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DISEASES of ARTERIES ARTERIOSCLEROSIS (“Hardening of the Arteries”): General Term Reflecting Arterial Wall Thickening and Loss of Elasticity

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DISEASES of ARTERIES ARTERIOSCLEROSIS (“Hardening of the Arteries”): General Term Reflecting Arterial Wall Thickening and Loss of Elasticity DISEASES OF ARTERIES ARTERIOSCLEROSIS (“hardening of the arteries”): general term reflecting arterial wall thickening and loss of elasticity 3 patterns •Atherosclerosis: involves the the aorta and the large arteries •Mönckeberg sclerosis: calcific deposits in the media of middle-sized arteries in persons >age 50 •Arteriolosclerosis: involves the small arteries and arterioles in association with hypertension or diabetes ATHEROSCLEROSIS Multifactorial, slowly progressive chronic degenerative-inflammatory disease of the aorta and the large arteries, such as • coronary arteries • circle of Willis • popliteal and tibial arteries Significance: > 50% of all death is attributed to atherosclerosis in well-developed countries Morphology Gross • Atheromatous plaque (pathognomic) - raised white-yellow lesion in the intima, protruding into the lumen • Large plaques in the aorta (> 2 cm) contain a yellow, grumous debris (”atheroma” - Greek word for gruel) Atheromatous plaque in the middle cerebral artery: raised white-yellow lesion in the intima, protruding into the lumen (formol-fixed brain) Aorta: the plaques contain a yellow, grumous debris (arrow) Structure of atheroma on LM • Intimal lesion • Central lipid core • Fibrous ”cap” subendothelially Central lipid core composed of lipids, cholesterol clefts, necrotic debris + calcium-salts, surrounded by foamy macrophages, T-lymphocytes, fibroblasts, small capillaries, and collagens and proteoglycans Types of plaques • Vulnerable plaques have large atheromatous cores, increased inflammatory cell content and thin fibrous caps high risk of rupture thrombosis • Stable plaques have minimal atheromatous cores and inflammation and thick fibrous caps 70% stenosis (critical stenosis) chronic ischemia distally Vulnerable plaque in the coronary artery Inflammatory infiltrates and capillaries around the lipid core. Lumen Intima Media Pathogenesis Response to chronic endocardial injury hypothesis • Cholesterol can’t dissolve in the blood. It is transported through the bloodstream by lipoproteins. • Low density lipoprotein (LDL) carries cholesterol to plaques (“bad cholesterol”). • High density lipoprotein (HDL) mobilizes cholesterol from plaques and transports it to the liver for biliary excretion (“good cholesterol”). Pathogenesis Response to chronic endocardial injury hypothesis Modifiable major risk factors • LDL-hypercholesterolemia (“bad cholesterol”) • Diabetic milieu (hyperglycemia plus dyslipidemia: trigliceridemia and reduced HDL-cholesterol [“good cholesterol”]). • Obesity • Hypertension • Smoking • Reduced physical activity Nonmodifiable risk factors • Male gender (in women, atherosclerosis is not significant before menopause) • Increasing age • Family history Pathogenesis Chronic endothelial injury due to risk factors, turbulence at branch points and other factors • Endothelial dysfunction: insudation of LDL- cholesterol into the intima + migration of monocytes into the intima + adhesion of platelets to the endothelial layer (PDGF ) • Transformation of monocytes to macrophages (GFs ) • Smooth muscle cell precursors (SMCPs) appear in the intima from the media and the circulation • Macrophages oxidate and engulf LDL-cholesterol foamy macrophages: GFs • SMCPs transform into fibroblasts collagens and other ECM material are produced • Vitious circle Course of atherosclerosis • Starts in teenagers/young adults • Insidious development of plaques within 15- 35 years • Clinical disease manifests as consequence of plaque complications in the age between 45-65 ys • Course of atherosclerosis • Starts in teenagers/young adults • Insidious development of plaques within 15- 35 years • Clinical disease manifests as consequence of plaque complications in the age between 45-65 ys • Sudden death can be the first manifestation of atherosclerosis Plaque complications • Rupture, ulceration of the luminal surface thrombus formation In arteries: within approx. 