Mechanisms and treatment outcomes of ostial right coronary artery in-stent restenosis.

Background: Despite a high rate of in-stent restenosis (ISR) after stenting the right coronary artery (RCA) ostium, the mechanism of ostial RCA ISR is not well understood.

Aims: We aimed to clarify the cause of ostial RCA ISR using intravascular ultrasound (IVUS).

Methods: Overall, 139 ostial RCA ISR lesions were identified with IVUS, pre-revascularisation. Primary ISR mechanisms were classified as follows: 1) neointimal hyperplasia (NIH); 2) neoatherosclerosis; 3) ostium not covered by the stent; 4) stent fracture or deformation; 5) stent underexpansion (old minimum stent area <4.0 mm or stent expansion <50%); or 6) a protruding calcified nodule.

Results: The median duration from prior stenting was 1.2 (first quartile 0.6, third quartile 3.1) years. The primary mechanisms of ISR were NIH in 25% (n=35) of lesions, neoatherosclerosis in 22% (n=30), uncovered ostium in 6% (n=9) (biological cause 53%, n=74), stent fracture or deformation in 25% (n=35), underexpansion in 11% (n=15), and protruding calcified nodules in 11% (n=15) (mechanical cause 47%, n=65). Including secondary mechanisms, 51% (n=71) of ostial RCA ISRs had stent fractures that were associated with greater hinge motion of the ostial-aorta angle during the cardiac cycle. The Kaplan-Meier rate of target lesion failure at 1 year was 11.5%. When the mechanically caused ISRs were treated without new stents, they suffered a higher subsequent event rate (41.4%) compared with non-mechanical causes or mechanical causes treated without restenting (7.8%, unadjusted hazard ratio 6.44, 95% confidence interval: 2.33-17.78; p<0.0001).

Conclusions: Half of the ostial RCA ISRs were due to mechanical causes. Subsequent event rates were high, especially in mechanically caused ISRs treated without the implantation of a new stent.