European Journal of Cardiovascular Medicine

Percutaneous coronary intervention (PCI) involving totally Occluded and tortuous coronary arteries poses significant technical challenges and risks. One such complication is stent fracture, a recognized cause of in-stent restenosis following drug-eluting stent (DES) implantation. Although relatively uncommon, stent fractures are associated with serious adverse outcomes such as stent thrombosis, coronary aneurysm formation, and in rare cases, coronary perforation.

Several case reports highlight the devastating consequences that can arise from stent fractures. Harish et al. described the development of a coronary aneurysm at a stent fracture site in the left anterior descending artery (LAD) two years post- DES implantation, while Choi et al. reported a massive 4-cm coronary aneurysm in the mid-right coronary artery (RCA) following a stent fracture, resulting in cardiac tamponade within three months. Hoshi et al. detailed a fatal case involving a pseudoaneurysm at the RCA ostium secondary to stent fracture, culminating in cardiopulmonary arrest shortly after diagnosis. 1

Management strategies for complications arising from stent fractures vary depending on the severity and clinical presentation. Conservative management with careful monitoring is recommended in stable cases without major bleeding, while more aggressive interventions, such as implantation of covered stents or surgical repair, may be required in cases of worsening hemorrhage or risk of vessel rupture.1–3,

In the present case, a stent fracture occurred immediately after the removal of the balloon and guidewire from a previously occluded and tortuous RCA. Notably, a myocardial bridge, previously masked by total occlusion, became evident after stent deployment. Prompt recognition and intervention were critical to prevent adverse events such as stent thrombosis. An immediate strategy was adopted involving careful re-crossing of the fractured segment, sequential balloon dilations, and deployment of an overlapping drug-eluting stent, resulting in a successful outcome with restored TIMI III flow and no procedural complications.

A 70-year-old male smoker presented with complaints of a sudden onset compressive type of compressive-type central chest pain, associated with sweating and radiation to the left shoulder since last 1 hour. It was not associated with nausea, vomiting, breathlessness, or syncope and there were no other conventional risk factors of coronary artery disease (CAD). In the emergency room, he was anxious with a pulse rate of 54 beats/min and a blood pressure of 130/80 mmHg. The neck veins were not distended. His room air oxygen saturation was 99%, with normal heart sounds and there were no murmurs or rales on auscultation.

An electrocardiogram (ECG) showed sinus rhythm, sinus bradycardia with ST-segment elevation in lead II, III, aVF with reciprocal changes in leads I and aVL, which suggested acute inferior ST-elevation myocardial infarction (STEMI). Transthoracic echocardiogram showed hypokinesia of the basal and mid-inferior wall with mild mitral regurgitation and mildly impaired left ventricular ejection fraction (LVEF – 45%). He was promptly transferred to the catheterization laboratory after loading with 325 mg of aspirin, 180 mg of ticagrelor, and 80 mg of atorvastatin. Coronary angiogram via right femoral access showed total thrombotic occlusion at the proximal right coronary artery (RCA) with minimal disease of the left coronary artery and its branches. the patient was taken immediately for primary percutaneous coronary intervention (PCI) after explaining potential risks and safeguards of the procedure.

Figure 1: ECG of the patient on Admission

PCI was done through a 7F femoral artery sheath. RCA was engaged using a 7F JR 3.5 guiding catheter. Repeat acquisition was done after crossing the RCA lesion with a 0.014″ Hi-Torque Balance Middleweight™ (Abbott Vascular). Thrombus aspiration was done using a 6F X-change aspiration catheter (Purple Microport Cardiovascular Private Limited) to achieve TIMI II Flow. Severe (90%) lesion was present in the proximal segment of RCA, which was the culprit for STEMI. The lesion was pre-dilated using NC TREK™ RX - Coronary Balloon Dilatation Catheter (Abbott Vascular) 2.00 mm x 8 mm, single inflation up to 16 ATM. A 3.5×28 mm Promus PREMIER™ Everolimus-Eluting Platinum Chromium Coronary Stent (Boston Scientific) was deployed in the proximal RCA segment and inflated up to 11 ATM. The suitable stent diameter was estimated by comparing the proximal healthy part of the artery with the diameter of the guiding catheter. The Stent was post dilated with NC TREK™ RX 3.5 mm x 8 mm Balloon and inflated up to 16 ATM to achieve good stent opposition with good final angiographic results with TIMI flow III.

