Iatrogenic coronary artery dissection is a rare but serious complication of PCI and represents one of the major mechanisms of acute vessel closure. The reported incidence of iatrogenic coronary dissection during PCI ranges from 0.8% to 1.4% (7–9). Iatrogenic coronary artery dissection most commonly results from noncoaxial catheter or guide engagement, forceful contrast injection against a dampened pressure waveform, inadvertent deep seating of the guide catheter, or excessive manipulation of stiff guiding catheters (7–9). Aggressive advancement or withdrawal of interventional devices and the use of polymer-jacketed guidewires may further propagate a dissection flap. In addition, balloon rupture, particularly in the presence of a calcified lesion, can result in an aortocoronary dissection (7–9). Importantly, although mechanical injury typically initiates the dissection, subsequent contrast injections may propagate a hydraulic dissection, further extending the intramural hematoma and potentially leading to vessel occlusion (10).

Patient-related factors include advanced age, female sex, and presentation with ACS (11). Angiographic risk factors include calcified, eccentric, long, or complex lesions (ACC/AHA type B or C), as well as vessel tortuosity (11). Procedural risk factors include a large balloon-to-artery ratio (>1.2), noncoaxial guide alignment, and deep seating of the catheter (11). Dissection is typically visualized on coronary angiography. Once a dissection is identified, further antegrade contrast injection should be avoided (10). Intravascular imaging, particularly IVUS, can facilitate accurate diagnosis and delineation of the dissection's extent (10).

In addition, underlying connective tissue disorders and pathogenic collagen or extracellular matrix gene variants have been associated with an increased risk of spontaneous coronary artery dissection, and syndromic conditions such as Loeys-Dietz syndrome have been reported as rare causes of SCAD (12, 13). However, the extent to which these genetic conditions independently increase the risk of iatrogenic coronary dissection during PCI remains unclear.

Iatrogenic coronary dissection is classified by the National Heart, Lung, and Blood Institute (NHLBI) into six types (A-F) as shown in Figure 1 (14). Type A represents a minor radiolucent line within the vessel lumen without persistent contrast staining after dye clearance. Type B is characterized by parallel tracts or a double-lumen appearance that also disappear following dye clearance, similar to Type A. Type C involves extraluminal contrast staining that persists after dye clearance, indicating deeper vessel wall involvement. Type D is identified by a spiral luminal filling defect that compromises flow within the true lumen, while Type E presents as a persistent luminal filling defect within the coronary artery lumen. Type F represents the most severe form, defined by total vessel occlusion with complete loss of antegrade flow (14). The NHLBI classification correlates with both clinical outcomes and management strategies. Types C through F are typically clinically significant and often require intervention, whereas Types A and B are usually benign and may be managed conservatively (14). The risk of acute vessel closure increases with the severity of dissection, progressing from Type A to Type F (14). Types B and C are associated with relatively low incidences of acute vessel closure (3% and 10%, respectively), while Types D, E, and F carry substantially higher risks, with incidences of approximately 30%, 37%, and 69%, respectively (14). The specific management strategies for coronary dissection are discussed in the dedicated dissection section below.

Management of guide catheter-induced dissection generally requires stent implantation, and the procedural approach depends on whether the guidewire has already crossed the lesion (10, 15). IVUS can help confirm whether the wire is positioned in the true or false lumen (10). If the wire is already across the lesion and located in the true lumen, a stent should be placed proximally to seal the entry point of the dissection and compress the hematoma (10). When the distal extent of the dissection is visualized, consider stenting the distal edge first to prevent further propagation (10, 15). If TIMI flow remains <3 after proximal stenting, this suggests persistent distal hematoma or occlusion; in such cases, balloon dilation or use of a cutting balloon may be considered to decompress the hematoma and restore flow (10, 15). If rewiring is necessary, IVUS should be used to ensure entry into the true lumen. IVUS is also useful for determining the length of the dissection, appropriate stent sizing, and optimization of stent deployment (10). Although optical coherence tomography (OCT) has been successfully used in some cases of catheter-induced dissection, its use should be approached with caution, as forceful contrast injection required for blood clearance can exacerbate the dissection (16).

