Aortic, renal, subclavian, and carotid interventions

Key points

Endovascular aneurysmal repair (EVAR) for abdominal aortic aneurysm (AAA) is a minimally invasive procedure that involves the placement of a bifurcated or tubular endoluminal stent graft over the AAA to exclude the aneurysm from arterial circulation suitable for patients at increased perioperative risk for open surgical repair (OSR).
In patients with symptomatic atherosclerotic renal artery stenosis (RAS), renal artery stenting is reasonable for hemodynamically significant RAS causing resistant (refractory) hypertension despite guideline-recommended medical therapy, declining renal function, and those with cardiac destabilization syndromes.
A moderately severe (indeterminate) RAS (50%–70%) should have the lesion’s hemodynamic significance confirmed. Renal artery stenting with an optimally sized bare-metal stent is the revascularization procedure of choice.
The indications for subclavian artery stenosis revascularization are subclavian steal syndrome, coronary-subclavian steal syndrome, and arm claudication.
Carotid artery stenting with embolic protection device is recommended as an alternative to carotid endarterectomy in average-surgical-risk symptomatic patients when the anticipated risk of periprocedural stroke or mortality is less than 6%.
Carotid artery stenting may be considered in highly selected asymptomatic patients with 60% or greater angiographic stenosis.

Introduction

The technical skills necessary to perform coronary intervention are transferable to the peripheral vasculature. Proper selection and management of peripheral vascular patients, however, require specific training and a knowledge base obtained (preferably) in a formal fellowship training program. Appropriate preparation and training include understanding the value of a multidisciplinary team approach.

Abdominal aortic interventions

Abdominal aortic aneurysm

An aortic diameter greater than 3.0 cm is generally considered aneurysmal. An aortic size index (ASI), determined by formulas that adjust for age and/or body surface area, is more predictive of clinical events. The incidence of abdominal aortic aneurysm (AAA) is much higher in men than in women. The prevalence is 41 to 49 per 100,000 men and 7 to 12 per 100,000 women. The risk factors for development of AAA include smoking, older age, hyperlipidemia, hypertension, and family history ( Table 16.1 ).

Table 16.1

A: Risk Factors for the Development of Abdominal Aortic Aneurysm

(Adapted from Lederle FA, Johnson GR, Wilson SE, et al. Relationship of age, gender, race, and body size to infrarenal aortic diameter. The Aneurysm Detection and Management [ADAM] Veterans Affairs Cooperative Study Investigators. J Vasc Surg. 1997;26:595–601.)

Risk Factor	Odds Ratio (OR)
History of smoking	3.59 (3.0–4.28)
Family history	1.88 (1.58–2.24)
Age	1.52 (1.44–1.62)
Hyperlipidemia	1.46 (1.29–1.65)
Hypertension	1.14 (1.02–1.26)
B: Rates of Rupture Based on Aneurysm Diameter
Maximal Diameter	5-Year Rupture Rate
<4.0 cm	2%
4.0–4.9 cm	3%–12%
5.0–5.9 cm	25%
6.0–6.9 cm	35%
>7.0 cm	75%

Detection

Most aortic aneurysms are diagnosed incidentally on abdominal imaging performed for unrelated indications. Physical examination can be helpful if an AAA is large (>5.5 cm). Abdominal ultrasonography is the most commonly used imaging modality for diagnosis and follow-up, which has sensitivity and specificity approaching 100% for an aortic diameter greater than 3.0 cm. Computed tomographic angiography (CTA) is the modality of choice for planning of endovascular or surgical intervention because it provides low interobserver variability and helps determine the anatomic eligibility for endovascular repair.

For asymptomatic patients, the U.S. Preventive Services Task Force recommends one-time screening for AAA with abdominal ultrasonography in men older than 65 with a smoking history ( Table 16.2 ). Screening is recommended to be selective in men who have never smoked and not recommended for women who have never smoked. There is insufficient evidence to make a recommendation for screening in women who have a smoking history or a family history of AAA.

Table 16.2

United States Preventive Services Task Force (USPSTF) Recommendations for Abdominal Aortic Aneurysm Screening

Population	Recommendation
Men aged 65–75 years who have ever smoked	The USPSTF recommends one-time screening for abdominal aortic aneurysm (AAA) with ultrasonography in men aged 65–75 years who have ever smoked.
Men aged 65–75 years who have never smoked	The USPSTF recommends that clinicians selectively offer screening for AAA in men aged 65–75 years who have never smoked rather than routinely screening all men in this group.
Women aged 65–75 years who have ever smoked	The USPSTF concludes that the current evidence is insufficient to assess the balance of benefits and harms of screening for AAA in women aged 65–75 years who have ever smoked.
Women who have never smoked	The USPSTF recommends against routine screening for AAA in women who have never smoked.

