As with many breakthroughs in medicine, endovascular therapy began as an accident. In 1963, Charles Dotter inadvertently recanalized a chronically occluded iliac artery with a rigid intravascular dilator while performing a renal artery angiogram via retrograde femoral artery access.¹ Dotter recognized the therapeutic potential of this approach and pursued translational studies in cadaveric peripheral vessels.² Dotter and Melvin Judkins subsequently published the first series of transluminal angioplasties in 1964 for treatment of patients with severe femoral and popliteal artery occlusive disease considered at prohibitive risk for surgical intervention.³ Dilating catheters of up to 3.2 mm in diameter were passed percutaneously from the contralateral femoral artery with encouraging results, thereby fostering the development of percutaneous peripheral and coronary interventions.^{2 , 3} In 1974, Andreas Grüntzig performed the first successful balloon angioplasty for treatment of superficial femoral and iliac artery occlusive disease, and in 1977, adapted this technology to enable coronary balloon angioplasty.^{4 , 5} Dotter also described the use of a tubular coiled wire stent graft in canines in 1969.⁶ Tillet and Garner isolated streptokinase in 1933, but it was not until the 1950s that Clifton first reported its use as a thrombolytic agent.^{7 , 8} In 1960, Luessenhop and Spence first described intravascular embolization to treat a cerebral arteriovenous malformation using a handmade plastic pellet.⁹

Percutaneous transluminal angioplasty (PTA) is indicated for symptomatic arterial or venous occlusive lesions or asymptomatic lesions at high risk for associated morbidity should progression to complete occlusion occur. Stenting after angioplasty is indicated in the presence of a flow-limiting dissection, a residual stenosis >30%, or a significant pressure gradient across the treated lesion. Primary stent placement is common for carotid and renal interventions and practiced selectively for iliac artery disease, particularly TASC C and D lesions, including stenotic regions >10 cm and chronic total occlusions (CTOs) >5 cm. Selective stenting of infrainguinal arterial lesions based on the outcome of initial angioplasty has been standard clinical practice¹⁰ with more recent randomized trials supporting the benefits of primary stenting of the superficial femoral artery (SFA) for patients with intermittent claudication.^{11 , 12} Nonetheless, the potential benefits of drug-coated balloon (DCB) technology continue to evolve for TASC C and D femoropopliteal lesions.

The exact roles for adjunctive percutaneous mechanical thrombectomy and pharmacologic thrombolytic therapy are debated, but these modalities are predominantly applied in the setting of acute arterial or venous thrombosis, including maintenance and salvage of bypass and dialysis access grafts. The ability to debulk an atherosclerotic lesion using directional, rotational, or laser atherectomy remains appealing, but there remains limited evidence demonstrating enhanced long-term patency by atherectomy alone and risks of distal embolization persist.

Indications for transarterial embolization include control of hemorrhage, particularly because of pelvic trauma, treatment of vascular anomalies, exclusion of aneurysmal segments, branch vessels covered by an endograft, or chemoembolization of tumor vasculature.

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  History and physical examination, as well as noninvasive physiologic and imaging studies, establishes the location and severity of vascular disease.

  
  
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  If angioplasty or stenting is planned, preprocedural administration of antiplatelet therapy with aspirin (81 mg daily) or clopidogrel (75 mg daily) is recommended for 5 days before the procedure. If patients have not received clopidogrel, an oral loading dose of 300 mg can be administered after the procedure.

  
  
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  Medical optimization is warranted for all patients with peripheral arterial disease, including counseling on smoking cessation and glycemic control for diabetics, as well as statin therapy and antiplatelet therapy.¹³

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  Dissection. The risk of inadvertent arterial dissection is decreased through use of soft atraumatic guidewires, careful wire technique with frequent “twirling” of the wire tip, with confirmation of its intraluminal location through use of angiography if the wire position is in doubt. Dissection after angioplasty occurs in the setting of a bulky heavily calcified plaque or after overdilation of a vessel. Although angioplasty-associated dissections are not typically flow limiting, stenting can be performed as needed.

  
  
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  Rupture. Vessel rupture may occur with wire manipulation causing perforation, balloon angioplasty, or insertion of other devices, such as a large sheath through small, tortuous, or calcified vessels. Circumferential and highly eccentric calcified lesions are at high risk of rupture and should be approached cautiously. Subintimal angioplasty may also increase the risk of perforation compared with intraluminal procedures.

