Stent balloon fracture, endarterectomy, and lithotripsy balloon rupture following percutaneous coronary intervention: A case report

Abstract

BACKGROUND

Severe coronary calcification remains one of the most challenging scenarios in interventional cardiology, predisposing to stent underexpansion, device entrapment, and procedural complications.

CASE SUMMARY

A 71-year-old man had a history of hypertension and dyslipidemia for 14 years, and presented with exertional chest pain for two days before admission. During initial percutaneous coronary intervention (PCI) for a calcified left anterior descending artery (LAD) lesion, the coronary stent balloon shaft fractured and became entrapped. Percutaneous retrieval failed; emergent open-heart surgery with coronary endarterectomy successfully extracted the fractured coronary stent balloon shaft and two embedded stents, followed by saphenous vein grafting. Two months later, recurrent angina with dynamic electrocardiographic changes prompted coronary computed tomography angiography, revealing native LAD occlusion at the anastomosis with significant diagonal branch disease. During re-PCI, intravascular ultrasound (IVUS) identified a 270° calcific arc; intravascular lithotripsy (IVL) balloon rupture occurred on the second pulse cycle. The balloon was retrieved; high-pressure non-compliant balloon dilatation achieved calcium fracture, and three drug-eluting stents were implanted with TIMI 3 flow.

CONCLUSION

This case sequentially documents three rare complications with complete photographic documentation, providing practical lessons on calcium preparation, coronary endarterectomy as salvage, IVUS guidance, and IVL rupture management.

Key Words: Coronary calcification; Coronary stent balloon shaft fracture; Coronary endarterectomy; Intravascular lithotripsy; Coronary artery bypass grafting; Case report

Core Tip: This case report describes a patient who sequentially experienced three rare complications—balloon shaft fracture requiring surgical endarterectomy, early native vessel occlusion after coronary artery bypass grafting, and intravascular lithotripsy (IVL) balloon rupture—with complete imaging documentation. The case highlights the importance of intravascular ultrasound -guided calcium modification before stenting and demonstrates that IVL balloon rupture can be managed safely with prompt retrieval and backup balloon dilatation.

INTRODUCTION

Severe coronary calcification is a major predictor of adverse outcomes after percutaneous coronary intervention (PCI), increasing the risks of stent underexpansion, malapposition, and stent thrombosis[1]. When calcification is not adequately modified prior to stenting, target lesion revascularization rates increase 2- to 3-fold[2].

Intravascular lithotripsy (IVL) has emerged as a breakthrough technology that uses pulsatile sonic pressure waves to selectively fracture calcium while sparing soft tissue[3]. However, uncommon complications can still occur. Coronary stent balloon shaft fracture during PCI is rare, with a reported incidence of 0.1%-0.5%[4], and most cases can be managed percutaneously. Requiring open-heart surgery with coronary endarterectomy for retrieval is exceptionally rare. IVL balloon rupture occurs in approximately 1%-3% of cases[5], but real-world reports remain limited[6]. The combination of these rare events in a single patient has never been reported.

Herein, we report a patient who experienced three rare events in sequence: Coronary stent balloon shaft fracture requiring open-heart surgery with coronary endarterectomy, early native vessel occlusion after coronary artery bypass grafting (CABG) accompanied by dynamic electrocardiogram (ECG) changes, and subsequent evaluation via computed tomography angiography (CTA) confirmation, and IVL balloon rupture during re-PCI under intravascular ultrasound (IVUS) guidance, providing a practical framework for managing this “trilogy of catastrophes”.

CASE PRESENTATION

Chief complaints

A 71-year-old man complained of recurrent chest tightness for 14 years, and acute onset of chest pain for 2 days before admission.

History of present illness

The patient’s symptoms typically appeared during physical activity, lasted 5-10 minutes, and were relieved by rest. Over the preceding 6 months, the frequency and severity of symptoms had gradually increased, with episodes triggered by minimal exertion. Two days prior to admission, the patient experienced acute onset of chest pain at rest, which persisted for approximately 30 minutes and was not relieved by rest or sublingual nitroglycerin. The pain was described as retrosternal pressure without radiation to the neck, jaw, or left arm. No associated symptoms of syncope, palpitations, orthopnea, or paroxysmal nocturnal dyspnea were reported. The patient had no prior history of myocardial infarction or revascularization.

History of past illness

The patient had a 14-year history of hypertension, which was well-controlled on amlodipine, and a history of dyslipidemia managed with atorvastatin. He had no prior myocardial infarction, PCI, CABG, or known drug allergies. There was no family history of premature coronary artery disease. He was a non-smoker and did not consume alcohol regularly.

Personal and family history

There was no family history of premature coronary artery disease.