Indications for intervention

Symptomatic AAA

There are three main clinical presentations of AAA: (1) rupture or impending rupture, (2) embolic or thrombotic complications, and (3) compression of adjacent structures because of mass effect.

The classic clinical triad of AAA rupture includes sudden onset of abdominal or lower back pain, pulsatile abdominal mass, and hypotension; however, this triad is present in less than 40% of patients. The prognosis of ruptured AAA is very poor with an in-hospital mortality of around 40% to 50%. It is estimated that 80% of the mortality from AAA is secondary to rupture, highlighting the importance of early detection and intervention.

Asymptomatic AAA

The decision to treat an asymptomatic AAA should include the risk of rupture, the procedural risk, and the patient’s life expectancy. The maximum aneurysmal diameter is currently accepted as the most primary determinant of the risk of rupture. In general terms, the risk of rupture increases substantially when the diameter is greater than 5 cm ( Fig. 16.1 ). Additionally, rapidly expanding aneurysms defined as a greater than 1 cm increase in diameter over 1 year represent a higher risk of rupture and constitute an indication for intervention. The operative mortality of elective open AAA is reported to be between 5% and 8%.

Aneurysm repair can be accomplished using open surgical repair (OSR) or endovascular aneurysm repair (EVAR) techniques. The choice between OSR and EVAR should be individualized, taking into account the patient’s age, risk factors for perioperative morbidity and mortality, anatomic factors, and the experience of the surgeon. EVAR is associated with a lower risk of perioperative morbidity compared with OSR for asymptomatic, symptomatic, and ruptured AAA. Long-term mortality after elective AAA repair, however, is not significantly different between the techniques.

Endovascular aneurysm repair.

Conceptually, during EVAR, an endoluminal stent graft connects the proximal “normal” nondilated portion of the aorta proximal to the aneurysm to the distal nondilated arteries, therefore excluding the aneurysm from the circulation. Excluding the aneurysm decreases the pressure on the wall and lowers the risk of rupture. With contemporary techniques, including custom-made fenestrated and branched devices, most patients can be considered candidates for EVAR in experienced endovascular centers.

The EVAR-1 and Dutch Randomized Endovascular Aneurysm Repair (DREAM) trials randomized patients who were suitable for both EVAR and OSR, showing similar 2-year all-cause mortality but lower aneurysm-related deaths for the EVAR group (4% vs. 7%; p = .04 in EVAR-1 and 2% vs. 6% in DREAM). Since then, EVAR has gained significant acceptance as the treatment of choice for most asymptomatic AAAs requiring repair. A recent systemic review and meta-analysis, however, have demonstrated that although the hazard of all-cause and aneurysm-related death within 6 months of surgery was significantly lower after EVAR, with further follow-up, the pooled hazard estimate moved in favor of OSR; in the long term (>8 years), the hazard of aneurysm-related mortality was significantly higher in patients who underwent EVAR. The risk of secondary intervention, aneurysm rupture, and death caused by rupture was significantly higher after EVAR. These data have led the British National Institute for Health and Care Excellence (NICE) to issue a recommendation that patients should not be offered EVAR if OSR is suitable.

Moreover, not all patients are anatomically suitable for EVAR. Preprocedural planning is the cornerstone of a successful procedure. CTA is the modality of choice for anatomic evaluation before endovascular repair. The critical anatomic elements that determine the patient’s suitability for EVAR are:

1)
A patent superior mesenteric artery (SMA) or celiac trunk: The inferior mesenteric artery is usually excluded with the graft. One of the worse complications of EVAR is ischemic colitis, which occurs in less than 2% of elective cases. The risk of colon necrosis is higher if the patient has had previous abdominal surgery that interrupts the collateral circulation from the SMA and celiac arteries or if there is significant preexisting stenosis of these arteries.
2)
An infrarenal neck diameter of less than 32 mm and greater than 10 to 15 mm in length is needed to appropriately land the proximal end of the graft and create a complete seal. The most common reason for a patient with AAA to be considered unsuitable for EVAR is the anatomy of the proximal aortic neck. In a series of 526 patients, EVAR performed in subjects with a hostile neck—defined as length less than 10 mm, angle greater than 60 degrees, diameter greater than 28 mm, or more than 50% circumferential thrombus or calcification—was associated with higher rates of intraprocedural type I endoleak (poor edge sealing).
3)
No more than 90 degrees of circumferential calcification or mural thrombus in the infrarenal neck: This would interfere with appropriate anchoring and sealing of the device.
4)
The minimal diameter of the external iliac arteries is large enough to allow the passage of the device (Currently 14 French [F]).
5)
Distal fixation requires 10 to 15 mm in length of normal vessel in the common iliac segment, similar to that required for proximal fixation.
6)
The diameter of the common internal iliac artery should be less than 20 mm. If this is not the case, an additional cuff is required to extend the graft into the external iliac artery with coiling of the internal iliac artery (see later).

