Aneurysms of Aorta
•   Defined as abnormal localized dilatation of a blood vessel or wall of the heart.
•   True Aneurysms: Bound by arterial wall or heart.
•   False Aneurysms: Breach in wall of vessel, extravascular hematoma,
    connection with lumen is retained, pulsating hematoma e.g. post myocardial
    infarction rupture.
•   Aneurysms are most important clinically when involve aorta.
•   Two most important causes of aortic aneurysms are atherosclerosis and cystic
    medial degeneration. However any artery may be involved by this condition if
    wall gets weakened due to: trauma, congenital defects (Berry An), infections
    e.g. Mycotic, Syphilis, Systemic diseases like vasculitis.
•   Mycotic aneurysms: Due to septic embolization and weakening e.g. infective
    endocarditis, due to extension from adjacent process and by circulating
    organisms infecting the wall directly.
•   Macroscopic types: Saccular, are spherical involving a portion of wall, 5-20
    cm, partially or completely filled with thrombus. Fusiform, may involve up to
    20 cm of the aortic wall.
Abdominal Aortic Aneurysms
• Atherosclerosis in men above 50 years of age the most
  frequent cause which destroys the underlying tunica media
  thereby weakening the wall.
• Abdominal aorta is most frequently affected, other parts
  including arch of aorta, common iliac arteries and thoracic
  aorta are also affected with less frequency.
• Part of abdominal aorta most commonly involved is below
  the origin of renal arteries.
• Aneurysm is usually fusiform measuring 15 x 25 cm.
• Mural thrombosis is frequent which may be complete and
  may involve the lumen partially. Aortic aneurysms may
  also be accompanied by similar lesions in iliac arteries.
• Occasionally the origins of renal and superior mesenteric
  artery may also be affected directly or by thrombosis. The
  atheromatous lesions in the aneurysms are ulcerated with
  mural thrombi. Atheroemboli can lodge in the vessels of
  kidneys or lower extremities.
• Variants: two variants. 1- Inflammatory: characterized by
  dense periaortic fibrosis containing an abundant
  lymphoplasmacytic infiltration, many giant cells and
  macrophages. Cause is uncertain.
• 2- Mycotic abdominal aneurysm: Aortic atherosclerotic
  aneurysms infected by deposition of circulating organisms
  in the wall, particularly salmonella gastroenteritis. This
  leads to suppuration and further destruction of media.
Pathogenesis of Aneurysms.
• Atherosclerosis along with other factors in men above 50
  years of age.
• Have been showing to be familial, in addition to the
  familial factors responsible for atherosclerosis and
  hypertension..
• Genetic defects e.g. Marfans syndrome in structural
  components of aorta can also cause aneurysms and
  dissections.
• There is evidence that matrix metalloproteins and
  plasminogen activators, which degrade extracellular matrix
  contribute to aneurysm formation.
Clinical Features
•   Depend on location and size.
•   Rupture into body cavities with massive hemorrhage.
•   Occlusion of a branch vessel.
•   Embolism from thrombosis or atheroma.
•   Compression of surrounding structures, e.g. ureter.
•   Presentation as abdominal mass.
Syphilitic Aneurysms
• Tertiary syphilis is marked by cardiovascular and nervous
  system complications.
• Endarteritis obliterans involves small muscular arteries and
  arterioles; most devastating when it involves the vasa
  vasorum of aorta which can lead to aneurysm of thoracic
  aorta along with dilatation of aortic annulus.
Morphologic Features.
• Medial destruction is the key process in tertiary syphilis.
• Inflammatory process starts in the aortic adventitia, esp.
  vasa vasorum, surrounded by lymphoplasmacytic
  infiltration.
• There is ischemic injury to aortic media, patchy loss of
  elastic tissue and smooth muscle cells followed by
  inflammation and later on scarring.
• Aorta loses its elastic support, becomes dilated.
• Luetic involvement of aorta favors superimposed
  atherosclerosis inducing further florid atheromatosis.
• Location in thoracic aorta an differentiate the luetic
  aneurysms from those purely due to atherosclerosis.
• Luetic aortic aneurysms also cause, dilatation of aortic
  valve ring, producing aortic valve insufficiency, valves get
  damaged as well.
• Left ventricle becomes hypertrophied with consequent
  marked cardiomegaly (cor bovinum).
Clinical Features.
• Both types of aneurysms produce signs and symptoms due
  to:
• Encroachment on mediastinal structures.
