Disclosure
Atherosclerosis of peripheral vessels, or peripheral vascular disease (PVD) is the most common cause of symptomatic stenosis in human vascular tree. The pathogenetic mechanisms that lead to PVD are similar to those of coronary artery disease (CAD). The risk factors are also similar and include a positive family history, cigarette smoking, diabetes, hypertension, dyslipidemia, advanced age, and physical inactivity, among others. Approximately 10 million Americans have PVD, only one half of whom manifest symptoms. PVD is the leading cause of limb amputation; the annual rates of limb loss are 2% in nondiabetic patients and 7% in diabetic patients. The prevalence of PVD in those older than 65 years is even greater. The most common symptom is pain in 1 or both legs (claudication), which usually occurs walking. In advanced cases, ulcers or gangrene can develop. Therapeutic goals for PVD include relief of symptoms and preservation of organs and tissues. Aggressive risk-factor reduction and pharmacologic treatments are the keystones in patient care. Once the affected luminal diameter is compromised by 75% or more, the risk of ischemia and limb loss becomes high. After this point, medical therapy, such as antiplatelet and vasodilators, become less effective, and revascularization becomes necessary. In the past, surgical revascularization has been performed with an acceptable risk. The work of pioneers, such as Dotter and Gruntzig, has opened up a novel era of percutaneous revascularization with techniques such as percutaneous transluminal angioplasty (PTA), a less invasive option in the management of PVD. Over the past 30 years, PTA has experienced steady growth and recently, it has become the first-line therapy for PVD. Increased emphasis on containing and reducing the healthcare expenditures has also enhanced the use of PTA (as compared with surgical procedures), which can be performed as a same-day procedure that saves overall costs. For excellent patient education resources, visit eMedicine's Circulatory Problems Center and Cholesterol Center. Also, see eMedicine's patient education articles Peripheral Vascular Disease, High Cholesterol, and Cholesterol FAQs.
Risk factors Risk factors for iliofemoral disease are similar to those for CAD and include diabetes mellitus, cigarette smoking, high blood pressure, positive family history of premature atherosclerosis, and hypercholesterolemia. The progression of PVD and its complications are accelerated in patients with diabetes mellitus and a history of cigarette smoking. Diabetes is the strongest predictor of serious complications of PVD. Gangrene occurs 6 times more frequently in patients with diabetes than in others. Diabetes has been associated with more than 50% of major amputations in patients with iliofemoral PVD. Smoking is another major predictor of complications. In a study, nondiabetic patients who quit smoking after the development of intermittent claudication did not progress to rest pain, whereas 16% of those who continued to smoke progressed to rest pain. Because the risk of limb loss is 20% in patients with intermittent claudication who are diabetic or use tobacco, revascularization procedures should be strongly considered in these patients. The incidence of atherosclerotic disease in the distal aorta and iliofemoral arteries varies with age. Symptomatic patients younger than 40 years frequently have aortoiliac disease. Femoropopliteal disease, on the other hand, accounts for more than two thirds of PVD cases in patients older than 40 years; these patients present with claudication. Additionally, approximately two thirds of patients with iliac disease have discrete stenoses, whereas two thirds of patients with femoral disease have long segmental occlusions. Morbidity and mortality Long-term survival is reduced in patients with iliofemoral obstructive disease, compared with survival of the healthy population. Concomitant CAD is the most common cause of death. Patients with PVD have an all-cause mortality rate 3 times higher and a cardiovascular mortality rate 6 times higher than those of the healthy population. The usual cause of death in these patients is acute myocardial infarction or stroke. The progression to severe limb ischemia or amputation is unusual in patients with intermittent claudication (1.4% per year). The major risk factors for limb loss are diabetes and tobacco abuse.