Available devices.

Presently, several devices have received U.S. Food and Drug Administration (FDA) approval for the treatment of AAA in the United States ( Table 16.3 ). The overall performance among the available devices is similar.

Table 16.3

Currently Available Endovascular Aneurysm Repair Devices in the United States

Company	Device	Largest Main Body Diameter (mm)	Delivery System Profile	Fixed Location
Cook Medical	Zenith Flex	36	20, 23, 26 F	Suprarenal
Endologix	Powerlink	28	21 F	Infrarenal
W.L. Gore & associates	Excluder AAA endoprosthesis	28.5	18 F	Infrarenal
Medtronic Vascular	Endurant	36	16, 18, 20 F	Infrarenal
TriVascular	Ovation Prime	30	15 F	Suprarenal

AAA, Abdominal aortic aneurysm; F , French.

The basic EVAR system includes three main components: a delivery system, a stent graft, and iliac extensions. Advanced devices can be used in challenging anatomy, such as fenestrated, branched, or chimney grafts.

Preprocedural evaluation.

Preprocedural risk assessment should be performed in EVAR patients because there is a small risk that the endovascular repair may need to be converted to an OSR. Before endograft placement, antibiotic prophylaxis is recommended within 30 minutes of the skin incision. Prophylactic renal artery stenting may be considered in selected patients with severe renal artery stenosis and preexisting renal insufficiency. Hypogastric (internal iliac) artery embolization also can be considered in selected patients. A small study suggested use of preoperative methylprednisolone as a prophylaxis for acute flu-like postimplantion inflammatory syndrome.

Technique.

There is some variation in technique depending on the type of endograft used. There is, however, a common workflow for most EVAR procedures:

1.
Aortogram: After bilateral femoral access is obtained, a marked pigtail is inserted through the contralateral side to the main graft and positioned just above the level of the renal arteries. A digital subtraction angiogram is performed and the level of the lowest renal artery is identified.
2.
Embolization of internal iliac artery when necessary: If the common iliac arteries are aneurysmal, the distal limb of the device can be anchored in the external iliac artery. However, collateral flow into the ipsilateral internal iliac artery can result in a type II endoleak (see later). Prophylactic embolization with coils of the internal iliac artery can be performed during EVAR or in a staged manner before the procedure.
3.
Introduction and deployment of the endograft: Once the lowest renal artery is identified, the sheath containing the endograft is positioned just below it. It is important to adjust the angulation of the x-ray camera to be perpendicular to the plane of the infrarenal aorta for appropriate positioning (see Fig. 16.1 ). The pigtail used for aortography should be removed before deployment. Postpositioning ballooning is often required and depends on the device used.
4.
Deployment of the contralateral limb: For modular endografts, one needs to deploy a separate iliac limb graft in the contralateral side. A wire should be introduced into the main limb of the endograft via the contralateral femoral artery. Once the wire is successfully placed in the suprarenal aorta through the already deployed endograft, the sheath with the iliac endograft is advanced into the main body of the endograft. The final step is to deploy the contralateral limb.
5.
Dilation of the endograft: Although stent grafts are self-expanding, balloon expansion of the proximal and distal attachment sites should be performed, as well as the junction of the modular components.
6.
Completion angiogram: A completion angiogram with a power injector is performed at completion of the procedure and identifies endoleaks.

Endoleaks

Immediate type I and type III endoleaks are generally treated with additional ballooning or the placement of additional endograft components ( Fig. 16.2 ; Table 16.4 ).

Table 16.4

Classification of Endoleaks

Type	Definition	Causes	Treatment
1	Arises from the distal and proximal attachment sites	Undersizing of the stent, poor sealing, neck dilatation, and stent migration	Postdilatation of the stent
2	Retrograde filling of the aneurysmal sac from lumbar or internal iliac arteries that were excluded with the endograft	Collateral circulation	Benign course. If needing treatment, translumbar embolization or surgical ligation
3	Limb separation or fabric wear	Mainly occur with modular grafts at the sites of attachment	Regrafting
4	Extravasation through graft material	Because of porosity of the fabric material	Benign course, usually aneurysmal sac thrombosis without clinical consequence
5	Endotension: Space between aortic graft and the native aorta has elevated pressure without demonstrable endoleak	Missed endoleaks, thrombosed endoleaks, hygroma, infection	Unknown

Postoperative care

Postoperative care includes pain control, fluid therapy, peripheral pulse exam assessment at regular intervals, and resumption of antithrombotic therapy.