  
  
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  Embolization. Crossing any lesion can lead to inadvertent embolization, but irregular, ulcerated, or complex lesions, especially those that are symptomatic, or aneurysmal with the presence of irregular thrombus, are at increased embolic risk. Judicious use of anticoagulation and cautious passage of atraumatic wires and intravascular devices through these lesions will help minimize embolization. A distal embolic protection device or flow reversal system can minimize embolization after carotid angioplasty and stenting or after treatment of other lesions at increased risk of embolization.

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  Antibiotic prophylaxis. Antibiotic prophylaxis is not recommended for diagnostic angiography, angioplasty, bare metal stenting, and thrombolysis or during the course of placement of a vena cava filter, central venous access catheter, or closure device. Periprocedural antibiotics are also not indicated for arteriovenous fistula and graft angioplasty, stent placement, or thrombectomy, nor is prophylaxis recommended for endovenous ablation of varicose veins.¹⁴

  
  
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  Antibiotic prophylaxis is recommended for planned treatment with a stent graft, tunneled dialysis catheter, hepatic embolization, splenic embolization (>70% splenic volume), TIPS procedure, or treatment of a vascular malformation. Antibiotic prophylaxis is also recommended if a central venous access catheter will be placed in an immunocompromised patient and for vena cava filter retrieval with bowel penetration on cross-sectional imaging.

  
  
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  Anticoagulation. Heparinization is not required for most diagnostic studies, but is recommended before complex wire and catheter maneuvers within the aortic arch. Heparinization is administered at an intravenous dose of 50 to 100 units/kg before all interventional procedures, but the dose may be reduced or precluded in the presence of traumatic injuries. Heparin activity is monitored by the activated clotting time (ACT) with TASC II guidelines¹⁵ recommending a target ACT of 200 to 250 seconds for peripheral vascular interventions and Society for Vascular Surgery guidelines recommending a target ACT of >300 seconds for endovascular aortic aneurysm repair (EVAR). ¹⁶ ACT can vary between device brands, with ACT values lower for the Medtronic system (ACT Plus® System, Medtronic, Minneapolis, MN) compared with the Hemochron device (Hemochron Signature Elite System, Werfen, Bedford, MA). The normal range for ACT in the absence of anticoagulation is 70 to 120 seconds. A common target range for ACT during most vascular procedures is between 250 and 300 seconds.

  
  
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  Heparin neutralization. Selective reversal of heparin in patients at increased risk of bleeding may reduce the risk of postprocedural hemorrhagic complications. Protamine sulfate is used to reverse the anticoagulant effects of heparin and dosed at 1 to 1.5 mg of protamine for every 100 units of heparin administered, not to exceed 50 mg, accounting for heparin’s half-life of 60 to 90 minutes and guided by ACT. Administration of protamine may cause mild hypotension from histamine release or severe hypotension from anaphylaxis and, as a consequence, is given slowly after an initial test dose of 5 to 10 mg. The onset of action is approximately 5 minutes.

  
  
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  Nonheparin alternatives. A history of heparin-induced thrombocytopenia (HIT) is a contraindication to heparin and requires the use of a direct thrombin inhibitor, such as argatroban or bivalirudin (Angiomax). Argatroban is metabolized in the liver, has a half-life of 50 minutes, and is monitored by ACT with a target of >250 seconds. An initial intravenous bolus dose of 350 μg/kg is administered with a continuous infusion of 25 μg/kg/min. The ACT is assessed 5 to 10 minutes after the bolus dose is completed. If the ACT is <250 seconds, an additional intravenous bolus dose of 150 μg/kg can be administered and the infusion dose increased to 30 μg/kg/min, with the ACT reassessed after 5 to 10 minutes. If the ACT is >450 seconds, the infusion rate should be decreased to 15 μg/kg/min. Bivalirudin is cleared by the kidneys and has a half-life of 25 minutes. An initial intravenous bolus dose is administered at 0.75 mg/kg with an infusion of 1.75 mg/kg/hr during the procedure with ACT monitoring.

  
  
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  Procedural planning. All interventional procedures follow a series of strategic steps beginning with vascular access and placement of an appropriate sheath. Selection of the puncture site, as well as the choice of the number and type of sheaths to be used, including size and length or steerable tip, and their sequence of use, along with wires, catheters, and other adjuncts are dependent on the location of the lesion. For example, if both inflow and outflow lesions are suspected in the presence of unilateral lower extremity ischemia and diminished ipsilateral pulses, access through a retrograde puncture in the contralateral common femoral artery will allow treatment of an inflow lesion using a 6-Fr sheath and 0.035-inch system followed by treatment of the distal outflow lesion through a long 4-Fr sheath and 0.014-inch system placed within the 6-Fr sheath. An alternative strategy would be treatment of the inflow lesion alone through a retrograde puncture on the affected side followed by treatment of the outflow lesion via a separate antegrade puncture.