Posts filed under ‘Aortic aneurysm’

Aneurysm

The Facts on Aneurysm

An aneurysm is a weak point in a blood vessel wall, most commonly in an artery. Blood pressure tends to push the weakened section of an arterial wall outward, forming a balloon-like projection. This condition by itself isn’t especially harmful, but the artery is prone to rupture. A ruptured aneurysm breaks the artery and allows uncontrolled bleeding to occur, which can be fatal.Aneurysms can form in different places. The most common type of aneurysm is an abdominal aortic aneurysm (AAA). The aorta is the body’s largest artery, carrying blood from the heart to every organ except the lungs. It leaves the heart flowing upwards in the chest, makes a U-bend, and flows down the spine from the chest to the abdomen. Several branches leave the aorta in the abdomen, going to the kidneys, liver, and intestines.

Other locations for aneurysms are

the bottom of the brain

the most common type of cerebral aneurysm is called a berry aneurysm

thoracic aortic aneurysm (the thorax is the chest) –

of the thoracic aneurysms, the most common subtype is the aneurysm of the ascending aorta (between the heart and the U-bend)

Aneurysms tend to occur in older Caucasian men; women are less at risk

By age 80, over 5% of Caucasian men have developed an aneurysm. People of African descent rarely develop aneurysms.

Ruptured abdominal aortic aneurysms are the 10th most common cause of death in Canadians over age 55, killing over 4,000 people every year in Canada. About 44% of these deaths are due to a hemorrhagic stroke (also called subarachnoid hemorrhage) from cerebral aneurysms. Of the rest, 22% are due to thoracic aneurysms, and the remaining third to abdominal aneurysms.

Causes of Aneurysm

A person’s risk of developing an aneurysms may be inherited

 Ascending aortic aneurysms and berry aneurysms are especially likely to run in families. The men of an affected family are more likely to develop aneurysms than are the women. Scientists haven’t yet identified the responsible genes in humans, though they have identified some in mice. About half of all people with ascending aortic aneurysms are born with deformations known as Marfan’s syndrome. Such people are unusually tall with long extremities. Abraham Lincoln is thought to have had Marfan’s syndrome. They also have a weakness in the aortic wall, just where the aorta leaves the top of the heart.

Two other types of aneurysms are mycotic and atherosclerotic aneurysms

 Mycotic aneurysms are caused by bacterial or fungal infection. Almost any such organism can damage the arteries, but the infection must be very deep and severe. Salmonella and syphilis both seem to have a special liking for arterial walls.

Atherosclerotic aneurysms are linked to the process that causes coronary artery disease – the build-up of fatty deposits on the inner wall of the arteries. In reality, the picture’s not so clear. Even someone with severe atherosclerosis may not develop an aneurysm if they are not already genetically predisposed.

High blood pressure, high cholesterol, inactivity, smoking, and obesity, which are risk factors for heart disease, are also risk factors for aneurysms.

 Severe aneurysms are probably due to a combination of genes and poor cardiovascular health. Occasionally, aneurysms develop where stab or gunshot wounds have perforated an artery.

Symptoms and Complications of Aneurysm

Aneurysms often cause no pain:

Often, they’re detected accidentally in body scans. The most likely way you will notice a cerebral, thoracic, or abdominal aneurysm is if it grows big enough to press against nerve-bearing tissue. Unfortunately, this means the aneurysm has grown recently, so the warning comes late. Fast-growing aneurysms are the ones most likely to rupture. Even large aneurysms often cause no symptoms.

Cerebral (brain) aneurysms occasionally cause some of these symptoms as they start to swell:

  • double vision
  • facial pain
  • loss of vision
  • severe headaches from minor bleeding
  • squinting
  • tremors or uncontrollable movement of an eye or eyelid

With thoracic aneurysms, symptoms are rare but may include:

  • chest pain, upper back pain, or both
  • coughing-up of blood
  • difficulty swallowing
  • hoarseness
  • Horner’s syndrome – drooping eyelid, absence of sweating on one side of the face
  • wheezing

Abdominal aneurysms are more likely to cause symptoms that:

  • pulsate in the abdomen
  • cause upper abdominal pain, severe lower back pain, or both

The symptom of a ruptured abdominal aneurysm is intense pain and tenderness in the stomach or lower back area.

