Multiple PCI Failures Due to Excessive Coronary Hinge Motion

Abstract

Background

Excessive vessel movement due to hinge motion (HM) may be one of the major contributors to in-stent thrombosis and subsequent stent fractures.

Case Summary

A 53-year-old man was admitted due to an acute myocardial infarction. Emergency angiography revealed thrombotic right coronary artery occlusion associated with excessive HM. After stenting, he was readmitted for in-stent thrombosis, and in-stent total occlusion and stent fractures were observed at 1-year follow-up; the stent fracture site is precisely located at the HM. Considering the persistent severe HM, coronary artery bypass grafting was recommended.

Discussion

Chronic mechanical stress due to HM of the vessel may play an important role in stent fracture. Stent implantation should be avoided in coronary regions with curves due to severe HM. Shorter stent, drug-coated balloons, or coronary artery bypass grafting should be prioritized.

Take-Home Messages

Stent implantation should be avoided in regions with severe HM. Shorter stents, drug-coated balloons, or coronary artery bypass grafting should be considered.

Visual Summary

Visual Summary.

Timeline of the Case Progression

PCI = percutaneous coronary intervention.

History of Presentation

A 53-year-old man was admitted with a 1-month history of chest tightness and limb weakness. On admission, he was diagnosed with inferior ST-segment elevation myocardial infarction.

Take-Home Messages

• •In vessels with excessive HM, stent implantation may not mitigate its adverse effects; therefore, stenting across these hinge points should be avoided when feasible.
• •Accordion phenomenon at the stent edge may predispose to edge thrombosis.

Past Medical History

Past medical history included hypertension and left-sided limb weakness due to previous ischemic stroke.

Investigations

On admission, cardiac troponin I was 0.10 ng/mL (reference: <0.03 ng/mL). The admission electrocardiogram (ECG) showed ST-segment elevation in leads II, III, and aVF, with accompanying T-wave changes (Figure 1A). Emergency coronary angiography (CAG) found mild stenosis in the left circumflex and left anterior descending arteries (Figures 1B and 1C). Severe stenosis was found in the middle of right coronary artery (RCA), where 4 bending points of hinge motion (HM) were revealed during cardiac cycle. Among the 4 bending points, the minimum systole-to-diastole angle change was Δ18°, and the maximal angle change was Δ47° (Figures 1D and 1E, Video 1).

Figure 1.

Admission Electrocardiogram and Coronary Angiography

(A) Admission electrocardiogram. (B and C) Left coronary angiography. (D) Right coronary artery (RCA) during diastole. (E) During systole, the mid RCA demonstrated prominent angle change due to hinge motion. ΔAngle, systolic and diastolic angle change.

Differential Diagnosis

Acute coronary syndrome

Because of chest tightness, elevated troponin, and inferior-lead ST-segment elevation on ECG, acute coronary syndrome was the primary diagnosis.

Pulmonary embolism

Despite limb weakness due to being poststroke, a negative D-dimer and no deep vein thrombosis in lower extremity veins made pulmonary embolism unlikely.

Aortic dissection

The patient had no high-risk features (tearing pain, pulse, or blood pressure asymmetry) and no proximal aortic findings; therefore, aortic dissection was unlikely.

Management

Based on the angiographic findings, the RCA was identified as the culprit vessel (Figure 2A). Intravascular ultrasound (IVUS) demonstrated moderate plaque burden and a layered structure suspected to be mural thrombus (Figure 2B, Video 2). Predilation was performed using a 2.5- × 15-mm semicompliant balloon (Boston Scientific), and a 3.5- × 30-mm drug-eluting stent (DES) (Medtronic) was deployed to cover the lesion under IVUS guidance (Figure 2C). Postdilation was then performed with a 4.0- × 15-mm noncompliant balloon (Boston Scientific). Angiography and final IVUS demonstrated adequate stent expansion without dissection at the landing zone (Figures 2D and 3A, Video 3). However, a guidewire-induced accordion phenomenon was observed at the proximal stent edge (Figure 3B, Video 3). After guidewire withdrawal, the native curvature in the proximal RCA recovered (Figure 2E, Video 4). Subsequently, dual antiplatelet therapy (aspirin and clopidogrel) was prescribed.

Figure 2.

Right Coronary Intervention and Intravascular Ultrasound

(A) Baseline right coronary artery (RCA) angiography. (B) Intravascular ultrasound demonstrated the suspected adherent thrombus. (C) Landing zone of stent. (D) The proximal RCA straightened by the guidewire. (E) The proximal curvature recovered after guidewire withdrawal.

Figure 3.

Intravascular Ultrasound of the Right Coronary Artery after stenting

(A) Intravascular ultrasound of the right coronary artery (RCA) after stenting. (B) Accordion phenomenon at the proximal stent edge of the RCA.

