Update on the Diagnosis and Treatment of Coronary Complications of Percutaneous Coronary Interventions

J INVASIVE CARDIOL 2024. doi:10.25270/jic/24.00260. Epub November 18, 2024.

Prevention, prompt diagnosis, and rapid treatment are crucial for improving outcomes of complications that occur during percutaneous coronary intervention (PCI). The authors summarize studies on PCI complications published between January 1, 2023, and May 1, 2024, including coronary dissection, no reflow, perforation, and equipment loss/entrapment.

Early diagnosis and treatment of coronary complications, such as acute vessel closure, perforation, and equipment loss or entrapment is critical for optimizing the outcomes of percutaneous coronary intervention (PCI).^1-3 We performed a systematic review of studies on PCI complications published between January 1, 2023, and May 1, 2024 to provide an update on contemporary diagnosis and practical management of these complications, based on real-world experience.

Search strategy

A systematic review of articles published in PubMed (National Institutes of Health) from January 1, 2023, to May 1, 2024, was conducted to evaluate the management of complications associated with PCI. The search terms included “complications,” “percutaneous coronary intervention,” “PCI,” “dissection,” “perforation,” “no-reflow,” and “entrapped equipment.”

Inclusion and exclusion criteria

Articles that discussed practical management strategies for PCI complications were included.

Review process and categorization

Two independent reviewers screened all identified articles for eligibility. Each reviewer assessed the articles to determine their relevance to the management of PCI complications. Any discrepancies in categorization were resolved through discussion and consensus. The articles were categorized into 4 primary coronary complication types: coronary dissection, no-reflow, perforation, and equipment loss/entrapment.

Data extraction

Relevant data from the included articles was extracted and summarized. Of the 184 retrieved articles, 78 were excluded because they did not discuss specific management of PCI complications. Moreover, 34 articles were excluded because their primary focus was not on PCI complications. Another 16 articles were excluded because they focused on complications from non-PCI procedures. A total of 56 studies met the inclusion criteria and were included in this review.

Iatrogenic coronary artery dissection is one of the main mechanisms leading to acute vessel closure. If unclear angiographically, the diagnosis of dissection can be confirmed by intravascular imaging.⁴  Rarely, a type A aortic dissection can lead to coronary dissection, causing an acute coronary syndrome, as reported in a patient who presented with an acute inferior ST-segment elevation myocardial infarction (STEMI).⁵

In a single-center study of 10 278 PCIs performed between 2014 and 2019, the incidence of coronary dissection was 1.4% (141 cases).⁶ The most common mechanism leading to dissection was guidewire advancement (30%), followed by stenting (22%), and balloon angioplasty (20%), and the most common treatment was stenting. Wire position was not maintained or lost in 64 cases (45%). Losing guidewire position significantly hinders treatment of the dissection, as rewiring the true lumen can be challenging, with the wire preferentially entering the dissection planes. Soft-tip guidewires, such as the Suoh 03 (0.3 grams distal tip load) (Asahi)⁷, can facilitate true lumen wiring in dissection cases. Having a “safety” guidewire in the donor vessel is routinely recommended in chronic total occlusion (CTO) PCI to help maintain catheter position and also to allow prompt treatment in case of dissection.⁸ Rarely, a coronary dissection may be diagnosed after coronary angiography, sometimes requiring stenting.^9,10

Aorto-coronary dissections can lead to an ascending aortic dissection that may require surgery on rare occasions. When an aorto-coronary dissection occurs, contrast injections should stop, followed by stenting from the coronary artery into the aorta. Intravascular ultrasound can help visualize the coronary artery without contrast injection and confirm complete stent coverage of the coronary ostium.¹¹ In a large CTO-PCI series published in 2023, the incidence of aorto-coronary dissection was  0.2% (n = 27), with most occurring in the right coronary artery cusp (96.3%, n = 26). Of the 27 patients with aortocoronary dissection, 19 (70.4%) were treated with ostial stenting, and 8 (29.6%) were treated conservatively without subsequent adverse clinical outcomes. No patients required emergency surgery.¹² Serial imaging with computed tomography (CT) angiography can help ensure healing of the dissection.

