Acute vessel closure


CTO PCI Manual Online cases: 38 , 92 , 98 , 112 , 125

PCI Manual Online cases: 18 , 21 , 40 , 44 , 57 , 68 , 72 , 81

Acute vessel closure is defined as (partial or complete) decrease in antegrade coronary flow that occurs during or immediately after percutaneous coronary intervention.

Fig. 25.1 outlines a step-by-step algorithm for approaching such lesions.

Figure 25.1
Approach to acute vessel closure. ACT , activated clotting time; CABG , coronary artery bypass graft surgery; GP IIa/IIIa , glycoprotein IIb/IIIa; Rx , treatment.

Maintain guidewire position

Acute vessel closure can lead to significant patient and operator stress, which may in turn lead to inadvertent removal of the previously delivered guidewire. Losing guidewire position can have catastrophic consequences, especially if acute vessel closure is due to a dissection, and should be avoided at all cost . Losing guidewire position can be the result of guide catheter manipulation, hence continuous attention to the guide catheter position is recommended throughout the procedure.

Remaining calm and maintaining true lumen guidewire position (if the guidewire was placed in the true lumen prior to the complication) is key for successfully managing acute vessel closure.

Determine the cause of acute vessel closure and treat accordingly

Treatment of acute vessel closure depends on the cause ( Table 25.1 ). The key differentiation is between dissection (that requires stenting) and distal embolization (that may actually worsen from stenting and requires physical removal of thrombus or debris and/or vasodilator administration).

Table 25.1
Causes of acute vessel closure.
Mechanism Risk factors Diagnosis Treatment
1. Dissection
  • SCAD

  • Iatrogenic from guide catheter or guide catheter extension, guidewire, lesion preparation, stent

  • Severe tortuosity

  • Aortic dissection

Angiography OCT, IVUS
2. Thrombosis
  • Suboptimal anticoagulation and antiplatelet Rx

  • Suboptimal stent implantation

  • Angiography

  • IVUS

  • OCT

  • Optimize anticoagulation/antiplatelet Rx

  • Thrombectomy

  • Balloon angioplasty

  • Stenting

3.1. Embolization—thrombus
  • Suboptimal catheter preparation

  • Suboptimal balloon/stent/indeflator preparation

  • Thrombus formation in sheath

  • Angiography

  • IVUS

  • OCT

  • Optimize anticoagulation/antiplatelet Rx

  • Thrombectomy

  • Balloon angioplasty

  • Stenting

3.2. Embolization—plaque
  • Lipid-rich lesions

  • Atherectomy

  • Angiography

  • IVUS

  • OCT

  • Aspiration

  • Vasodilators

  • Balloon angioplasty (if epicardial embolization)

3.3. Embolization—air
  • Inadequate catheter preparation

  • Angiography

  • ECG changes

  • 100% oxygen

  • Aspiration

  • Vasodilators

  • IC epinephrine

4. Side branch occlusion after stenting
  • Ostial disease

  • Dissection

  • Large plaque burden

  • Angiography

  • ECG changes

  • Rewire branch

  • Balloon angioplasty, including kissing balloon inflation

  • Stenting

5. Spasm
  • Catheter manipulation

Angiography+response to vasodilators
  • Vasodilators

6. Pseudolesions •Severe tortuosity Angiography
  • Remove equipment from tortuous vessel

7. Equipment entrapment
  • Calcification

  • Tortuosity

  • Poor lesion preparation

  • Rotational atherectomy

  • Equipment advancement through stents

Angiography
8. Intramural hematoma •SCAD, large lipid-rich plaque, use of cutting balloons IVUS, OCT
  • Stent distally first, then proximally

  • Cutting balloon

  • Medical therapy

Note: ECG , electrocardiographic; IC , intracoronary; IVUS , intravascular ultrasound; OCT , optical coherence tomography; Rx , treatment; SCAD , spontaneous coronary artery dissection; STAR , subintimal tracking and re-entry

Dissection

In coronary dissection there is separation of the various layers of the coronary arterial wall. Angiographically, a dissection appears as a linear or spiral filling defect within the vessel lumen, although in severe cases complete vessel occlusion may occur ( Section 6.8.6 ).

The consequences of dissection depend on:

  • the severity of coronary flow obstruction (none, partial, or complete cessation of coronary flow), and

  • the location of the dissection (more proximal dissections, such as in the left main, can have more profound consequences as they cause a larger area of ischemia, potentially leading to arrhythmias and hemodynamic compromise).

Causes:

  • Injection of contrast despite dampened pressure waveform ( Chapter 5 : Coronary and graft engagement, Section 5.6 ).

  • Non-coaxial guide catheter position.

  • Guidewire crossing attempts ( Chapter 8 : Wiring, Section 8.6 , Section 8.7 , Section 8.8 ).

  • Lesion preparation (balloon angioplasty, atherectomy, laser, especially use of oversized balloons).

  • Balloon rupture ( Fig. 25.2 ).

