A Case of Coronary Artery Aneurysm Occurring After Drug-Coated Balloon Intervention for De Novo Chronic Total Occlusion

Abstract

Drug-coated balloons (DCBs) have been proposed as a viable alternative to drug-eluting stents (DES) for managing chronic total occlusion (CTO), reducing adverse reactions associated with DES. However, adverse events after DCB treatment are rarely reported. We present a case of coronary artery aneurysm (CAA) formation after DCB treatment. A 55-year-old active smoker presented with exertional chest pain and positive ischemic response on the exercise stress test. Diagnostic coronary angiography revealed CTO in the mid-left anterior descending (mid-LAD) coronary artery with collateral circulation arising from the contralateral side. The patient underwent DCB treatment using a paclitaxel-coated balloon after predilatation with a noncutting balloon and a semi-compliant balloon. The final angiogram showed minimal recoil, type B coronary dissection nonflow limiting, and thrombolysis in myocardial infarction (TIMI) grade 3 flow. A follow-up coronary angiogram at 6 months revealed a fusiform aneurysm at the treated lesion with DCB. Despite the asymptomatic nature of the patient, good distal flow in the LAD, and the patient achieving a TIMI grade 3 flow, a decision was made to observe and closely monitor the patient. Despite potential risks, DCB remains a viable alternative to DES in CTO cases. Our case suggests that, although CAA occurred, it did not lead to significant adverse cardiac events. Further research is needed to understand the predictors and long-term outcomes of CAA.

In the modern era, percutaneous coronary intervention (PCI) with a drug-eluting stent (DES) has been the primary approach for managing chronic total occlusion (CTO). Nevertheless, there is an elevated risk of experiencing late adverse events.

Recent studies suggest that drug-coated balloons (DCBs) could serve as a viable alternative to DES for de novo CTO. ¹ DCB reduces the likelihood of maladaptive biological reactions linked to DES, which can lead to restenosis and thrombosis, ² while also promoting a positive natural healing process in the vascular system. Nevertheless, the related adverse events after DCB treatment are rarely reported. Here, we report one case of coronary artery aneurysm (CAA) formation after DCB treatment.

Case Presentation

A 55-year-old man, an active smoker, complained of exertional typical chest pain. He had a positive ischemic response to the exercise stress test. His baseline electrocardiogram showed normal sinus rhythm. Echocardiography revealed normal ejection fraction and normal valves.

Diagnostic angiography demonstrated a normal left main, a CTO of mid-left anterior descending (mid-LAD) coronary artery, with collateral arising from contralateral vessels ( Fig. 1 ). Left circumflex coronary artery is nondominant and normal, and the right coronary artery is dominant and normal. The overall impression was single vessel coronary artery disease with CTO of mid-LAD with a Japanese CTO score of 1.

Fig. 1.

Left anterior descending artery coronary angiography before percutaneous coronary intervention.

Coronary angioplasty was performed via a right radial access, and a 6-Fr Extra Backup 3.5 guiding catheter was engaged to the ostium of the left coronary artery. A Pilot 50 guidewire was successfully advanced into distal LAD. The lesion was dilated with a 3.0 × 10 mm noncutting balloon and a 3.5 × 10 mm semi-compliant balloon. There was minimal recoil, and a type B coronary dissection without flow limitation was observed during angiography. After predilatation, the lesion was treated with a drug (paclitaxel) coated 3.5 × 20 mm balloon, inflated at 6 atm for 30 seconds ( Fig. 2 ). The final angiogram showed minimal recoil, type B coronary dissection with no flow limitation, and a thrombolysis in myocardial infarction (TIMI) grade 3 flow ( Fig. 3 ).

Fig. 2.

Drug-coated balloon deployment.

Fig. 3.

Coronary angiography after drug-coated balloon deployment.

A follow-up coronary angiogram at 6 months showed a fusiform aneurysm at the site of the treated lesion with DCB ( Fig. 4 ). Considering that the patient was asymptomatic, the distal flow of the LAD was good, and the patient achieved a TIMI grade 3 flow, we decided to observe and closely monitor the patient.

Fig. 4.

Coronary angiography at the 6-month follow-up showing coronary artery aneurysm.

Discussion

A true CAA is defined as the dilatation of the coronary artery by 50% or more than the reference vessel diameter. ³ The incidence rate of CAA is 3.9% and 0.2 to 2.3% after percutaneous transluminal coronary angioplasty (PTCA) and first-generation of DES, respectively. ^{4 5}

Overstretching of the stent strut, delayed re-endothelialization, inflammatory changes of the medial wall, hypersensitivity reactions to the drug on the DES, or incomplete healing secondary to the local antiproliferative drug are reported to be associated with aneurysm formation after stent implantation. ^{6 7 8}

Several theories have been proposed as the mechanism of CAA aneurysms due to DCB treatment. Initially, lesion preparation preceding DCB implantation typically involves employing high-pressure and prolonged balloon inflation. It is advised to inflate the DCB itself for 30 to 60 seconds to achieve optimal outcomes. ^{9 10} The repetitive trauma from this process may induce intimal dissection, potentially resulting in aneurysm formation. Furthermore, drug delivery via DCB results in significantly higher tissue concentration (300 µg/g tissue) compared with DES (3.2 + 1.8 µg/g tissue), ^{11 12} intensifying the localized drug effect. This effect includes reducing neointimal hyperplasia and fostering positive remodeling, which may contribute to arterial thinning and aneurysm development. Finally, inadequate adherence of the balloon to the artery's curvature can lead to uneven drug distribution, thereby influencing differential healing and possibly promoting CAA. ¹³ In our case, the aforementioned mechanisms might have existed.

An angiogram in our case revealed a non-flow-limiting type B dissection following the deployment of DCB. Subsequently, after 6 months, a CAA was observed at the same site as the dissection. A plausible explanation suggests that an intimal dissection may have been unintentionally formed during lesion preparation and DCB deployment. This led to the contact of paclitaxel drug with the vessel wall, effectively suppressing vascular intimal hyperplasia and cell proliferation. However, it also hindered the healing of blood vessels by impairing the intima's ability to repair itself. Consequently, the arterial wall thinned, and the damaged area in the intima and middle layer enlarged, resulting in CAA formation. Although not all dissections result in an aneurysm, research indicates that the severity of the dissection raises the risk of CAA development. ¹ Further investigations are essential to identify the contributing factor of CAA development during DCB treatment.

The management of CAA formation without coronary stenosis is still unclear. Treatment approaches are personalized based on patient characteristics, CAA size and morphology, and clinical features. ¹⁴ Given our patient was asymptomatic and stable, the decision made was to observe closely and conduct regular follow-ups. This finding aligns with another study that found no significant major adverse cardiac events linked to aneurysms. ¹

Conclusion

In summary, although the data are still scarce regarding the use of DCB in CTO with no randomized trials available comparing DCB with DES directly, the use of DCB could be an alternative to DES in CTO cases. In our case, there is a potential risk of CAA to be formed, but it is not associated with major adverse cardiovascular events. Further research is needed regarding the mechanism of CAA occurrence in DCB treatment and its association with clinical outcomes over a longer period.