Despite recent advances, CTO PCI is associated with higher complication rates, especially for CTOs involving bifurcations.¹³ Branch occlusion may occur because of an extension of a dissection, known as a "subintimal shift" (SIS).¹³ The management of SIS is not yet standardized, but direct stenting in CTOs can help restore blood flow quickly. Intravascular imaging can help assess the risk of branch occlusion. A guidewire should be inserted in both bifurcation branches prior to stenting whenever feasible; occasionally puncturing the true lumen through an intimal flap with stiff tapered wires may also be necessary.¹³

Cardiac CT may be utilized to detect iatrogenic aortic dissection that was initially missed during conventional angiography,¹⁴ as well as coronary involvement in patients with type A aortic dissection.⁵ Coronary CT angiography can also be useful in identifying why patients develop chest pain both early and late after PCI.⁹ Finally, when true lumen wiring with standard techniques fails, the parallel wire technique or subintimal tracking and reentry (STAR) can help salvage a dissection that caused abrupt closure or severe reduction in flow.¹⁵ 

The no-reflow phenomenon is the failure to restore normal myocardial blood flow despite treating the epicardial coronary artery obstruction. No-reflow is usually caused by distal embolization leading to microvascular damage and local edema.^2,16 Risk factors for no-reflow include large thrombus burden, atherectomy,¹⁷ and PCI of lesions with a large lipid burden.

No-reflow is usually treated by intracoronary administration of adenosine, nicardipine, nitroprusside, a non-dihydropyridine calcium channel blocker, or epinephrine and thrombus aspiration.^18,19 Intracoronary epinephrine may also be effective for reversing refractory no-reflow,²⁰ as is super-selective intracoronary injection of saline through a thrombus aspiration catheter (SALINE technique).²¹ In a study of 1471 STEMI patients who underwent PCI from May 2015 to June 2020, 168 developed no-reflow. After propensity score matching, 75% of the patients treated with SALINE achieved ST-segment resolution of at least 70% compared with only 19% in the control group (P < .004). The SALINE group also had a higher final Thrombolysis in Myocardial Infarction (TIMI) flow grade and better 3-year outcomes.²¹

The incidence of no-reflow in STEMI patients undergoing primary PCI ranges from 2.3% to 30%, and significantly impacts prognosis.^22,23 Compared with patients who did not develop coronary no-reflow after primary PCI for STEMI, those who did had higher in-hospital (8.2% vs. 4.3%, P = .04) and 5-year (22.2% vs. 16.2%, P = .04) mortality.²⁴ Large thrombus is associated with a higher risk of no-reflow.²⁵ Intracoronary thrombolytics did not reduce the risk of no-reflow,²⁵ whereas thrombus aspiration (4-5 times) did, without increasing the incidence of stroke.²⁶ Primary stenting (after thrombus aspiration) may be beneficial in STEMI patients with a high thrombus burden, as predilatation has been associated with a higher risk of no-reflow.^27,28 Primary stenting should, however, be used with caution to avoid the risk of stent underexpansion if directly deployed in resistant fibrotic or calcified lesions. The use of intracoronary imaging could help guide such a decision.

Coronary artery perforation occurs in approximately 0.51% of PCIs.²⁹ The incidence of perforation is higher in CTO PCI (4.9% to 5.8%),^30,31 especially when using the retrograde approach through ipsilateral epicardial collaterals.^32,33 In an online survey of CTO-PCI operators, 19% of respondents had experienced coronary artery perforation during the prior month.³⁴ In a national Polish registry of CTO PCI, operators who performed at least 40 CTO cases annually had lower perforation rates compared with lower volume operators.³⁵ The PROGRESS-CTO perforation score includes 5 parameters (patient age ≥ 65 years, moderate/severe calcification, blunt/no stump, use of antegrade dissection and re-entry, and use of the retrograde approach) and can help assess the risk of perforation during CTO PCI.³⁶

There are 3 main types of perforation depending on location: large vessel, distal vessel, and collateral vessel perforation.³⁷ A fourth type of perforation is “cavity spilling,” in which the blood flow enters another cardiac chamber. Cavity-spilling perforations into a low pressure cavity, such as the right ventricle or the coronary sinus, may not cause tamponade and may not require specific treatment, as they often spontaneously resolve during follow-up.³⁸ A conservative strategy has been recommended for cavity-spilling perforations if the patient remains asymptomatic and does not develop a pericardial effusion.³⁸   

Large vessel perforations are often due to balloon and stent inflation, which interrupt the intima and create a crater that penetrates the external layers of the vessel wall,³⁹ while distal vessel perforations are usually caused by guidewire exit.²⁹ Severe lesion calcification is a risk factor for perforation: the C-type Calcified and residual Thin plaque sign (C-CAT sign: 270-degree calcified C-type eccentric plaque and a thin contralateral plaque) on intravascular ultrasound (IVUS) has been associated with an increased risk of perforation, likely because of an overstretch of the minimally diseased side of the artery and failure to modify the larger area of plaque.⁴⁰ Whether intravascular lithotripsy can reduce the risk of perforation in these lesions remains to be investigated. 