Thoracic aneurysms cause excruciating pain in the upper chest that spreads to the back and sometimes down the trunk. Blood loss and failure of vital organs such as the kidneys can lead to fatal consequences in cases of thoracic and abdominal aneurysms. Ruptured cerebral aneurysms cause a hemorrhagic stroke, with all of its symptoms.

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December 19, 2008 at 10:38 am

Causes and Risk Factors of Aortic Aneurysms

Definition of Aortic Aneurysms

An aortic aneurysm is a weak spot in the wall of the aorta, the primary artery that carries blood from the heart to the head and extremities

Description of Aortic Aneurysms

An aneurysm is an abnormal enlargement of a blood vessel.
Some 15,000 Americans die suddenly each year from rupture of an aneurysm in the aorta, which is the ninth leading cause of death in men over age 55. Aortic aneurysms are four times more common in men than in women and usually occur in those over age 50. Approximately one percent of men between the ages of 55 and 64 will have a significant aneurysm, and the likelihood increases to about four to six percent of those men over the age of 75.

The aorta is the largest artery in the body. All of the blood leaving the heart to go to the body leaves through the aorta and is then distributed to the smaller arteries. The aorta leaves the heart traveling towards the head, then makes a u-turn, and travels down the body just to the left of the spine before branching into two arteries in the pelvis which feed the separate leg. An aortic aneurysm is a weak spot in the wall of the aorta allowing the vessel to expand which increases in diameter.

Aneurysms are first classified by where they occur in the body. If they are in the thorax (above the diaphragm), they are thoracic aortic aneurysms. Aneurysms below the diaphragm are abdominal aortic aneurysms. Abdominal aortic aneurysms are further classified into those that extend above the renal arteries and those that do not (infrarenal).

They are then classified by whether or not they involve a dissection, a tear in the inner lining of the artery. Blood is then pushed into this tear under pressure from the heart which causes the tear to expand. This tear may extend in between the three concentric walls of the artery and travel down through the walls creating a new channel. The new channel may become so big that it compresses the normal flow of blood depriving organs of blood flow and oxygen.

More commonly, aneurysms do not start with a large tear, but result from a gradual weakening in the walls, especially of the muscular lining that maintains the shape of the vessel. With this weakness, the wall stretches further and the constant pressure from the pumping blood causes it to slowly expand.

Causes and Risk Factors of Aortic Aneurysms

Most aneurysms occur in older patients with a history of hypertension and atherosclerosis. However the causes of aneurysms are poorly understood.

Thoracic aortic dissections or aneurysms can occur in young people. The dissecting tear can begin as the result of trauma such as a car accident. Patients with Marfan’s syndrome (a problem with collagen which makes the vessels weak) or with an abnormal aortic valve, which increases stress on the artery, can cause it to dilate. Several basketball players have undergone surgery to correct this type of aneurysm. The actor John Ritter reportedly had an abnormal valve which led to an aortic dissection.
The causes of abdominal aortic aneurysms are less well-understood. The wall may become weak because atherosclerosis (cholesterol deposits) make the artery less healthy and cause it to weaken. Some studies have suggested low-grade inflammation in the arterial wall slowly digests the wall making it weak. There are some families that have multiple aneurysms suggesting that at least some cases are related to a genetic disorder.

 Symptoms of Aortic Aneurysms

Aneurysms can be small, or grow to the size of a grapefruit. Most produce no symptoms, especially when small. The most common symptom is a throbbing, or pulsation, in the abdomen. Sometimes, abdominal or lower back pain occurs.

Dissections, or dissecting aneurysms, on the other hand often cause excruciating pain. Those that occur in the chest may be mistaken for a heart attack and the two are occasionally related. The pain of this dissection is often described as “ripping” or “tearing”. It may travel, first being located in the chest, then moving to the back between the shoulder blades, and then lower in the body. Similarly, dissections in the abdominal aorta cause a traveling pain that tends to start at the level of the stomach and then migrates down, often to one leg or the other.
Aneurysms may also cause symptoms when they embolize. The inside layer of the ballooning section will usually be lined with blood that has clotted; if a piece of this clot breaks loose it is called an emboli. The symptoms associated with embolization will vary depending on where the embolus goes – if it goes to the brain, it will cause a stroke. More often, it will travel down the legs towards the feet. The area of the leg downstream from the clot will become cool, pale, and usually painful. It will eventually take on a bluish discoloration if the problem is not corrected.
Aneurysms may also rupture – the ballooning segment may pop. This is usually a fairly catastrophic event. Severe pain is usually followed quickly by low blood pressure and then death. This happens because the blood leaves the arteries and bleeds internally.

