CAD Flashcards
Coronary Artery Disease Mechanisms
- gradual enlargement of plaque, eventually obstruct blood flow to degree of causing ischemia
- Unstabilized plaque will rupture creating acute thrombosis and acute MI if total occlusion or near occlusion occurs
CAD pathogenesis
Abnormal lipid metabolism
Excessive intake of cholesterol/ sat. fats
genetic predisposition
CAD pathogenesis 1st phase - Fatty Streaks
focal thickening of intima w/ increase in smooth muscle cells and extracellular matric
migration of smooth muscle cells into intima w/ proliferation
accumulation of intracellular lipid deposits or extracellular lipids or both
FATTY STREAK is created!
CAD 2nd phase - Fibrous Plaques
Evolve from Fatty Streaks via accumulation of connective tissue w/ an increased number of smooth muscle cells laden with lipids and often a deeper extracellular lipid pool
CAD 3rd phase - Advanced Lesions
fibrous plaque becomes revascularized
contains necrotic lipid rich core
calcification occurs and remodeling
Positive remodeling: smoother margins and more stable
Negative remodeling: smaller lumen and more unstable, seen w/ ACS
Vessel diameter may also increase initially
CAD contributors
Endothelial dysfunction:
impaired vascular reactivity
induced by dyslipidemia - oxidized LDL, worsened by smoking
improved w/ corrections of lipids, statin therapy, ace inhibitor therapy, antioxidants
Endothelial dysfunction factors
Increased age Family Hx of CHD Smoking Hyperlipidemia - Increased serum cholesterol low serum HDL HTN Increased serum homocysteine Diabetes mellitus Obesity High-fat diet
Endothelial function improvements
L-arginine Estrogen Antioxidants Smoking cessation Cholesterol lowering ACE inhibitors Exercise Homocysteine lowering
Dyslipidemia
high LDL, low HDL
LDL accumulates in cholesterol-enriched macrophages - FOAM CELLS
Foam cells lead to mitochondrial dysfunction, apoptosis, necrosis (unstable plaque)
Inflammatory process - increase in platelet aggregation
Inflammation Key role in CAD
both cellular and humoral pathways
Macrophages modified by oxidized LDL release variety of inflammatory substances,
cytokines and growth factors
Plaque Hemorrhage in CAD
As plaque develops and expands, develops its own microvascular network from adventitia thru the media into the thickened intima.
Vessels prone to disruption and hemorrhage occurs.
Plaque Rupture in CAD
Unstable environment
Plaque ruptures>Inflammatory process>Platelets activated>Platelets adhere>Thrombus formation> Occlusion of vessel>MI
CP - Low Risk
Atypical CP, minimal or no risk factors, young
CP - Intermediate Risk
Age > 70 Male Hx of Diabetes Hx of PVD/CVA Previous EKG changes
CP - High Risk
Ischemic discomfort Hx of CAD Hx of CHF New EKG changes Elevated Biomarkers
CP clinical presentation
Symptoms: duration, location, radiation, ppting activities, w. exertion or rest, reproducible
Assoc. Sx: dyspnea, nausea/vomiting, dizziness/syncope, diaphoresis
CP DX testing
EKG - baseline w/ CP & again in am to compare
Cardiac Enzymes - Troponin ^ 2 hrs. after event, check again in another 2-4 hrs. stay elevated 1-2 wks
Lipid panel
Screen for Diabetes
CP stress testing
Graded exercise stress testing
Pharmacological stress testing
Imaging - Echocardiography, nuclear imaging
Ischemic Heart Disease
Chronic ischemia - supply & demand mismatch
Ppted by activity, eating, cold weather, emotional stress.
Acute Coronary Syndrome - typically plaque ruptures w/ sudden onset of symptoms
Acute Coronary Syndrome
Unstable Angina
Non-ST Elevated MI
ST Elevated MI
Acute Coronary Syndrome
EKG changes: ST Depression,
Transient ST Elevation
T wave Inversion
MI Biomarkers - released from necrotic cardiac tissue
Myoglobin: 2-4 hrs, lasts 24 hrs (rises quickly w/i 2 hrs of event, in 2 hrs should double if having MI
CK-MB: 4-8 hrs, lasts 48-72 hrs
Troponin I: 6-12 hrs, lasts 7-10 days (starts to go up at 2 hrs, 6 hrs, 12 hrs
Large area MI
Hypotension Tachycardia Third Heart Sound Fourth Heart Sound Rales - backup of fluid in lungs (fine crackles)
Unstable Angina TX
Anti-ischemic medical therapy
Anti-Thrombotic medical therapy
Revascularization
