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Aneurysms & dissection 7

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  • 1. Aneurysms and DissectionsAneurysm: A localized abnormal dilation of a blood vesselor wall of heart. When aneurysm is bounded by arterial wallcomponents or attenuated wall of heart calledtrue aneurysm. Atherosclerotic, syphilitic, and congenital vascularaneurysms and left ventricular aneurysm that canfollow a myocardial infarction are true aneuryms.
  • 2.  False aneurysm (also called pseudoaneurysm) isa breach in vascular wall leading to extravascularhematoma that freely communicates withintravascular space (pulsating hematoma ). The most common false aneurysms are: Post-myocardial infarction rupture. Leak at junction (anastomosis) of vascular graftwith natural artery.
  • 3. Dissection: Arises when blood enters the wall of artery asa hematoma and dissecting between its layers . Dissections may, but do not always, arise inaneurysmal arteries. Both true and false aneurysms, also dissections,can rupture.Causes of Aneurysm: The two most important causes ofaortic aneurysms are:o Atherosclerosis.o Cystic medial degeneration of arterial media.
  • 4.  Other causes include:o Trauma: traumatic aneurysms or arteriovenousaneurysms.o Congenital defects such as berry aneurysms:small spherical dilatations most frequentlyoccur in brain.o Infections (mycotic aneurysms).o Syphilis.o Systemic diseases: in some vasculitides.
  • 5.  Aneurysms can be classified by shape and size :-o Saccular aneurysms: spherical and vary in sizefrom 5 to 20 cm , often partially or completelyfilled by thrombus.o Fusiform aneurysms: involving a long segment,many involve the entire ascending and transverseportions of aortic arch.o These shapes and sizes are not specific for anydisease or clinical manifestations.
  • 6. ABDOMINAL AORTIC ANEURYSMS ( AAA ):Atherosclerosis is the most frequent etiology.Morphology:o Usually positioned below renal arteries and abovebifurcation of aorta.o Saccular or fusiform.o Prime sites for formation of athero emboli.
  • 7. Arteriograph showing abdominal aortic aneurysm
  • 8. Gross appearance of abdominal aortic aneurysm
  • 9. Pathogenesis: AAAs rarely develop before age 50 andare more common in men. There is a genetic susceptibility to AAA beyondthe genetic predisposition to atherosclerosis. As in Marfan syndrome: genetic defects inconnective tissue component which isresponsible for strength of aorta .
  • 10.  An altered balance of collagen degradationand synthesis mediated by local inflammatoryinfiltrates and destructive proteolytic enzymesthey produce and regulate. In this regard, matrix metalloproteinases (MMPs)in macrophages implicated in development ofaortic aneurysms through increased proteolysisof extracellular matrix proteins.
  • 11.  These enzymes have capacity to degrade allcomponents of EC matrix in arterial wall (collagens,elastin, proteoglycans, laminin, fibronectin). Decreased level of tissue inhibitor ofmetalloproteinases (TIMP) also reported inaortic aneurysms.
  • 12. Clinical Course: Rupture into peritoneal cavity or retroperitonealtissues with massive fatal hemorrhage. Obstruction of vessel (iliac, renal, or mesenteric)leading to ischemic tissue injury. Embolism from atheroma or mural thrombus. Impingement on adjacent structures such ascompression of ureter, or erosion of vertebrae. Presentation as an abdominal mass (often pulsating)that simulates a tumor.
  • 13. SYPHILITIC (LUETIC) ANEURYSMS : Obliterative endarteritis, characteristic oftertiary stage of syphilis (lues), showspredilection for small vessels. Syphilitic involvement of vasa vasorum ofthoracic aorta can lead to aneurysmal dilation. Thoracic aortic aneurysms can give rise to signsand symptoms:1. Respiratory difficulties: due to encroachment onlungs and airways.
  • 14. 2. Difficulty in swallowing: due to compressionof esophagus.3. Persistent cough: due to irritation of or pressureon recurrent laryngeal nerves.4. Pain: caused by erosion of bone (ribs and vertebralbodies).5. Cardiac disease: aortic valve dilation with valvularinsufficiency, or narrowing of coronary ostiacausing myocardial ischemia.6. Rupture.
