1. Keep Smiling….! “ It will help you to grow up in greater happiness & Love for each other. Mother Teresa Roman Catholic Missionary

2. Chapter 11 Blood vessels

3. TOPICS Vascular wall responses Congenital Anomalies Atherosclerosis Arteriosclerosis Hypertension Aneurysms Vasculitides Raynaud “phenomenon” Veins Lymphatics Tumors Interventions

4. Taking blood to the tissues and back Arteries, Arterioles, Capillaries, Venules, Veins,

5. NORMAL VESSELS Arterial walls are thicker than veins To accommodate pulsatile flow and higher blood pressures.

6. ARTERIES – WALLS ARE THICKER DUE TO GREATER SMOOTH MUSCLE, HENCE STRONGER & CAN WITHSTAND HIGH PRESSURE

7. Structure of blood vessels Tunica intima – Endothelium and connective tissue Tunica media – Smooth muscle and elastic tissue Tunica externa or tunica adventitia – Connective, nerve fibers and vasa vasorum 7

9. Arteries Large arteries or elastic arteries – Aorta and its branches, subclavian, common carotid artery, pulmonary artery Ileac artery Medium arteries are muscular arteries Coronary and renal arteries. Small arteries and arterioles are With in tissue and organs.

10. Arterioles are the main unit in regulating the systemic arterial Blood pressure

11. Capillaries Only a single layer of endothelium and a basement membrane and no media Connect arterioles and venules Exchange of diffusible substances between blood and tissues. Capillary network of most tissues are high and Myocardium has highest density of capillaries. 11

13. Veins Relatively thin; less elastic Larger in diameter than arteries Have valves to prevent backflow of blood Flow to heart is assisted by contraction of skeletal muscles.. 13

14. veins are more prone to dilation, compression, and easy penetration by tumors and inflammatory processes.

15. Lymphatics are thin-walled, endothelium-lined channels that drain excess interstitial tissue fluid eventually returning it to blood via the thoracic duct. Lymphatic make pathway for the spread of the disease by transporting bacteria and also tumor cells to distant sites.

16. The main cellular components of the walls of vessels are: 1) endothelial cells 2) smooth muscle cells 3)ECM including elastin, collagen, and glucosamine glycans

17. 1)Endothelial cells: a)Maintenance of permeability barrier. b)Elaboration of,anticoagulant,antithrombotic and fibrinolytic regulators. c)Elaboration of prothrombotic molecules., VWF, Tissue factor, Plasminogen activator

18. d) Regulation of inflammation and immunity e) Extracellular matrix production f)Regulation of cell growth Growth stimulators, PDGF,FGF Growth inhibitors, TGF beta, heparin

19. The term endothelial dysfunction is defined as an altered phenotype that impairs vasoreactivity or induces a surface that is thrombbogenic or abnormally adhesive to inflammatory cells, is responsible for initiation of thrombus formation,

20. Endothelial activation. The EC responds to various patho physiological stimuli by adjusting their usual functions and expressing newly acquired properties is called as Endothelial activation.

21. Inducers 1.cytokines and bacterial products 2.advanced glycosylation of end products (involved in pathogenesis of diabetes) 3. viruses, 4.complement components 5.hypoxia 6.Lipid products. 7.Hemodynamic forces.

22. Activators Activated endothelial cells also elaborate adhesion molecules, other cytokines and chemokines, growth factors, molecules of the major histocompatibility complex (MHC), procoagulant or anticoagulant factors and vasoactive molecules that are involved either in vasoconstriction or in vasodilatation.

23. Smooth muscle cells are capable:  to mediate vasoconstriction,  to mediate vasodilatation, by  to synthesize the collagen, elastin, and proteoglycans,  to elaborate the growth factors and cytokines,  to proliferate, and to migrate to the intima. They play important role in normal vascular repair and atherosclerosis.