 Diagnosis of Aortic Aneurysms

There are two ways to diagnose an aneurysm prior to it causing symptoms: through physical examination or through a medical imaging study. During a physical examination, your doctor should listen to your abdomen and palpate (feel) your abdomen. Some aneurysms create a bruit, which is a certain kind of noise, that can be heard with a stethoscope. The palpation can be felt at about the level of the belly button. Even large aneurysm can be impossible to feel in subjects with a large amount of abdominal fat. On the other hand, thin people may be able to feel, or even see, the pulsations in their abdomen. In this case, one simply needs to measure how wide the area of pulsation is to determine whether or not it is normal.
Oftentimes, aneurysms are detected during some sort of imaging study. For instance, a doctor orders a CAT scan to look at the kidneys and the aneurysm is seen, or it is seen on a chest X-ray in someone thought to have pneumonia.

If an aneurysm is found or suspected, it should be further studied with some sort of dedicated imaging study. This may be a CAT scan, an MRI, or an ultrasound depending on its location. It is important to known how big the aneurysm is (its greatest diameter) and where it begins and where it ends.

Treatment of Aortic Aneurysms

The treatment for an aneurysm depends on many factors: where it is, how big it is, how quickly it is enlarging, and whether or not it has caused any symptoms. The major decision is whether or not surgery is needed to correct it.

For small aneurysms that are found incidentally, the treatment is usually watchful waiting. This involves medications to control blood pressure and repeating an imaging study in approximately six months. If it is increasing rapidly in size, surgery may need to occur sooner. Aneurysms less than four centimeters (cm) in diameter can be safely monitored, and those bigger than six cm should usually be repaired. There is a gray area in the middle; treatment for these size aneurysms will depend on many factors, especially the degree of risk of the surgery for each particular patient.
Some physicians will prescribe a blood thinner, such as coumadin, in addition to blood pressure medications. This medication will hopefully break apart any blood clots before they can cause damage, but there is a risk of too much bleeding.Immediate surgery is usually required for a dissecting aortic aneurysm, especially those in the thorax. Aneurysms that start further down the aorta may be managed with medications.

If surgery is necessary, the type of surgery and the degree of risk of the surgery depend on the location of the aneurysm. If it is in the thorax near the heart, the surgery may require cardiopulmonary bypass which increases the risk of the surgery. In the abdomen, if the aneurysm starts below the renal arteries, it may be repaired by inserting a synthetic graft. This material (similar to Gore-Tex) is attached to a small tube and threaded up from the leg and positioned inside of the aneurysm. When it is deployed, it creates a strong inner lining to the aorta, preventing it from expanding further or rupturing. This procedure does not involve a large incision and the recovery time is fairly quick, but it should only be done by someone with a fair deal of experience with the procedure. If the aneurysm involve the renal arteries, an open surgery is necessary to repair it and ensure that blood flow to the kidneys is maintained.

 Questions To Ask Your Doctor About Aortic Aneurysms

  • Where is the aneurysm located?
  • What type of aneurysm is it?
  • What is its size?
  • Is it rapidly growing?
  • What threat does it pose?
  • Is surgery indicated?
  • What are the risks involved?
  • How often have you performed this surgery?

December 15, 2008 at 11:00 am

Angiotensin II, atherosclerosis, and aortic aneurysms

The importance of angiotensin II (Ang II) in the pathogenesis of cardiovascular disease has become increasingly clear as evidence has mounted for the clinical benefits of angiotensin-converting enzyme (ACE) inhibitors. Three pivotal heart failure trials in the 1980s (CONSENSUS, SOLVED, and SAVE) showed significantly increased survival among subjects treated with ACE inhibitors rather than conventional therapy. An interesting aspect of these trials was a 25% decrease in myocardial infarctions, suggesting that inhibition of the renin-angiotensin-aldosterone system (RAAS) by these drugs prevents atherosclerosis . Recently, the HOPE trial showed forcefully that chronic ACE inhibition can reduce cardiovascular events in patients with multiple risk factors for atherosclerosis.