Upon removal of the balloon and guidewire from the RCA an unexpected and rather unique occurrence was observed, there was a sudden fracture of the distal end of the previously deployed well opposed stent, along with the evidence of a strong myocardial bridge in the proximal RCA, which had not been apparent earlier due to total vessel occlusion and tortuosity.

An immediate decision was made to address the stent fracture to prevent complications such as acute stent thrombosis. With much difficulty the same BMW guidewire was reinserted through the fractured segment and an attempt was made to cross the fractured stent with a 3.0 × 8 mm NC Trek balloon, but was unsuccessful due to the severity of the fracture at the distal end. Subsequently, a smaller 2.0 × 8 mm NC Trek balloon was carefully advanced across the fractured segment and inflated at 16 ATM to create a pathway for a larger Balloon and stent. Following this, the distal stent segment was predilated further with a 3.0 × 8 mm NC Trek balloon. A new drug-eluting stent, 3.5 × 38 mm Promus PREMIER™ was then crossed through the previously implanted stent and successfully deployed in the proximal RCA at 11 ATM. The stent was then post-dilated using a 3.5 × 8 mm NC TREK™ Balloon at 16 ATM. The final angiographic result demonstrated adequate stent expansion with TIMI III flow, and no procedural complications were encountered.

Figure 2: Coronary Angiography Showing Total thromboticocclusion of Right Coronary Artery

Figure 3: A. BMW Guidewire in RCA, B. RCA Thermojunction , C. Post thrombosuction and Predilation RCA Angiogram

Figure 4: A, B Stent deployment in RCA C, D - Post Stenting diastolic cine angiography Frame C – In diastole D- In systole

Figure 5: A,B Distal Stent Fracture with crossed ballonC - Balloon dilation of Distal Fractures stent D- Baloon dilation of proximal Fractured stent

Figure 6: A,B,C – New stent deployment in RCA

Figure 7: A,B – Post Balloon dilation cine angiography and stent boost film C – Final Cine Angiography showing proper stent placement in RCA without any complications

Figure 7: Post PCI Electrocardiogram

Further, the course in the hospital was uneventful, and the patient was discharged in a stable condition on the third day of hospitalization. At discharge, the patient was put on Aspirin, Ticagrelor, Atorvastatin, and beta-blocker.

Discussion:

Acute Coronary Syndrome (ACS) typically results from the rupture or erosion of an atherosclerotic plaque, leading to thrombus formation and subsequent myocardial ischemia4. However, in certain cases, unique anatomical variants such as myocardial bridging (MB) can contribute to myocardial ischemia, either independently or synergistically with atherosclerosis. In our patient, the rare combination of ACS complicated by the presence of a myocardial bridge, and later by stent fracture post-primary percutaneous coronary intervention (PCI) in the right coronary artery (RCA), presents an instructive and complex clinical scenario.

Myocardial bridging refers to an intramyocardial course of a segment of an epicardial coronary artery, most commonly the left anterior descending (LAD) artery and Left Circumflex artery (LCX ) and occasionally the Right coronary Artery (RCA)

5. While often considered a benign anatomical variant, MB can sometimes provoke ischemia, arrhythmias, or even myocardial infarction, especially when associated with significant systolic compression6. Several mechanisms underlie the ischemic potential of MB, including altered hemodynamics with systolic narrowing, endothelial dysfunction, and a pro-atherogenic environment proximal to the bridge7.

Fig: 8- Anatomy of Coronary Myocardial Bridge 8

In our patient, while the MB was located in the culprit RCA which is less common than LAD.9,10 the overall predisposition to coronary events in the presence of structural anomalies must be considered. Moreover, the Myocardial Bridge can complicate coronary interventions if present at or near the site of stenting due to

dynamic forces exerted by myocardial contraction, predisposing the stent to mechanical stress, fracture, and restenosis.