Balloon tamponade is the first line of treatment for all perforations. Prolonged balloon inflation can sometimes seal a large perforation, but the balloon inflation site matters.⁴¹ In a case of a mid-left anterior descending artery (LAD), a 2.75 × 12-mm balloon was inflated for 15 minutes, with a 2-minute break for blood perfusion without sealing the perforation. The balloon was subsequently inflated proximal to the perforation for 10 minutes, achieving perforation sealing.⁴² Hence, balloon inflation proximal to the perforation site may be advantageous compared with ballooning over the perforation.⁴² Balloon inflation may cause ischemia, especially in proximal vessel locations, such as the proximal LAD. A perfusion balloon (Ringer, Teleflex) was recently approved for clinical use in the United States,⁴³ but ischemia can also be prevented by inserting a microcatheter or thrombus aspiration catheter distal to the balloon inflation site and using it to inject oxygenated blood (aspirated from the guide catheter) through the over-the-wire lumen (Figure 1).⁴⁴

 

 

Delivering a blocking balloon can be challenging. For treating perforations during retrograde CTO PCI, especially through saphenous vein grafts, retrograde-balloon (and sometimes covered-stent) delivery can sometimes be performed.⁴⁵ Retrograde-balloon delivery has also been described through septal collaterals (“septal retrograde ping pong technique”).⁴⁶

If balloon inflation fails to seal a large vessel perforation, a covered stent is usually required. The use of low-profile covered stents, such as the PK Papyrus (Biotronik) can facilitate delivery, but delivery can still be challenging, especially in heavily calcified vessels. The use of the “tunnel in landslide” technique (TILT) (balloon inflation alongside a guide catheter extension) can simultaneously achieve hemostasis and facilitate delivery of the covered stent (Figure 2).^47,48 Covered-stent deployment at a bifurcation will cause occlusion of the side branch. The PK Papyrus stent can be fenestrated using stiff guidewires followed by ballooning and stenting to restore perfusion of the side branch.^49,50

 

 

Distal vessel perforations may lead to delayed tamponade for hours or even days after PCI (after two⁵¹  and four⁵² days in recent case reports). Some patients with perforation may develop pericardial thickening and recurrent effusions after a few months, occasionally causing constriction that requires pericardiectomy.⁵³

In some perforation cases, especially distal vessel perforations, the vessel may need to be occluded to stop bleeding into the pericardium. Coils or pericardial fat are usually used for distal embolization. Some coils, such as the low-profile 0.0135-inch Ruby coils (Penumbra), can be delivered through an over-the-wire balloon while maintaining distal hemostasis with inflation of the balloon (“plug and seal technique”).⁵⁴ Alternatively, they can be delivered through standard 0.014-inch microcatheters. However, coils may not be available in all catheterization laboratories. The “umbrella technique” involves cutting the distal portion of an angioplasty balloon and delivering it to the perforation site by pushing it with another balloon. The downside of this technique is that, once delivered, the balloon fragment cannot be retrieved.⁵⁵

If all other treatments fail, emergency cardiac surgery may be needed to treat a perforation; however, this surgery is associated with high mortality. Emergency coronary artery bypass surgery was performed in 0.12% of 14 512 CTO PCIs between 2012 and 2023 in the PROGRESS-CTO registry, and perforation caused 70.6% of these cases.⁵⁶ Perioperative mortality was 35.3%.⁵⁶ Tamponade was the cause of 58% of all periprocedural deaths after CTO PCI in the same registry.⁵⁷

Several types of equipment, such as coronary guidewires, microcatheters, atherectomy devices, and balloons can become entrapped or lost during PCI.^58,59,60 The risk of equipment loss/entrapment is high in complex PCI, with an incidence of 0.4% in a large 2024 CTO-PCI series,⁶⁰ and has been associated with a high incidence of myocardial infarction, need for emergency CABG, and death. Most cases can be treated with percutaneous techniques,^60,61 but emergency CABG may sometimes be required.⁶²

