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.