Archive for November, 2008

Aortic Aneurysm in the Differential for Panic Attacks

Case Report
Mr. Z. is a 65-year-old White male with a long history of recurrent depression; historical diagnosis of alcohol dependence, which has been in remission for 20 years; and dependent personality disorder. For the last 14 months, the patient experienced anxiety symptoms, including shortness of breath, nonspecific chest pain (without radiation, left arm pain, nausea, or vomiting), diaphoresis, fear of dying, and palpitations that peaked in 15 to 20 minutes and resolved in 5 to 6 hours. Mr. Z. also experienced free-floating anxiety symptoms with much lower intensity that lasted for up to a day at a time. Mr. Z. did not endorse muscle tension, irritability, or feeling on edge. An increase in mental health contact over the past 14 months related to his recent worsening anxiety and panic symptoms.
Mr. Z.’s admission medications included albuterol (two puffs four times a day), amlodipine (5 mg every day), doxazosin (1 mg every night), ranitidine (150 mg every day), nitroglycerin (0.4 mg sublingual) as required for chest pain, enteric coated aspirin (325 mg every day), and isosorbide dinitrate (slow release 40 mg twice a day). There were no changes in his medication regimen that coincided with an increase in his anxiety symptoms. Repeat lab reviews over the 14 months showed normal complete blood count, chemistry panels, RPR, urinalysis, urine drug screen, liver function tests, thyroid screen, cardiac enzymes, oxygen saturation, and arterial blood gases. He had a normal heart catheterization within the past year. A chart review noted that a routine chest x-ray 1 year ago showed a widened mediastinum. This was followed up by a computed topography (CT) scan showing a thoracic aortic aneurysm of 6.3 cm. Aside from some mild hypertension necessitating an increase in amlodipine (10 mg once a day), Mr. Z. was medically stable. A current CT scan showed fusiform aneurysmal dilatations of the descending aorta from the aortic arch extending down to the celiac axis, 7 cm in diameter with a thrombus without dissection. Surgeons concurred that this expanding aneurysm could indeed be resulting in anxiety symptoms. Emergency surgery was scheduled, but Mr. Z. died before surgery.

A number of psychiatric and medical causes that can produce anxiety were stable during the 14-month period of worsening anxiety symptoms. Several CT scans showed an enlarging aneurysm that temporally coincided with Mr. Z.’s worsening anxiety symptoms. With numerous causes for anxiety symptoms, we recognize that his enlarging aneurysm was probably not the sole contributor to the anxiety symptoms.

The sympathetic nervous system has been implicated in the pathophysiology of panic attacks. Theoretically, an enlarging aneurysm may have a mass effect on the nearby sympathetic ganglion, which may result in panic-like symptoms. The symptoms of aortic aneurysms can vary widely with many being asymptomatic unless dissection is present. The natural progression of untreated aortic aneurysms is enlargement, rupture, and death. Enlarging thoracic aneurysms may compress the left recurrent laryngeal nerve producing hoarseness. Dissection of an aortic aneurysm is usually accompanied by pain; chest pain is most common (80% of patients) along with back pain (30%) and neck, epigastric, and arm and leg pain. Substernal or back pain, cough, dyspnea, and dysphagia may also be present. The dissecting aneurysm may produce ischemia of the brain, spinal cord, or peripheral nerves with syncope, stroke, or paraplegia. The risk of rupture is directly related to the diameter of the aneurysm. For example, the risk of rupture of a 6-cm abdominal aortic aneurysm is 25%–30% at 5 years, and for an 8-cm abdominal aortic aneurysm is 75 percent at 5 years. Therefore most vascular surgeons recommend elective repair of aortic aneurysms larger than 5–6 cm in diameter if the patient’s condition warrants.It is impossible to quantify the contribution of the enlarging aneurysm to the panic symptoms. However, it is important that cardiovascular causes are ruled out because of the overlap of symptoms. We have not seen any reports in the psychiatric or medical literature that include an aortic aneurysm in the differential for anxiety or panic symptoms. We hope that this case report results in creating a broader differential for anxiety disorders. This in turn may result in more appropriate and possibly earlier interventions for what is a very serious medical and life-threatening condition.


November 29, 2008 at 9:44 am

Endovascular Stent-Graft in Abdominal Aortic Aneurysms

The Relationship between Patent Vessels that Arise from the Aneurysmal Sac and Early Endoleak

Purpose: To determine the association of patent sac branch vessels (lumbar and inferior mesenteric arteries [IMAs]) with early endoleak rate after stent-graft repair of abdominal aortic aneurysm (AAA).

Materials And  Methods: Pre- and postoperative computed tomographic (CT) angiograms in 158 patients who underwent stent-graft AAA repair were retrospectively reviewed to determine the preoperative patency of IMAs and other sac branch vessels (feeders) and presence or absence of immediate postoperative endoleak. Relationships of early endoleak rate with total branch vessel, IMA, and lumbar artery patency and graft type were evaluated.

Results: There was a significant association between patency of sac feeders and rate of early endoleak, especially type 2. As total patent feeders increased from zero to three to four to six, total endoleak rate increased from 6% (one of 17) to 35% (30 of 86); type 2 endoleak rate, from 0% to 25%. IMA patency was significantly associated with total early endoleak rate. Increasing lumbar artery patency also was associated with significantly higher total and type 2 endoleak rates: With zero to three lumbar arteries, the total endoleak rate was 17% and type 2 endoleak rate was 13%, as compared with 60% and 50%, respectively, with more than six patent lumbar arteries.