Clinical presentationSigns and symptoms The 2 most important symptoms of iliofemoral disease are intermittent claudication and rest pain. Intermittent claudication is described as a deep-seated, uncomfortable, aching sensation in the calf, thigh, or buttock that is precipitated by walking and relieved within minutes by rest. Symptoms develop when the vascular flow or supply does not meet the demand for blood flow to the exercising lower-extremity muscles. The amount of exertion needed to induce claudication varies little from one day to another. Symptoms of intermittent claudication may affect both legs. Claudication is generally brought on more rapidly by walking uphill than by walking on level ground. Patients frequently learn to pace themselves or avoid most activities that involve climbing a graded surface. The differential diagnosis of intermittent claudication includes pseudoclaudication. Pseudoclaudication Pseudoclaudication and cauda equina syndrome are caused by spinal stenosis. In pseudoclaudication, leg pain may occur after sitting for long periods of time in one position or immediately upon rising from a seated position. Walking may provide partial relief with pseudoclaudication but not with true claudication. True claudication Patients with true claudication have decreased or absent peripheral pulses at the level of the popliteal, dorsalis pedis, or posterior tibialis arteries. They may also have femoral bruits or absent femoral pulses. Some patients may also have arterial ulcerations that involve the toes or the feet below the malleolar line (in contrast to venous ulcers, which usually occur above the malleolar line and which may be associated with brawny edema). Rest pain Rest pain occurs when the blood supply does not meet the nutritional demands of the muscles and other tissues of the affected extremity, resulting in critical limb ischemia leading to tissue loss, ulceration, or gangrene. Often, the symptoms are most severe in the toes and feet and relieved by placing the affected foot in a slightly dependent position. Physical examination often shows evidence of dependent rubor and absent pedal pulses. The differential diagnosis includes acute limb ischemia, among other conditions. Acute limb ischemia may also arise as a result of an embolism or acute thrombosis that forms after an intravascular procedure. If acute sensorimotor deficits persist longer than 6 hours, irreversible tissue injury may have occurred. The examination shows intact pedal pulses. Other possible diagnoses should also be considered; these include small-vessel disease and cholesterol-embolization syndrome. DiagnosisBoth noninvasive and invasive modalities are used for diagnostic evaluation. Noninvasive testing includes Doppler ultrasonography and magnetic resonance angiography (MRA). Doppler sonography and evaluation of the ankle-brachial index For Doppler sonography, pneumatic cuffs are placed along the leg and inflated to suprasystolic pressures. During controlled cuff deflation, a Doppler probe placed over the dorsalis pedis artery or posterior tibial artery to detect the onset of flow. Normally, the systolic blood pressure in the leg is slightly higher than that in the arm; therefore, the normal ankle-brachial index (ABI) of systolic blood pressure should be 1.0 or slightly greater. An ABI less than 0.95 is considered abnormal. Patients with leg claudication typically have an ABI less than 0.8. In patients with ischemia at rest, the ABI is frequently less than 0.4. Magnetic resonance angiography MRA is another noninvasive approach for imaging the peripheral circulation. It does not involve the risk of intravascular catheterization or conventional contrast agents. Angiography Invasive imaging with contrast arteriography is still required when the diagnosis remains unclear or endovascular procedures are planned. |
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Medical managementExercise is the cornerstone of therapy that can improve symptoms, exertional capacity, and quality of life in patients with PVD. Risk-factor reduction to the same magnitude as that recommended for prevention of coronary atherosclerosis is of paramount importance. Patients who smoke must be emphatically counseled about complete smoking cessation. Quitting smoking retards the progression of symptoms, decreases the requirement for vascular procedures, and improves graft patency. Aggressive cholesterol goals are recommended for patients with PVD in the National Cholesterol Education Program (NCEP) Adult Treatment Panel III (ATP III) guidelines, which consider PVD a coronary risk equivalent. Hypercholesterolemia must be brought under control with statin therapy. Hypertension must also be controlled with use of angiotensin converting enzyme inhibitors or selective beta1-blockers, and weight reduction must be emphasized. Glycemic control in patients with PVD is critical because, in the presence of diabetes, PVD progresses aggressively to ischemic rest pain and ulceration. Some of the newer risk factors for atherosclerosis in PVD that should be managed as well include hyperhomocystinemia, familial dysbetalipoproteinemia type III (with modest elevations of triglycerides and cholesterol), high lipoprotein(a), and elevated C-reactive proteins. Medications Several medications can be used for symptom abatement and improvement in functional capacity. Cilostazol, a phosphodiesterase III inhibitor, can be used for symptomatic claudication relief. It causes smooth muscle relaxation, vasodilatation, platelet inhibition, and modest improvement in lipoprotein profile. Pentoxifylline, a methylxanthine derivative, is approved for symptomatic relief, as