Three months later, the patient was readmitted with worsening chest tightness despite adherence to optimal medical therapy. Troponin I was 1.13 ng/mL (reference: <0.03 ng/mL), and the ECG showed T-wave inversions in leads II, III, and aVF (Figure 4A). The patient was diagnosed with non–ST-segment elevation myocardial infarction. CAG demonstrated prominent stenoses at the proximal and distal edges of the RCA stent (Figure 4B, Video 5). IVUS revealed in-stent thrombosis (IST) at stenosis segments (Figures 4C1 and 4C2, Video 6). Due to a SYNTAX score <22, isolated RCA involvement and the patient's willingness, percutaneous intervention was selected instead of coronary artery bypass grafting (CABG). Given the uncertain benefit of drug-coated balloon (DCB) for thrombotic lesions, stent implantation was performed. Two 3.5- × 29-mm and 3.5- × 33-mm DESs (Shandong Jiwei Medical Products) were implanted to the distal and proximal RCA stent (Figures 4D1 and 4D2). Under IVUS guidance, postdilation was performed using a 4.0- × 15-mm noncompliant balloon (Medtronic). Poststenting angiography demonstrated a newly formed significant stenosis at the proximal edge of the stent, which was suspected to be a result of accordion phenomenon, and remained unchanged after intracoronary nitroglycerin (Figure 4E). Final IVUS showed no evidence of dissection at the proximal edge of the stent (Figure 5, Video 7). After guidewire withdrawal, the native curvature of the RCA recovered from the accordion phenomenon (Figure 4F, Video 8).

Figure 4.

Second Percutaneous Coronary Intervention After 3 Months

(A) The readmission electrocardiogram showing T-wave inversions in leads II, III, and aVF. (B) Stenosis at the proximal and distal edges of the right coronary artery (RCA) stent. (C1 and C2) Intravascular ultrasound demonstrated in-stent thrombosis. (D1 and D2) Two drug-eluting stents were implanted in the RCA. (E) Poststenting angiography demonstrated a newly formed significant stenosis at the proximal RCA, suspected to be a result of accordion phenomenon. (F) After guidewire withdrawal, the native curvature of the RCA recovered from the accordion phenomenon.

Figure 5.

Intravascular Ultrasound Demonstrated the Landing Zone of the Proximal Stent and Accordion Phenomenon at the Proximal RCA After the Second Percutaneous Coronary Intervention

Five days after the second percutaneous coronary intervention (PCI). The patient experienced sudden chest pain and loss of consciousness in hospital during the early morning. The emergency ECG showed ventricular fibrillation (Figure 6A). After defibrillation, the patient restored sinus rhythm with ST-segment elevation in leads III and aVF (Figure 6B). Emergency angiography revealed total occlusion of the proximal RCA (Figure 6C). CAG demonstrated significant IST (Figure 6D), which was confirmed by IVUS (Figure 6E). We identified HM as the primary driver of the stent thrombosis. However, repeat stenting was performed as a pragmatic measurement for the rapid restoration of RCA flow. Aspiration thrombectomy and balloon dilation was performed. A 4.0- × 15-mm DES (Medtronic) was then implanted at the ostium of RCA (Figure 6F). Postdilation was performed with a 4.5- × 15-mm noncompliant balloon (Medtronic). Final angiography showed restoration of normal RCA flow (Figures 6G and 6H, Video 9). Final IVUS demonstrated that the stent was expanded symmetrically without intraluminal thrombus and stent fracture (SF) (Figure 7, Video 10). Given recurrent IST and no apparent abnormalities of platelet function, pharmacogenetic testing was undertaken. The CYP2C19 genotype indicated an intermediate-metabolizer phenotype, indicating reduced clopidogrel activation. Accordingly, clopidogrel was switched to ticagrelor, and low-molecular-weight heparin was administered for anticoagulation during hospitalization.

Figure 6.

Third Percutaneous Coronary Intervention After In-Hospital ST-Segment Elevation Myocardial Infarction

(A) Electrocardiogram (ECG) showing ventricular fibrillation. (B) Postdefibrillation ECG showing ST-segment elevation in leads III and aVF. (C) Emergency angiography demonstrating total occlusion of the proximal right coronary artery (RCA). (D) Angiography demonstrated in-stent thrombosis (IST). (E) Intravascular ultrasound showed IST. (F) Stent was implanted at the ostium of the RCA. (G and H) Final angiography demonstrated restoration of normal RCA flow.

Figure 7.

IVUS After the Third Percutaneous Coronary Intervention

(A) Postprocedural intravascular ultrasound (IVUS) showed no evidence of intraluminal thrombus and stent fracture. (B) Postprocedural IVUS longitudinal view after percutaneous coronary intervention.

Outcome and Follow-Up

At 1-year follow-up, the patient reported exertional chest tightness. Coronary computed tomography angiography revealed in-stent total occlusion of the RCA (Figure 8A). Angiography confirmed total occlusion of the proximal RCA (Figure 8B). Fluoroscopy revealed 4 points of SF (Figure 8C). These 4 points of SF accurately coincided with 4 bending points of HM identified by the baseline CAG (Figures 8D to 8H, open arrows). We postulated that the HM might contribute to the original intracoronary thrombus, recurrent IST, and multiple SFs.

