Other complex lesions


In addition to calcification, thrombus, and CTOs, other complex lesion types include:

  • Spontaneous coronary artery dissection (SCAD) (PCI Manual Online case 72 ),

  • Stent failure (in-stent restenosis and stent thrombosis),

    CTO Manual Online cases: 19 , 52 , 54 , 58 , 72 , 84 , 91 , 101 ; PCI Manual Online cases: 63 , 89 , 94

  • Small and large vessels, and

  • Long lesions.

Spontaneous coronary artery dissection

SCAD is defined as an epicardial coronary artery dissection that is not associated with atherosclerosis or trauma and is not iatrogenic . The predominant mechanism of myocardial injury occurring as a result of SCAD is coronary artery obstruction caused by formation of an intramural hematoma (IMH) or intimal disruption rather than atherosclerotic plaque rupture or intraluminal thrombus .

Planning

SCAD should be suspected in young women, especially in the peripartum setting ( Fig. 22.1 ) .

Figure 22.1, Acute anterior myocardial infarction in a term pregnant woman.

Monitoring

Given high risk of complications and hemodynamic deterioration, careful monitoring is needed throughout the procedure.

Medications

Anticoagulation and oral antiplatelet therapy is administered as in non-SCAD cases. Glycoprotein IIb/IIIa inhibitors and cangrelor should generally be avoided given risk of extending an IMH.

Access

Femoral access is preferred for coronary angiography of patients with suspected SCAD, given a threefold higher risk for catheter-induced iatrogenic dissection with radial access observed in one series .

Engagement

Coronary engagement should be performed with extreme care aiming for coaxial positioning, and avoiding deep coronary artery intubation .

Angiography

Strong contrast injections should be avoided to reduce the risk of iatrogenic dissection .

Identification of SCAD can be challenging and requires awareness and careful angiographic interpretation. There are three angiographic types of SCAD ( Fig. 22.2 ) :

Figure 22.2, The Saw SCAD angiographic classification.

Type 1 : Classic appearance of multiple radiolucent lumens or arterial wall contrast staining.

Type 2 : Diffuse stenosis that can be of varying severity and length (usually >20 mm). Variant 2A is diffuse arterial narrowing bordered by normal segments proximal and distal to the IMH, and variant 2B is diffuse narrowing that extends to the distal tip of the artery.

Type 3 : Focal or tubular stenosis, usually <20 mm in length. Type 3 mimics atherosclerosis and requires intracoronary imaging (if safe) to diagnose SCAD.

Selecting target lesion(s)

PCI of SCAD lesions carries high risk of complications and is often quoted as “a temptation to be avoided.” Conservative management is preferred (if feasible), however in patients with active ischemia or hemodynamic instability coronary revascularization may be required, as follows :

  • Stable patients without left main or proximal two-vessel coronary dissection: in-hospital observation for 3–5 days without revascularization.

  • Stable patients with left main or proximal two-vessel coronary dissection: CABG versus continued in-hospital observation.

  • Unstable patients or active ischemia: PCI or CABG depending on anatomy.

Wiring

Given the risk of subintimal guidewire entry, polymer-jacketed guidewires should be avoided in patients with suspected SCAD.

Lesion preparation

Direct stenting has been proposed for SCAD lesions to minimize the risk of IMH expansion. A cutting balloon can sometimes be used to decompress the hematoma, but it carries a risk of perforation.

The cutting balloon has been used for fenestration of an IMH with luminal compression at multiple sites prior to stenting .

Stenting

Implanting long stents that extend 5–10 mm on both sides of the IMH has been proposed in SCAD patients to minimize the risk of subintimal hematoma expansion . The stent diameter should generally be smaller than the size used in similar atherosclerotic lesions to avoid hematoma expansion.

Closure

Access closure is performed as described in Chapter 11: Access Closure .

Coronary physiology

Coronary physiology has limited role in SCAD cases.

Intravascular imaging

Intravascular imaging, especially OCT, can confirm the diagnosis of SCAD, but may also cause extension of the dissection and should, therefore, be used cautiously.

Hemodynamic support

Because of high risk of acute vessel closure during PCI of SCAD lesions, access to hemodynamic support devices, such as VA-ECMO is recommended (PCI Manual Online case 72 ).

Stent failure

Stent failure can manifest as stent thrombosis or in-stent restenosis . Stent thrombosis is a life-threatening complication and usually presents as ST-segment elevation acute myocardial infarction. In-stent restenosis usually presents with stable angina but can sometimes present as an acute coronary syndrome.

Stent thrombosis is often caused by stent underexpansion or insufficient antithrombotic therapy. Stent thrombosis is rarely caused by stent fracture.

Planning

Special emphasis should be given to a detailed history of prior percutaneous coronary interventions, including stent types, stent sizes, prior stent failure (stent thrombosis or in-stent restenosis), and prior brachytherapy [that requires lifelong dual antiplatelet therapy due to continued risk of very late (>1 year) stent thrombosis].

Moreover, it is important to know the current antiplatelet therapy and compliance with the therapy, any recent antiplatelet therapy discontinuation and any recent noncardiac surgery.

Monitoring

Given high risk of complications and hemodynamic deterioration of stent thrombosis patients, careful monitoring is needed throughout the procedure.

Medications

Lifelong dual antiplatelet therapy is recommended after development of stent thrombosis unless the patient is at high risk of bleeding.

Cilostazol may decrease the risk of in-stent restenosis, but is contraindicated in patients with heart failure.

Access

Radial or femoral access can be used. Radial access is generally preferred in stent thrombosis patients presenting with a STEMI.

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