well. Prostaglandins are potent vasodilators and have been used in patients with critical limb ischemia. L-Carnitine, a skeletal muscle metabolic co-factor, can help normalize skeletal muscle metabolism. L-Arginine enhances vascular endothelial production of nitric oxide and can cause vasodilatation and anti-atherosclerotic effects. Protein and gene-based angiogenic growth factors, such as basic fibroblast growth factor and vascular endothelial growth factor, hold promise for the future. Peripheral interventionsRevascularization by percutaneous catheter techniques or surgery is required when intermittent claudication progresses to rest pain or tissue ischemia (ABI < 0.20), threat of limb loss, acute arterial occlusion, and difficult to heal ulcers. It may also be needed for patients with lifestyle-limiting claudication and significant symptoms. Endovascular interventions initially begin with the desire to avoid the morbidity and operative risk of surgical revascularization. However, interventional techniques have become more common. Recent growth in the application of peripheral angioplasty is a result of rapid technologic advances that include smaller catheter and balloon profiles, better balloon and guidewire construction, superior imaging equipment, and the introduction of stents. Both short- and long-term outcomes of PTAs have improved tremendously. Some yet-unsolved issues include the problems of restenosis and difficulty in opening diffusely diseased or occluded arteries. Patients also seem to prefer less invasive PTA over surgery. Often, the lower risk of partial revascularization with PTA may be more acceptable than total surgical revascularization, which may potentially cause more morbidity. For example, a patient with a limb-threatening ischemic ulcer may benefit from even a short-term resumption of blood flow that can expedite ulcer healing. The prevalence of PVD is higher in the elderly. The availability of PTA for this subgroup of patients, who often have associated comorbidities and involvement of multiple vascular beds, has made PTA a first-line treatment for PVD. Indications Indications for PTA or stenting include (1) intermittent claudication that causes severe disabling symptoms (eg, claudication when the patient walks <200 m), (2) the presence of rest pain, or (3) the presence of ischemic ulceration. Procedures The techniques of peripheral intervention include PTA, a stent procedure, and the use of stent grafts. Generally, PTA is the procedure of choice for shorter, more discrete stenoses. Variables that favor PTA include stenosis exposed following thrombolytic therapy and short stenoses. The latter include stenoses less than 5 cm in iliac artery, those less than 10 cm in the superficial femoral artery, and those less than 2 cm in the tibial artery. Aortoiliac PTA and stenting PTA or stenting may be the preferred treatment for focal lesions in the distal abdominal aorta and common iliac and external iliac arteries when the lesional length is less than 5 cm in the iliac artery. Femoropopliteal PTA and stenting Some patients with intermittent claudication and femoropopliteal disease may be candidates for PTA or stenting. However, stents are not indicated as an initial approach and should be reserved for salvaging extensive dissection or thrombosis following PTA. Focal stenosis of generally less than 3 cm in length in the common or superficial femoral artery is appropriate for PTA. Newer approaches High rates of restenosis are prevalent in femoropopliteal interventions. Vascular brachytherapy utilizing gamma or beta radiation can be administered through a catheter-based approach. Infrapopliteal PTA Infrapopliteal PTA has a limited advantage in patients with claudication and is generally needed in those with refractory claudication and limb ischemia. Outcome of PTA procedures The acute procedural success rate for PTA is 90% and the patency rates are 80% at 1 year, 70% at 3 years, and 60% at 5 years. Stent placement, especially in the iliac arteries, may be associated with higher success rates. The 1-year restenosis rates are less than 5%. The success rates in stenoses below the inguinal ligaments are lower than for those in the iliac arteries. In addition, success rates are better for revascularization procedures performed in the setting of good distal runoff or intermittent claudication than in critical limb ischemia. In infrainguinal locations, the rates of repeat intervention are approximately identical after the use of stents versus balloon angioplasty in the femoropopliteal segment. Complications Most complications arise from access-site problems. Events such as hematomas, pseudoaneurysms, or thromboses occur in 2-5% of patients. Atheroemboli causing blue-toe syndrome occur in less than 1% of patients. Future trendsNewer therapies, such as angiogenesis, seem promising for future medical interventions. Availability of newer stents, especially drug-eluting stents, may increase the therapeutic options and result in patients with femoropopliteal and infrapopliteal disease. Surgical intervention The indications for bypass reconstruction of the femoral-popliteal and femoral-tibial segments are generally more stringent than those for aortofemoral reconstruction because the likelihood of long-term success is lower and the risk of limb-threatening complications is higher than they are for iliofemoral disease. Inflow to the level of the profunda femoris is important in maintaining collateral circulation to the infrapopliteal segment. Adjunctive therapy Whenever an endovascular or surgical treatment is undertaken, concomitant medical therapy must also be strictly enforced along with aggressive risk reduction.