24. Smooth muscle cell Promoters PDGF Endothelin, Inter ferongama FGF and thrombin Inhibitors, NO, TGF beta Heparn sulfate, Angiotensin II, Catecholamines

25. Diseases of arterias A) Congenital anomalies B) Atherosclerosis C) Hypertensive vascular disease D) Inflammatory disease – Vasculitis E) Raynaud disease F) Aneurysms a dissections

26. Congenital anomalies AVM (Arterio Venous malformations) Abnormal communication between the high pressure arteries and low pressure veins. Usually congenital but acquired by trauma or inflammation. Most often described in Brain as AVM Asymptomatic or hemorrhage or pressure effect.

27. Berry Aneurysm Saccular dilation typically found around the circle of Willis and base of the brain. Risk factors Normal hemodynamic stress Presence of HT of any cause Coarctation of aorta Atherosclerosis Associated with Polycystic kidney disease

29. Most common causes of Subarachanoid hemorrhage Berry aneurysm rupture. Extension of traumatic hematoma hypertensive intracranial hemorrhage into ventricular system.

30. Berry aneurysm

31. Fibromuscular dysplasia -  leads to -renal artery stenosis Common in females and younger age group. pathogenesis--Fibrous or Fibromuscular thickening of the media and intimal layers due to hyperplasia and fibrosis.

32. The lesions leads to constriction or series of narrowing the middle or distal portion of the renal artery and may be bilateral involvement Clinical features- Essential hypertension Renal artery bruit in some cases Lab-elevated level of Plasma Renin Treatment –Good response to ACE inhibitors

35. Diseases of arterias. ARTERIOSCLEROSIS(Hardening of the arteries) It is a generic term for three patters of vascular disease that have in common thickening and loss of elasticity of arterial walls: 1) Atherosclerosis – characterized by the formation of intimal fibrous plaques that often have a central core rich in lipid (fibrofatty plaques)..

36. Monckeberg medial calcific sclerosis 2.Monckeberg arteriosclerosis (medial calcific sclerosis) involves the media of medium sized muscular arteries, most typically the radial and ulnar arteries, persons older than 50 years of age. It does not obstruct arterial flow because the intima is not involved.

37. This is Monckeberg's medial calcific sclerosis, which is the most insignificant form of arteriosclerosis. Note the purplish blue calcifications in the media; note that the lumen is unaffected by this process. Thus, there are usually no real clinical consequences.

39. a. Ring-like calcifications in the media of the arteries are characteristic. b. Stiff, calcific "pipestem" arteries. Common in elderly person,

40. 3.Arteriolosclerosis Hardening of the small arteries and arterioles especially in the kidneys and usually associated with Hypertension /diabetes mellitus. Two variants are 1.Hyaline arteriolosclerosis 2.Hyperplastic arteriolosclerosis

41. Hyaline Arteriolosclerosis This vascular lesion consists of a homogeneous pink hyaline thickening of the walls of arterioles with loss of underlying structural detail and with narrowing of the lumen. Present in Elderly patients, whether normo tensive or hypertensive, Patients with hypertension. It is also common as part of the characteristic of diabetes.(Benign nephrosclerosis)

42. Benign nephrosclerosis Sclerosis of renal arterioles and small arteries. Vessel wall thickening with narrowing of the lumen. Seen mainly in benign Hypertension and Diabetics, and old age individuals.

43. Benign nephrosclerosis

44. HISTOPATHOLOGY of ESSENTIAL HYPERTENSION “HYALINE” = BENIGN HTN. “HYPERPLASTIC” = MALIGNANT HTN. SYS>200 1) ONION SKIN 2) “FIBRINOID” NECR.

45. Hyperplastic Arteriolosclerosis Malignant hypertension200/120 mm Hg (typically, diastolic pressures over 120 mm Hg associated with acute cerebral and/or renal injury). Hyperplastic arteriolosclerosis is associated with "onion-skin," concentric, laminated thickening of the walls of arterioles with luminal narrowing. The laminations consist of SMCs and thickened, duplicated basement membrane.

46. In malignant hypertension, these hyperplastic changes are accompanied by fibrinoid deposits and vessel wall necrosis (necrotizing arteriolitis), particularly prominent in the kidney.

48. Malignant hypertension. This slide is a gross specimen showing multiple hemorrhages on the surface of the kidney. This is called a flea- bitten kidney...