Conclusion: Sac branch vessel patency is associated with significantly higher early total and type 2 endoleak rates after stent-graft repair of AAAs; thus, patent sac branches play an important role in the pathogenesis of endoleaks.

November 25, 2008 at 9:31 am Leave a comment

Endovascular Management of Mycotic Aortic Aneurysms and Associated Aortoaerodigestive Fistulas

We evaluated the short- and intermediate-term results of endovascular aneurysm repair (EVAR) for mycotic aneurysms. We reviewed all patients undergoing EVAR for mycotic aneurysms at our institution. To be consistent with the existing literature, patients with associated aortoaerodigestive fistulas were included. Aneurysm location, demographics, clinical findings, EVAR success, morbidity, and short- (<30 days) and long-term mortality were reviewed. From 2000 to 2007, 326 patients underwent EVAR. Nine of these (3%) had treatment of a mycotic aneurysm. The average age was 72 years (range 53-86), and seven patients were male. Four of the aneurysms were located in the thoracic aorta, two in the abdominal aorta, and three in the thoracoabdominal aorta. Four patients presented with gastrointestinal bleeding, two with hemoptysis, one with hemothorax, and two with fever. Etiologies included bacteremia from endocarditis and central catheter infection, erosion of anastomotic aneurysms from a previous aortic repair or endograft, erosion of a penetrating ulcer with pseudoaneurysm, infected aortic repair, left chest empyema, and unknown in one patient. Methicillin-resistant Staphylococcus aureus was the only bacteria isolated in 56% of the patients. EVAR successfully excluded the aneurysm or fistula in all nine patients; however, five patients experienced at least one postoperative complication. Two patients expired within 30 days. After 30 days, four additional patients expired; three of these deaths were procedure/aneurysm-related. Of the three survivors, over a mean follow-up of 257 days (range 60-417), one has required excision of an infected endograft with extra-anatomic bypass grafting but is now alive and well. All three surviving patients and two out of four patients expiring after 30 days had received long-term postoperative antibiotics. Despite an in-hospital mortality of 22.2%, EVAR can be used to treat acute complications from mycotic aneurysms and associated aortoaerodigestive fistulas, such as gastrointestinal bleeding, hemoptysis, or hemodynamic instability. As a definitive treatment, EVAR remains suspect and therefore should be considered a bridge to open surgical repair.

November 21, 2008 at 9:20 am

Vascular wall flow-induced forces in a progressively enlarged aneurysm model.

The current study is focused on the numerical investigation of the flow field induced by the unsteady flow in the vicinity of an abdominal aortic aneurysm model. The computational fluid dynamics code used is based on the finite volume method, and it has already been used in various bioflow studies. For modelling the rheological behaviour of blood, the Quemada non-Newtonian model is employed, which is suitable for simulating the two-phase character of blood namely a suspension of blood cells in plasma. For examining its non-Newtonian effects a comparison with a corresponding Newtonian flow is carried out. Furthermore, the investigation is focused on the distribution of the flow-induced forces on the interior wall of the aneurysm and in order to study the development of the distribution with the gradual enlargement of the aneurysm, three different degrees of aneurysm-growth have been assumed. Finally and for examining the effect of the distribution on the aneurysm growth, a comparison is made between the pressure and wall shear-stress distributions at the wall for each growth-degree.

November 17, 2008 at 8:58 am

Abdominal Aortic Aneurysm

Abdominal aortic aneurysms (AAAs) represent a degenerative process of the abdominal aorta that is often attributed to atherosclerosis; however, the exact cause is not known. A familiar clustering of AAAs has been noted in 15-25% of patients undergoing repair of the problem. Degenerative aneurysms account for more than 90% of all infrarenal AAAs. Other causes include infection, cystic medial necrosis, arteritis, trauma, inherited connective-tissue disorders, and anastomotic disruption.The disease generally affects elderly white men. Smoking appears to be the risk factor most strongly associated with AAA.

History of the Procedure

Vesalius described the first AAA in the 16th century. Before the development of a surgical intervention for the process, attempts at medical management failed. The initial attempts at control used ligation of the aorta, with the expected consequences. In 1923, Matas performed the first successful aortic ligation on a patient. Attempts were made to induce thrombosis by inserting intraluminal wires. In 1948, Rea wrapped reactive cellophane around the aneurysm in order to induce fibrosis and limit expansion. This technique was used on Albert Einstein in 1949, and he survived 6 years before succumbing to rupture. In 1951, Charles Dubost performed the first AAA repair using a homograft.

Prior to this, aortic aneurysms were treated using a variety of methods, including ligation, intraluminal wiring, and cellophane wrapping. Unfortunately, early homografts became aneurysmal because of preservation techniques. In 1953, Blakemore and Voorhees repaired a ruptured AAA using a Vinyon-N graft (ie, nylon). Later, these grafts were replaced by Dacron and Gore-Tex (ie, polytetrafluoroethylene [PTFE]) fabrics. The final advance was abandonment of silk sutures, which degenerated, in favor of braided Dacron, polyethylene, and PTFE (ie, Gore-Tex) sutures, all of which retain tensile strength.