Mechanics of peripheral angioplasty While surgical treatment of arterial stenosis involves direct visualization and remodeling of the stenosed segment by using forceps, a scalpel, and sutures, the basic premise behind treating a stenosis through peripheral angioplasty is to apply a strong but carefully controlled centrifugal force from within the vascular lumen. For this, a small, elongated polymer balloon attached to 1 end of a long catheter is percutaneously introduced through a small peripheral arterial puncture and then inflated for a few seconds. Balloons come in various shapes, diameters, and lengths, and they are chosen according to the diameter of the artery in the adjacent nonstenosed segment and the length of the stenosed segment, respectively. The mechanism of PTA involves outward dilatation of the stenosis by straddling an initially uninflated balloon under negative pressure attached through the airtight fluid-filled lumen of the balloon catheter to an inflation device capable of generating several atmospheres of pressure. The outward radial force, called hoop stress, stretches or separates the components of the arterial wall. This radial force is a product of the pressure applied and the area against which it is applied. The Laplace law describes this force: hoop stress = pressure X diameter. Equipment The equipment for PTA includes balloon catheters of different designs and compliance; guide catheters with various tip shapes; and guidewires, including standard, steerable, and slick guidewires. Preprocedural activities Several activities should be done before the procedure. These include selecting patients, obtaining informed consent, performing routine measures in terms of medications and other preparations, setting up the procedure room, completing sterile patient preparation, and conducting studies such as fluoroscopy and cine imaging. Procedure The procedure involves numerous components: monitoring, conscious sedation of the patient, gaining peripheral access, reviewing diagnostic images, placing guides, advancing guidewires, administering intraprocedural pharmacologic agents (eg, for anticoagulation or vasodilation), preparing and inserting the balloon, positioning and inflating the balloon, treating the patient after dilation, placing the stent, other interventions (eg, atherectomy, laser procedures, use of a transluminal extraction catheter), and removing the catheter. Postprocedural activities Post-PTA care involves access-site management, use of closure devices, routine postprocedural management, and the provision of discharge instructions and follow-up.
Epidemiology Atherosclerotic disease producing stenosis of more than 50% in at least 1 renal artery is encountered in 30% of patients with CAD, 38% of patients with abdominal aortic aneurysms (AAAs), and 39% of patients with peripheral vascular (iliofemoral) disease. In approximately one third of the instances, renal artery disease is bilateral. About 11% of renal arteries with stenoses of greater than 60% progress to total occlusion within 2 years. Clinical presentation Most patients have no overt symptoms. Generally, the renal artery stenoses are found during flush aortography in patients undergoing cardiac catheterization who have difficult-to-control hypertension. The most common consequences of renal stenosis include hypertension, ischemic nephropathy, and volume overload. Diagnostic assessment Captopril renography has been used in the past for diagnosis of bilateral renal artery stenosis. Renal atherosclerosis can just as accurately be predicted by the presence of clinical parameters, such as advanced age, female sex, atherosclerosis in other vascular beds, recent onset of hypertension, smoking, abdominal bruits, elevated creatinine level, and hypercholesterolemia. MRA has emerged as a potentially useful noninvasive imaging method for diagnosing renal artery stenosis. Flush abdominal aortography in patients undergoing coronary arteriography can be performed when the likelihood of renovascular disease is high. This imaging is usually performed by placing a pigtail catheter at the level of the first lumbar vertebra and injecting contrast material at a rate of 20 mL/s for a total contrast-agent volume of 6-12 mL. Renal angioplasty and stenting Indications for angioplasty and stenting include uncontrolled hypertension requiring the use of 3 or more agents. The best treatment for renal artery stenoses is not known. When balloon angioplasty alone was compared with medical therapy, no significant differences or favorable trends in serum creatinine levels were observed between the treatment groups during 3- to 54-month follow-up. Stenting of renal arteries has a higher rate of angiographic success than balloon angioplasty. The technical success rate of renal arterial stenting is 95-99%. Approximately 4-18% of patients undergoing renal artery stenting achieve a cure of hypertension and as many as 22-61% of patients show moderate change in blood pressure control. The procedural mortality rate is less than 1.3%, whereas surgical revascularization for renal artery stenoses is associated with an operative mortality rate as high as 9%. The restenosis rates after renal artery stenting are in the range of 11-19% at 1 year.