51. HYPERTENSION High blood pressure Elevated blood pressure exceeding 140 over 90 mmHg -- a systolic pressure above 140 or a diastolic pressure above 90. Hypertensions is higher among blacks and older persons, especially older women.

52. Silent Killer – painless – dizziness, headache, and visual difficulties, It is the leading risk factor – MI, Stroke and R.F Responsible for the majority of office visits, Complications bring to diagnosis but late… Chronic, end organ & vascular damage

53. Classification www.nhlbi.nih.gov

54. Isolated Systolic Hypertension Systolic B.P more than 160 mm Hg and diastolic pressure less than 90 mmHg is called as systolic hypertension. SBP should be primarily considered during treatment and not just diastolic BP. Systolic BP is more important cardiovascular risk factor after age 50.

55. White coat hypertension BP recording in hospital or clinic is high. But recording the BP at home will remain normal. Labile HT- BP remain high at certain time of the day and remain normal. Malignant HT- Systolic BP higher than 200 and diastolic remain above 110 mm of Hg associated with papilledema, headache,

56. Regulation of BP: BP = Cardiac Output x Peripheral Resistance Endocrine Factors – Renin, Angiotensin, ANP, ADH, Aldosterone. Neural Factors – Sympathetic & Parasympathetic Blood Volume – Sodium, Mineralocorticoids, ANP Cardiac Factors – Heart rate & Contractility.

58. Renin  Angiotensin  Aldosterone AXIS (RAAS) If the perfusion of the juxtaglomerular apparatus in the kidneys decreases, then the juxtaglomerular cells release the enzyme renin.juxtaglomerular apparatuskidneysenzymerenin Renin cleaves an inactive peptide called angiotensinogen, converting it into angiotensin I.peptide angiotensinogenangiotensin I Angiotensin I is then converted to angiotensin II by angiotensin-converting enzyme (ACE), which is found mainly in lung capillaries.angiotensin II angiotensin-converting enzymelungcapillaries Angiotensin II is the major bioactive product of the renin-angiotensin system. Angiotensin II acts as an endocrine, autocrine/ paracrine, and intracrine hormone. endocrineautocrineparacrineintracrine

59. HYPERTENSION “ESSENTIAL” 95% “SECONDARY” 5%

60. Primary hypertension Also called essential or idiopathic hypertension 92- 95 % of all cases No specific cause identified Can happen with retention of sodium and water → increased blood volume. Also low dietary potassium, calcium and magnesium intakes 60

61. GENETIC vs.ENVIRONMENTAL GENETIC  UN-CONTROLLABLE ENVIRONMENTAL  CONTROLLABLE – STRESS – OBESITY – SMOKING – PHYSICAL ACTIVITY – NaCl INTAKE

62. Suspected causes Interaction of genetics and environment Overactivity of sympathetic nervous system Overactivity of renin / angiotensin/ aldosterone system Salt and water retention by kidneys And others 62

63. SECONDARY Renal Acute glomerulonephritis Chronic renal disease Polycystic disease Renal artery stenosis Renal artery fibromuscular dysplasia Renal vasculitis Renin-producing tumors Endocrine Adrenocortical hyperfunction (Cushing syndrome, primary aldosteronism, congenital adrenal hyperplasia, licorice ingestion) Exogenous hormones (glucocorticoids, estrogen [including pregnancy-induced and oral contraceptives], sympathomimetics and tyramine-containing foods, monoamine oxidase inhibitors) Pheochromocytoma, Acromegaly, Hypothyroidism (myxedema), Hyperthyroidism Pregnancy-induced Cardiovascular : Coarctation of aorta, Polyarteritis nodosa (or other vasculitis) Increased intravascular volume MISC: Increased cardiac output, Rigidity of the aorta, Neurologic, Psychogenic, Increased intracranial pressure, Sleep apnea, Acute stress, including, surgery

64. GENETIC ACQUIRED

67. Complications of hypertension CVS-Left ventricular hypertrophy Myocardial infarction and Atherosclerosis CNS-Stoke Intracerebral hematoma due to charcot Bouchard aneurismal rupture Berry aneurysm  subarachnoid hemorrhage Lacunar infarct due to small infarcts due to hyaline arteriolosclerosis. Renal system-Benign nephrosclerosis Renal failure Eyes-Hypertensive retionopathy.