If the wire has not crossed the lesion, an antegrade wiring attempt should be performed, followed by stenting once true lumen access is accessed (10, 15). When the initial wire lies within the false lumen, IVUS may be left in place alongside the first wire to provide real-time imaging guidance during the parallel wire technique. This approach allows the subintimal wire to tamponade the false lumen while a second wire is advanced into the true lumen (10). The subintimal transcatheter withdrawal (STRAW) technique may also be used to aspirate and decompress a subintimal hematoma that prevents distal reentry (17).

If antegrade wiring fails, alternative reentry techniques can be performed, including wire-based dissection reentry, reentry using a Stingray reentry system, or a retrograde approach (10, 15). The subintimal tracking and reentry (STAR) technique involves advancing a knuckled polymer-jacketed wire through the subintimal space until it spontaneously reenters the distal true lumen (18). Modified antegrade reentry methods, such as mini-STAR and limited antegrade subintimal tracking (LAST), have been developed to achieve earlier and more controlled reentry, minimizing the dissection plane and vessel trauma (18). The Stingray balloon system facilitates controlled subintimal navigation and targeted reentry into the true lumen using a flat, dual-lumen balloon and a specialized reentry wire (18). In selected cases with suitable collateral vessels, a retrograde approach may be performed.

Prevention of iatrogenic coronary dissection includes avoiding contrast injection when a dampened pressure waveform is observed, preventing deep catheter engagement, maintaining coaxial guide alignment, minimizing aggressive wire manipulation, and exercising caution with polymer-jacketed guidewires (19). Preprocedural IVUS imaging can assist in lesion assessment and guide appropriate lesion preparation to minimize the risk of dissection (10).

Aortocoronary dissection may extend into the aortic cusp or ascending aorta. The reported incidence of iatrogenic aortocoronary dissection ranges from 0.02% to 0.2%, with most cases originating from the right coronary cusp (7, 20). The majority of these dissections can be managed with ostial stenting, which seals the entry tear (20).

The Dunning classification provides an angiographic framework for characterizing aortocoronary dissections based on the extent of aortic involvement: Class I dissections are confined to the aortic cusp, Class II extend less than 4 cm into the ascending aorta, and Class III extend more than 4 cm into the ascending aorta (21). This classification correlates with both prognosis and management strategy. Higher Dunning classes are associated with an increased likelihood of surgical intervention and higher mortality, reported as 0% for Class I, 4.3% for Class II, and 6.5% for Class III (8). Most Class I cases can be successfully treated conservatively or with ostial stenting, whereas 17.4% of Class II and 40.3% of Class III cases require surgical repair (8). IVUS should be used to guide stent placement to ensure complete ostial coverage and seal the dissection entry point (22).

Large-vessel coronary perforation most commonly occurs due to the use of oversized or overinflated balloons and stents, or as a complication of atherectomy devices such as rotational atherectomy (86). These perforations are typically classified as Ellis Type III, representing the most severe form of coronary perforation (85, 86). Clinically, large-vessel perforation can lead to rapid hemodynamic deterioration due to cardiac tamponade, often requiring emergent pericardiocentesis and hemodynamic support (86). The sudden onset of acute chest pain or hemodynamic instability during balloon inflation or stent deployment should raise suspicion for coronary artery perforation, which can be promptly confirmed by angiographic visualization of contrast extravasation.

Management of coronary artery perforation involves both general supportive measures applicable to all cases and specific strategies based on the vessel size and perforation severity. General management includes hemodynamic stabilization with fluid resuscitation, vasopressor support if needed, and pericardiocentesis in cases of cardiac tamponade (81). Importantly, in cases of ongoing extravasation or persistent localized tamponade, particularly in patients with prior CABG, where the pericardial space may not be amenable to complete percutaneous drainage, emergent surgical intervention, including creation of a pericardial window or operative repair, may be required to restore and maintain hemodynamic stability (87).