Physical examination

Physical examination revealed the following: Blood pressure 138/82 mmHg, heart rate 76 bpm, and unremarkable cardiovascular findings. No murmurs, gallops, or peripheral edema were noted. The lungs were clear on auscultation. Peripheral pulses were palpable and symmetric bilaterally.

Laboratory examinations

On admission, laboratory examinations revealed the following abnormalities: Creatine kinase-MB 33.00 U/L; monocyte count 0.64 × 10⁹/L; hemoglobin 112 g/L; high-sensitivity cardiac troponin T (hs-cTnT) 0.238 ng/mL; myoglobin 143.00 ng/mL; D-dimer 0.72 μg/mL; N-terminal pro-B-type natriuretic peptide 1250.0 pg/mL. The following day, repeat cardiac biomarkers showed: Lactate dehydrogenase 249.00 U/L; creatine kinase 312 U/L; creatine kinase-MB 37.00 U/L; hs-cTnT 0.898 ng/mL. The dynamic elevation of hs-cTnT from 0.238 ng/mL to 0.898 ng/mL was consistent with non-ST-elevation myocardial infarction.

Imaging examinations

ECG on admission showed sinus rhythm with ST-T changes. Transthoracic echocardiography on the same day revealed post-CABG status, mild mitral and tricuspid regurgitation, and normal left ventricular systolic function (ejection fraction 68%).

MULTIDISCIPLINARY EXPERT CONSULTATION

The first coronary angiography showed severe calcific stenosis of the mid-left anterior descending artery (LAD) with the involvement of the second and third diagonal branches (D2 and D3) (Figure 1A and B). The right coronary artery was not severely diseased (Figure 1C).

Figure 1 Coronary stent balloon shaft fracture during initial percutaneous coronary intervention. A and B: Baseline angiography: Calcified left anterior descending artery (LAD) with D2/D3 involvement; C: Right coronary artery: No significant stenosis; D: Guidewire advancement and predilation; E: Coronary stent balloon shaft fracture extending 50 cm from mid-LAD into the ascending aorta after stent dislodgement and failed withdrawal.

SYNTAX score of the patient was 34 (intermediate-high complexity) based on the baseline angiographic results, which showed the complexity of the coronary artery disease involving the LAD bifurcation and diffuse calcification. GRACE risk score was 89, which indicated intermediate risk of major adverse cardiac events at 6 months[7]. The presence of severe calcification was an additional adverse prognostic factor[1].

FINAL DIAGNOSIS

Acute non-ST-elevation myocardial infarction; essential hypertension (grade 2, very high-risk); hepatic impairment; and hyperlipidemia.

TREATMENT

The chronological sequence of events and corresponding management of this patient are summarized in Table 1.

Table 1 Timeline of clinical events from initial presentation to one-month follow-up.

Date	Event
Day 0	Initial PCI with coronary stent balloon shaft fracture and stent dislodgement
Day 0 (same day, hours later)	Emergent open-heart surgery with coronary endarterectomy and SVG grafting to mid-LAD
Month 2	Recurrent exertional chest pain; dynamic ECG changes (pseudonormalization → ST depression and T-wave inversion); hs-cTnT elevation; CTA confirms native LAD occlusion at anastomosis with D2/D3 severe stenosis
Month 2 + Day 4	Re-PCI with IVUS guidance; IVL balloon rupture on second pulse cycle; NC balloon achieves calcium fracture; 3 DES implanted; TIMI 3 flow restored
Month 2 + 1 month	One-month follow-up: Symptom-free, adherent to DAPT, ECG stable

PCI: Percutaneous coronary intervention; SVG: Saphenous vein graft; LAD: Left anterior descending artery; ECG: Electrocardiogram; CTA: Computed tomography angiography; TnT: Troponin T; D2: Second diagonal branch; D3: Third diagonal branch; IVUS: Intravascular ultrasound; IVL: Intravascular lithotripsy; NC: Non-compliant; DES: Drug-eluting stent; TIMI: Thrombolysis in myocardial infarction; DAPT: Dual antiplatelet therapy.

Initial PCI and complication (Figure 1): Following predilation with a 2.0 mm × 15 mm balloon inflated to 12 atm, an attempt was made to deploy the stent. After the implantation of the first stent (2.5 mm × 20 mm), a second overlapping stent (3.0 mm × 20 mm) was implanted. The delivery system was not removable, which led to the dislodgement of stents. The second stent was placed, but its proximal part did not expand completely. Further attempts to withdraw the stent balloon led to partial fracture of the balloon shaft (Figure 1E). The trapped stent-balloon assembly was left in the mid-LAD, and the rest of the fractured shaft was left to protrude about 50 cm into the ascending aorta. An attempt was made to snare but failed.