Subclavian and brachiocephalic artery diseaseRisk factors Risk factors for atherosclerotic disease of the upper extremity include smoking and diabetes. Nonatherosclerotic causes include Takayasu arteritis, radiation-induced atherosclerosis, trauma, and thoracic outlet obstruction. Signs and symptoms Patients with atherosclerotic disease of an upper extremity may develop symptoms of ischemia, but these occur less commonly than symptoms of iliofemoral disease. This difference is partially explained by a lower incidence of severe obstruction in the subclavian and brachiocephalic (innominate) arteries than in the iliofemoral systems and also by the increased tendency for collateral development around the shoulder and scapula. Most patients with atherosclerotic obstruction of the subclavian or brachiocephalic arteries are asymptomatic. Usually, the condition is incidentally discovered when a difference in blood pressure measurements between a patient's arms is noticed or when evidence of obstructive disease is observed during angiography or a noninvasive evaluation. After coronary artery bypass surgery, patients may have incomplete relief of angina when flow in the left internal mammary artery is jeopardized by an obstruction of the proximal left subclavian artery due to atherosclerosis. Careful attention should be given to preoperative bilateral arm pressure measurements and the use of selective subclavian angiography. Treatment Percutaneous treatment of atherosclerotic obstructions of the subclavian or brachiocephalic vessels can be considered in patients who have hand claudication or subclavian steal syndrome. A syndrome of large-vessel atheroembolism from the brachiocephalic artery to the central nervous system or retina (amaurosis) can be successfully treated with angioplasty and stenting. Treatment should also be considered for patients who need improved inflow for distal grafts, such as internal mammary coronary artery bypasses, axilloaxillary bypasses, or dialysis bridge grafts and fistulas. Experience with subclavian or brachiocephalic stenting is limited to case reports and small series. However, stenting appears to be superior to balloon dilatation alone. In a small series, 18 consecutive patients were treated with 100% success and no complications. These results compared favorably with those of surgical series. Carotid artery diseasePrevalence Stroke is the third leading cause of death in the United States, after heart disease and cancer. More than half a million Americans have new or recurrent strokes each year, resulting in almost 3 million stroke survivors with varying degrees of disability. Types of stroke The various types of stroke include ischemic stroke, cardioembolic stroke, and others. Ischemic stroke Ischemic stroke, unlike myocardial infarction, has multiple pathogenic mechanisms. Carotid artery disease is responsible for approximately 25% of strokes in the general population and causes about 30% of strokes in the population older than 65 years. Atherosclerosis of the internal carotid artery causes strokes primarily by embolizing platelets and plaque debris into the cerebral circulation. Complete occlusion of an isolated internal carotid stenosis is a less common cause because more than 75% of patients with an isolated complete carotid occlusion are protected against stroke by collateral flow. Ischemic stroke can also occur from the embolization associated with severe atherosclerotic disease of the ascending aorta or arch. The occlusion of small end-arteries may cause lacunar strokes. They usually take place in the internal capsule or thalamus and occur most commonly in hypertensive, diabetic, or elderly patients. Cardioembolic stroke Cardiac embolism accounts for 20% of strokes in adults aged 45-60, and is associated with the following: atrial fibrillation, recent myocardial infarction, dilated cardiomyopathy, prosthetic or native valvular heart disease, endocarditis, and a patent foramen ovale with paradoxical embolism. Other The least common mechanism for ischemic stroke is a reduction in total cerebral blood flow. Signs and symptoms Patients with carotid artery disease may be asymptomatic, they may have evidence of transient ischemia, or they may have sustained irreversible neurologic injury in the anterior circulation. Transient ischemic attacks (TIAs) last an average of 14 minutes and may produce temporary contralateral sensorimotor deficits, dysphasia (dominant hemisphere), neglect (nondominant), or ipsilateral amaurosis fugax. Diagnostic evaluation A diagnosis of carotid artery disease by means of physical examination alone is probably inaccurate. Only 40% of patients with a significant internal carotid stenosis have a cervical bruit. Of those with a cervical bruit, only 20% have a significant carotid stenosis. To complicate matters further, only about 50% of strokes in patients with carotid disease have ischemia and disease in the ipsilateral carotid distribution. The anatomic diagnosis of carotid disease can be confirmed with noninvasive or invasive angiographic approaches. Some authors advocate the use of duplex and transcranial Doppler ultrasonography as the first step in the evaluation of carotid disease; this approach is accurate in 90% of cases. MRA is also emerging as a noninvasive means of visualizing the carotid, vertebrobasilar, and major intracranial vessels, but it provides less detail than contrast-enhanced methods. When the combination of MRA and Doppler ultrasonography is used, however, nearly 100% specificity in defining the hemodynamic severity of carotid stenoses is achieved. Treatment TIAs afflict approximately 50,000 people in the United States per year. Stroke develops in one third of these patients, usually within 1 year of the transient attack. The goal of therapy is to prevent the progression to ischemic stroke. Carotid endarterectomy Several randomized studies have compared carotid endarterectomy (CEA) with medical therapy, but debate continues about whether prophylactic endarterectomy is useful in asymptomatic patients. Between 1987 and 1993, investigators in the