4 hours, complete occlusion of the lumen tissue ischemia, then infarction distally In aorta: mural thrombi Coronary occlusion due ulceration of the plaque leading to thrombosis Plaque complications • Rupture, ulceration of the luminal surface • Hemorrhage into a plaque sudden expansion of the plaque or plaque rupture • Cholesterol microembolism. Rupture of large plaques can discharge debris into the blood • Calcification destruction of elastic fibers in tunica media of aorta • Plaques compress the tunica media atrophy of aortic wall thinning aneurysmal dilation CONSEQUENCES OF ATHEROSCLEROSIS 1. Coronaries • Rupture of vulnerable plaques thrombosis: sudden cardiac death or acute myocardial infarction • Slow progression of stable plaques chronic myocardial ischemia congestive heart failure 2. Circle of Willis Thrombosis in middle cerebral artery – cerebral infarct contralateral hemiplegia, prolonged bed rest • Thrombosis in basilar artery – death • Thrombosis of internal carotid artery - cerebral infarct - no consequence, if the circle of Willis functions well Cerebral infarct involving the internal capsule contralateral hemiparesis 3. Aorta Most severe lesions in the abdominal aorta • Mural thrombi embolism in the lower extremities • Thinning of aortic wall aneurysm rupture: may lead to lethal bleeding • Plaque rupture cholesterol microembolism, renal failure Abdominal aorta: mural thrombi Celiac artery Superior Renal artery mesenteric artery Cholesterol microembolism in the arcuate artery of the kidney 4. Superior mesenteric artery Thrombosis of a vulnerable plaque at the orifice: infarction of small bowels death Thrombosis of sup. mesenteric artery: bowel infarction 5. Unilateral renal artery stenosis at the orifice - renovascular hypertension 6. Arteries of lower extremities • Stenosis: intermittent claudation (clinical diagnosis for pain in the calf muscles, which occurs during exercise and is relieved by short period of rest) • Complete occlusion: gangrene of leg LDL-hypercholest- Smoking Physical erolemia inactivity ATHEROSCLEROSIS Myocardial Cerebral Leg infarction infarction gangrene ATHEROSCLEROSIS Obesity Diabetes Hypertension Note: Prophylacticallly administered platelet aggregation inhibitors reduce the incidence of myocardial and cerebal infarction. ANEURYSMS OF AORTA • Aneurysm: circumscribed dilation of aorta, arteries • True aneurysm: bounded by all three vessel wall layers (intima, media, and adventitia); the layers can be individually attenuated • False aneurysm: extravascular hematoma that communicates with the intravascular space, part of the vessel wall is destructed Abdominal aortic aneurysm • Usually in smoking men older than age 50 • Wall thinning through medial destruction secondary to atheromatous intimal plaques • Between the renal arteries and the aortic bifurcation • Can be - saccular (saclike bulging on one side of the artery) - fusiform (symmetrical spindle shaped) - up to 15 cm in diameter and 25 cm in length Complications • Mural thrombi impair blood flow to the renal, mesenteric, vertebral, or iliac arteries ischemia of the kidneys, bowels, spinal cord, or legs • Embolism acute obstruction, usually in the leg(s) culminating in gangrene • Expansion compression of an ureter or erosion of vertebrae • Rupture (above 5 cm) often fatal retroperitoneal or peritoneal bleeding Ruptured aneurysm of abdominal aorta leading to retroperitoneal bleeding and shock (the probe indicates the rupture) Iliac arteries Therapy Surgical, either by open placement of tubular prosthetic grafts or with endoluminal insertion of stented grafts Thoracic aortic aneurysm Etiologic factors include • hypertension • + atherosclerosis • + poor intrinsic quality of the vessel matrix associated with elastic tissue loss Consequences • Aortic root dilation: aortic valve insufficiency • Compression of esophagus: dysphagia airways: dyspnea recurrent laryngeal nerves: persistent cough • Rupture: hemothorax, and death Saccular aneurysms in the thoracic aorta. Note mural thrombi DISSECTION OF AORTA •A dissection occurs when blood enters the aortic wall and separates the various layers •The most common catastrophe of the aorta Pathogenesis •Insidious degeneration of the tunica media •Mainly in men aged 40 to 60, who are often hypertensive •Younger individuals with connective tissue disorder that give rise to abnormal aortic extracellular matrix (e.g., Marfan’s sy: mutation in the fibrillin-1 gene progressive loss of elastic tissue matrix) LM of media degeneration: fragmentation and loss of elastic fibers, formation of cleft-like spaces filled with ECM material Alcian blue Elastin Consequences • Spontaneously developing long tears in the intima forceful separation of the intima from the media by the blood, extending toward the heart or the descending aorta • Most frequent site of tears: the first 10 cm of the aortic arch, measured from the aortic valve • Rupture of the adventitia: hemopericardium and cardiac tamponade or hemothorax Dissection of aorta: intimal tear Dissection of aorta, hemopericardium Clinical features • Sudden onset of excruciating pain, usually beginning in the anterior chest, radiating to the back, and moving downward as the dissection progresses • Lethal if surgical treatment is not available REGULATION OF BLOOD PRESSURE (BP; for details see pathophysiology) • BP is determined by the cardiac output and the vascular resistance • Cardiac output is determined by heart rate and stroke volume. The determinant of stroke volume is the filling pressure which is regulated through renal sodium excretion or resorption • Vascular
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