• Respiratory difficulties.
• Swallowing difficulties.
• Persistent cough- recurrent laryngeal nerve.
• Pain following erosion of ribs and vertebral bodies.
• Cardiac disease.
• Rupture of aneurysm.
Aortic Dissections
• Aortic dissection is catastrophic disease, characterized by dissection of
  blood in between and along the laminar planes of media forming blood
  filled channel. Usually dilatation of aorta is minimal.
• Two groups of patients are affected e.g. men between 40-60 years in
  whom chronic hypertension, second group consists of younger persons
  having systemic or localized abnormality of connective tissue of aorta
  e.g. Marfans syndrome.
• Dissection may occur as complication of arterial catheterization.
• Arterial dissections may occur in aorta or coronaries during
  pregnancy, reason is unknown.
• Dissection is uncommon in advanced atherosclerosis due to scarring in
  the tunica media of aorta.
Morphologic Features.
• Starts mostly with intimal tear that occurs within 10 cm of
  aortic valve.
• Tears are usually 1-5 cm in length.
• Dissection may extend proximally or distally, may involve
  the aorta up to the iliacs and femoral artery.
• Spreads along with laminar planes, between outer and
  middle one third of the wall of aorta.
• The channel may again rupture in to the aorta through a
  secondary tear (double barrel aorta), this avoids fatal extra
  aortic rupture and fatal hemorrhage.
• Most common cause of death is rupture into one of the
  body cavities.
• Clinical manifestations may also be due to extension of the
  dissection to the origins of aortic branches, like coronary,
  renal, mesenteric or iliac arteries causing obstructions to
  vascular flow.
• Histologically the most frequent and detectable lesion is
  cystic medial degeneration. The lesions consist of elastic
  tissue fragmentation and separation of elastic and
  fibromuscular elements of tunica media that creates cleft
  like or cystic spaces filled with amorphous extracellular
  matrix. Inflammation is absent.
• Cystic medial degeneration is frequently found in patients
  with Marfans syndrome.
• Cystic medial degeneration is frequently found at autopsy
  in persons who had experienced no symptoms of
  dissection.
Pathogenesis
• Hypertension is the major risk factor, but contribution to
  CMD is uncertain, no good correlation between CMD and
  dissection.
• Some dissections are due to inherited connective tissue
  defects e.g. Marfans autosomal dominant disorder.
• Complications of Marfans syndrome include; aortic
  dissection, aortic and mitral valve prolapse; other
  manifestations include; skeletal and occular.
• The triggering factors for intimal tear and intramural
  hemorrhage is unknown. But once the process has started,
  hypertension plays an important role in the progression.
Clinical Features.
• Depend on level of aorta affected.
• Sudden onset of excruciating pain, beginning in the front
  of chest, radiating to back, can be readily confused
  clinically with that of acute myocardial infarction.
• The diagnosis may be based on various investigations,
  including angiography, two dimensional cardiac
  ultrasound, CT scan and MRI.
• Prognosis has recently improved due to development of
  surgical techniques.
Varicose Veins
• Varicose veins have narrowed or abnormally dilated
  lumina along with incompetence of valves leading to
  venous stasis. These are tortuous, dilated, elongated and
  scarred.
• Loss of support of vessel walls and increased intramural
  pressure.
• Leg veins are affected due to posture, so occupations are
  important in its aetiology.
• Prolonged erect posture also results in simple orthostatic
  oedema.
• Condition is more common over 50 years, obese people
  and during pregnancy.
Morphologic Features.
• There is marked variation in the thickness of the wall.
  There may be thrombosis and valvular deformities.
• Microscopically changes consist of variations in thickness
  of the wall caused by dilatations and compensatory
  hypertrophy of smooth muscle and subintimal fibrosis.
Clinical Features
• Venous stasis, congestion, oedema and thrombosis.
• Embolism is rare in contrast to deep vein thrombosis.
• Distension is painful.
• Persistent varicose veins produce oedema of legs along
  with trophic changes leading to stasis dermatitis and
  ulcerations.
• Varicose veins are also seen in lower esophagus, in
  patients of cirrhosis, due to portal hypertension.
Aneurysms and dissections
Aortic Dissection With Double Lumen
Aortic Dissection




 aortic dissecting aneurysm from intimal tear, blood clot present in the adventitial layer
 may accumulate in the thorax, causing hemothorax.