Balloon tamponade remains the first-line procedural intervention and should be performed by inflating a balloon at or just proximal to the perforation site for 5–10 min using a balloon-to-artery ratio of 1:1 at low inflation pressure (81). Because prolonged balloon inflation can compromise distal myocardial perfusion and lead to ischemia or infarction, a specialized device known as the Ringer perfusion balloon has been developed. This helical-shaped inflatable balloon opposes the vessel wall while maintaining antegrade coronary perfusion through a hollow central lumen (88). In a recent study, the Ringer perfusion balloon demonstrated a high procedural success rate, achieving cessation of contrast extravasation in 84.6% of cases and maintenance of TIMI grade 2–3 flow in 100% of patients (88). Intravenous anticoagulant and antiplatelet therapies should be withheld immediately following the recognition of a coronary artery perforation. Reversal of anticoagulation may be considered once all interventional equipment has been withdrawn from the coronary artery. Recent evidence further supports the safety of this approach (89). In a single-center retrospective study 160 patients with coronary perforations during CTO PCI, protamine administration after complete device removal was associated with significantly lower rates of in-hospital mortality and cardiac tamponade, with no observed cases of acute stent thrombosis (89). These findings reinforce that appropriately timed heparin reversal can be safely utilized in select cases of coronary artery perforation.

If balloon tamponade fails to control the bleeding, covered stent implantation should be performed (15). The goal of a covered stent is to seal the perforation using an impermeable barrier layer, thereby restoring vessel integrity and preventing further extravasation (90, 91). Two main types of covered stents are currently available. The Graftmaster (Abbott Vascular) has a traditional “sandwich” design, consisting of a bilayer metallic framework with a thin, biocompatible polytetrafluoroethylene (PTFE) membrane between the layers. It typically has a larger diameter and requires a larger guide catheter for delivery (91). The PK Papyrus (Biotronik) has a single-layer cobalt-chromium platform covered with a highly elastic polyurethane membrane, offering a smaller profile, improved flexibility, and compatibility with smaller guide catheters and standard 0.014-inch guidewires (90, 91).

The deployment technique depends on the guide catheter size and stent type. If the guide catheter is large enough, the “block-and-deliver” technique can be used with a single guide catheter (92). In this method, a second guidewire is advanced while the balloon remains inflated at the perforation site. The balloon is briefly deflated to allow guidewire passage, then reinflated to maintain hemostasis while the covered stent is advanced proximally. Once positioned, the balloon is deflated and withdrawn, allowing deployment of the covered stent at the perforation site (92).

When the initial guide is too small, the “ping-pong” (dual-guide) technique can be performed (93). In this approach, a second guide catheter is introduced while maintaining balloon inflation. The balloon is briefly deflated to allow passage of the second guidewire and covered stent, to the perforation site. After the stent is positioned, the first guidewire and balloon are withdrawn, and the covered stent is deployed to seal the perforation (93).

Despite their efficacy, covered stents cause side-branch occlusion, which may result in myocardial ischemia. Evidence comparing different covered stent types remains limited. Observational study in patients with large-vessel perforations successfully sealed with a covered stent reported that the PK Papyrus was associated with a significantly lower rate of target lesion revascularization at 30 days compared with the Graftmaster, although no differences were observed in 30-day or 1-year MACE (94).

Although covered stents provide rapid and effective sealing of large-vessel perforations, several concerns remain regarding their long-term performance, including higher rates of restenosis and stent thrombosis (91). While these devices were conceptually designed to reduce in-stent restenosis by creating a mechanical barrier that limits neointimal proliferation through the stent struts, randomized data in SVG-PCI have not demonstrated a reduction in restenosis compared with bare-metal stents (95, 96). A retrospective study reported a definite stent thrombosis rate of 8.6% among patients with Ellis Grade III perforation treated with a covered stent, and registry data similarly show a higher incidence of stent thrombosis within one year in covered stents compared with other stent platforms (96, 97). These findings underscore the need for optimal deployment technique and high-pressure post-dilation.

Perforations occurring in or near coronary bifurcations represent a particularly challenging scenario, as management must balance rapid hemostasis with preservation of side-branch flow. Initial treatment follows standard principles, including immediate balloon tamponade and hemodynamic stabilization, with precise localization of the perforation relative to the bifurcation determined using angiography and intravascular imaging. When bleeding persists, covered stent implantation is often required; however, bifurcation perforations may necessitate intentional side-branch jailing to achieve complete sealing (98). A systematic review of Ellis grade III perforations involving left main distal bifurcation lesions demonstrated that crossover covered stenting is the most commonly employed strategy, while alternative approaches, including covered stent implantation with the jailed balloon technique or simultaneous kissing covered stents, may improve side-branch preservation in selected cases (98). Side-branch sacrifice is sometimes unavoidable to achieve definitive hemostasis, with subsequent reaccess using high tip-load guidewires and dual-lumen catheters when clinically indicated. These principles are illustrated by a recent case report describing a complex bifurcation core perforation managed with a dual-covered stent strategy, in which intentional side-branch jailing was required for sealing, followed by advanced rewiring techniques to restore coronary blood flow (99).