Postoperative surgical mortality rates initially remained high (>25%) because the aneurysm sac generally was excised. Nearly simultaneously in 1962, Javid and Creech reported the technique of endoaneurysmorrhaphy . This advancement dramatically reduced mortality. Today, operative mortality rates range from 1.8-5%.In the late 1980s, Parodi et al described endovascular repair using a large Palmaz stent and unilateral aortofemoral and femorofemoral crossover Dacron grafts.1 Currently, many devices are used for the endovascular treatment of AAA


Aneurysms are defined as a focal dilatation with at least a 50% increase over normal arterial diameter. Thus, an enlargement of at least 3 cm of the abdominal aorta fits the definition. In large ultrasound screening studies, increasing age; male sex; African American race; and increased height, weight, body mass index, and body surface area all were associated with increased infrarenal aortic diameter.

Most cases of AAA begin below the renal arteries and end above the iliac arteries. They generally are spindle shaped; however, size, shape, and extent vary considerably. Of AAA cases, 10-20% have focal outpouchings or blebs that are thought to contribute to the potential for rupture. The wall of the aneurysm becomes laminated with thrombus as the blebs enlarge. This can give the appearance of a relatively normal intraluminal diameter in spite of a large extraluminal size.


AAAs are uncommon in African Americans, Asians, and persons of Hispanic heritage.

United States

In autopsy studies, the frequency rate of AAA ranges from 0.5-3.2%. In a large US Veterans Administration screening study, the prevalence rate was 1.4%.2 The frequency of rupture is 4.4 cases per 100,000 persons.

AAA is 5 times more common in men than in women and is 3.5 times more common in white males than in African American males. The likelihood of development varies from 3-117 cases per 100,000 person-years. In men, the process appears to begin at approximately age 50 years and reaches peak incidence at approximately age 80 years. In women, the onset is delayed and appears to begin at approximately age 60 years. The reported incidence of rupture varies from 1-21 cases per 100,000 person-years.


The frequency rate of asymptomatic AAA is 8.2% in the United Kingdom, 8.8% in Italy, 4.2% in Denmark, and 8.5% in Sweden (in males only). The frequency rate of AAA in females is much lower, 0.6-1.4%. The frequency of rupture is 6.9 cases per 100,000 persons in Sweden, 4.8 cases per 100,000 persons in Finland, and 13 cases per 100,000 persons in the United Kingdom.

Risk factors

The peak incidence of AAA occurs in people aged 70 years. The male-to-female incidence ratio in people younger than 80 years is 2:1. When older than 80 years, the ratio changes to 1:1.

A family history of AAA is a risk factor for AAA. Approximately 25% of cases are in persons with first-degree relatives with AAA. Other risk factors include previous aneurysm repair or peripheral aneurysm (popliteal or femoral), smoking, coronary artery disease, and hypertension (1-15%).


AAA is thought to be a degenerative process of the aorta, the cause of which remains unclear. It is often attributed to atherosclerosis because these changes are observed in the aneurysm at the time of surgery. Atherosclerosis fails to explain the development of occlusion, which is observed in the disease process.

AAA appears to have a familial prevalence rate of 15-25%. Studies by Majumder and associates suggest the genetic predisposition is isolated to a single dominant gene with low penetrance that increases with age. Tilson et al described the potential for an autoimmune basis for the development of AAA involving the DRB1 major histocompatibility locus. This locus has been identified as a basis for inflammatory AAA.The other causes of AAA include infection, cystic medial necrosis, arteritis, trauma, inherited connective-tissue (structural collagen) disorders, and anastomotic disruption producing pseudoaneurysms.


A multidisciplinary research program supported by the US National Heart, Lung, and Blood Institute identified proteolytic degradation of aortic wall connective tissue, inflammation and immune responses, biomechanical wall stress, and molecular genetics as mechanisms important in the development of AAA.5

The aortic wall contains smooth muscle, elastin, and collagen arranged in concentric layers in order to withstand arterial pressure. The number of medial elastin layers from the proximal thoracic aorta to the infrarenal aorta is markedly reduced, with medial thinning and intimal thickening. A reduction in collagen and elastin content is noted from the proximal to the distal aorta. Elastin is the principal load-bearing element in the aorta. Elastin fragmentation and degeneration are observed in aneurysm walls. The decrease in content coupled with the histological changes of this matrix protein in aneurysms may explain the propensity for aneurysm formation in the infrarenal aorta.Immunoreactive proteins are found more conspicuously in the abdominal aorta, and this may contribute to the increased frequency of aneurysms in this location.

The aortic media appear to degrade in AAA by means of a proteolytic process. This implies an increase in the concentration of proteolytic enzymes relative to their inhibitors in the abdominal aorta as the individual ages. Reports have documented increased expression and activity of matrix metalloproteinases (MMPs) in persons with AAAs. MMPs and other proteases have been shown to be secreted into the extracellular matrix of AAAs by macrophages and aortic smooth muscle cells. MMPs and their inhibitors are present in normal aortic tissue and are responsible for vessel wall remodeling. In aneurysmal tissue, a tendency exists for increased MMP activity favoring the degradation of elastin and collagen. The mechanism that tips the balance in favor of degradation of elastin and collagen in the aortic wall of AAAs by MMPs and other proteases is presently unknown.

