Restenosis pathophysiology

Acute vessel recoil, chronic remodeling, and intimal hyperplasia were the mechanisms involved in this process (1-4). However, after the introduction of stents in the daily practice during interventional procedures, intimal hyperplasia became the mechanism associated in the pathophysiology of in-stent restenosis (5-9). Therefore, its prevention should be related with therapies that inhibit smooth muscle cell proliferation. 

In the past, several clinical studies with corticosteroids failed to demonstrate a significant reduction in coronary restenosis after percutaneous transluminal coronary angioplasty (35,36). However, as we mentioned previously, after balloon angioplasty, there were other mechanisms involved in the pathophysiology of coronary restenosis (such as acute wall recoil or chronic remodeling) that explained the negative results of those studies (35,36). 

Lau K-W Sigwart U. Restenosis—an accelerated arteriopathy pathophysiology, preventive strategies and research horizons. In Edelman ER, Levy RJ, eds. Molecular Interventions and Local Drug Delivery. London W. B. Saunders Co. Ltd., 1995 1-28. 

Landzberg BR, Frishman WH, Lerrick K. Pathophysiology and pharmacological approaches for prevention of coronary artery restenosis following coronary artery balloon angioplasty and related procedures. Prog Cardiovasc Dis 1997 39 361-398. 

Restenosis implicates three pathophysiological mechanisms thrombosis, recruitment, and proliferation. These complex phenomena may be subdivided into eight main initiating or contributory factors to postangiplasty restenosis ... 

Restenosis is the reobstruction of the artery following angioplasty procedure. Proliferation of the smooth muscle cells of the arterial wall in response to the injury due to balloon angioplasty is considered as the main reason for the pathophysiology of restenosis ". ... 

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