Distal-vessel perforation typically occurs in distal coronary segments, side branches or collaterals in patients undergoing CTO PCI, most commonly resulting from guidewire-related injury. Previous studies have shown that the majority of guidewire-associated perforations are caused by hydrophilic guidewires (100). Compared with large-vessel perforation, small-vessel perforation carries a lower risk of immediate hemodynamic compromise, but it may lead to delayed cardiac tamponade, which can develop hours to days after PCI (101). Diagnosis is usually established by coronary angiography, which should include prolonged image acquisition with panning of the distal vessel to visualize subtle or delayed contrast extravasation. Adjunctive imaging with transthoracic echocardiography, including contrast-enhanced echocardiography, can determine the presence and location of ongoing extravasation, differentiate pericardial from intracardiac leakage, and guide the need for additional interventions such as coil embolization or covered stent placement.

Management principles are similar to those used in large-vessel perforation and begin with prolonged balloon inflation (15). If balloon tamponade fails to achieve hemostasis, a microcatheter should be advanced as close as possible to the perforation site for embolization therapy (15). Coil embolization is the preferred therapeutic option for sealing distal or small-vessel perforations vessel (81, 102, 103). Based on their delivery mechanism, coils are categorized into two main types. Pushable coils are non-retrievable once deployed and have a less predictable final position, whereas detachable coils permit controlled, reversible delivery, allowing for more precise placement at the target site (81, 103). During coil delivery, a second guidewire and balloon can be inflated proximally to the perforated branch to control bleeding, using the block-and-deliver technique (92).

In case where coils are unavailable, several alternative embolic agents may be used to achieve hemostasis. These include autologous fat, typically harvested from the abdomen or groin and delivered through a microcatheter; autologous blood clot, which serves as a natural occlusive material; and thrombin, which promotes localized thrombosis at the site of perforation to effectively seal the vessel (81). A negative suction technique using a microcatheter connected to a syringe has also been reported to achieve successful hemostasis by collapsing the perforated distal vessel (104). More recently, a novel technique involving the delivery of silk or absorbable suture fragments via microcatheter has been reported, effectively occluding distal perforations and achieving durable hemostasis (105). If embolization fails to seal the perforated branch, a covered stent can be deployed in the main vessel to seal the ostium of the perforated side branch, thereby preventing further extravasation (15).

The incidence of guidewire entrapment or fracture ranges from 0.1%–0.2%, increasing to approximately 0.5% in CTO interventions (109, 111, 112). Risk factors for guidewire entrapment and fracture include guidewire jailing, excessive rotation (>180°), aggressive wire manipulation, use of multiple guidewires, and advancing an atherectomy burr over a kinked wire (113, 114). Anatomical features include marked vessel angulation, heavy calcification, bifurcation lesions, and CTO morphology further increase the risk of entrapment (113, 114). Entrapment may lead to wire fracture and retained fragments, particularly when excessive traction is applied. Advancing a rotational atherectomy burr against kink or immobile wire can also cause transection (113, 114).

Diagnosis of guidewire fracture is typically made by identifying loss of wire continuity on fluoroscopy or confirmed using IVUS (115). Retained guidewire fragments can result in serious complications, including thrombosis, coronary dissection, perforation, arrhythmia, or systemic embolization (116). Structurally, guidewires consist of inner and outer components; unraveling of the outer coil increases thrombogenicity and may cause luminal obstruction or distal embolism (109).