AAAs demonstrate a chronic adventitial and medial inflammatory infiltrate upon histological examination. Infiltration of AAAs with lymphocytes and macrophages may trigger protease activation via various cytokines (interleukin [IL]–1, IL-6, IL-8, and tumor necrosis factor-alpha). Further study has defined a matrix protein that is immunoreactive with immunoglobulin G in the aneurysm wall. This autoantigen appears to be a collagen-associated microfibril. Certain infectious agents have been associated with the development of this protein, including Chlamydia pneumoniae and Treponema pallidum; however, a direct cause-and-effect relationship has not been demonstrated.

AAAs arise as a result of a failure of the major structural proteins of the aorta (elastin and collagen). The inciting factors are not known, but a genetic predisposition clearly exists. Surgical specimens of AAA reveal inflammation, with infiltration by lymphocytes and macrophages; thinning of the media; and marked loss of elastin . Recent research has focused on the role of the metalloproteinases, a group of zinc-dependent enzymes responsible for tissue remodeling.

In general, AAAs gradually enlarge (0.2-0.8 mm/y) and eventually rupture. Hemodynamics play an important role. Areas of high stress have been found in AAAs and appear to correlate with the site of rupture. Computer-generated geometric factors have demonstrated that aneurysm volume is a better predictor of areas of peak wall stress than aneurysm diameter. This may have implications in determining which AAAs require surgical repair.

Additionally, molecular genetics has provided some insight into the development of AAAs. Through gene microarray analysis, various genes involved in extracellular matrix degradation, inflammation, and other processes observed in AAA formation have been shown to be up-regulated, while others that may serve to prevent this occurrence are down-regulated. The combination of proteolytic degradation of aortic wall connective tissue, inflammation and immune responses, biomechanical wall stress, and molecular genetics represents a dynamic process that leads to aneurysmal deterioration of aortic tissue.


  • Asymptomatic: Most patients present without an asymptomatic pulsatile abdominal mass . The aortic bifurcation is located just above the umbilicus. Occasionally, an overlying mass (pancreas or stomach) may be mistaken for an AAA. An abdominal bruit is nonspecific for a nonruptured aneurysm. Patients with popliteal artery aneurysms frequently have AAAs (25-50%).
  • Rupture: Persons with AAAs that have ruptured may present in many ways. The most typical manifestation of rupture is abdominal or back pain with a pulsatile abdominal mass. However, the symptoms may be vague, and the abdominal mass may be missed. Symptoms may include groin pain, syncope, paralysis, or flank mass. The diagnosis may be confused with renal calculus, diverticulitis, incarcerated hernia, or lumbar spine disease.
  • Peripheral emboli: Atheroemboli from small AAAs produce livedo reticularis of the feet or blue toe syndrome
  • Acute aortic occlusion: Occasionally, small AAAs thrombose, producing acute claudication.
  • Aortocaval fistulae: AAAs may rupture into the vena cava, producing large arteriovenous fistulae. In this case, symptoms include tachycardia, congestive heart failure (CHF), leg swelling, abdominal thrill, machinery-type abdominal bruit, renal failure, and peripheral ischemia.
  • Aortoduodenal fistulae: Finally, an AAA may rupture into the fourth portion of the duodenum. These patients may present with a herald upper gastrointestinal bleed followed by an exsanguinating hemorrhage.

Physical examination

Bilateral upper extremity blood pressures are discernible in patients with AAAs. Hypertension may trigger a workup for renal artery stenosis. Unequal blood pressures (>30 mm Hg) indicate subclavian artery stenosis, and perioperative monitoring is important.

Cervical bruits may indicate carotid artery stenosis. Abdominal examination includes palpation of the aorta and an estimation of the size of the aneurysm. Bruits may indicate the presence of renal or visceral artery stenosis; a thrill is possible with aortocaval fistulae.

Regarding the peripheral pulses, palpate femoral popliteal and pedal pulses (dorsalis pedis or posterior tibial) to determine if an associated aneurysm (femoral/popliteal) or occlusive disease exists. Flank ecchymosis (Grey Turner sign) represents retroperitoneal hemorrhage.

With respect to rectal aspects of the physical examination, guaiac-positive stool is present with associated colon cancer.

Most persons with AAAs are asymptomatic. Patients may describe a pulse in the abdomen and may actually feel a pulsatile mass. At times, AAAs may cause symptoms from local compression, including early satiety, nausea, vomiting, urinary symptoms, or venous thrombosis from venous compression. Back pain can be caused by erosion of the AAA into adjacent vertebrae. Other symptoms include abdominal pain, groin pain, embolic phenomenon to the toes, and fever. Transient hypotension should prompt consideration of rupture because this finding can progress to frank shock over a period of hours. Temporary loss of consciousness is also a potential symptom of rupture.

Most clinically significant aneurysms are palpable upon routine physical examination; however, the sensitivity of the technique is based on the experience of the examiner, the size of the aneurysm, and the size of the patient. In a recent study, 38% of AAA cases were detected based on physical examination findings, while 62% were detected incidentally based on radiologic studies obtained for other reasons.