Complications

Complications related to EVAR occur in 10% of cases, including vascular access bleeding, technical failure, endoleak, and open conversion.

Surveillance after EVAR

EVAR offers the advantage of lower perioperative morbidity but is associated with a concern for device-related complications, such as endoleaks, migration of the stents at the aortic and iliac landing zones, graft thrombosis, and separation of the device components. Because of these potential complications, lifelong surveillance is mandatory. Current standard of care includes serial studies at 1, 6, 12 months, and yearly thereafter. Since the advent of EVAR, this has largely been accomplished with serial CTA with delayed images. Compared with CTA, duplex ultrasonography (DU) is cost effective and has no risk of contrast and radiation exposure. The reported specificity of endoleak identification by DU is high (89%–97%).

Renal artery interventions

Renal artery stenosis (RAS) is the most common cause of secondary hypertension. It affects 25% to 35% of patients with secondary hypertension, is associated with progressive renal insufficiency, and causes cardiovascular complications, such as refractory heart failure and flash pulmonary edema. A critical issue is the appropriate patient selection for interventional procedures.

Clinical syndromes associated with RAS

Renovascular hypertension

Resistant hypertension is defined as blood pressure above goal on three different classes of antihypertensive medications, ideally including a diuretic drug. Current American Heart Association (AHA)/American College of Cardiology (ACC) guidelines recommend renal artery stenting for RAS with accelerated, resistant, or malignant hypertension; hypertension with unilateral small kidney; and hypertension with medication intolerance (Class IIa, LOE B).

Ischemic nephropathy

RAS is a potentially reversible form of renal insufficiency. In 73 patients with chronic renal failure (estimated glomerular filtration rate [eGFR] < 50 mL/min) and clinical evidence of RAS, renal stenting demonstrated an improved renal function in 34 of 59 patients (57.6%). Current AHA/ACC guidelines and appropriate use criteria recommend renal artery stenting for patients with ischemic nephropathy if they have progressive chronic kidney disease (CKD) with bilateral RAS (Class IIa, LOE B), progressive CKD with RAS to a solitary functioning kidney (Class IIa, LOE B), or CKD with unilateral RAS (Class IIb, LOE C; Fig. 16.3 ).

Cardiac destabilization syndromes

The most widely recognized example of a cardiac destabilization syndrome is “flash” pulmonary or Pickering syndrome. In patients with either congestive heart failure (CHF) or an acute coronary syndrome (ACS), successful renal stent placement resulted in a significant decrease in blood pressure and symptom improvement in 88% (42 of 48) of patients. For those patients who presented with unstable angina, renal artery stenting improved the Canadian Class Society (CCS) symptoms at least by one regardless of concomitant coronary intervention (see Fig. 16.3 ). Current AHA/ACC guidelines recommend renal artery stenting for RAS with recurrent, unexplained heart failure decompensation, or sudden unexplained pulmonary edema (Class I, LOE B) and for hemodynamically significant RAS and medically refractory unstable angina (Class IIa, LOE B).

Diagnostic testing

Doppler ultrasound evaluation

Significant RAS is associated with a peak systolic velocity (PSV) greater than 180 cm/sec and a ratio of the PSV of the stenosed renal artery to the PSV in the aorta that is greater than 3.5. PSV greater than 395 cm/s and renal artery ratio (RAR) greater than 5.1 are the most predictive of angiographically significant in-stent restenosis (ISR) in more than 70% of cases.

Computed tomographic angiography

CTA can provide high-resolution cross-sectional imaging of RAS while supplying three-dimensional angiographic images of the aorta, renal, and visceral arteries, allowing localization and enumeration of the renal arteries, including accessory branches. CTA can be used to follow patients with prior stents to detect ISR, an advantage over magnetic resonance angiography (MRA) in which metallic stents generate artifact.

Magnetic resonance angiography

This imaging modality allows for localization and enumeration of the renal arteries and characterization of the stenosis. Limitations for MRA include the association of gadolinium with nephrogenic systemic fibrosis when administered to patients with an eGFR of less than 30 mL/1.73m ² . Metal also causes artifacts on MRA and, therefore, it is not a useful test for patients with prior renal stents.

Treatment strategies

You're Reading a Preview

Become a Clinical Tree membership for Full access and enjoy Unlimited articles

Become membership

If you are a member. Log in here