  • 15. Morphology: Inflammatory involvement begins in aortic adventitia,particularly involving vasa vasorum. Inducing obliterative endarteritis rimmed byan infiltrate of lymphocytes and plasma cells(syphilitic aortitis). The narrowing of lumina of vasa causes ischemicinjury of aortic media, with patchy loss of medialelastic fibers and muscle cells, followed byinflammation and scarring.
  • 16.  With destruction of media, the aorta loses itselastic recoil and become dilated. Luetic aortitis may also cause aortic valve ringdilation resulting in valvular insufficiency, Through stretching of valve cusps, widening ofcommissures, and thickening and rolling of freemargins. Owing to aortic insufficiency, left ventricular wallcan undergo volume overload hypertrophy,sometimes to 1000 gm (three times normal weight),referred to (cows heart).
  • 17. Figure 1: A large swelling on left sideof anterior chest wall.Figure 2: Chest roentgenogram showingwidening of mediastinum witha radiopaque mass extending into superiormediastinum occupying left upper andmid-zone with right tracheal shift.
  • 18. Figure 3: Three-dimensionalreconstructive image ofcardiac angiogram showinganeurysm of arch of aortaand ascending aortaindicated by arrows.Figure 4: Elastic Van-Gieson stain showingwall of aneurysm composed of fibrohyalinetissue with fragmented elastic fibers .
  • 19. AORTIC DISSECTION (DISSECTING HEMATOMA) : Dissection of blood between and along laminarplanes of media, with formation of blood-filledchannel within aortic wall which often rupturesoutward causing massive hemorrhage. Aortic dissection may or may not be associatedwith marked dilatation of aorta. For this reason the older term "dissecting aneurysm"is discouraged.
  • 20.  Aortic dissection occurs principally intwo groups of patients:o More than 90% occur in men between agesof 40 and 60 with antecedent hypertension.o The second major group of patients,usually younger, has a systemic or localizedabnormality of connective tissue that affectsaorta (Marfan syndrome).
  • 21.  Dissection can also be iatrogenic,as a complication of arterial cannulation(during diagnostic catheterization orcardiopulmonary bypass). Rarely, for unknown reasons, dissection of aortaor its branches including coronary arteriesoccurs during or following pregnancy
  • 22. Morphology: Detectable aortic wall pathology is not alwayspresent in dissection. The most frequent histologically detectable lesionis medial degeneration (cystic medial degeneration). Characterized by elastic tissue fragmentation andseparation of elastic and fibro muscular elementsof tunica media by small cleft like spaces. These are not truly "cysts“.
  • 23.  Thus, the term "cystic medial necrosis" is inaccuratebecause neither necrosis nor cysts are present. Inflammation is absent.This aortic dissection occurred just abovethe aortic root in a patient with Marfanssyndrome.
  • 24. Microscopically, the tear (arrow) in this aorta extends through the media,blood also dissects along the media (asterisk).
  • 25. Pathogenesis: Hypertension is the major risk factor , but itscontribution to aortic medial damage is uncertain. Some dissections are related to inherited connectivetissue disorders (Marfan syndrome) an autosomaldominant disease of connective tissue fibrillincharacterized by skeletal, cardiovascular, andocular manifestations. The cause of spontaneous dissections not associatedwith hypertension or genetic disorders is unknown.
  • 26. Clinical Course: Depend strongly on level of aorta affected. Classified into two types :o More common (more serious ) proximal lesions:involving either ascending portion only, or bothascending and descending aorta (type A).o Distal lesions: not involving ascending part andusually occur distal to subclavian artery (type B).
  • 27.  The classic clinical symptom is sudden onset ofexcruciating pain, beginning in anterior chest,radiating to back, and moving downward asdissection progresses. This intense pain can be confused with that ofacute myocardial infarction. The most common cause of death is rupture ofdissection outward into any of three body cavities(pericardial, pleural, or peritoneal).
  • 28.  Retrograde dissection into aortic root can causedisruption of aortic valvular apparatus. Extension of dissection into great arteries of neck ;or into coronary, renal, mesenteric, or iliac arteries,causing critical vascular obstruction. Compression of spinal arteries may causetransverse myelitis. Aortic dissection was usually fatal.