November 13, 2008 at 8:31 am

Thoracic Aortic Aneurysm


Thoracic aortic aneurysm represents aneurysmal dilatation of ascending, arch, or descending thoracic aorta. Aneurysm is defined as a localized or diffuse dilatation of more than 50% normal diameter of the aorta. It occurs with the highest frequency of all of the diseases of the thoracic aorta that require surgical treatment. Atherosclerosis or connective tissue disorders may be contributing underlying disorders that facilitate aortic dilatation. Frequently associated factors include advanced age, hypertension, smoking, atherosclerosis, and aortic dissection.Thoracic aneurysms are classified by the portion of aorta involved: the ascending thoracic aorta, the arch, or the descending thoracic aorta. This anatomic distinction is important because the etiology, natural history,and treatment of thoracic aneurysms vary for each of these segments.Aneurysms of the descending aorta are most common, followed by aneurysms of the ascending aorta, whereas arch aneurysms occur less often. In addition, descending aortic thoracic aneurysms may extend distally to involve the abdominal aorta and create a thoracoabdominal aortic aneurysm.Sometimes, the entire aorta may be ectatic, with localized aneurysms seen at sites in both the thoracic and abdominal aorta. Interestingly, thoracic aortic aneurysms are less common than aneurysms of the abdominal aorta.


Cystic medial necrosis Aneurysms of the ascending thoracic aorta most often result from the process of cystic medial degeneration (or cystic medial necrosis).Histologically, cystic medial degeneration has the appearance of smooth muscle cell necrosis and elastic fiber degeneration, with the presence in the media of cystic spaces filled with mucoid material. Although these changes occur most frequently in the ascending aorta, in some cases the entire aorta may be similarly affected.The histologic changes lead to weakening of the aortic wall, which in turn results in the formation of a fusiform aneurysm. Such aneurysms often involve the aortic root and may consequently result in aortic regurgitation. The term annuloaortic ectasia is often used to describe this condition.Cystic medial degeneration is found in virtually all cases of Marfan syndrome and may be associated with other connective tissue disorders as well, such as Ehlers-Danlos syndrome. Marfan syndrome is an autosomal dominant heritable disorder of connective tissue that has been discovered to be due to mutations in one of the genes for fibrillin, a structural protein that helps direct and orient elastin in the developing aorta.These mutations result in a decrease in the amount of elastin in the aortic wall, together with a loss of the normally highly organized structure of elastin. As a consequence, a marfanoid aorta exhibits markedly abnormal elastic properties and increased systemic pulse wave velocities from an early age, and over time, the aorta exhibits progressively increasing degrees of stiffness and dilatation.In patients without Marfan syndrome, however, it is not possible to recognize the histologic diagnosis of cystic medial degeneration prospectively (eg, without surgery or necropsy). This fact has significantly limited our understanding of medial degeneration and its natural history, and it remains unclear to what extent this syndrome may represent an independent disease process versus a manifestation of another disease state.It has long been suspected that some patients who have annuloaortic ectasia and proven cystic medial degeneration without the classic phenotypic manifestations of Marfan syndrome may, in fact, have a variation, or forme fruste, of Marfan syndrome, although this theory remains unproved. On the contrary, many patients with ascending thoracic aortic aneurysms appear to have nothing more than idiopathic cystic medial degeneration.


Atherosclerotic aneurysms infrequently occur in the ascending aorta and, when they do, tend to be associated with diffuse aortic atherosclerosis. Aneurysms in the aortic arch are often contiguous with aneurysms of the ascending or descending aorta. They may be due to atherosclerotic disease, cystic medial degeneration, syphilis, or other infections.The predominant etiology of aneurysms of the descending thoracic aorta is atherosclerosis. These aneurysms tend to originate just distal to the origin of the left subclavian artery and may be either fusiform or saccular. The pathogenesis of such atherosclerotic aneurysms in the thoracic aorta may be similar to that of abdominal aneurysms but has not been extensively examined.


Syphilis was once a common cause of ascending thoracic aortic aneurysm, but today it has become a rarity in most major medical centers as a result of aggressive antibiotic treatment of the disease in its early stages.The latent period from initial spirochetal infection to aortic complications is in the range of 5-40 years, but it is most commonly 10-25 years. During the secondary phase of the disease, spirochetes directly infect the aortic media, most commonly involving the ascending aorta. The muscular and elastic medial elements are destroyed by the infection and inflammatory response and are replaced by fibrous tissue that frequently calcifies.Weakening of the aortic wall from medial destruction results in progressive aneurysmal dilatation. In addition, the infection may spread into the aortic root, and the subsequent root dilatation may result in aortic regurgitation.

Infectious aortitis

This rare cause of aortic aneurysm may result from a primary infection of the aortic wall causing aortic dilatation with the formation of fusiform or saccular aneurysms.More commonly, infected or mycotic aneurysms may arise secondarily from an infection occurring in a preexisting aneurysm of another etiology. When an infected aneurysm involves the ascending aorta, it is often the consequence of direct spread from aortic valve bacterial endocarditis.


Other causes of thoracic aortic aneurysms include giant cell arteritis, aortic trauma, and aortic dissection.


United States

The population incidence of detected thoracic aortic aneurysms is estimated to be 5.9 new aneurysms per 100,000 person-years. The lifetime probability of rupture in thoracic and thoracoabdominal aneurysms is 75 to 80%, with 5-year untreated survival rates or 10-20%. In nondissecting aneurysms, the median time to rupture has been reported to be 2-3 years.



