remember

• AGA is ongoing and progressive - transplantation does not stop future loss
• Medications (finasteride, minoxidil, PRP, LLLT) must continue alongside transplant to preserve surrounding hair
• The surgeon must always plan for future hair loss when designing the hairline
• Hair color, shaft caliber, and donor density all affect the final cosmetic result
• Dermatology 2-Volume Set 5e; Goldman-Cecil Medicine; Healthline Hair Transplant Guide

Finasteride - Complete Overview

1. Composition & Drug Class

2. Mechanism of Action

Testosterone  ──[5α-reductase]──►  DHT
                  ↑
             BLOCKED by Finasteride

• In the scalp: DHT binds to androgen receptors in hair follicles of genetically predisposed individuals, causing progressive miniaturization of terminal hairs into thin vellus hairs → eventual baldness
• In the prostate: DHT drives prostate cell growth → benign prostatic hyperplasia (BPH) and enlarged prostate volume

• Reduces serum DHT by ~70%
• Reduces intraprostatic DHT by ~90%
• Does NOT reduce testosterone to castration levels (type I 5α-reductase in skin and liver continues to produce some DHT)
• Reduces serum PSA by ~50% (important: must double PSA value to correct for this when screening for prostate cancer)
• Campbell Walsh Wein Urology; Katzung's Pharmacology 16th Ed.

3. Indications & Dosing

• Finasteride and minoxidil are the only two FDA-approved medications for male pattern hair loss
• Must be used continuously - stopping leads to reversal of benefit within ~12 months for hair loss

4. Pharmacokinetics

5. Side Effects

Sexual Side Effects (Most Common)

In most men, these resolve with continued therapy or upon discontinuation.

Post-Finasteride Syndrome (PFS) - Serious Concern

• Persistent erectile dysfunction
• Decreased libido
• Depression and anxiety
• Brain fog (cognitive impairment)
• Fatigue and insomnia
• Testicular pain
• Suicidal ideation (rare)

Other Side Effects

• Katzung's Basic and Clinical Pharmacology 16th Ed.; Lippincott Illustrated Reviews Pharmacology

6. Contraindications

7. Drug Interactions

• No major pharmacokinetic drug interactions identified
• Caution with other CYP3A4 inhibitors (may increase finasteride levels)
• No interaction with antihypertensives, digoxin, warfarin, or theophylline (studied in trials)

8. Key Points Summary

• Sources: Katzung's Basic and Clinical Pharmacology 16th Ed., p. 1690; Lippincott Illustrated Reviews Pharmacology, p. 1513; Campbell Walsh Wein Urology; FDA Topical Finasteride Alert