Intimal Tear in Aortic Dissection
Aortic Dissection
Aortic Dissection




 Aortic aneurysm dissecting into the muscular layer. The blood dissecting proximally may
 block the carotids and distally may shut the coronaries.

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Aneurysms and dissections

  • 1. Aneurysms of Aorta • Defined as abnormal localized dilatation of a blood vessel or wall of the heart. • True Aneurysms: Bound by arterial wall or heart. • False Aneurysms: Breach in wall of vessel, extravascular hematoma, connection with lumen is retained, pulsating hematoma e.g. post myocardial infarction rupture. • Aneurysms are most important clinically when involve aorta. • Two most important causes of aortic aneurysms are atherosclerosis and cystic medial degeneration. However any artery may be involved by this condition if wall gets weakened due to: trauma, congenital defects (Berry An), infections e.g. Mycotic, Syphilis, Systemic diseases like vasculitis. • Mycotic aneurysms: Due to septic embolization and weakening e.g. infective endocarditis, due to extension from adjacent process and by circulating organisms infecting the wall directly. • Macroscopic types: Saccular, are spherical involving a portion of wall, 5-20 cm, partially or completely filled with thrombus. Fusiform, may involve up to 20 cm of the aortic wall.
  • 2. Abdominal Aortic Aneurysms • Atherosclerosis in men above 50 years of age the most frequent cause which destroys the underlying tunica media thereby weakening the wall. • Abdominal aorta is most frequently affected, other parts including arch of aorta, common iliac arteries and thoracic aorta are also affected with less frequency. • Part of abdominal aorta most commonly involved is below the origin of renal arteries. • Aneurysm is usually fusiform measuring 15 x 25 cm. • Mural thrombosis is frequent which may be complete and may involve the lumen partially. Aortic aneurysms may also be accompanied by similar lesions in iliac arteries.
  • 3. • Occasionally the origins of renal and superior mesenteric artery may also be affected directly or by thrombosis. The atheromatous lesions in the aneurysms are ulcerated with mural thrombi. Atheroemboli can lodge in the vessels of kidneys or lower extremities. • Variants: two variants. 1- Inflammatory: characterized by dense periaortic fibrosis containing an abundant lymphoplasmacytic infiltration, many giant cells and macrophages. Cause is uncertain. • 2- Mycotic abdominal aneurysm: Aortic atherosclerotic aneurysms infected by deposition of circulating organisms in the wall, particularly salmonella gastroenteritis. This leads to suppuration and further destruction of media.
  • 4. Pathogenesis of Aneurysms. • Atherosclerosis along with other factors in men above 50 years of age. • Have been showing to be familial, in addition to the familial factors responsible for atherosclerosis and hypertension.. • Genetic defects e.g. Marfans syndrome in structural components of aorta can also cause aneurysms and dissections. • There is evidence that matrix metalloproteins and plasminogen activators, which degrade extracellular matrix contribute to aneurysm formation.
  • 5. Clinical Features • Depend on location and size. • Rupture into body cavities with massive hemorrhage. • Occlusion of a branch vessel. • Embolism from thrombosis or atheroma. • Compression of surrounding structures, e.g. ureter. • Presentation as abdominal mass.
  • 6. Syphilitic Aneurysms • Tertiary syphilis is marked by cardiovascular and nervous system complications. • Endarteritis obliterans involves small muscular arteries and arterioles; most devastating when it involves the vasa vasorum of aorta which can lead to aneurysm of thoracic aorta along with dilatation of aortic annulus.
  • 7. Morphologic Features. • Medial destruction is the key process in tertiary syphilis. • Inflammatory process starts in the aortic adventitia, esp. vasa vasorum, surrounded by lymphoplasmacytic infiltration. • There is ischemic injury to aortic media, patchy loss of elastic tissue and smooth muscle cells followed by inflammation and later on scarring. • Aorta loses its elastic support, becomes dilated. • Luetic involvement of aorta favors superimposed atherosclerosis inducing further florid atheromatosis. • Location in thoracic aorta an differentiate the luetic aneurysms from those purely due to atherosclerosis.
  • 8. • Luetic aortic aneurysms also cause, dilatation of aortic valve ring, producing aortic valve insufficiency, valves get damaged as well. • Left ventricle becomes hypertrophied with consequent marked cardiomegaly (cor bovinum).
