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What is Atherosclerosis?

chronic inflammatory response in the walls of arteries, largely due to the deposition of lipoproteins
"hardening of the arteries"

HALLMARK: formation of multiple plaques within the arteries


What cellular components are involved in the development of atheroclerosis?

endothelial cells, smooth muscle cells, platelets, leukocytes and a wide variety of chemotactic and inflammatory mediators

Atherogenesis is a result of complex and incompletely understood interactions that exist between these cellular elements and other biologic processes


What biological processes contribute to atherosclerosis?

Vasomotor function, thrombogenicity of the blood vessel wall, activation of the coagulation cascade, the fibrinolytic system, smooth muscle cell migration and proliferation, and adrenergic stimulus are interrelated biological processes that contribute to atherogenesis


”response-to-injury” theory

the most widely accepted mechanism of action in atherosclerosis

Endothelial injury --> vascular inflammation + fibroproliferative response --> plaque formation

Triggered by by any other number of insults, such as:
- Physical injury or stress as a result of direct trauma or HTN
- Turbulent blood flow, esp where arteries branch
- Circulation of reactive oxygen species (free radicals)
- Hyperlipidemia
- Chronically elevated blood glucose levels
- Homocysteinemia, which is toxic to endothelium
- infectious agents
- chemical toxins


Describe the atherosclerotic process

Circulating monocytes infiltrate the intima of the vessel wall --> monocytes differentiate into macrophages, which ingest oxidized LDL, slowly turning into large "foam cells“ --> Foam cells eventually die, and further propagate the inflammatory process


What is the earliest grossly visible pathologic lesion of atherosclerosis? Why does it occur?

the fatty streak: occurs as a result of focal accumulation of serum lipoproteins within the intima of the vessel wall
lipid-laden macrophages, T lymphocytes, and smooth muscle cells in varying proportions

Fatty streatks are observed in the aorta and coronary arteries of most individuals by 20 years of age.
*fatty streaks do not impair the lumen size


How is smooth muscle involved in atherosclerosis?

SM cells migrate to and proliferate in the intima and are responsible for deposition of extracellular connective tissue matrix forming a fibrous cap (plaque) that overlies a core of lipid-laden foam cells, extracellular lipid, and necrotic cellular debris.


What is Angina Pectoris? What causes it?

Paroxysmal and usu recurrent attacks of chest pain (constricting, squeezing, choking, or knifelike)

Caused by transient (15 seconds to 15 minutes) myocardial ischemia that falls short of inducing the cellular necrosis that defines MIs.


Common symptoms of angina

• Chest pain: usu across anterior precordium; severe tightness, squeezing pain or intense weight or pressure on the chest; may radiate to the jaw, neck, arms, back, and epigastrium
• Dyspnea: may occur as an isolated complaint; often indicates poor ventricular compliance in the setting of acute ischemia
• Diaphoresis
• Anxiety
• Lightheadedness and syncope
• Cough/wheezing
• Nausea and vomiting or abdominal
*Women (40-50%) do not present with typical cardiac symptoms: dyspnea & SOB are more common presentations


Stable Angina
When do Sxs occur?

Cardiac ischemia that is usually due to a fixed lesion in a coronary artery
Sxs generally occur only upon exertion and are usu relieved by rest and/or medications which dilate arteries (nitrates)


Variant Angina (Prinzmetal)
When do Sxs occur?

Pathophysiology Unknown, but intermittent vasospasm appears to be key to development of sxs

Sxs: Pain often occurs at rest and may be well controlled by vasodilators such as calcium channel blockers


Unstable Angina

Pattern: increasing frequency or intensity of chest pain; Often includes pain at rest
* Prolonged episode of unstable angina pectoris may precede the development of a myocardial infarction


What is an acute myocardial infarction?

the development of myocardial necrosis caused by a prolonged critical imbalance between the amount of oxygen supplied to the myocardium and the metabolic demand of the myocardium.


