IHD Patho 2012_Student Version (1)

Toxic to the bv cells triggers immune response

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toxic to the BV cells Triggers immune response Inflammation WBC (macrophages & T-lymphocytes) absorb oxidized LDL and form “foam cells” These foam cells cannot degrade LDL and eventually rupture release more oxidized LDL triggers more WBC “fatty streak” grows in size artery lining becomes inflammed stimulates BV smooth muscle cells to enlarge and form a hard cover over the affected area (Fibrous athermatous plaque) further narrows the artery
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Sites of  Atherosclerosis  Development Mostly affects larger, high- pressure vessels: coronary, renal, femoral, cerebral, and carotid arteries Mostly affects larger, high- pressure vessels: coronary, renal, femoral, cerebral, and carotid arteries
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Clinical Manifestations of Atherosclerosis Atherosclerosis Peripheral  arterial  disease CHD Cerebrovascular  disease Acute  coronary  syndrome Angina Sudden  death Heart failure Arrhythmias
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Coronary Heart Disease Blockages of coronary arteries caused by atherosclerosis “Umbrella” term Ischemic heart disease (IHD) is the primary etiology of CHD Disorders of myocardial blood flow due to stable or unstable coronary atherosclerotic plaques
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Spectrum of CHD Chronic IHD Chronic stable angina Variant angina (Prinzmetal’s angina) Silent myocardial ischemia Acute coronary syndrome (ACS) Non-ST-segment elevation ACS (NSTE ACS) Unstable angina (UA) NSTE MI ST-segment elevation MI (STE MI)
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Spectrum of CHD
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Development of Atherosclerosis Fatty streak Fibrous atheromatous plaque Complicated lesion
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Fatty Streaks Accumulation of lipid and inflammatory cells Macrophages and smooth muscle cells become distended with lipids and form foam cells Foam cells rupture, release LDL, attract more inflammatory cells cycle restarts Yellow, intimal discolorations progressively enlarge by becoming thicker and slightly elevated as they grow in length Can occur as early as 1 st decade of life
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Fibrous Atheromatous Plaque Accumulation of intracellular and extracellular lipids Proliferation of vascular smooth muscle cells Formation of scar tissue Leads to elevated thickening of vessel intima Core composed of lipids Covered by fibrous cap of connective tissue and smooth muscle Can be thin / weak (unstable cap) or thick / sturdy (stable cap)
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Complicated Lesion Thin / weak fibrous cap at risk of rupturing Rupture/ulceration of plaque occurs Thrombus formation Occurs in ACS only!! Non-complicated lesion = Stable angina where the plaque does NOT rupture and is “stable”
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Plaque Vulnerability Determinants of plaque vulnerability to rupture Size and consistency of lipid-rich atheromatous core Larger lipid cores within plaque risk of rupture More solid consistency (calcification) stabilizes plaque risk of rupture Thickness of fibrous cap covering the core Thin fibrous cap risk of rupture
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toxic to the BV cells Triggers immune response Inflammation...

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