Asymptomatic Carotid Atherosclerosis Study (ACAS) enrolled 1,659 patients aged 40-79 years. The main results of the study supported the use of CEA for selected asymptomatic patients with carotid artery disease, and the overall risk reduction for stroke was 55% when this procedure was used. For symptomatic patients with carotid disease, the benefits of CEA are more pronounced. In the North American Symptomatic CEA Trial, 595 patients with carotid artery stenoses of more than 70% were randomly assigned to CEA or medical therapy. Surgery was associated with an absolute reduction of 17% and a relative reduction of 65%. Formal guidelines recommend CEA for symptomatic patients or asymptomatic patients with stenosis of more than 60%, so long as the operative mortality/morbidity rates are less than 3%, 5%, and 7% for asymptomatic disease, TIA, and prior stroke, respectively. Carotid stenting To the authors' knowledge, no controlled studies of carotid stenting versus endarterectomy have been reported. At the current time, CEA is the treatment of choice for most patients with symptomatic or asymptomatic severe carotid disease. In certain situations, however, carotid stenting should be considered. Situations in which carotid stenting may be preferred may involve patients with the following: restenosis after prior endarterectomy, radiation therapy to the neck, and inaccessible intracranial and difficult-to-access intrathoracic disease, coexisting severe medical illnesses, and acute neurologic syndromes. In all cases in which carotid stenting is contemplated, a vascular surgeon or neurosurgeon should evaluate the patient for CEA. If the risks of surgery are excessive, he or she should refer the patient to an experienced interventionalist for possible carotid stenting. It is also important to tell the patient that carotid stenting remains experimental. The largest uncontrolled experience with carotid stenting was reported by Wholey et al, who assembled a collection of investigator-reported experiences in 5,210 patients treated at 34 centers. These authors reported a 98.4% success rate. Investigator-reported complications within 30 days after carotid stenting in their registry included the following: 134 TIAs (2.8%), 129 minor strokes (2.7%), and 71 major strokes (1.5%). A total of 41 deaths (0.9%) occurred within the 30-day postprocedural follow-up period. Mathur et al observed that advanced age, the presence of stenoses longer than 10 mm, and multiple stenoses are predictors of stroke after carotid stenting. Because of the increased complication rates of carotid stenting in asymptomatic patients older than 80 years, the recommendation for medical therapy for this group is reasonable. Recently reported results from Stenting and Angioplasty with Protection in Patients at High Risk for Endarterectomy (SAPPHIRE) study in which carotid stenting with the use of a distal protection device was compared with surgery show that stenting is somewhat superior. Vertebral artery diseaseThe reported experience with balloon angioplasty and stenting for vertebrobasilar insufficiency is limited to a small series of patients. Although vertebrobasilar angioplasty with stent insertion is technically feasible, embolic complications (eg, in the brainstem) can be life-threatening. It is also important to recognize that, if the contralateral vertebral artery is patent and the carotid arteries are normal, the patient is unlikely to have vertebrobasilar insufficiency. About 25% of patients with vertebrobasilar insufficiency have carotid disease with symptoms that can be relieved with treatment. As more experience is gained, however, vertebrobasilar interventions may be offered as an alternative therapy to patients with medically refractory, posterior-circulation occlusive disease. No current evidence supports prophylactic vertebrobasilar interventions in asymptomatic patients. Carotid disease and severe CADSignificant carotid artery stenoses, even in asymptomatic patients, are responsible for as many as 30% of strokes that occur early after coronary artery bypass grafting. The perioperative stroke risk is less than 2% when carotid stenoses are less than 50%, 10% when stenoses are 50-80%, and 11-19% when stenoses are greater than 80%. Patients with bilateral, high-grade stenoses or occlusions have a 20% risk of having stroke. CEA is recommended for patients with severe extracranial carotid vascular disease before or at the same time as bypass surgery. CEA is associated with a lower risk of significant neurologic complications than that of bypass surgery in the presence of high-grade carotid stenoses. CEA performed in this setting carries a low mortality rate (3.5%), it reduces the early postoperative stroke risk to less than 4%, and it is associated with a 5-year stroke-free rate of 88-96%. The decision about who should undergo preoperative carotid screening remains controversial. Predictors of neurologic risk include the presence of carotid bruits, advanced age, female sex, known PVD, previous TIA or stroke, a history of smoking, and left main CAD. Many centers screen all patients older than 65 years with either duplex ultrasonography or cerebral angiography at the time of diagnostic coronary arteriography. When surgery for carotid and CAD is planned, the most common approach is to perform the operation in a staged manner. The patient first undergoes carotid surgery, which is followed by bypass surgery in 1-5 days. If the patient has compelling cardiac symptoms or coronary anatomy, the operations may be performed during a single period of anesthesia with the CEA immediately preceding the coronary bypass. Neither strategy has been established as being superior. In patients with refractory unstable coronary symptoms and incidentally discovered asymptomatic carotid disease, emergency bypass surgery is commonly performed first because of the insurmountable logistics of arranging for an emergency combined procedure. However, the risk of stroke is increased if a reversed-stage procedure is used where the coronary bypass operation precedes the CEA by more than 1 day.