72. ATHEROSCLEROSIS Etiology/Risk Factors Pathogenesis Morphology Clinical Expression

73. ATHEROSCLEROSIS Atherosclerosis is characterized by intimal lesions called atheroma or atheromatous plaques, which protrude into and obstruct vascular lumens and weaken the underlying media.

74. Risk Factors for Atherosclerosis MajorMinor NON-modifiable Increasing ageObesity Male genderPhysical inactivity Family historyStress ("type A" personality) Genetic abnormalitiesPostmenopausal estrogen deficiency High carbohydrate intake Modifiable HyperlipidemiaAlcohol HypertensionLipoprotein Lp(a) Cigarette smokingHardened (trans)unsaturated fat intake DiabetesChlamydia pneumoniae

75. There are a number of other less well-established risk factors for atherosclerosis, including: – High serum homocysteine levels Homocysteine is derived from the metabolism of dietary methionine Homocysteine inhibits elements of the anticoagulant cascade and is associated with endothelial damage. – Elevated serum C-reactive protein It may increase the likelihood of thrombus formation; Inflammation marker;

76. – Infectious agents The presence of some organisms (Chlamydia pneumoniae, herpesvirus hominis, cytomegalovirus) in atheromatous lesions has been demonstrated by immunocytochemistry, but no cause-and-effect relationship has been established. The organisms may play a role in atherosclerotic development by initiating and enhancing the inflammatory response

77. PATHOGENESIS “atherosclerosis is a chronic inflammatory response of the arterial wall initiated by injury to the endothelium”. Lesion progression is due to interaction between modified lipoproteins, monocyte derived macrophages, T lymphocytes and normal cellular constituents of arterial wall

78. Main features of the injury hypothesis: 1.Chronic endothelial injury 2.Insudation of lipoproteins into the vessel wall mainly LDL with high cholestrol content…….then oxidation of lesional lipoprotein 3.Adhesion of blood monocytes & other leukocytes to the endothelium, & their migration into the intima & their transformation into macrophages & foam cells 4.Adhesion of platelets 5.Release of factors from activated platelets, macrophages or vascular endothelial cells that cause migration of SMCs from media into the intima. 6.Proliferation of SMCs in the intima, elaboration of extracellular matrix, leading to accumulation of collagen & proteoglycans. 7.Enhanced accumulation of lipids within macrophages & SMCs & extracellularly

81. Chronic endothelial “injury” Atheroma 1

82. Chronic endothelial injury Hypertension Hyperlipedemia Homocysteine Smoking Viruses Toxins Hemodynamic factors Immune reactions

83. Endothelial dysfunction Monocyte adhesion and emigration 2 Atheroma

84. Macrophage activation Smooth muscle recruitment 3 Atheroma

85. Macrophages and smooth muscle cells engulf lipid Atheroma

86. Accumulation of lipoproteins Increase in the level of LDL Decrease in the levels of HDL Increase in the Lipoprotein (a) Other conditions that affect the circulating lipids 1.Nephrotic syndrome Hypothyroidism Diabetes and Alcoholism

87. The mechanism of Hyperlipidemia contributing to Atherosclerosis Endothelial impairment by chronic hyperlipidemia by increasing O 2 free radicals production Deactivates Nitric oxide Impair vaso dilation Impair endothelial function Oxidize the LDL

88. Intimal SMC proliferation and ECM deposits convert a fatty streak into atheroma

89. Oxidative modification of LDL 1.Is important in atherogenic process. 2.Oxidized LDL is toxic to endothelial cells, 3.Responsible for endothelial injury 4.It is chemo tactic to monocytes and immobilizes the macrophges favoring their accumulation at the site. 5.It is taken up by macrophages and smooth muscle cells(Through scavenger pathway)

90. Fatty streak is the earliest lesion in Atherosclerosis.

91. 1.Fatty dots not raised, so do not cause obstruction to the flow Multiple, yellow, flat spots < than 1mm in diameter composed of lipid laden foam cells 2.Fatty streaks =coalesce of multiple fatty dots Elongated, 1 cms longer or more contain T- lymphocytes & extracellular lipid < than plaques Appear in aorta in some children younger than 1 year & all children older than 10years, 3.Fatty streaks may be precursor of plaque but not all fatty streaks are converted into fibrous plaque or more advanced lesions

92. The white arrow denotes the most prominent fatty streak in the photo, but there are other fatty streaks scattered over the aortic surface. Fatty streaks are the earliest lesions seen with atherosclerosis in arteries.