In this issue of the JCI, Daugherty etal.  provide exciting insights into potential relationships between Ang II, atherosclerosis, and aortic aneurysm formation. These authors studied the effects of Ang II in apoE–/– mice, which have increased total cholesterol and VLDL/LDL levels and develop spontaneous atherosclerosis even when fed a low-fat, low-cholesterol diet . Ang II infusion dramatically promoted vascular pathology, including an increase in the extent of atherosclerosis, a change in the nature of lesions and surrounding adventitial tissue, and formation of large abdominal aortic aneurysms. Furthermore, since atherosclerosis and aneurysm formation were not observed in strain matched apoE+/+ mice, Ang II’s effects evidently depend on the hyperlipidemic state.

Because Ang II infusion does not cause hypertension in mice, the effects of this factor on vascular pathology must be direct and independent of changes in blood pressure. How, then, does Ang II increase vascular pathology in hyperlipidemia? The answer is that Ang II acts on multiple cell types — endothelial cells, smooth muscle cells, monocytes, and lymphocytes — and promotes an inflammatory reaction in the vessel wall. Mediating the effects of Ang II, most likely, is monocyte chemoattractant protein-1 (MCP-1), a product of endothelial and smooth muscle cells, whose expression is induced by Ang II. Deficiency of the major MCP-1 receptor (CCR2) reduces atherosclerosis in the apoE–/– mouse , so it appears that Ang II increases inflammation and stimulates atherosclerosis by stimulating MCP-1 expression.

Ang II is known to induce VCAM-1 expression by activating NF-κB–dependent gene expression, and it probably induces MCP-1 expression by a similar mechanism. In addition, Ang II stimulates production of reactive oxygen species (ROS) by inducing a vascular NADH oxidase ,possibly through its specific effects on expression or activity of Mox1, a subunit of the vascular smooth muscle cell NADH oxidase . Induction of vascular ROS by Ang II appears in rodent models to be significantly greater than by other vasoconstrictors, such as norepinephrine . Thus,it is logical to propose that Ang II promotes atherosclerosis by two redox mechanisms: first, by increasing levels of lipid-oxidizing ROS, which promote the loading of lipid into foam cells; and second, by inducing the expression of redox-sensitive gene products, such as VCAM-1 and MCP-1.

Another important mechanism by which Ang II promotes atherosclerosis is endothelial dysfunction, measured by impaired vasorelaxation in response to acetylcholine. Ang II causes endothelial dysfunction in animal models , and ACE inhibitors improve endothelial dysfunction in patients with coronary artery disease.While endothelial dysfunction may be in part related to a change in vascular redox state that decreases nitric oxide bioavailability, other aspects of endothelial dysfunction may represent more direct effects of Ang II. Both VCAM-1  and PAI-1  are induced by this factor, and both of these proteins promote inflammation and thrombosis. Perhaps of greater consequence is the recently demonstrated effect of Ang II on endothelial cell apoptosis. Clearly, endothelial apoptosis must have still more dramatic effects on binding of platelets and inflammatory cells than does endothelial dysfunction. The exciting possibility that the proapoptotic effects of Ang II are augmented in apoE–/– mice must await future studies.

Perhaps the most interesting aspect of the present study was the appearance of aneurysms in the Ang II–treated mice. Aortic aneurysms are characterized by weakening, dilation, and occasional rupture of the vessel wall. Development of aneurysms is associated with inflammation, tissue remodeling, and upregulation of matrix-degrading proteinases, and it correlates with atherosclerosis, aging, pulmonary emphysema, and high blood pressure . Matrix metalloproteinases (MMPs) can degrade a variety of extracellular matrix (ECM) molecules , and increased levels of MMP-2 (gelatinase A), MMP-9 (gelatinase B), and MMP-12 (macrophage elastase) have been found in the aneurysmal vessel wall. Conversely, inhibitors of MMPs have been shown to prevent aneurysmal degeneration and rupture in animal models. These data indicate that degradation of ECM molecules is a critical event leading to weakening of the vessel wall. It is also possible that fragments of ECM proteins, released by proteolysis, contribute to matrix remodeling during aneurysm development by upregulating production of MMPs, serving as chemoattractants for monocytes and macrophages, or altering cell growth responses.