In the largest modern series, survival rates for patients with thoracic aortic aneurysms not undergoing surgical repair were as follows: 65% survival at 1 year, 36% survival at 3 years, and 20% survival at 5 years. Aneurysm rupture occurs in 32-68% of patients not treated surgically, with rupture accounting for 32-47% of all deaths. Less than one half of patients with rupture may arrive at the hospital alive. The mortality rates for aneurysmal rupture are 54% at 6 hours and 76% at 24 hours. Hospital mortality rates for primary medical treatment remain relatively high, and a substantial percentage of patients require surgery during initial hospitalization. The main causes of death in both medical and surgical groups are rupture. Improvements in supportive medical care have increased patient survival. In the patients with aortic aneurysm, aortic dissection is the catastrophic event most feared. Rupture of a thoracic aortic aneurysm is more frequent than abdominal aortic rupture. The presence or absence of symptoms is another important predictor. Symptomatic patients have a poorer prognosis than those without symptoms. Onset of new symptoms is frequently a harbinger of rupture or death. Moreover, the high prevalence of additional cardiovascular disease in these patients may have a great impact on mortality. In fact, next to aneurysm rupture, the most common causes of death in persons with aortic aneurysm are other cardiovascular diseases.


The incidence or thoracic aortic aneurysm is more common with increasing age.



The DeBakey and Stanford classifications are the 2 most widely used methods to describe the type of aortic dissection.In the DeBakey classification, types I, II, and III are based on the origin and extent of the dissecting process.In the Stanford system, type A signifies involvement of the ascending aorta, with or without involvement of the arch or the descending aorta (regardless of the site of the primary intimal tear). Type B represents all others, or dissections that do not involve the ascending aorta.

Dissection and rupture

The aortic layers, beginning at the innermost wall, are the intima, the media, and the adventitia.In aortic dissection, a tear in the intima allows blood to escape from the true lumen of the aorta, rapidly dissecting the inner from the outer layer of the media and expanding the aorta to above normal size. A false channel forms in the outer half of the aortic media, whose walls are exceedingly thin and highly susceptible to rupture.Size is an important predictor of the risk of aneurysm rupture.

Acute versus chronic dissections

Dissections or rupture detected within 14 days of the onset of pain or other initial clinical symptom related to the dissection are classified as acute, and death may occur suddenly or within the first hours or days after onset.Chronic dissection, which is diagnosed 2 weeks after the initial tear, may expand in the weakened aortic wall to develop an aneurysm. As in aortic aneurysm, causative factors are difficult to establish. The risk of rupture within 1 year for aneurysms with diameters of 6 cm is 43%. The risk with diameters of 8 cm and greater is 80%, and the risk for those with diameters smaller than 5 cm is 4%.


Dapunt and colleagues monitored 67 patients with thoracic aortic aneurysms by means of serial CT and found a mean rate of expansion of 0.43 cm/y. The only independent predictor of rapid expansion (>0.5 cm/y) was an initial aortic diameter larger than 5 cm.Growth rates were as follows: for aneurysms 5 cm or smaller, 0.17 cm/y, and for aneurysms larger than 5 cm, 0.79 cm/y. Only 1 of 25 aneurysms 4 cm or smaller at baseline showed rapid growth. No aneurysm smaller than 5 cm ruptured during the follow-up period. The only predictor of survival was initial aneurysm size.For dissecting aneurysms, the median time to rupture is approximately 3 days in patients with acute dissection. Patients with aneurysms 5 cm or larger, those with documented aneurysm enlargement, or those with chest or back pain indicating expansion are considered candidates for elective surgery.

Clinical Details

Signs and symptoms associated with aortic dissection are variable and depend on the extent of aortic and branch vessel involvement. Patients with the ultimate diagnosis of aortic dissection are often initially thought to have other conditions such as myocardial ischemia, congestive heart failure, or pulmonary embolus. Several clinical syndromes are particularly suggestive of aortic dissection: pain that progresses over hours or days from chest to neck to arms to abdomen, chest pain with concomitant neurologic deficits, and chest pain with pulse deficits.Approximately 40% of patients with thoracic aortic aneurysms are asymptomatic at the time of diagnosis. Aneurysms are typically discovered as incidental findings on a routine physical examination or chest radiography. When patients experience symptoms, the symptoms tend to reflect either a vascular consequence of the aneurysm or a local mass effect.Vascular consequences include (1) aortic regurgitation from dilatation of the aortic root, which is often associated with secondary congestive heart failure; (2) sinus of Valsalva aneurysms that may rupture into the right side of the heart and cause a continuous murmur and congestive heart failure; and (3) thromboembolism causing stroke, lower extremity ischemia, renal infarction, or mesenteric ischemia.A local mass effect from an ascending or arch aneurysm may cause superior vena cava syndrome as a result of obstruction of venous return via compression of the superior vena cava or innominate veins.Aneurysms of the arch or descending aorta may compress the trachea or main stem bronchus and produce tracheal deviation, wheezing, cough, dyspnea (with symptoms that may be positional), hemoptysis, or recurrent pneumonitis. Compression of the esophagus may produce dysphagia, and compression of the recurrent laryngeal nerve may cause hoarseness.Chest pain occurs in 37% of nondissecting aneurysms and back pain, in 21%. These result from direct compression of other intrathoracic structures or the chest wall or from erosion into adjacent bone. Typically, the pain is steady, deep, boring, and sometimes severe.As with abdominal aortic aneurysms, the most worrisome consequence of thoracic aneurysms is leakage or rupture.