Aortic aneurysmAortic aneurysm and rupture Aneurysms can affect any arterial bed, but infrarenal AAAs account for most arterial aneurysms. An aortic aneurysm is defined by a diameter of greater than 3 cm. Most AAAs are incidentally discovered during abdominal ultrasonography or angiographic examinations performed for other indications. The growth rate for AAAs is variable, but averages 0.3-0.5 cm/y. Whether an aneurysm ruptures is most strongly related to its size. In a database of 2257 patients followed up with serial ultrasonographic examinations, risk factors for rupture included size greater than 5 cm, female sex, high mean arterial pressure, and current smoking habit. The number of ruptures per 100 patient-years was 0.3, 1.5, and 6.5 for aneurysms measuring less than 4, 4-4.9, and 5-5.9 cm, respectively. Mortality rates Approximately 16,000 patients die from ruptured aortic aneurysms per year in the United States. The overall mortality rate for a ruptured AAA is 80%, and 25% of patients die before they reach the hospital. After admission to the hospital, the mortality rate averages 1% per hour, which underscores the importance of early diagnosis and treatment. Diagnostic evaluation Accurate sizing requires the performance of abdominal ultrasonography, CT scanning, or MRI. Aortography does not provide a clear delineation of the size of the aneurysm because the presence of laminated thrombus may result in an underestimation of its size. Surgical treatment Elective surgical therapy of AAAs is associated with a mortality rate of 3-5%. The procedure involves making an incision into the aneurysm and inserting a synthetic graft. Complete aortobifemoral bypass surgery is often necessary in the presence of coexisting severe iliac disease. The surgical treatment of abdominal aneurysms is associated with an operative mortality of 4-6% overall and 2% in low-risk patients. Conditions that increase the risk of surgical intervention include patient age greater than 75 years, myocardial infarction within 6 months, renal insufficiency or the need for renal artery bypass surgery, inflammatory aneurysms, and the presence of a horseshoe kidney. Endovascular repair with stent-grafts Experience with the endovascular repair of AAAs is increasing, as several new devices have been developed. Moore et al compared the experience of their first 100 patients undergoing endovascular stent-grafting versus open repair. Length of hospital stay was significantly reduced (2 vs 7 d). They noted no significant difference in the rate of postoperative complications. The endovascular group had a trend toward fewer postoperative myocardial infarctions (1% vs 5%) and more wound infections (5% vs 1%), and the investigators observed no difference between the endovascular group and the open group in operative mortality rates (2% vs 3%) or actuarial survival rates (65% vs 72%). Another center compared cardiac mortality and morbidity rates in 83 patients undergoing endovascular AAA repair with the rates in 63 concurrent patients undergoing open surgical repair. The rates of perioperative myocardial infarction, congestive heart failure, or deterioration of cardiac origin were similar in the 2 groups (6% vs 5%). One cardiac death occurred in the series (in the cardiovascular group). In another nonrandomized comparison of endovascular methods versus surgical techniques, 250 patients with infrarenal aneurysms underwent treatment at 12 study sites. A total of 190 patients underwent endovascular repair with the Medtronic AneuRx stent-graft (Sunnyvale, Calif), and 60 underwent open surgical repair. The patients who underwent stent-grafting had significant reductions in blood loss, time to extubation, days in the intensive care unit and the hospital, and time to return of function. The major morbidity rate was reduced from 23% in the surgery group to 12% (P <.05) in the stent-graft group. Combined morbidity or mortality rates did not differ between the 2 groups. At 30 days, the primary and secondary procedural success rates did not differ between the groups. The primary graft patency rate at 6 months was 98% in the surgery group and 97% in the stent graft group. The aneurysm exclusion rate at 1 month and at 6 months was 100% in patients who underwent surgery and 91% in patients who underwent stent-grafting. Stent-graft migration occurred in 3 patients and resulted in late endoleaks, but each endoleak was corrected with the endovascular placement of a stent-graft extender cuff. Postimplantation inflammatory syndrome A noninfectious systemic illness called postimplantation inflammatory syndrome may arise after endograft placement in 1-4% of patients; this syndrome manifests as fever and leukocytosis. Cultures are negative. Supportive care and the prevention of graft or access-site