93. Fatty streaks

94. Common sites: 1.Abdominal aorta compared to thorasic aorta & lesions are more common around the ostia of major branches 2.Other common arteries in descending order after aorta is coronaries, popliteal, internal carotid & cicle of Willis 3.Vessels of the upper extremities are usually spared 4.Mesenteric & renal arteries are also spared but ostias can be involve

95. COMPONENTS OF ATHEROMATOUS PLAQUE (MP) 1.*Superficial fibrous cap is composed of SMCs & relatively dense collagen 2. *cellular zone containing, SMCs, macrophages, Lymphocytes (T cells) *Foam cells : are monocytes derived from blood & SMCs can also become foam cells 3.*Deep to the fibrous cap is central necrotic core, containing a disorganized mass of lipids( cholestrol& cholestrol esters) cholestrol clefts, debris from dead cells, foam cells, fibrin

96. 3.*Below & to the sides of cap ( shoulder) is a cellular area consisting of macrophages, SMCs, T lymphocytes 4.At the periphery area of neovascularization is present Generally plaque undergo remodelling ( degeneration, synthesis of ECM & organization of thrombus.

97. PLAQUE

98. American heart association classified ATH into six types or stages Type I – Fatty dots - Foam cells Type II – Fatty streak Type III – Intermediate stage (Extracellular lipid pool) Type IV – Atheroma – Core of lipid Type V – Fibroatheroma – Fibrotic layer Type VI – Complicated lesion ( Ulcer, Ca+ Hemorrhage, thrombus, embolism, aneurysm).

99. Atheroma Aorta:

101. Atheroma Coronary Artery: Calcification

102. COMPLICATIONS & clinical significance A) Advanced lesions of atheromas are vulnerable to following pathological changes:

103. Complications MI, Rupture or ulceration Erosion or thrombus formation Aneurysms Arrhythmias Cerebral infarct Renal infarct, Atheroembolism And Death

104. 1.Thrombosis & calcification 2.Emboli formation, cholestrol emboli or atheroemboli which are discharged into blood stream. 3.Rupture, ulceration, erosions. 4.Hemorrhage: due to rupture of fibrin cap or thin walled capillaries that vascularize the plaque & contained hematoma expand & rupture the plaque 5.Aneurysmal dilatation: Fusiform, dissecting, or berry etc., due to pressure or ischemic atrophy of media with loss of elastic tissue causing weakness & rupture.

105. This is severe atherosclerosis of the aorta in which the atheromatous plaques have undergone ulceration along with formation of overlying mural thrombus.

106. A coronary thrombosis is seen microscopically occluding the remaining small lumen of this coronary artery. Such an acute coronary thrombosis is often the antecedent to acute myocardial infarction.

107. The aorta shows a large atheroma. Cholesterol clefts are numerous in this atheroma. The surface shows ulceration and hemorrhage.

108. Prevention Three factors need improvement 1. life style, cigarette smoking 2.Reduced consumption of cholestrol & saturated animal fat & control of hypertension 3. Prevention of recurrences in those who have previously suffered from serious ATH related clinical events

110. PLAQUE DEPOSIT ORIGINAL DIAMETER

111. Mild fibrous plaques

112. Aneurysm An aneurysm is a localized abnormal dilation of a blood vessel or the heart. There are two types of aneurysm. 1.Trueaneurysm 2.False aneurysm

113. True Aneurysm When an aneurysm involves all three layers of the arterial wall (intima, media, and adventitia) or the attenuated wall of the heart.