    Figure 25.2, Dissection due to pinhole balloon rupture. An undilatable mid LAD lesion was ballooned with a 3.0×8 mm noncompliant balloon at 30 atm ( arrow , panel A). A pinhole balloon shaft rupture created a subintimal dissection ( arrows , panels C and D), that was treated with stenting and an excellent final result ( arrows , panel E).

  • Heavily calcified and tortuous lesions.

  • Stenting ( Chapter 10 : Stenting, Sections 10.2.3 and 10.2.13).

  • Spontaneous coronary artery dissection ( Chapter 22 : Other complex lesion types, Section 22.1 ).

  • Aortic dissection: aortic dissection may involve the coronary ostia causing partial or complete occlusion.

Prevention:

  • Do not inject contrast if there is dampened pressure waveform.

  • Achieve coaxial catheter position.

  • Avoid aggressive wiring strategies; avoid using polymer-jacketed guidewires as workhorse.

  • Avoid use of oversized balloons and very high-pressure balloon inflations.

  • Preparation of calcified lesions.

Treatment:

  • Small, non-flow limiting dissections do not require treatment. OCT ( Chapter 13 : Coronary intravascular imaging) is very sensitive in identifying dissections (as compared with IVUS) . Proximal edge dissections after stenting most often do not require treatment, as the stent prevents forward propagation of the dissection .

  • If wire position is maintained into the distal true lumen, stenting is performed.

  • If there is no wire into the distal true lumen, various guidewires can be used in an attempt to enter into the distal true lumen (parallel wiring).

  • IVUS can help confirm distal true lumen position. Injection of a collateralizing vessel, if available, can also help opacify the distal true lumen. Alternatively a microcatheter can be advanced distally and contrast injected, however, if the wire is subintimal, contrast injection will enlarge the subintimal space and make reentry into the distal true lumen more challenging. A safer strategy is to advance the microcatheter distally and then attempt to advance a workhorse guidewire. If the guidewire is in the true lumen it will reach the distal vessel without resistance. If the guidewire is in the subintimal space, significance resistance will be encountered when attempting to advance it.

  • If wiring into the true lumen fails, CTO techniques (such as use of the Stingray balloon , retrograde crossing , or STAR [subintimal tracking and reentry]) can be used to achieve wire crossing into the distal true lumen.

  • Avoid contrast injections; if they are absolutely needed they should be performed nonselectively with the catheter disengaged from the coronary ostium to avoid propagation of the dissection.

  • Rapid stent delivery and deployment is needed, especially for proximal dissections, such as left main dissections .

  • If a stent cannot be delivered due to significant tortuosity, calcification, or other reasons, balloon angioplasty or using a guide catheter extension may be needed first. Sometimes prolonged balloon angioplasty alone may be sufficient (although stenting is preferable, if feasible).

  • If attempts to advance a guidewire into the distal true lumen fail, emergent surgery may be needed (e.g., left main dissections). Medical therapy may suffice in patients with small dissected vessels.

  • If the cause of an ostial lesion is aortic dissection, emergency cardiac surgery is required with replacement of the aortic root.

Aorto-coronary dissection

CTO Manual Online case: 10 , 112 , 118 PCI Manual Online cases: 45 , 79

Aorto-coronary dissection is a rare complication which can occur with any PCI, but is more common with CTO PCI (especially retrograde procedures) (frequency was 0.8% to 1.8% in two contemporary series ) and most commonly occurs in the right coronary artery ( Fig. 25.3 ) . Dissection may be limited to the coronary sinus, but may extend to the proximal ascending aorta or even beyond the ascending aorta .

  • Causes ( Fig. 25.4 ) :

    • Deep coronary engagement and utilization of aggressive guide catheters, such as 8 French Amplatz left catheters.

    • Guide catheter pressure dampening.

    • Forceful contrast injection, especially through “wedged” guide catheters with dampened pressure waveform.

    • Predilation of the coronary ostium.

    • Balloon rupture.

    • Retrograde wire advancement into the subintimal and subaortic space during the reverse CART procedure.

    • Antegrade attempts to recanalize a true aorto-ostial CTO.

    • Aortic dissection extending into the coronary ostia.

    Figure 25.4, Examples of aorto-coronary dissection. (Panel A) Anteroposterior cranial view showing a class 2 aorto-coronary dissection caused by a retrograde approach to a proximal CTO lesion of the RCA. Guide catheter: left Amplatz 1 (Cordis). Presumed mechanism: contrast injection with a wedged catheter. (Panel B) Left anterior oblique view showing class 1 (limited to right sinus of Valsalva) aorto-coronary dissection caused by an antegrade approach of the ostial CTO lesion of the RCA. Guide catheter: Judkins right 4 (Cordis). Presumed mechanism: catheter trauma. (Panel C) Anteroposterior view showing class 2 aorto-coronary dissection with a parietal hematoma ( arrow ) caused by a retrograde approach to the proximal CTO lesion of the RCA. Guide catheter: right Amplatz 1. Presumed mechanism: catheter trauma. CTO , Chronic total occlusion; RCA , right coronary artery.

  • Prevention:

    • Consider using anchor techniques (Section 3.6.5) as an alternative to aggressive guide catheter intubation to enhance guide catheter support.