Management of an entrapped guidewire typically begins with percutaneous retrieval techniques. A microcatheter can be advanced as distally as possible over the trapped wire, followed by gradual withdrawal to facilitate release (15, 117). Alternatively, a small-profile balloon may be advanced, inflated at the site of entrapment, and gently pulled back to dislodge the trapped segment (117). Excessive traction should be avoided, as the guidewire core may unravel proximally and extend into the aorta. This unravelling can be difficult to visualize angiographically and is highly thrombogenic, emphasizing the importance of controlled retrieval rather than forceful pulling. If percutaneous retrieval fails, intentional wire transection can be performed. This technique has been described using rotational atherectomy to cut the entrapped guidewire, retrieve the proximal broken end, and leave the remaining distal fragment securely jailed beneath a stent, thereby reducing the risk of embolization (118). Surgical removal considered if the fragment poses thrombotic or embolic risk (117).

In setting of retained guidewire fragments, management should be individualized based on the location and extent of the retained wire, given its thrombogenic potential and the limited evidence regarding long-term outcomes. Conservative management may be appropriate in selected cases, particularly when the fragment is confined to a small, distal, or chronically occluded vessel, or when the risks of percutaneous or surgical retrieval outweigh potential benefits (111). Several studies have reported a benign clinical course in patients with retained fragments confined to chronically occluded or distal vessels, or in cases where retrieval attempts were unsuccessful (111, 119).

However, if the wire fragment extends into the aorta, removal is recommended due to the risk of thrombus formation and systemic embolization (111). Percutaneous retrieval techniques include the snare technique and the double- or triple-wire twisting method, in which additional guidewires are advanced alongside the fractured segment and rotated using a torquer to entangle and retrieve the wire (111, 120, 121). The knuckle-twister technique, a modification using a polymer-jacketed tapered wire formed into a knuckle, can be advanced distal to the fracture, then rotated and withdrawn to capture and extract the fragment, with high reported success and reproducibility (122). If percutaneous retrieval fails, surgical removal should be considered (111, 120).

For fragments confined within the coronary artery, several percutaneous strategies are available, including the snare technique, wire-twisting technique, small-balloon inflation and withdrawal, or stent deployment to seal and exclude the fractured wire from the lumen (111, 117, 120). When these percutaneous approaches are unsuccessful or carry excessive procedural risk, surgical removal should be pursued, whereas conservative management may be reserved for high-risk or clinically stable cases (111, 117).

Coronary guidewire entrapment can be reduced by careful lesion assessment, appropriate wire selection, and avoidance of excessive wire rotation (>180°), particularly with hydrophilic or polymer-jacketed guidewires. Resistance during manipulation should prompt reassessment rather than forceful advancement, guidewire jailing should be minimized, and rotational atherectomy should not be performed over kinked or immobile guidewires, with frequent fluoroscopic confirmation of wire position in complex anatomy.

Previous studies have reported an incidence of approximately 0.4%–1% of procedures (123). The rotational burr, coated with diamond particles, ablates plaque in a unidirectional manner. When burring is halted within a tight or calcified segment, particularly distal to the lesion, the burr may become irretrievably trapped (124). One common mechanism is the “Kokesi phenomenon”, named after the Japanese doll with a bulb-shaped head and hollow body (124). This occurs when a small burr is advanced at high rotational speed through a narrow, rigidly calcified lesion, mimicking the insertion of the doll's neck into its body, allowing rotation but preventing withdrawal (124). Conversely, using an oversized burr in a severely calcified vessel or maintaining a high burr-to-artery ratio can also increase the risk of entrapment (125). Additionally, performing rotational atherectomy on a recently implanted, underexpanded stent may predispose to burr entrapment, as the stent struts impede burr movement (125).

When burr entrapment occurs, percutaneous retrieval should be attempted prior to emergency surgery. The initial management involves balloon dilation of the lesion to enlarge the lumen and release the burr. This can be achieved by introducing a second guidewire, either via a second guiding catheter or by removing the rotablation advancer sheath to allow wire passage (125, 126). After successful wiring, balloon angioplasty at or proximal to the burr may facilitate its retrieval (125). Additional techniques include pulling the RotaWire, burr, and guiding catheter as a single unit, using the distal wire bulb to transmit traction and dislodge the burr, as well as disconnecting the burr from the housing and rotating it in reverse while maintaining gentle traction to free it from the lesion. If unsuccessful, deep guide catheter intubation or the use of a guide-extension (“mother-and-child”) system, advancing a guide-extension or smaller guide catheter toward the burr, may assist in extraction (125, 127, 128). The snare technique has also been reported as an effective percutaneous retrieval method (129). If all percutaneous attempts fail, emergent surgical removal should be performed (125, 130).