114. False aneurysm (pseudoaneurysm) is a breach in the vascular wall leading to an extravascular hematoma that freely communicates with the intravascular space ("pulsating hematoma").

115. True Aneurysms Atherosclerotic. Syphilitic Congenital Ventricular aneurismal follow a MI False aneurysms 1.Post myocardial infarction rupture 2.Leak at the junction (anastomosis) of vascular graft with natural artery.

116. Fusiform – Spindle-shaped involving whole circumference can involve extensive portions of the aortic arch, abdominal aorta, or even the iliacs Saccular – Small segment of wall ballooning due to localized weakness – they vary from 5 to 20 cm in diameter and often contain thrombi.

118. Fusi form Saccular form

119. Risk factors – Smoking, – Hypertension, Hypercholesterolaemia

120. Most common causes of aneurysm Atherosclerosis Hypertension

121. Rare causes of aneurysms Congenital – Marfan’s syndrome, Berry aneurysms Post-stenotic – Coarctation of the aorta, Cervical rib, Popliteal artery entrapment syndrome Traumatic – Gunshot, stab wounds, arterial punctures Inflammatory – Takayaso’s disease, Behcet’s disease

122. Rare causes of aneurysms Mycotic – Bacterial endocarditis, syphilis Pregnancy associated – Splenic, cerebral, aortic, renal, iliac & coronary

123. Aortic Aneurysms Laplace’s Law Tension varies directly with radius when pressure is constant T = P x R T - Tension P - Pressure R - Radius

124. Aortic Aneurysms Decrease in elastin and collagen in arterial wall Elastin becomes fragmented-->arterial elongation and dilatation Increase in the collagenase and elastase activity.

126. Pathogenesis 1.The intrinsic quality of the vascular wall connective tissue is poor Eg. Marfan syndrome Loeys Deitz syndrome Ehlers Danlos syndrome

127. 2.The balance of collagen synthesis and degradation is altered by inflammatory. Infiltration and destructive proteolytic enzymes. Increased production of MMP by macrophages in atherosclerosis or vasculitis Also decreased in tissue MMP inhibitors

128. 3.The vascular wall weakened through loss of smooth muscle cells. Hypoxia due to athermanous plaque and leads to ischemia and HT in turn leads to smooth muscle loss and scarring and decreased synthesis of ECM and increased amount of gycosaminoglycons called as cystic medial degeneration seen in Marfan syndrome and scurvy.

129. Most abdominal aortic aneurysms (AAA) occur between the renal arteries and the bifurcation of the aorta

130. Abdominal Aortic Aneurysm Atherosclerosis, the most common cause of aneurysms, causes thinning and weakening of the media secondary to inti.mal plaques Site-. Atherosclerotic aneurysms occur most frequently in the abdominal aorta (abdominal aortic aneurysm, often abbreviated AAA), but the, Associated with iliac aneurysms in 30% Associated with popliteal aneurysms in 10% can also be involved

131. Pathogenesis AAA More frequently in men and rarely develops before age 50.Male to female (4:1) since the incidence is less than 5% in men older than 60 years,

132. Two AAA variants Inflammatory AAAs are characterized by dense periaortic fibrosis containing abundant lympho plasmacytic infiltrate with many macrophages and often giant cells. Their cause is uncertain.

133. Mycotic AAAs are atherosclerotic lesions infected by lodging of circulating microorganisms in the wall, particularly in the setting of bacteremia from a primary Salmonella gastroenteritis. In such cases, suppuration further destroys the media, potentiating rapid dilation and rupture.

134. Clinical features of AAA Asymptomatic in 75% – Incidentally discovered during clinical exam.or radiographic investigation Pain – Central abdominal radiating to the back – Chronic due to stretching the vessel wall or compression/erosion of surrounding structures – Acute pain due to rupture

135. Clinical features of AAA Asymptomatic in 75% – Incidentally discovered during clinical exam.or radiographic investigation Pain – Central abdominal radiating to the back – Chronic due to stretching the vessel wall or compression/erosion of surrounding structures – Acute pain due to rupture

136. Clinical features The clinical features depend on the consequences of the AAA Rupture into peritoneal cavity leads to fatal hemorrhage Obstruction into the branch leads to ischemic injury Embolism

137. Compression of the adjacent structures like ureter or vertebral erosion The risk of rupture depends upon the sizes a abdominal mass.

