Bioresorbable stents: The future of interventional cardiology?

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ABSTRACTThe introduction of stents has drastically reduced target-lesion restenosis rates associated with percutaneous coronary angioplasty. Bare-metal stents were the first introduced, followed by drug-eluting stents, both of which had significant impacts on the complication rates. Stents, however, have resulted in the emergence of stent thrombosis and stent restenosis, which can cause life-threatening cardiac complications. Three new technological approaches are being investigated to overcome these complications: stents coated with bioresorbable polymers, stents without polymers, and completely bioresorbable stents. Initial results are encouraging, but more data are needed to ascertain their implications for clinical practice.


  • Stents have dramatically improved outcomes associated with percutaneous coronary angioplasty.
  • Bare-metal stents were the first stents developed, followed by first- and second-generation drug-eluting stents, which have progressively reduced complication rates.
  • Despite the improvements with conventional stents, persistent rates of restenosis and stent thrombosis remain, which can lead to increased coronary morbidity and mortality.
  • New stent technologies include stents coated with bioresorbable polymers, stents without polymers, and completely bioresorbable stents.



Interventional cardiology has made great strides in the last few decades. Percutaneous coronary intervention (PCI) is among the most commonly performed medical procedures globally.1 At the time of inception, PCI was plagued by high complication rates—balloon catheters had a 50% target-lesion restenosis rate at 6 months and required emergency bypass surgery in up to 6% patients.2 With passage of time, the complication rate of PCI has markedly decreased.

Reduction of restenosis rates by stent type
Figure 1. Reduction of restenosis rates by stent type.

The introduction of stents had a dramatic impact on lowering the complication rates. Initially, the bare-metal stents (BMS) reduced the stent restenosis rate to 10% to 15%. Drug-eluting stents (DES) have further revolutionized the field (Figure 1), significantly lowering rates of stent thrombosis (less than 0.5% in 1 year) and risk of restenosis (less than 5% in 1 year).3–6 The second-generation DES widely used in contemporary practice have made even more reductions owing to their improved designs and metallic and polymer composition; and concurrent advancements in the medical management, including use of antithrombotic and antiproliferative drugs, have further contributed to improved rates.

Second- vs first-generation drug-eluting stents
Figure 2. Second- vs first-generation drug-eluting stents.

What, then, is to be hoped for? Unfortunately, with the advent of stents, complications such as stent thrombosis and stent restenosis also emerged. These complications can be life-threatening in the form of post-procedural or late myocardial infarction and cardiac death. Thus, although the US Food and Drug Administration (FDA) assesses target-lesion failure (defined as a composite of cardiac death, target vessel myocardial infarction, or ischemia-driven target vessel revascularization) at 1 year, patients can have complications for the remainder of their lives. Despite the advancements attained by the second-generation DES over their predecessors, the issue of stent thrombosis and restenosis continues to plague second-generation DES with a 2% to 2.5% increased rate of target-lesion failure each year, seemingly forever (Figure 2).7,8

This article will briefly discuss the stent design and pathophysiology driving stent thrombosis and restenosis along with potential strategies to mitigate the problem. It pays special emphasis to bioresorbable stents, given their increasing interest among interventional cardiologists and patients, and given their potential to transform the practice of PCI.


Contemporary DES essentially consist of three components:

  • A metallic alloy with a mesh-like design serves as the platform for the stent.
  • This framework is coated with a multi-layered polymer that holds and releases the active drug in a controlled manner so that its effects can be extended.
  • Components of drug-eluting and bioresorbable stents
    Figure 3. Components of drug-eluting and bioresorbable stents.
    An antiproliferative drug (absent in the bioresorbable stents) that inhibits the smooth muscle proliferation and neointimal hyperplastic response: sirolimus or paclitaxel in first-generation DES; everolimus or zotarolimus in second-generation DES (Figure 3).


Several theories and pathophysiological mechanisms have been proposed to explain these late adverse events (Table 1). However, our overall understanding of the cause remains modest at best. The major factor seems to be persistent presence of polymer on the stent and the ensuing inflammation. The second issue appears to be related to neoathero­sclerosis that is generally defined as lipid or calcified neointima. Neoathero­sclerosis is especially problematic for the second-generation DES. Neoatherosclerosis eventually predisposes to the development of thin cap fibroadenoma, and the rupture of thin cap leads to stent thrombosis and restenosis.

Autopsy studies suggest that approxi­mately 50% of first- and second-generation DES start developing neoatherosclerosis within 1 to 3 years of implantation.9 Turbulence created by thick strutted stents or incomplete impaction of stents to the vessel wall predisposes the stents to platelet aggregation and fibrinogen deposition, thereby increasing the risk of neoatherosclerosis. Despite these pathologic insights, no treatment strategy has been shown to attenuate the problem, with the exception of high-dose statins.

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