Preventive strategies include avoiding excessive forward force, refraining from stopping burr rotation within or distal to the lesion, and preventing abrupt deceleration of rotational speed (125). Appropriate burr sizing and gradual advancement using a pecking motion remain essential procedural principles to minimize the risk of entrapment (125).

Balloon entrapment is an uncommon but can lead to abrupt vessel closure and myocardial ischemia. It may occur secondary to balloon shaft fracture, balloon rupture, failure to deflate, or interaction with a previously implanted stent struts (131). The mechanisms underlying failure to deflate include elastic recoil of a severely calcified lesion compressing the balloon, premature withdrawal into the guide catheter before complete deflation, or kinking or damage to the hypotube (132).

Management of failure to deflate includes using an indeflator filled with normal saline rather than contrast, attempting gentle balloon withdrawal without full deflation, or puncturing the balloon with another guidewire (133). Increasing the proportion of saline in the contrast mixture reduces viscosity and shortens balloon deflation time (132). If these steps are unsuccessful, high-pressure inflation to intentionally rupture the balloon may be used; however, this approach should be reserved for large-caliber vessels due to the high risk of coronary dissection or perforation (132).

When balloon entrapment occurs, and the cause is failure to deflate, the above steps should be followed. Otherwise, strategies include repeated gentle inflation and deflation, or gently forward-backward manipulation to release the trapped balloon (15, 131). Several techniques can be performed for retrieval of an entrapped balloon. The balloon-trapping technique involves advancing a second balloon into the guide catheter and inflating it to secure the entrapped balloon shaft, allowing the entire system to be withdrawn as a single unit. Alternatively, advancement of a guide-extension catheter over the trapped balloon shaft can facilitate its release by providing additional support and coaxial alignment. The snare technique may also be used when the balloon is accessible (15, 131). In cases where entrapment is caused by a heavily calcified lesion, plaque modification using a second guidewire and balloon to dilate the vessel distal to the trapped segment can modify the and release the entrapped balloon (134). The mini-STAR technique has also been described as an effective bailout option (135).

Balloon shaft fracture may occur as a result of kinking or excessive manipulation. Management depends on the location of the retained fragment (131). If a portion of the fragment remains within the guide catheter, a balloon-trapping maneuver or snare device may be used for retrieval (131). Surgical removal should be considered if percutaneous efforts are unsuccessful. When the fragment extends beyond the guide catheter, retrieval can be attempted by inflating another balloon alongside the retained segment to facilitate extraction or by using a snare system (131). Rotational atherectomy has also been successfully used to modify calcified plaque surrounding a retained balloon fragment, followed by stent implantation to secure the material and prevent distal embolization (136).

Preventive strategies include adequate lesion preparation, particularly with atherectomy for severely calcified lesions, avoiding very high-pressure balloon inflation, and avoiding forceful advancement of a balloon through resistant or underprepared segments.

The mechanisms include over-torquing, forceful advancement through heavily calcified or tortuous vessels, and use of the microcatheter without an internal guidewire for support (131). These factors increase friction and mechanical stress along the shaft, predisposing to device entrapment or structural failure.

The management approach is generally similar to that used for other types of device entrapment (15, 131). Management options include percutaneous retrieval, surgical removal, or conservative management, depending on the fragment's location and clinical impact. Among percutaneous strategies, the trapping technique is often effective (15, 131, 137). Additional options include the snare technique or plaque-modification maneuvers, such as advancing a second guidewire with balloon angioplasty to relieve mechanical impingement and facilitate removal (15, 131). If percutaneous retrieval fails, surgical extraction may be required, though conservative management can be reasonable when a small fragment remains confined to a distal branch and the procedural risk outweighs the benefit (15, 131).

Preventive strategies focus on minimizing mechanical stress during catheter manipulation. Operators should avoid excessive rotation and refrain from aggressive advancement through resistant or heavily calcified segments. Selecting microcatheters with reinforced or stiffer distal tips may further reduce the risk of tip fracture or deformation (138).