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Cardiovascular Block > CAD Pathology > Flashcards

Flashcards in CAD Pathology Deck (12):
1

Syndromes of Ischemic Heart Disease

Stable: angina occurs during exercise

Acute coronary syndromes: unstable angina (pain at rest usually associated with plaque rupture), cell death with MI, and sudden cardiac death

Chronic ischemic heart disease: congestive heart failure

2

Types of Arteriosclerosis

Arteriosclerosis = hardening of the arteries (general term)

Arteriolosclerosis = affects small arteries and arterioles

Atherosclerosis = hardening of medium and large arteries due to atheromatous plaque

3

Atherosclerotic Plaque

Components:
Cellular components: smooth muscle cells, macrophages, and T cells
ECM with intracellular and extracellular lipids

Fibrous Cap = collagen, smooth muscle cells
Edges = macrophages, T cells, smooth muscle cells
Lipid Core = macrophages, cholesterol esters, and foam cells

Primary lesion is the intima

4

Risk Factors for Atherosclerosis

1. Chronic Inflammatory Disorders like CRP, homocysteine levels, stressful personality

2. Metabolic Syndrome (3/5): waistline, high TG, low HDL, HTN, and glucose

3. Many others: lipoprotein A

5

Coronary Reperfusion Injury

Want to get fresh blood back to the heart ASAP
Tissue plasminogen activator = t-PA

Internal mammary artery or greater saphenous vein = bypass graft

Ideally: want blood flow back in 6 hours; greater than 12 is little salvage

6

Lab Dx of MI

Less than ideal is myoglobin because not very specific (can happen with normal muscle damage) but is the first one to go up with sign of MI (goes up and down first)

Creatine kinase MB (CK-MB) is most sensitive and fairly specific (not perfect) increases 4-6 hours after MI and peaks at 24 hours, and back to normal within 48 hours

Cardiac troponin I and T: elevation within 4-6 hours and peak at 24, but remain for 7-10 days; gold standard

7

Wavefront Phenomenon

Initially after MI, most vulnerable area is subendocardial and then over time is completely transmural for the area of necrosis

8

Occlusion Types

LAD: widow maker; infarction of anterior wall of ventricle near apex and anterior septum

L circumflex: lateral wall sparing the apex

RCA: affects inferior and posterior L ventricle predominantly and posterior septum

9

Patterns of Infarction

ST elevated MI = STEMI; transmural necrosis

Non ST elevated MI = NSTEMI; subendocardial necrosis

Hemorrhagic: reperfusion injury

10

Gross Morphologic Changes in MI

Grossly within 12 hours will not see much

After 12 hours = reddish discoloration/ dark mottling

1-3 days see yellow necrosis with soft center

3-10 see red granulation tissue that progresses to fibrosis at periphery

11

Microscopic Changes in MI

0-12 hours: wavy fibers, edema, and non-specific

12-24 hours: coagulative necrosis, myocyte eosinophilia

1-3 days: neutrophilic infiltrate

3-10 days: cell disintegration, macrophage phagocytosis, granulation tissue

10 days – 2 months: granulation tissue, progressive fibrosis

12

MI Complications

First problem with low O2 supply: contractile dysfunction and arrhythmia (causes sudden cardiac death)

L ventricle may rupture leading to blood accumulation in pericardium = cardiac tamponade can occur

Papillary muscle rupture can lead to mitral regurgitation

Weakened myocardium can cause aneurysm with ballooning and blood stasis and formation = lead to thromboembolism if dislodged

Pericarditis