General Principles of Endovascular Therapy: Angioplasty, Stenting, Recanalization, and Embolization

Historical Background

Angioplasty was first used by Dotter and Judkins in 1964 for the treatment of peripheral vascular lesions using rigid intravascular dilators. Although relatively unnoticed in the United States, this approach was used to treat large numbers of patients in Europe. Grüntzig substituted a balloon-tipped catheter for the rigid dilator and performed the first peripheral balloon angioplasty in 1974. Dotter also described the use of a tubular coiled wire stent graft in canines in 1969. Tillet and Garner isolated streptokinase in 1933, but it was not until the 1950s that Clifton and Grunnet first reported its use as a thrombolytic agent. In 1960 Luessenhop and Spence first described intravascular embolization to treat a cerebral arteriovenous malformation using a handmade plastic pellet.

Indications

Indications for percutaneous transluminal angioplasty (PTA) of specific anatomic sites are detailed in later chapters but typically include an occlusive lesion that is symptomatic or at high risk for causing significant morbidity should progression to complete occlusion occur. Specific indications for stenting after an initial angioplasty include flow-limiting dissection, residual stenosis of more than 30%, or the presence of a significant pressure gradient across the treated lesion. Primary stent placement is commonly practiced for carotid and renal interventions or for a lesion that is embolizing but has not proved beneficial over selective stenting in the iliac system. It is common to selectively stent infrainguinal lesions based on the postangioplasty results, and long-term outcomes for superficial femoral artery (SFA) stents, stent grafts, and drug-eluting stents are evolving.

The exact roles for adjunctive percutaneous mechanical thrombectomy and pharmacologic thrombolytic therapy are debated, but these modalities are predominantly considered in the setting of acute arterial or venous thrombosis. Atherectomy for chronic peripheral lesions is advocated by some, but its role is controversial with a paucity of randomized data.

Indications for intravascular embolization include control of hemorrhage, treatment of vascular anomalies, exclusion of aneurysmal segments or vessels that have been treated with an endograft, and interruption of tumor vasculature.

Preoperative Preparation

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

• If angioplasty or stenting is planned, preprocedural administration of antiplatelet therapy with aspirin (325 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.

Pitfalls and Danger Points

• Inadvertent 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 help minimize embolization.

• Dissection. Dissection may occur as a consequence of wire or catheter manipulation or after primary angioplasty. Dissection from a guidewire may be avoided by frequent “twirling” of the wire tip to ensure an intraluminal position. If the position of the catheter is in doubt, contrast angiography should be performed to identify a subintimal plane of dissection. Dissection after angioplasty occurs most frequently in the region of significant plaque burden or after overdilation of a vessel. Most iatrogenic dissections are clinically silent and are not flow limiting, but if a flow-limiting dissection is present, stenting is required.

• Rupture. Vessel rupture can occur with wire manipulation, balloon angioplasty, or insertion of other devices, such as a large sheath. Rupture after angioplasty is often secondary to overdilation of the lesion. Circumferentially and highly eccentric calcified lesions are at high risk of rupture and should be approached cautiously. Subintimal angioplasty may also increase the risk for perforation compared with intraluminal procedures.