Emergent surgical salvage (same day, hours later) (Figure 2): Since the percutaneous retrieval had failed, and the heart team was informed of the presence of an entrapped calcified stent-balloon assembly in the mid-LAD, the heart team was immediately consulted. It was decided to continue with emergent open-heart surgery. Coronary endarterectomy was performed[8]. The mid-LAD was incised longitudinally (Figure 2A). The calcified core containing stents and fractured shaft was removed as a block (Figure 2B and C). An saphenous vein graft (SVG) was anastomosed to the distal LAD (Figure 2D). The patient was able to tolerate the procedure and was weaned off cardiopulmonary bypass without any problems. Postoperative recovery was uneventful, and the patient was transferred to the cardiac care unit for further monitoring.

Figure 2 Surgical salvage with coronary endarterectomy. A: Longitudinal arteriotomy of mid-left anterior descending artery (black arrowheads); B: Retrieved specimen: Coronary stent balloon fracture approximately 50 cm in length and two bare metal stents embedded in calcified tissue; C: Reconstructed plaque with protruding stent ends; D: Patch closure of arteriotomy.

Two months post-CABG, ECG showed pseudonormalization of T waves in leads V2-V4 (Figure 3A), followed by ST-segment depression and deep T-wave inversions (Figure 3B). The post-procedural electrocardiogram of second PCI demonstrated notable recovery of the T-waves in leads V2-V6 (Figure 3C). hs-cTnT increased from 0.238 ng/mL on admission to 0.898 ng/mL the following day, consistent with non-ST-elevation myocardial infarction. Coronary CTA confirmed a patent SVG to the LAD but native LAD occlusion at the anastomotic site with significant D2 and D3 disease (Figure 4).

Figure 3 Serial electrocardiogram changes. A: Admission electrocardiogram (ECG): Pseudonormalization of T waves in V2-V4; B: ECG during recurrent angina: New ST depression and deep T-wave inversions in V2-V6, confirming active ischemia; C: Post-procedural 12-lead electrocardiogram of second percutaneous coronary intervention showing significant recovery of T-waves in leads V2-V6, suggesting improved myocardial reperfusion.

Figure 4 Coronary computed tomography angiography following coronary artery bypass grafting. A: Left anterior descending artery (LAD): Proximal calcified plaque with diffuse narrowing, suspected mid-to-distal occlusion; B: D2: Ostial severe stenosis with mid-segment calcification; C: D3: Proximal severe stenosis with tortuosity; D: 3D reconstruction: Patent saphenous vein graft to LAD, occluded native LAD at anastomosis. B-LAD: Saphenous vein bypass graft to the left anterior descending coronary artery; D2: Second diagonal branch; D3: Third diagonal branch; LAD: Left anterior descending artery; R-PDA: Right posterior descending artery.

As shown in Figures 5 and 6, two months after CABG, re-PCI was performed. IVUS revealed 270° circumferential calcification in the proximal LAD and a calcified nodule at the LAD ostium (Figure 6C and D). A 3.0 mm × 10 mm Saihe^® IVL balloon (Saihe Medical, China) was positioned at the calcified segment and inflated to 6 atm for energy delivery. During the second pulse cycle, balloon rupture occurred (Figure 5C). The balloon was retrieved intact. High-pressure non-compliant balloon dilatation (up to 22 atm) achieved calcium fracture, and three drug-eluting stents were implanted (Figure 5D). Postprocedural IVUS confirmed adequate stent expansion, complete strut apposition, and fracture of the calcified plaque at the treated segment (Figure 6E and F).

Figure 5 Re-percutaneous coronary intervention with intravascular lithotripsy rupture and successful stenting. A and B: Baseline angiography: Patent saphenous vein graft, severe anastomotic restenosis, occluded mid-left anterior descending artery; C: Intravascular lithotripsy balloon rupture on fluoroscopy; D: Final angiography: TIMI 3 flow after three stents.

Figure 6 Intravascular ultrasound findings during re-percutaneous coronary intervention. A: Mid-left anterior descending artery (LAD): Myocardial bridging, no plaque; B: Mid-LAD (post-endarterectomy): Hypoechoic plaques, no calcification; C: Proximal LAD: 270° circumferential calcification; D: LAD ostium: Calcified nodule (acoustic shadowing), prompting IVL; E: Full drugeluting stent implantation apposition of 270° circumferential calcification; F: Adequate drugeluting stent implantation apposition of calcified nodule.