  • 9. Clinical Features. • Both types of aneurysms produce signs and symptoms due to: • Encroachment on mediastinal structures. • Respiratory difficulties. • Swallowing difficulties. • Persistent cough- recurrent laryngeal nerve. • Pain following erosion of ribs and vertebral bodies. • Cardiac disease. • Rupture of aneurysm.
  • 10. Aortic Dissections • Aortic dissection is catastrophic disease, characterized by dissection of blood in between and along the laminar planes of media forming blood filled channel. Usually dilatation of aorta is minimal. • Two groups of patients are affected e.g. men between 40-60 years in whom chronic hypertension, second group consists of younger persons having systemic or localized abnormality of connective tissue of aorta e.g. Marfans syndrome. • Dissection may occur as complication of arterial catheterization. • Arterial dissections may occur in aorta or coronaries during pregnancy, reason is unknown. • Dissection is uncommon in advanced atherosclerosis due to scarring in the tunica media of aorta.
  • 11. Morphologic Features. • Starts mostly with intimal tear that occurs within 10 cm of aortic valve. • Tears are usually 1-5 cm in length. • Dissection may extend proximally or distally, may involve the aorta up to the iliacs and femoral artery. • Spreads along with laminar planes, between outer and middle one third of the wall of aorta. • The channel may again rupture in to the aorta through a secondary tear (double barrel aorta), this avoids fatal extra aortic rupture and fatal hemorrhage. • Most common cause of death is rupture into one of the body cavities.
  • 12. • Clinical manifestations may also be due to extension of the dissection to the origins of aortic branches, like coronary, renal, mesenteric or iliac arteries causing obstructions to vascular flow. • Histologically the most frequent and detectable lesion is cystic medial degeneration. The lesions consist of elastic tissue fragmentation and separation of elastic and fibromuscular elements of tunica media that creates cleft like or cystic spaces filled with amorphous extracellular matrix. Inflammation is absent. • Cystic medial degeneration is frequently found in patients with Marfans syndrome. • Cystic medial degeneration is frequently found at autopsy in persons who had experienced no symptoms of dissection.
  • 13. Pathogenesis • Hypertension is the major risk factor, but contribution to CMD is uncertain, no good correlation between CMD and dissection. • Some dissections are due to inherited connective tissue defects e.g. Marfans autosomal dominant disorder. • Complications of Marfans syndrome include; aortic dissection, aortic and mitral valve prolapse; other manifestations include; skeletal and occular. • The triggering factors for intimal tear and intramural hemorrhage is unknown. But once the process has started, hypertension plays an important role in the progression.
  • 14. Clinical Features. • Depend on level of aorta affected. • Sudden onset of excruciating pain, beginning in the front of chest, radiating to back, can be readily confused clinically with that of acute myocardial infarction. • The diagnosis may be based on various investigations, including angiography, two dimensional cardiac ultrasound, CT scan and MRI. • Prognosis has recently improved due to development of surgical techniques.
  • 15. Varicose Veins • Varicose veins have narrowed or abnormally dilated lumina along with incompetence of valves leading to venous stasis. These are tortuous, dilated, elongated and scarred. • Loss of support of vessel walls and increased intramural pressure. • Leg veins are affected due to posture, so occupations are important in its aetiology. • Prolonged erect posture also results in simple orthostatic oedema. • Condition is more common over 50 years, obese people and during pregnancy.
  • 16. Morphologic Features. • There is marked variation in the thickness of the wall. There may be thrombosis and valvular deformities. • Microscopically changes consist of variations in thickness of the wall caused by dilatations and compensatory hypertrophy of smooth muscle and subintimal fibrosis.
  • 17. Clinical Features • Venous stasis, congestion, oedema and thrombosis. • Embolism is rare in contrast to deep vein thrombosis. • Distension is painful. • Persistent varicose veins produce oedema of legs along with trophic changes leading to stasis dermatitis and ulcerations. • Varicose veins are also seen in lower esophagus, in patients of cirrhosis, due to portal hypertension.
  • 19. Aortic Dissection With Double Lumen
  • 20. Aortic Dissection aortic dissecting aneurysm from intimal tear, blood clot present in the adventitial layer may accumulate in the thorax, causing hemothorax.
  • 21. Intimal Tear in Aortic Dissection
  • 23. Aortic Dissection Aortic aneurysm dissecting into the muscular layer. The blood dissecting proximally may block the carotids and distally may shut the coronaries.