Several previous studies have also linked Ang II to aneurysm formation. Thus, Huang et al. showed that ACE inhibitors exert beneficial effects in a rat aneurysm model, and Nishijo etal. found that Ang II stimulated aneurysm formation in hypertensive mice . Ang II may promote development of aneurysms by contributing to the inflammatory response in the vessel wall — as seen in the present study  — or may act by altering smooth muscle cell migration , inducing ECM and MMP production , or stimulating ROS formation . In summary, the present study by Daugherty etal. provides additional rationale for inhibiting the RAAS to limit the progression of atherosclerosis; it also suggests benefits for ACE inhibition in peripheral vascular disease and aortic aneurysms, as well as coronary artery disease and myocardial infarction.

December 11, 2008 at 10:15 am

Thoracoabdominal aortic aneurysms- preoperative and intraoperative factors

Thoracoabdominal aortic aneurysms

preoperative and intraoperative factors determining immediate and long-term results of operations in 605 patients:

Graft inclusion and vessel reattachment to openings made in the graft were employed in the treatment of 605 patients with thoracoabdominal aortic aneurysms. These patients were divided into four groups on the basis of the extent of aneurysm. Group I consisted of those patients with involvement of most of the descending thoracic and upper abdominal aorta; group II involved most of the descending thoracic aorta and most or all of the abdominal aorta; group III involved the distal descending thoracic aorta and varying segments of abdominal aorta; and group IV involved most or all of the abdominal aorta including the segment from which the visceral vessels arose. The cause of aneurysm formation was medial degenerative disease in 80%, and dissection in 17%; other causes were responsible in the remaining 3%. The median age was 65 years and associated diseases including aneurysms involving other segments, atherosclerotic occlusive disease, heart disease, chronic obstructive pulmonary disease (COPD), hypertension, and renal insufficiency were frequent. The aneurysm was symptomatic in 70% of cases and rupture had occurred in 4% of cases. There were 54 (8.9%) early (30-day) deaths and 151 late deaths; 400 (66%) patients were still alive 3 months to 20 years after operation, including 60% at 5 years. Statistically significant pre- and intraoperative variables by univariate analysis that were predictive of increased risk of early death were advancing age, associated diseases that included COPD, renal artery occlusive disease, atherosclerotic heart disease, renal insufficiency, and long aortic clamp time. Three of these (age, clamp time, and the presence of COPD) retained significance by multivariate analysis. Variables predictive of risk of late death were age, dissection, extent of aneurysm, rupture, heart disease, cerebrovascular disease, COPD, hypertension, and poor renal function. Age, rupture, renal dysfunction, extent of aneurysm, and dissection retained their significance by multivariate analysis. Variables predictive of neurologic disturbances of the lower extremities included rupture, reattachment of intercostal and lumbar arteries, clamp time, dissection, extent and age. Rupture, reattachment of vessels, dissection, and extent of aneurysm retained significance by multivariate analysis. Thus, the risk of this complication was greatest in patients with extensive lesions (group II) with aortic dissection. The greatest risk of renal failure after operation that required dialysis was in patients who had impaired renal function before operation. Methods employed did not prevent these complications.

December 7, 2008 at 10:13 am

Abdominal Aortic Aneurysm Expansion

Risk Factors and Time Intervals for Surveillance

Background

Intervention to reduce abdominal aortic aneurysm (AAA) expansion and optimization of screening intervals would improve current surveillance programs. The aim of this study was to characterize AAA growth in a national cohort of patients with AAA both overall and by cardiovascular risk factors.

Methods and Results

In this study, 1743 patients were monitored for changes in AAA diameter by ultrasonography over a mean follow-up of 1.9 years. Mean initial AAA diameter and growth rate were 43 mm (range 28 to 85 mm) and 2.6 mm/year (95% range, –1.0 to 6.1 mm/year), respectively. Baseline diameter was strongly associated with growth, suggesting that AAA growth accelerates as the aneurysm enlarges. AAA growth rate was lower in those with low ankle/brachial pressure index and diabetes but higher for current smokers (all P<0.001). No other factor (including lipids and blood pressure) was associated with AAA growth. Intervals of 36, 24, 12, and 3 months for aneurysms of 35, 40, 45, and 50 mm, respectively, would restrict the probability of breaching the 55-mm limit at rescreening to below 1%.

Conclusions

Annual, or less frequent, surveillance intervals are safe for all AAAs 45 mm in diameter. Smoking increases AAA growth, but atherosclerosis plays a minor role.

December 3, 2008 at 9:53 am

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.

Discussion
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

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