What is the most common cause/pathogenesis of an MI

plaque rupture within a coronary artery

Subsequent subendothelial exposure results in platelet aggregation, thrombus formation, fibrin accumulation, hemorrhage into the plaque, and varying degrees of vasospasm --> either partial or complete occlusion of the vessel and subsequent myocardial ischemia


Less common other causes of MI

• Emboli to coronary arteries (dt cholesterol or infxn)
• Coronary artery vasospasm
• Coronary anomalies (irregular/absent coronary arteries or aneurysms)
• Hypoxia dt underlying pulmonary disease.
• Hypoxia due to CO poisoning or inhaled toxins.
• Arteritis


Process of an MI

Decreased oxygen flow to myocardium → conversion from aerobic to anaerobic metabolism → decreased ATP synthesis (within 1-2 min; reduced to 50% by 10 min) → disruption of the Na+/K+ ATPase membrane channel → marked increase in the membrane permeability of involved cardiac muscle cellsmyocytes swell and metabolic functions deteriorate; Ca activates various degradative enzymes (lipases, proteases and nucleases) → Irreversible cell death approx. 15 to 20 minutes from onset of injury --> possible sudden cardiac death


What will dramatically reduce morbidity and mortality from MIs?

reperfusion of the affected myocardium within a time period of 1 to 6 hours


Describe the gross and histopathology changes S/P Myocardial Infarction at
0 - .5 hours

Gross: None
Histopath: None


Describe the gross and histopathology changes S/P Myocardial Infarction at 0.5 - 4 hrs

Gross: Usu none
Histopath: GLYCOGEN DEPLETION, as seen with a PAS Stain and poss. waviness of myocardial fibers at borders


Describe the gross and histopathology changes S/P Myocardial Infarction at 4 - 12 hours

Gross: Slight mottling; Edematous, pale to sl. blue in color
Histopath: Initiation of COAGULATION NECROSIS, edema, hemorrhage


Describe the gross and histopathology changes S/P Myocardial Infarction at 12 - 24 hours

Gross: Dark mottling; Darker areas of hemorrhage appear deep blue or purple
Histopath: Ongoing coagulation necrosis, HYPEREOSINOPHILIA, contraction band necrosis in margins, beginning of neutrophil infiltration


Describe the gross and histopathology changes S/P Myocardial Infarction at 1 - 3 days

Gross: Infarct center becomes tannish-yellow (bruise-like)
Histopath: Continued coagulation necrosis, Loss of myocardial cell nuclei and striations, increased infiltration of NEUTROPHILS to interstitium


Describe the gross and histopathology changes S/P Myocardial Infarction at 3 - 7 days

Gross: Hyperemia at border with softening yellow-tan center, with decreased wall thickness and coagulation necrosis
Histopath: Beginning of DISINTEGRATION OF DEAD Mm FIBERS, necrosis of neutrophils, beginning of macrophage removal of dead cells at border


Describe the gross and histopathology changes S/P Myocardial Infarction at 10 - 30 days

Gross: Red-gray with depressed borders
Histopath: MATURE GRANULATION TISSUE with type I collagen


Describe the gross and histopathology changes S/P Myocardial Infarction at 2 - 8 weeks

Gross: Gray-white granulation tissue
Histopath: Increased COLLAGEN DEPOSITION, decreased cellularity


Describe the gross and histopathology changes S/P Myocardial Infarction at > 2 months

Gross: Completed scarring


How long after a MI are cardiac aneurysms most likely occur?

2-8 weeks due to formation of thin scar tissue


How does a drop in BP may be due to a massive heart attack cause a Pt to end up with pump failure?

With posterior or right sided infarct that is close to the R vagal N (which affects BP)


Appearance of an MI Pt

Pt may appear normal and entirely asymptomatic; OR quite anxious, agitated, pale and diaphoretic


How to HTN and hypoTN relate to MIs?

• Hypertension may precipitate a MI or reflect elevated catecholamines due to pain and anxiety
• Hypotension: may indicate a large infarct; is frequently seen with R ventricular infarctions