infection are the mainstays of management. Approximately 1% of patients may have atheroembolism syndrome after graft implantation; this manifests as nonoliguric renal failure or blue-toe syndrome. The natural history of postimplantation inflammatory syndrome takes place over 3-6 months and consists of a subacute phase of microvascular insufficiency caused by mechanical obstruction and a chronic phase of further small-vessel obstruction caused by inflammation secondary to cholesterol emboli. Although many therapies have been tried, none has been proven successful. Supportive care, close attention to fluid management, and prevention of skin breakdown are the most important approaches to the management of this syndrome. Atheroembolization syndromePrevalence and risk factors Cholesterol embolization is a rarely recognized complication of invasive vascular procedures. When it occurs, however, the consequences can be catastrophic. The prevalence of the cholesterol embolization syndrome is not accurately known, but it probably occurs in 0.15-0.2% of patients who undergo angiographic studies of the abdominal aorta, the aortic arch, the carotid arteries, or the coronary arteries. Coronary guide catheters often scrape atheromatous particles from the aorta and contribute to the occurrence of the syndrome after coronary angioplasty and stenting. The use of an anticoagulant such as warfarin or heparin is the second most common precipitating factor of the cholesterol embolization syndrome. Cases of cholesterol embolism after the use of tissue plasminogen activator for acute myocardial infarction have also been reported. Signs and symptoms The organs involved by cholesterol embolization depend on the location of the embolic source. Because a shaggy, atherosclerotic abdominal aorta is the most common source during invasive procedures, the legs, gastrointestinal tract, and the kidneys are most often affected. Leg involvement is manifest by calf myalgias and acrocyanosis of the toes with intact peripheral pulses (blue toe syndrome). Skin findings include livedo reticularis, ischemic ulcers, and splinter hemorrhages. The appearance of cutaneous signs can be delayed. In one series, 50% of patients had skin signs of atheroembolism more than 30 days after their procedure. Diagnostic evaluation Results of laboratory tests for the diagnosis are nonspecific. Although 80% of patients develop an elevated erythrocyte sedimentation rate during the subacute phase and although 14% develop eosinophilia, the only reliable diagnostic test is biopsy. Renal involvement often results in hypertension, progressive renal failure, and volume overload several weeks after an invasive procedure is performed. Treatment No specific therapy for cholesterol embolization syndrome has been identified, although many types of treatment have been tried. Supportive care includes pain relief; dialysis; prevention of tissue breakdown; and, possibly, antiplatelet therapy. Anticoagulants should probably be avoided. Prevention Because no specific therapy has been identified, the prevention of cholesterol embolization syndrome is critical. Patients who have noninvasive evidence of atherosclerotic aortic debris should probably undergo an upper-extremity approach to reduce the likelihood of cholesterol embolization. Dialysis shunt thrombosisPrevalence Approximately 360,000 patients in the United States have end-stage renal disease. These patients may undergo hemodialysis and require functioning dialysis grafts. Most patients have polytetrafluoroethylene bridge grafts, which have a 1-year patency of only 41-75%. Maintaining the patency of these grafts is estimated to cost $750 million annually in the United States. Pathogenesis The pathogenesis of graft closure is related to the formation of a flow-mediated, fibrotic stenosis in the outflow vein, and stasis and thrombosis of the graft. The development of the outflow stenosis may be detected before the graft thrombosis occurs. Treatment Thrombectomy of dialysis grafts is a 4-step procedure. The success rate for catheter-based thrombectomy of dialysis grafts is approximately 90%. Approximately 1% of patients experience clinically significant pulmonary embolism or distal arterial embolization. Contraindications to percutaneous treatment include graft infection, a central right-to-left shunt, pulmonary hypertension, and recent surgical revision less than 30 days before thrombosis. Although surgical results are better than percutaneous interventional results, the catheter-based approach is increasingly recommended because no additional venous length is consumed during the interventional approach. The primary goal of therapy is to prolong each graft so that moving to a new access site is not necessary.
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