Peripheral Interventions



Peripheral Interventions


Jayendrakumar S. Patel, MD

Samir R. Kapadia, MD

Mehdi H. Shishehbor, DO, MPH, PHD



INTRODUCTION

Peripheral artery and venous disorders are becoming more prevalent and clinically apparent in developed countries owing to the growth of the aging population. Advanced age and comorbid conditions prohibit many patients with peripheral vascular disorders from conventional surgical therapies. For such cases, percutaneous options have become firstline. Over the past decade, the field of peripheral intervention has realized significant advances in technique, devices, and pharmacotherapy making it possible to treat complex disease. In this chapter, we present a technical review of the most common arterial and venous peripheral interventions.


ARTERIAL INTERVENTIONS


Carotid Arteries

Carotid artery stenting (CAS) has been shown to offer similar or possibly better long-term outcomes in carefully selected patients with symptomatic or asymptomatic carotid stenosis when performed by experienced centers with low periprocedural morbidity and mortality rates (<6%).1,2 Age ≥70 to 80 years, presence of chronic kidney disease, complex plaque morphology (including long lesion length), and calcified complex arch anatomy have been associated with higher rates of stroke or death at 1 month.1,3,4,5 Current American Heart Association/American Stroke Association guidelines recommend CAS for symptomatic patients who have internal carotid artery stenosis of 70% to 99% by noninvasive imaging or 50% to 99% by angiography.6 Asymptomatic patients who undergo CAS should have 70% to 99% stenosis by Doppler or 60% to 99% stenosis by angiography.6



Noninvasive Imaging







FIGURE 23.1 Abnormal carotid artery duplex ultrasound. An arterial duplex is often the first test that is obtained for patients with suspected carotid artery stenosis and is highly sensitive and specific (>85%-90%).7 Areas of severe stenosis will typically exhibit aliasing on color flow Doppler owing to flow acceleration. In this study, mosaic color is observed in the right internal carotid artery and is due to high-velocity blood flow (A). Spectral Doppler waveform of the distal common carotid artery reveals a normal peak-systolic velocity of 92 cm/s with brisk upstroke (B). However, the peak-systolic and diastolic velocities at the origin of the internal carotid artery are markedly elevated (C). There is also evidence of turbulent flow on spectral waveform (flow below the baseline during systole and filing of the spectral window (D). In the distal segment of the internal carotid artery, spectral waveform demonstrates a parvus-tardus pattern (E and F). Importantly, duplex ultrasound may not be able to differential subtotal from complete occlusions.7







FIGURE 23.2 Computed tomography angiography (CTA), axial slices. In cases where duplex ultrasound is equivocal or nondiagnostic, CTA can be quite helpful but requires intravenous contrast and ionizing radiation.7 The test has a high sensitivity and negative predictive value7. A, demonstrates both common carotid arteries without significant stenosis. B, shows the right internal carotid artery (red circle). A focal area of severe stenosis (red arrow) is seen just distal to the origin of the right internal carotid artery (C). D, CTA, sagittal slice. The right common carotid (solid arrow), internal carotid (arrowhead), and external carotid arteries (broken arrow) are labeled. A 99% stenosis (asterisk) demonstrating the string sign is seen just distal to the origin of the right internal carotid artery.


Angiographic Evaluation and Treatment







FIGURE 23.3 Arch aortography. At the start of the procedure, arch aortography is performed and carefully studied to understand the extent and location of aortic atheroma and assess the complexity of arch anatomy. The aortic arch is classified based on the vertical distance from the origin of the innominate artery to the outer curvature, with the reference diameter being the width of the left common carotid artery (A). The type I arch is most common, with arch vessels arising from the outer curvature in the same plane (B). In a type II arch, the vertical distance from the outer curvature of the arch to the origin of the innominate artery is 1-2 diameters of the left common carotid artery (C). In a type III arch, the vertical distance from the origin of the innominate artery to the outer curvature is >2 diameters of the left common carotid artery (D). A type III aortic arch and proximal common carotid tortuosity portends a difficult procedure and is associated with higher rates of periprocedural stroke, death, and other complications.3,8,9







FIGURE 23.4 A, Engaging the carotid artery. After administering heparin to a therapeutic activated clotting time of 250-300 s, the carotid artery can be engaged. A diagnostic preshaped catheter (JR, Simons, V Tek) is used to engage the carotid or innominate artery. Selective carotid angiography is performed to create a roadmap reference image (B). A Wholey or glidewire is advanced into the external carotid artery to ensure that the sheath will not touch the internal carotid artery lesion. The diagnostic catheter is advanced into the external carotid artery, and the sheath is subsequently advanced over the diagnostic catheter up to the proximal innominate or common carotid artery (C). After reaching the desired location, the diagnostic catheter and wire are slowly removed, the system is deaired, and selective carotid and cerebral angiography are performed. Courtesy of Samir Kapadia and Jay S. Patel, Cleveland Clinic Non Invasive Vascular Laboratory.