    • If a guide catheter extension is being used, avoid delivery into the coronary artery directly over the guidewire. Delivering the guide catheter extension over a balloon, for example, using the “ inchworming ” technique ( Section 30.3.3 and Fig. 30.28 ) is less likely to injure the vessel. Also use extreme caution when injecting through a guide catheter extension, as there is increased risk of hydraulic vessel dissection.

    • Use of guide catheters with side holes in occluded right coronary arteries may decrease the risk of barotrauma, but may also provide a false sense of security, as the pressure waveform may appear normal, but ischemia and aorto-coronary dissection can still occur.

    • Power injectors should also be avoided or used with caution after the proximal segment of a CTO vessel has been dilated; manual injections and contralateral injections from the donor vessel are preferred.

  • Treatment:

    • Stop injecting contrast into the coronary a (as injections can expand the dissection plane).

    • Stent the ostium of the dissected coronary artery with a stent that can expand to a diameter that will seal the dissection. The stent should be protruding 1–2 mm into the aorta to cover the ostium of the dissected vessel.

    • Use intravascular ultrasonography to guide stent placement and ensure complete ostial coverage .

    • If contrast injection is considered absolutely essential to check the status of the distal vessel, it is best performed through a dual lumen microcatheter or an aspiration thrombectomy catheter (that allows better vessel filling, but is bulkier and harder to deliver) advanced into the distal vessel .

    • If the aorto-coronary dissection is large, perform serial non-invasive imaging (with computed tomography or transesophageal echocardiography) to ensure that the dissection has stabilized and/or resolved ( Fig. 25.5 ) . This is of particular importance if the dissection involves the ascending aorta. The blood pressure should be carefully controlled after the procedure.

      Figure 25.5, Computed tomography (CT) follow-up of the aorto-coronary dissection shown in panel A of Fig. 25.4 . (Panel A) Twenty-four hours after the procedure, CT angiogram examination showing dislocation of intimal calcification with an eccentric double lumen. (Panel B) One-month CT control examination demonstrating almost total resolution of the dissected thrombosed lumen. (Panel C) Six-month CT control examination demonstrating total resolution of the dissection.

    • Emergency surgery is rarely needed except in patients who develop aortic regurgitation, tamponade due to rupture into the pericardium, or extension of the dissection (>40 mm from the coronary ostia has been proposed as a cutoff ) ( Fig. 25.6 ) .

      Figure 25.6, Example of aorto-coronary dissection extending into the descending aorta after CTO intervention. Angiography demonstrating proximal long segment dissection of the right coronary artery, extending to sinus of Valsalva (panels A and B). After stenting with a 3.5×24 mm bare metal stent, the final angiogram revealed limited dissection to the sinus of Valsalva (panel B). Computed tomography imaging demonstrated a type A aortic dissection extending from the ascending aorta to the suprarenal abdominal level (panels C and D) with involvement of the aortic arch and celiac trunk (panel E).

    • Emergency replacement of the aortic root is needed in patients who present with aortic dissection involving the coronary ostia (in contrast to PCI-induced aorto-coronary dissections that rarely require surgery).

Figure 25.3, Illustration of an aorto-coronary dissection during retrograde CTO intervention. Retrograde CTO intervention was performed to recanalize a proximal right coronary artery CTO ( arrow , panel A), using the reverse controlled antegrade and retrograde tracking (reverse CART) technique (panel B). Staining of the aorto-coronary junction was observed with test injections during stent placement (panel C), that expanded when cine angiography was performed (panel D). Stenting of the right coronary artery ostium was performed ( arrow , panel E) without further antegrade contrast injections. The patient had an uneventful recovery. This case illustrates the importance of stopping antegrade contrast injections and stenting the vessel ostium if aorto-coronary dissection occurs, in order to seal the dissection flap at the entry point of the dissection.

Thrombosis

Causes:

  • Inadequate anticoagulant and antiplatelet treatment.

  • Suboptimal lesion treatment (such as stent underexpansion).

  • Hypercoagulable state, including heparin-induced thrombocytopenia.

  • Venous access failure resulting in inadequate intravenous administration of the anticoagulation agent.

Prevention:

  • Maintain therapeutic ACT (>250 [Hemotec] or >300 [Hemochron] seconds depending on lesion complexity and concomitant use of intravenous antiplatelet agents, such as glycoprotein IIb/IIIa inhibitors and cangrelor) throughout the case. ACTs measured using the Hemochron devices are higher than ACTs measured with the Hemotec device .

  • Administer a P2Y12 inhibitor (pretreatment is ideal for planned PCI).

  • Meticulous lesion preparation to achieve excellent stent expansion.

  • Use of intravascular imaging to confirm than an excellent PCI result has been achieved.

Treatment:

  • Treatment of intracoronary thrombus is performed as described in Chapter 20 , Acute coronary syndromes—thrombus.

  • Ensure optimal anticoagulation and antiplatelet therapy is achieved.

  • Thrombectomy may be needed in cases of large thrombus burden.

  • Occasionally stenting may trap thrombus and restore antegrade flow.

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