Rupture is accompanied by the dramatic onset of excruciating pain, usually in the region where less severe pain had previously existed. Rupture occurs most commonly into the left intrapleural space or the intrapericardial space and is manifested as hypotension. The third most common site of rupture is from the descending thoracic aorta into the adjacent esophagus (an aortoesophageal fistula), which causes life-threatening hematemesis.Acute aneurysm expansion, which may herald rupture, can cause similar chest or back pain.Thoracic aneurysms may also be accompanied by aortic dissection.

Preferred Examination

Although aortic dissection might be suspected on the basis of history and physical findings, diagnostic imaging is necessary to establish the diagnosis. A clear and efficient imaging strategy is required. The clinical team involved in the diagnosis and treatment of patients with aortic dissection should prospectively agree on a strategy. Their approach should consider the technology available at the institution and the ease of performing each test, especially after hours.The preferred examinations for diagnosis are aortic angiography, MRI, magnetic resonance angiography (MRA), and echocardiography.Aortography has been the criterion standard against which other modalities were measured, but it is rarely used with the advent of transesophageal echocardiography (TEE) and CT, though aortography is still the preferred modality for the preoperative evaluation of thoracic aortic aneurysms and for precise definition of the anatomy of the aneurysm and great vessels.CT is a reliable test for diagnosing aortic dissection, and it is the primary diagnostic test of choice in most institutions. CT scans usually show dilation of the aorta, an intimal flap, and both the false and true lumina. Rapid scanning after an intravenous bolus injection of contrast material allows the detection of differential filling rates in the true and false lumina.TEE is helpful due to the proximity of the esophagus to the aorta and the ability to use higher transducer frequencies help to better delineate the aorta. It is highly sensitive but less specific. TEE, however, is

excellent at detecting pericardial effusion and aortic regurgitation, and can be quickly performed at the patient’s bedside under sedation without radiation or the injection of contrast material. Evaluating the ascending aorta and proximal arch may be difficult.MRI is useful in defining thoracic aortic anatomy and detecting aneurysms and is of particular utility in patients with preexisting aortic disease. MRI is an appealing option in the detection of aortic dissection. Sensitivity and specificity are excellent, but it is time consuming and cumbersome to perform.MRA may prove especially useful in defining the anatomy of aortic branch vessels.Regarding echocardiography, TTE is not accurate for diagnosing thoracic aneurysms, and it is particularly limited in its ability to examine the descending thoracic aorta. TEE is a far more accurate method for assessing the thoracic aorta and has become widely used for detection of aortic dissection. There has been less experience with TEE, however, in the evaluation of nondissecting thoracic aneurysms.Reports have shown high sensitivity for TEE, CT, and MRI for the diagnosis of aortic dissection. However, the specificity of CT and MRI was significantly better than that of TEE.

November 9, 2008 at 7:22 am Leave a comment

Aortic Aneurysm Medical Treatment Signs,Symptoms and Diagnosis

An aortic aneurysm is a general term for any swelling (dilatation or aneurysm) of the aorta, usually representing an underlying weakness in the wall of the aorta at that location. While the stretched vessel may occasionally cause discomfort, a greater concern is the risk of rupture, which causes severe pain; massive internal hemorrhage; and, without prompt treatment, results in a quick death.


Aortic aneurysms are classified by where on the aorta they occur; aneurysms can appear anywhere. An aortic root aneurysm, or aneurysm of sinus of Valsalva, appears on the sinuses of Valsalva or aortic root. Thoracic aortic aneurysms are found on the thoracic aorta; these are further classified as ascending, aortic arch, or descending aneurysms depending on the location on the thoracic aorta involved. Abdominal aortic aneurysms, the most common form of aortic aneurysm, are found on the abdominal aorta, and thoracoabdominal aortic aneuryms involve both the thoracic and abdominal aorta.


The physical change in the aortic diameter can occur secondary to trauma, infection, an intrinsic defect in the protein construction of the aortic wall, or due to progressive destruction of aortic proteins by enzymes.

Signs, symptoms and diagnosis

 Most intact aortic aneurysms do not produce symptoms. As they enlarge, symptoms such as abdominal pain and back pain may develop. Compression of nerve roots may cause leg pain or numbness. Untreated, aneurysms tend to become progressively larger, although the rate of enlargement is unpredictable for any individual. Rarely, clotted blood which lines most aortic aneurysms can break off and result in an embolus. They may be found on physical examination. Medical imaging is necessary to confirm the diagnosis. Symptoms may include: anxiety or feeling of stress; nausea and vomiting; clammy skin; rapid heart rate.