OUTCOME AND FOLLOW-UP

The patient’s chest pain resolved immediately after the procedure. He was subsequently monitored closely in the cardiac care unit and was discharged on dual antiplatelet therapy [dual antiplatelet therapy (DAPT); aspirin 100 mg daily and clopidogrel 75 mg daily] in line with the recommendations from authoritative international guidelines (American Heart Association/American College of Cardiology, European Society of Cardiology)[9,10]. For patients with acute coronary syndrome, it is recommended that they receive this DAPT for at least 12 months to stabilize the condition and reduce the risk of recurrence. The dosage used was also within the standard recommended range, with aspirin recommended at 75-150 mg/day and clopidogrel at 75 mg/day for long-term administration. The patient reported full adherence to the prescribed DAPT regimen and experienced no bleeding or other adverse effects.

At one-month follow-up, repeat ECG showed stable T-wave changes without further dynamic evolution. The patient who remained in New York Heart Association functional class I, reported significant improvement in quality of life, and expressed satisfaction with the treatment outcomes. He remained symptom-free without recurrence of angina.

DISCUSSION

This case is unique in sequentially documenting the three rare complications with complete imaging documentation across six figures. Each carries distinct lessons.

During PCI coronary stent balloon shaft fracture occurs in 0.1%-0.5% of cases[4]. The underlying mechanism was entrapment due to severe calcific nodules, as pre-procedural calcium modification was not performed before stenting. For lesions with > 270° calcific arc on IVUS, dedicated calcium modification should precede stenting[3].

The open technique allowed direct visualization and en bloc extraction of the calcified mass. The retrieved specimen (Figure 2B) shows the stents embedded in calcified tissue, explaining why percutaneous retrieval failed. A meta-analysis of 63730 patients found that coronary endarterectomy with CABG was associated with significantly increased 30-day postoperative mortality and higher incidences of short-term postoperative complications compared with isolated CABG, particularly in the subgroup of patients with a high-risk profile and patients with diffuse disease in the LAD[11]. Nevertheless, there are a number of drawbacks to coronary endarterectomy. The procedure is technically challenging and has a greater risk of perioperative myocardial infarction, low cardiac output syndrome, and early graft failure than traditional CABG[11]. Competitive flow through the patent graft, intimal hyperplasia at the anastomotic site, or distal embolisation of debris is a recognised complication that occurs early after endarterectomy with distal graft anastomosis. The fact that the native LAD was rapidly occluded at the anastomosis within two months in this case highlights the importance of close clinical monitoring and early CTA or angiography in patients with recurrent symptoms following endarterectomy.

Pseudonormalization of T waves (Figure 3A) is an often-overlooked ischemia sign. Rapid native vessel occlusion with a patent graft occurs in 10%-20% of patients at 1 year, mediated by competitive flow[12]. CTA provides a critical roadmap for re-intervention.

IVL rupture occurs in approximately 2.6% of cases[5]. The mechanism was likely uneven energy reflection off the calcified ring. Prompt retrieval and backup non-compliant balloon dilatation achieved adequate calcium fracture. IVL balloon rupture can be managed safely; a successful outcome remains achievable.

IVUS identified the 270° calcification and confirmed calcium fracture after treatment. In patients undergoing complex PCI, intracoronary imaging guidance reduced the risk of MACE compared with angiography guidance, an effect that was driven by reducing the incidence of cardiac death, definite/probable stent thrombosis, and target vessel and target lesion revascularization[13].

Severe coronary calcification is one of the most difficult lesion subsets in interventional cardiology, inadequate lesion preparation is the leading cause of stent underexpansion, which in turn is the best predictor of stent thrombosis and restenosis. Available calciummodification strategies include noncompliant balloons (up to 30 atm), scoring/cutting balloons, rotational atherectomy, orbital atherectomy, and intravascular lithotripsy. Among these, IVL has gained rapid acceptance due to its favourable safety profile and efficacy in modifying deep calcium. This case illustrates that even with IVL, complications such as balloon rupture can occur, but they can be managed safely with prompt retrieval and backup strategies. The sequential nature of complications in this case underscores the principle that calcium modification should be performed before, not after, stent deployment, and that IVUS guidance is essential for both preprocedural planning and postintervention assessment.

This study has several limitations that should be acknowledged. This represents a single case report, and long-term follow-up extending beyond one month has not yet been completed. The mechanisms underlying device failures were deduced from imaging findings rather than verified through formal engineering analysis.

CONCLUSION

This case illustrates that a disastrous cascade of uncommon complications, coronary stent balloon shaft fracture necessitating surgical endarterectomy, early graft-related native vessel occlusion, and IVL balloon rupture can be effectively addressed through heart team collaboration, IVUS guidance, and a stepwise approach. In severely calcified lesions, IVUS-guided calcium modification prior to stenting is necessary to avoid device entrapment. IVL balloon rupture can be safely treated with prompt retrieval and support high-pressure balloon dilatation.

ACKNOWLEDGEMENTS

The authors thank the cardiac catheterization laboratory staff and the cardiothoracic surgery team for their excellent care of this patient.