The first step in managing dislodged stents is to determine whether to attempt retrieval or deploy/crush them against the vessel wall. Stent deployment or crushing is often preferred, as it is usually faster and safer. Attempts at stent retrieval may lead to coronary injury.⁶³ Retrieval can be achieved using simple techniques, such as the small-balloon technique, or more complex techniques, such as the twisted-wire technique or the use of microsnares,⁶⁴ but these strategies can result in guidewire position loss. The novel “guide extension catheter trapping technique” involves advancing the guide extension catheter over the guidewire to the site of the dislodged stent. Once in position, a balloon catheter is introduced to trap the dislodged stent against the inner wall of the guide catheter extension. The balloon is then inflated to secure the stent in place. The entire system, including the guide extension catheter, balloon catheter, and trapped stent, is then carefully withdrawn from the coronary artery.⁶⁵

Guidewire entrapment is infrequent, but, if it occurs, forceful withdrawal can lead to wire fracture and unraveling of the wire coil, sometimes requiring surgery. Rotational atherectomy (RA) can be used to cut the entrapped guidewire,⁶⁶ which can then be subsequently removed, avoiding unraveling. The operator should confirm the guidewire entrapment with fluoroscopy and prepare the RA system. The RA burr can be used at 150 000 to 200 000 rpm to cut the wire, and then the entrapped equipment can be retrieved with standard techniques, such as snaring or gentle traction.⁶⁶ Retrieval of guidewire fragments can also be achieved using the “knuckle-twister technique”, in which a polymer-jacketed guidewire is folded, transforming it into an open lasso that tightens when twisted next to a wire fragment. The pulling force generated in testing was 1.5 kg (Figure 3).⁶⁷ Alternatively, coronary snares might be used.

 

 

Balloon entrapment can lead to balloon shaft fracture. The remaining balloon fragment can be retrieved using a snare. If the balloon fragment is partially inside the guide catheter, a balloon can be advanced alongside the portion inside the guide and inflated at high pressure, followed by withdrawal of the entire system, trapping out the balloon. The same technique has also been described for retrieving a fractured IVUS outer sheath.⁶⁸ If retrieval is impossible, balloon fragments can be jailed by stenting over them.⁶⁹

The prevention, diagnosis, and treatment of PCI complications continue to evolve. The implementation of novel techniques and technologies can help with prevention, as well as early identification and treatment of PCI complications in real world settings.

Sant Kumar, MD¹; Ahmed Al-Ogaili, MD²; Allison Hall, MD³; Lorenzo Azzalini, MD, PhD⁴; Khaldoon Alaswad, MD⁵; Stéphane Rinfret, MD⁶; Jimmy Kerrigan, MD⁷; Jason Wollmuth, MD⁸; Anastasios Milkas, MD, PhD⁹; Subhash Banerjee, MD¹⁰; Yader Sandoval, MD²; Emmanouil S. Brilakis, MD, PhD²

Author Affiliations: ¹Department of Cardiology, Creighton University School of Medicine, Phoenix, Arizona; ²Minneapolis Heart Institute and Minneapolis Heart Institute Foundation, Abbott Northwestern Hospital, Minneapolis, Minnesota; ³NL Health Services/Memorial University of NL St John's, Newfoundland and Labrador, Canada; ⁴Division of Cardiology, Department of Medicine, University of Washington, Seattle, Washington; ⁵Henry Ford Hospital, Cardiovascular Division, Detroit, Michigan; ⁶Emory University, Atlanta, Georgia; ⁷Ascension Saint Thomas Heart, Nashville, Tennessee; ⁸Providence Heart Institute, Portland, Oregon; ⁹Department of Cardiology, Athens Naval Hospital, Athens, Greece; ¹⁰Baylor Scott & White Heart and Vascular Hospital, Dallas, Texas.

Disclosures: Dr Stephane Rinfret is a consultant for Abiomed, Boston Scientific, Medtronic, and Teleflex. Dr Brilakis receives a consulting/speaker honorarium from Abbott Vascular, the American Heart Association (associate editor, Circulation), Biotronik, Boston Scientific, Cardiovascular Innovations Foundation (Board of Directors), Cordis, CSI, Elsevier, GE Healthcare, IMDS, Medtronic, and Teleflex; research support from Boston Scientific and GE Healthcare; is the owner of Hippocrates, LLC; and is a shareholder in MHI Ventures, Cleerly Health, and Stallion Medical.

Address for correspondence: Emmanouil S. Brilakis, MD, PhD, Minneapolis Heart Institute and Minneapolis Heart Institute Foundation, Minneapolis, MN 55407, USA. Email: esbrilakis@gmail.com. X: @esbrilakis; @sant_j_kumar