Abdominal aortic aneurysm

Abdominal aortic aneurysms, hereafter referred to as AAAs, are the most common type of aortic aneurysm. One reason for this is that elastin, the principal load-bearing protein present in the wall of the aorta, is reduced in the abdominal aorta as compared to the thoracic aorta (nearer the heart). Another is that the abdominal aorta does not possess vasa vasorum, hindering repair. Most are true aneurysms that involve all three layers (tunica intima, tunica media and tunica adventitia), and are generally asymptomatic before rupture.The prevalence of AAAs increases with age, with an average age of 65-70 at the time of diagnosis. AAAs have been attributed to atherosclerosis, though other factors are involved in their formation.

An AAA may remain asymptomatic indefinitely. There is a large risk of rupture once the size has reached 5 cm, though some AAAs may swell to over 15 cm in diameter before rupturing. Before rupture, an AAA may present as a large, pulsatile mass above the umbilicus. A bruit may be heard from the turbulent flow in a severe atherosclerotic aneurysm or if thrombosis occurs. Unfortunately, however, rupture is usually the first hint of AAA. Once an aneurysm has ruptured, it presents with a classic pain-hypotension-mass triad. The pain is classically reported in the abdomen, back or flank. It is usually acute, severe and constant, and may radiate through the abdomen to the back.

The diagnosis of an abdominal aortic aneurysm can be confirmed at the bedside by the use of ultrasound. Rupture could be indicated by the presence of free fluid in potential abdominal spaces, such as Morison’s pouch, the splenorenal space (between the spleen and left kidney), subdiaphragmatic spaces (underneath the diaphragm) and peri-vesical spaces. A contrast-enhanced abdominal CT scan is needed for confirmation.

Only 10-25% of patients survive rupture due to large pre- and post-operative mortality. Annual mortality from ruptured abdominal aneurysms in the United States alone is about 15,000. Another important complication of AAA is formation of a thrombus in the aneurysm.

Medical treatment

 Medical therapy of aortic aneurysms involves strict blood pressure control. This does not treat the aortic aneurysm per se, but control of hypertension within tight blood pressure parameters may decrease the rate of expansion of the aneurysm.

Surgical treatment

The definitive treatment for an aortic aneurysm is surgical repair of the aorta. This typically involves opening up of the dilated portion of the aorta and insertion of a synthetic (Dacron or Gore-tex) patch tube. Once the tube is sewn into the proximal and distal portions of the aorta, the aneurysmal sac is closed around the artificial tube. Instead of sewing, the tube ends, made rigid and expandable by nitinol wireframe, can be much more simply and quickly inserted into the vascular stumps and there permanently fixed by external ligature

The determination of when surgery should be performed is complex and case-specific. The overriding consideration is when the risk of rupture exceeds the risk of surgery. The diameter of the aneurysm, its rate of growth, the presence or absence of Marfan Syndrome or similar connective tissue disorders, and other coexisting medical conditions are all important factors in the determination.

A rapidly expanding aneurysm should be operated on as soon as feasible, since it has a greater chance of rupture. Slowly expanding aortic aneurysms may be followed by routine diagnostic testing (ie: CT scan or ultrasound imaging). If the aortic aneurysm grows at a rate of more than 1 cm/year, surgical treatment should be electively performed.

The current treatment guidelines for abdominal aortic aneurysms suggest elective surgical repair when the diameter of the aneurysm is greater than 5 cm. However, recent data suggests medical management for abdominal aneurysms with a diameter of less than 5.5 cm.

Endovascular treatment of AAA

In the recent years, the endoluminal treatment of Abdominal Aortic Aneurysms has emerged as a minimally invasive alternative to open surgery repair. The first endoluminal exclusion of an aneurysm took place in Argentina by Dr. Parodi and his colleagues in 1991. The endovascular treatment of aortic aneurysms involves the placement of an endo-vascular stent via a percutaneous technique (usually through the femoral arteries) into the diseased portion of the aorta. This technique has been reported to have a lower mortality rate compared to open surgical repair, and is now being widely used in individuals with co-morbid conditions that make them high risk patients for open surgery. Some centers also report very promising results for the specific method in patients that do not constitute a high surgical risk group.

There have also been many reports concerning the endovascular treatment of ruptured Abdominal Aortic Aneurysms, which are usually treated with an open surgery repair due to the patient’s impaired overall condition. Mid-term results have been quite promising.[citation needed] However, according to the latest studies, the EVAR procedure doesn’t carry any overall survival benefit.

Endovascular treatment of other aortic aneurysms

The endoluminal exclusion of aortic aneurysms has seen a real revolution in the very recent years. It is now possible to treat thoracic aortic aneurysms, abdominal aortic aneurysms and other aneurysms in most of the body’s major arteries (such as the iliac and the femoral arteries) using endovascular stents and avoiding big incisions. Still, in most cases the technique is applied in patients at high risk for surgery as more trials are required in order to fully accept this method as the gold standard for the treatment of aneurysms.


Attention to patient’s general blood pressure, smoking and cholesterol risks helps reduce the risk on an individual basis. There have been proposals to introduce ultrasound scans as a screening tool for those most at risk: men over the age of 65.. The tetracycline antibiotic Doxycycline is currently being investigated for use as a potential drug in the prevention of aortic aneurysm due to its metalloproteinase inhibitor and collagen stabilising properties.


Stanford University is conducting research to gather information on AAA risk factors, and to evaluate the effectiveness of an exercise program at preventing the growth of small AAAs in older individuals.

November 5, 2008 at 6:27 am


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