FIGURE 23.5 Selective angiography of the common carotid artery. Note the presence of a string sign in the internal carotid artery (arrow). Percent stenosis of the target lesion is most commonly calculated by using the North American Symptomatic Carotid Endarterectomy Trial (NASCET) method, where the reference diameter is the region distal to the stenosis (dashed line).7 Branches of the external carotid artery are outlined. Lingual artery (1). Ascending pharyngeal artery (2). Facial artery (3). Maxillary artery (4). Superficial temporal artery (5). Occipital artery (6).







FIGURE 23.6 A-C, Selective angiography of the internal carotid artery is routinely performed both before and after CAS. Terminal branches of the internal carotid artery are labeled. ICA, internal carotid artery; MCA, middle cerebral artery; PCA, posterior cerebral artery; PCOM, posterior communicating artery.






FIGURE 23.7 Positioning and deployment of distal embolic protection device. A distal embolic protection device is carefully advan ced in the collapsed configuration into the distal segment of the internal carotid artery (A) and is subsequently deployed (B, arrow). An attempt should be made to deploy the filter in a segment of the internal carotid artery that is free of disease and vertical. Courtesy of Samir Kapadia and Jay S. Patel, Cleveland Clinic Non Invasive Vascular Laboratory.







FIGURE 23.8 Carotid stenting. After deployment of the embolic protection device, the severe internal carotid artery lesion is predilated at low pressure (A) to facilitate passage of the stent and ensure deformation of the lesion. A self-expanding stent is then positioned using a roadmap image and slowly deployed (B, bracket), taking care to avoid placing the distal edge of the stent at areas of extreme tortuosity. The stent is subsequently postdilated at the lesion site at nominal pressures, taking care to avoid the stent edge (C and D). Bradycardia may occur during stent deployment or balloon dilation owing to baroreceptor activation. The embolic protection device is retrieved. It is acceptable to have a residual 10%-20% stenosis, and further postdilation is not advisable (E).



Subclavian Arteries

Patients with severe subclavian artery stenosis due to atherosclerosis are usually asymptomatic and often incidentally diagnosed with the finding of differential arm blood pressures on routine physical examination. Those with symptoms may experience arm claudication or ischemia, syncope/neurologic symptoms (subclavian steal syndrome), or chest pain (coronary-subclavian steal) during arm exertion. Current American College of Cardiology/American Heart Association (ACC/AHA) guidelines give a class IIa recommendation for revascularization in patients with symptomatic severe subclavian artery stenosis.7 Revascularization should also be considered for patients before coronary bypass surgery to improve flow into the mammary arteries or to preserve axillary graft or dialysis conduits. Revascularization for asymptomatic patients carries a class III level of evidence C recommendation.7 The choice between surgical and percutaneous revascularization depends on anatomical and lesion characteristics, surgical risk, and patient preference. However, percutaneous revascularization is associated with a high success rate and low complication rate and is typically pursued for focal or short proximal stenoses that avoid the vertebral artery.


Noninvasive Imaging







FIGURE 23.9 Abnormal subclavian arterial duplex ultrasound. A, Demonstrates normal triphasic waveform with brisk upstroke. Note the absence of aliasing and spectral broadening (both characteristics of turbulent flow). B, shows a typical poststenotic waveform with delayed upstroke (tardusparvus) and spectral broadening. Interrogation of the ipsilateral vertebral artery (C) demonstrates retrograde flow, consistent with subclavian steel.



Angiographic Evaluation and Treatment







FIGURE 23.10 Arch aortography. An arch aortogram is performed in standard fashion in the LAO (A) and RAO (B) projections to create a roadmap for selective engagement of the subclavian artery and for treatment planning. Ascending aorta (Asc Ao), descending aorta (Des Ao), brachiocephalic (BC), right subclavian (RSc), right vertebral (RV), right common carotid (RCC), left common carotid (LCC), left subclavian (LSc) vessels are labeled. Note the severe stenosis at the origin of the left subclavian artery (red asterisk).