Primary PCI remains the standard of care in the management of ST-elevation myocardial infarction (STEMI) and other high-risk ACS presentations11. Our patient underwent a primary PCI of the RCA with the subsequent occurrence of stent fracture is recognized immediately after post-stent deployment angiography, though it is a relatively uncommon complication, but Serious clinical implications.

Stent fracture rates have been reported variably, ranging from 0.5% to as high as 20% in different series, depending on factors like stent type, vessel anatomy, and mechanical forces12. It is more frequently associated with drug-eluting stents (DES), particularly sirolimus-eluting stents, possibly due to their thinner struts and polymer coating13. In our case, the fracture was identified during follow-up evaluation for recurrent symptoms, highlighting the importance of vigilance even after an initially successful PCI.

Stent fracture has been defined and classified according to severity depending on the presence of isolated strut fractures (least severe), partial or complete stent fractures and fractures with separation of stent segments (being most severe).

Figure 9: Classification of stent Fracture 14

Multiple factors contribute to the risk of stent fracture:

• Anatomical Factors: Tortuous vessels, excessive vessel movement, and areas with high mechanical stress (e.g., RCA, due to its relatively mobile nature) are particularly susceptible.
• Stent-related Factors: Longer stent lengths, overlapping stents, and specific stent designs (closed-cell versus open-cell) can predispose them to fracture.
• Technical Factors: Aggressive post-dilatation or deployment in severely angulated segments can create focal points of mechanical stress.
• Biological Factors: Recurrent atherosclerotic progression or neo-atherosclerosis within the stent can also present mechanical challenges to stent integrity.

In our patient, the RCA’s inherent mobility during the cardiac cycle, combined with the presence of vessel angulation or flexion with myocardial bridge played a major role. The dynamic nature of myocardial motion, particularly in a heart already compromised by MB-induced functional changes, might have exaggerated these mechanical stresses.

Clinical Consequences of Stent Fracture

Stent fracture is associated with a spectrum of clinical outcomes. While some fractures may remain asymptomatic, others can precipitate in-stent restenosis, late stent thrombosis, and recurrent myocardial infarction. Our patient developed stent fracture immediately after the removal of guidewire which was recognised during the procedure itself. Timely recognition and intervention are therefore critical to prevent future complications

Diagnosis and Management Strategies3

The diagnosis of stent fracture often requires high-resolution imaging. Conventional coronary angiography with stent boost may detect gross displacement or restenosis, but can miss minor fractures. Intravascular imaging modalities like intravascular ultrasound (IVUS) or optical coherence tomography (OCT) offer superior detection capabilities, although not all centers have ready access.

Management strategies depend on the clinical impact:1

Asymptomatic fractures without restenosis might warrant conservative management and close monitoring.

Symptomatic fractures with restenosis or thrombosis necessitate reintervention. Options include balloon angioplasty, deployment of a new stent (often a drug-eluting stent with a different mechanical profile), or, less commonly, bypass surgery if PCI is not feasible

In our patient with severe stent fracture, immediate second stenting was successfully performed, with careful attention to lesion preparation and post- deployment optimization to minimize recurrence risk.

This case highlights the critical importance of anticipating and preventing stent fractures, particularly in anatomically challenging settings such as tortuous vessels and in the presence of myocardial bridges. Prevention begins with meticulous lesion preparation, careful stent sizing, minimizing unnecessary stent overlap, and selecting stent platforms with superior flexibility and fracture resistance. In certain high-risk cases, alternative strategies like drug-coated balloons or bioresorbable scaffolds may be considered, although further evidence is needed to support their widespread use.

Recognition of myocardial bridges as a contributing factor to altered coronary mechanical stress is essential during procedural planning. Stent fracture, though rare, must remain a differential diagnosis in patients presenting with recurrent ischemia post-PCI, especially in mobile segments like the RCA. A multidisciplinary approach involving advanced imaging, precise procedural techniques, and vigilant follow-up is vital to achieving optimal patient outcomes.

Future advances in stent design, computational modeling of coronary biomechanics, and refined PCI strategies tailored to complex anatomical variations offer promise in reducing the incidence of such complications. Continued vigilance and innovation will be essential in improving long-term outcomes in complex coronary interventions

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