Figure 8.

1-Year Follow-Up: Coronary Computed Tomography Angiography and Right Coronary Angiography

(A) Coronary computed tomography angiography demonstrating in-stent occlusion of the proximal right coronary artery (RCA). (B) Coronary angiography confirming the total occlusion of the proximal RCA. (C) Four points of stent fracture revealed on fluoroscopy. (D) Baseline RCA angiography before stenting; open arrows indicated 4 hinge motion sites. (E to H) Four fracture sites of the RCA stents.

Discussion

The RCA is particularly prone to HM. Tortuosity and HM subject an implanted stent to repetitive cyclic bending and axial deformation, predisposing it to malapposition, underexpansion at bends, neointimal proliferation at the edges, and SF.^1,2

Stent implantation within an HM segment is hypothesized to alter wall shear stress distribution across both the stented segments and the stent edges. Deploying low-compliance or closed-cell stents across sharp curvatures may accentuate arterial straightening, edge injury, and cyclic stress accumulation, thereby accelerating metal fatigue.² Prior research has clearly shown that HM correlates with a higher rate of in-stent restenosis and identifies a lesion angulation change (Δangle: ≥11.5°) as an independent predictor of adverse outcomes.³ Furthermore, stent fracture mechanically induced by HM, or wider inter-strut distance resulting in inadequate drug delivery and vessel injury, may represent a pivotal mechanism underlying ISR.⁴

In this patient, stent failure may have been multifactorial, involving vascular factors (eg, tortuosity, HM), device-related factors (eg, thinner struts, excessive stent length), and pharmacologic factors (including reduced clopidogrel effectiveness). Even with IVUS-guided PCI optimization, recurrent in-stent thrombosis occurred. The accordion phenomenon at the stent edges was observed on IVUS imaging. We infer that cyclic flexion at the stent edge likely caused recurrent intimal injury, promoting thrombosis. Although a subsequent stent was used to fully cover the curved segment, late occlusion developed, and the stent construct ultimately fractured.⁵

In this case, HM of the right coronary artery was probably associated with the primary thrombotic event at the patient's initial presentation, including subsequent IST, SF, and total occlusion. Ideally, CABG should have been considered at the time of the initial IST (3 months postprocedure). Unfortunately, a repeat stenting strategy was performed in an attempt to offset the adverse effects of HM. In retrospect, we underestimated the mechanical impact of HM, erroneously assuming that the new stent could withstand the repetitive cyclic flexion. This strategy finally led to complete occlusion and SF. Notably, at 1-year follow-up, 4 SF points corresponded precisely to the previously identified HM sites.

Although contemporary stent platforms have become progressively thinner, the underlying materials have not undergone fundamental changes. Although thinner struts enhance deliverability, they may compromise radial strength, longitudinal integrity, and fatigue resistance—particularly in chronic total occlusions, severely calcified lesions, and large-caliber vessels.^6,7 In markedly curved vessels with significant HM, the threshold for SF is lowered. Earlier-generation, thicker-strut stents are generally more resistant to SF caused by HM of vessel than the contemporary thinner-strut stents. Therefore, stent materials with excellent fatigue resistance may be required to withstand such pronounced HM of vessel.

Finally, the optimal management of this patient remains challenging. Despite IVUS-guided landing zone and optimal medical therapy, the outcome remained suboptimal. These subsequent complications underscore the biomechanical mismatch between a permanent metallic scaffold and a vessel segment with excessive HM. Consequently, the implanted stents could not mitigate the adverse effects of excessive HM. To minimize stent-related adverse events resulting from excessive HM, alternative approaches such as shorter stents, avoidance of HM points, DCBs, and CABG might be warranted.

Conclusions

This case highlights the hazards of stenting in the pronounced HM segments of the vessel. Despite IVUS-guided PCI optimization, the patient developed recurrent IST, total occlusion, and SF at follow-up. The management of such lesions is difficult, and shorter stent, avoidance of HM points, DCBs, and CABG might be preferable.

Funding Support and Author Disclosures

The authors have reported that they have no relationships relevant to the contents of this paper to disclose.

Appendix

Video 1

Baseline Coronary Angiography (Right Coronary Artery)

Video 2

Baseline Intravascular Ultrasound (Right Coronary Artery)

Video 3

Intravascular Ultrasound After First Percutaneous Coronary Intervention

Video 4

Coronary Angiography After First Percutaneous Coronary Intervention

Video 5

Coronary Angiography at 3-Month Follow-Up Demonstrating Stent Edge Stenosis

Video 6

Intravascular Ultrasound at 3-Month Follow-Up

Video 7

Intravascular Ultrasound After Second Percutaneous Coronary Intervention

Video 8

Coronary Angiography After Second Percutaneous Coronary Intervention

Video 9

Coronary Angiography After Third Emergency Percutaneous Coronary Intervention (3-Month Follow-Up)

Video 10

Intravascular Ultrasound After Third Emergency Percutaneous Coronary Intervention (3-Month Follow-Up)