FIGURE 23.11 Selective left subclavian angiography. For nonocclusive lesions, a diagnostic catheter (typically JL4) is used to engage the ostium of the subclavian artery. Angiography is then performed, taking note of lesion severity and location with respect to the ostium of the subclavian artery and proximity to vertebral and internal mammary artery. Note the presence of a severe proximal stenosis denoted by the red arrow and the absence of the vertebral artery likely due to retrograde flow (white arrow).







FIGURE 23.12 Left subclavian angioplasty and stenting. Intervention can be performed via the femoral approach using a 5- to 8-Fr guide. For total occlusions, a retrograde brachial artery approach may be warranted. A smaller caliber diagnostic catheter is telescoped through the guide (eg, H-1 or JR4) and the subclavian artery is subsequently engaged with the diagnostic catheter. After selective subclavian angiography, the lesion is crossed using a heavy-support coronary or 0.035-inch stiff angle glidewire or, if possible, a Wholey wire advanced into the axillary artery. The diagnostic catheter and sheath are gently advanced over the wire and positioned just proximal to the lesion. The glidewire can then be exchanged for a 0.035-inch Wholey wire if the lesion was not initially crossed with the Wholey. An undersized (typically 4-6 mm) balloon is then advanced into position, and predilation is performed to assist with sizing and ensure that the stent will expand (A). Angiography is then performed to assess for dissection or perforation (B), and a balloon-expandable stent is then advanced into position (C and D), taking care to avoid jailing of the vertebral or internal mammary arteries. Although randomized controlled trials are lacking, stent placement appears to be associated with lower rates of restenosis.10,11,12,13 The choice between balloon-expandable and self-expanding stents depends, in part, on lesion location, degree of calcification, and vessel anatomy. For ostial or proximal segment disease, balloon-expandable stents are preferred due to more precise positioning. Distal segment disease (past the internal mammary artery) or tortuous anatomy may be best treated with self-expanding stents. The stent is then deployed (E) and carefully postdilated (F) to match the size of the subclavian artery (usually between 5 and 8 mm). Further dilation should be avoided if the patient experiences pain.







FIGURE 23.13 Postprocedure subclavian arterial duplex ultrasound. A and B, Demonstrate normalization of the waveform with no evidence of color aliasing. Flow in the vertebral artery is now normal and antegrade (C).


Renal Arteries

Renal artery stenosis is most commonly due to atherosclerosis or fibromuscular dysplasia (FMD) and can result in treatment-resistant or malignant hypertension, recurrent flash pulmonary edema, or ischemic nephropathy. Invasive management of atherosclerotic renal artery stenosis remains somewhat controversial owing to lack of strong evidence of benefit from randomized trials. Indeed, the only class I indication for revascularization is in patients with hemodynamically significant stenosis and recurrent unexplained heart failure or pulmonary edema.14 However, it may also be beneficial in cases of failed medical therapy with fairly recent onset hypertension or progressive renal failure secondary to suspected ischemic nephropathy. There are no randomized trials available to guide revascularization for patients with FMD; however, hypertension is markedly and durably improved with angioplasty in the majority of patients. As such, revascularization is usually recommended for FMD if anatomically feasible. A percutaneous approach is preferred, with surgery reserved only for those patients with complex anatomy (eg, concomitant periaortic disease requiring surgery, aneurysmal disease, dissection).



Noninvasive Imaging







FIGURE 23.14 Abnormal renal artery duplex ultrasound in a patient with atherosclerotic renal artery stenosis. Renal artery duplex ultrasound is relatively inexpensive and provides both anatomical and functional information.15 A, Demonstrates laminar flow within the Ao at the level of the left renal artery (LRA). Color aliasing is noted at the proximal segment of the LRA and is suggestive of nonlaminar blood flow. Peak-systolic and end-diastolic flow velocities at the origin of the LRA are markedly elevated and consistent with a severe stenosis (B). Note the parvus-tardus waveform along with spectral broadening and turbulence in (C). The renal aortic ratio (D) can be calculated by comparing the peak-systolic velocity of the renal artery to the Ao. Values >3.5 are considered to be consistent with severe stenosis. The resistive index (B and C) can also be calculated and may be a useful prognostic tool.16,17







FIGURE 23.15 Abnormal renal artery duplex ultrasound in a patient with renal artery stenosis due to FMD. Unlike atherosclerotic disease, FMD typically involves the mid to distal segments of the renal arteries. A, Demonstrates normal peak-systolic velocity and waveform at the proximal segment of the right renal artery (RRA), and inspection of color Doppler reveals laminar flow without evidence of color aliasing. However, color Doppler assessment at the mid segment (B) reveals multiple areas of aliasing suggestive of turbulent flow and possible stenosis. This is corroborated by markedly elevated peak-systolic velocities recorded at the mid and distal segments (C and D) along with spectral broadening of the Doppler waveform.



