Development of an enhanced framework for arterial remodelling following percutaneous coronary intervention

The standard treatment for coronary artery disease is the percutaneous coronary intervention (PCI), using a balloon and a drug-eluting stent (DES). One of the major complications following this procedure is the development of in-stent restenosis (ISR).

ISR is a complex phenomenon whose triggering mechanism consists of the arterial wall damage due to the surgical procedure.

The mechanical damage causes a localized inflammation in the intima and media, where smooth muscle cells proliferate, and extracellular matrix is deposed in an abnormal way.

Many factors influence on ISR formation: the inflammatory response, the stent placement, the stent strut distribution, drug release and retention.

While some attention has been placed on mechanical damage-induced proliferation and drug transport alone, less research has been devoted to how these two phenomena concur to the arterial remodelling following the procedure.

In fact, while a mechanical damage enhances cellular proliferation, therefore leading to higher risk of ISR, drug retention would decrease the chances of development of ISR, due to its anti-inflammatory action.

The coupling of these two phenomena would provide a multiscale approach on vascular remodelling post intervention, capturing their impact on ISR.

Mathematical and computational tools that are able to address this challenge could help discover more in depth the mechanobiological processes behind ISR development after PCI, which would ultimately help to provide more tailored treatments to avoid the worsening of this pathology.