138. 1.0 to 1%/year if aneurysm size is less than 4 cm in diameter. 2.11% /year if aneurysm is 5 to 5.9 cm in diameter. 3.25%/year if aneurysm is more than 6 cm. Most aneurysm expand 0.2 to 0.3 c,/year.

139. Complications 1.Rupture into the peritoneal cavity or retroperitoneal tissues with massive hemorrhage. 2.Obstruction of the vessel(Mainly iliac, renal, mesentric) 3.Embolism from the atheroma 4.Pressure effect on adjacent structure (ureter or erosion of the vertebra) 5.present as a abdominal mass.

140. Syphilitic ( luetic) aneurysm. This aneurysm is a manifestation of tertiary syphilis, which has become rare with better treatment and control of the disease. It is caused by syphilitic aortitis, which is characterized by obliterative endarteritis of the vasa vasorum and necrosis of the media. Grossly, these changes result in a "tree-bark" appearance

142. The narrowing of the lumina of the vasa vasorum causes ischemic injury of the aortic media, with patchy loss of the medial elastic fibers and muscle cells, followed by inflammation and scarring, the aorta loses its elastic recoil producing an aneurysm. Contraction of fibrous scars may lead to wrinkling of intervening segments of aortic intima, grossly reminiscent of "tree bark."

143. Unlike atherosclerotic aneurysms, syphilitic aneurysms characteristically involve the ascending aorta. Dilation of the ascending aorta may widen the aortic commissures, leading to aortic valve insufficiency

144. FTA –ABS test FTA –ABS test reads Syphilis infection, Important to remember in a patient with Aortic aneurysm mainly thoracic or ascending aorta involved in Syphilitic aortitis

145. THORACIC ANEURYSMS – Hypertnesion is common cause – Marfan syndrome and loeys Dietz syndrome – Encroachment – Respiratory difficulties – Dysphagia – Cough – Pain – Aortic valve dilatation – Rupture

146. DISSECTION

147. Aortic Dissection Blood splays apart the laminar planes of the media to form a blood-filled channel within the aortic wall this channel often ruptures through the adventitia and into various spaces, where it causes either massive hemorrhage or cardiac tamponade

149. (1) men aged 40 to 60 years, with antecedent hypertension (more than 90% of cases of dissection), and (2) younger patients with systemic or localized abnormalities of connective tissue affecting the aorta. 3.Iatrogenic following catheterization or bypass surgery. 4.During and after pregnancy.

150. Hypertension is the major risk factor. There is medial hypertrophy of the vasa vasorum. Degenerative changes in the aortic media Loss of smooth muscle cells The medial weakness trigger the intimal tear. There is cystic medial degeneration.

151. Level of the aorta affected The more common (and dangerous) proximal lesions (called type A dissections), involving either the ascending aorta only or both the ascending and descending aorta. Distal lesions not involving the ascending part and usually beginning distal to the subclavian artery Type B.

153. . Stanford classification type A - A affects ascending aorta and arch – accounts for ~60% of aortic dissections – surgical management – may result in: – Aortic incompetence coronary artery occlusion rupture into pericardial sac with resulting cardiac tamponade

154. TYPE B - begins beyond brachiocephalic vessels – accounts for ~ 40% of aortic dissections – dissection commences distal to the left sub- clavian artery – medical management with blood pressure control.

156. CLINICAL FEATURES The classic clinical symptoms of aortic dissection are the sudden onset of excruciating pain, usually beginning in the anterior chest, radiating to the back between the scapulae, and moving downward as the dissection progresses; the pain can be confused with that of myocardial infarction.

157. The most common cause of death is rupture of the dissection into body cavities (i.e., pericardial, pleural, or peritoneal). Retrograde dissection into the aortic root can cause disruption of the aortic valvular apparatus. cardiac tamponade, aortic insufficiency, myocardial infarction

158. Extension of the dissection into the great arteries of the neck or Into the coronary, Renal, Mesenteric, or Iliac arteries