Angiographic Evaluation and Treatment







FIGURE 23.16 Invasive renal artery assessment. We routinely perform renal angiography and intervention using the “no-touch” technique to minimize contrast use and reduce aortic wall trauma.18 A 0.035-inch wire (A, white arrow) is first placed well above the renal arteries in the Ao and the guide catheter is then advanced over the wire to the L1-2 vertebral body level. While the 0.035-inch wire is still in place, the renal artery is wired using a 0.014-inch guide wire or fractional flow reserve (FFR) wire. The artery is subsequently engaged by retracting the 0.035-inch wire into the guide and advancing the guide over the 0.014-inch guide wire. Selective renal angiography can then be performed with 3 mL of contrast mixed with 3-4 mL of heparinized saline flush under digital subtraction angiography. Intravascular ultrasound (IVUS) (B) is then used to assess reference vessel size (C), plaque characteristics, and lesion severity and identify the true ostium. Once the true ostium is identified on IVUS (D), a fluoroscopic image is obtained to mark the ostium and guide stent placement. FFR assessment using a 0.014-inch pressure wire should be performed if there is a question of hemodynamic significance for stenoses between 50%-70% severity. A resting mean pressure gradient >10 mm Hg, systolic hyperemic pressure gradient >20 mm Hg, or Pd/Pa ≤0.80 is considered to be flow limiting.19,20 Intrarenal dopamine (not adenosine) or papaverine can be used to induce maximal hyperemia.







FIGURE 23.17 Renal artery stent positioning and deployment. Several studies have shown lower restenosis rates associated with stenting compared with angioplasty alone, and current ACC/AHA guidelines recommend stent placement if revascularization is performed for atherosclerotic renal artery stenosis.21,22,23,24,25 We routinely use IVUS to assess plaque characteristics and vessel size and identify the true ostium (A) as under-sizing or over-sizing leads to suboptimal results.26 A reference fluoroscopic image marking the true ostium is created and used to optimally position the stent. Careful predilation is performed using an undersized balloon if there is concern that the lesion will not expand during stent placement (B). An appropriately sized stent is then advanced into position (with about 1-2 mm extension into the Ao) using the reference image and deployed (C). We then perform angiography and IVUS to assess for edge dissection and malapposition. D, Shows final angiographic result after stent deployment.


Mesenteric Arteries

The most common cause of mesenteric artery stenosis is atherosclerosis, but other causes should be considered including median arcuate ligament compression, FMD, vasculitis, or dissection. Owing to the extensive collateral network of the mesenteric arterial system, severe stenosis in 1 artery rarely results in symptoms. Occasionally, patients can present with postprandial abdominal pain (intestinal angina), especially after a fatty meal, that tends to resolve over several hours. If left untreated, the patient may experience significant weight loss or develop intestinal infarction. Percutaneous angioplasty with stent placement is the preferred method of revascularization in severely symptomatic patients, and the superior mesenteric artery (SMA) is often targeted for treatment.27







FIGURE 23.18 FMD. Typical “string of beads” finding on renal angiography (A and B, white arrowhead). Note that the ostial and proximal segments of the artery are spared, which is characteristic in FMD. We routinely use IVUS preintervention to assess reference vessel size (C), visualize coexisting plaque burden, and identify the segment(s) with most severe stenosis. D and E, Demonstrate significant fibrous bands that are seen in FMD. In cases where it is unclear which renal artery requires intervention, we perform FFR assessment with the caveat that a false-negative result may be obtained if the webs are easily compressible by the FFR wire. In this case, mean resting pressure gradient in the LRA was 2 mm Hg, while gradient in the RRA was 20 mm Hg. Balloon angioplasty was subsequently performed on the RRA at the segment with the most severe narrowing identified by IVUS (F and G; arrowhead). We often perform FFR and IVUS assessment after angioplasty to document adequate treatment in cases where angiography is ambiguous or residual stenosis >30% suspected (H). Postangioplasty FFR assessment, in this case, demonstrated a residual gradient of >15 mm Hg. After repeat angioplasty, the residual gradient was <6 mm Hg. Note that stenting is reserved for failure or complications resulting from balloon angioplasty.

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May 3, 2019 | Posted by in CARDIOLOGY | Comments Off on Peripheral Interventions

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