Coronary aneurysms after stent placement: A suggestion of altered vessel wall healing in the presence of anti-inflammatory agents

Abstract

Coronary aneurysms are rare after conventional angioplasty and have not been reported after coronary stenting. Coronary artery stent sites were examined by follow-up angiography at a median of 4 months in 29 patients who received the Cook stent (Gianturco-Roubin) for acute coronary closure. Nineteen patients were treated with glucocorticoids administered intravenously or orally, or both, with or without colchicine and results were compared with those in 10 patients who were treated with neither agent. Standard therapy for all patients included routine administration of aspirin and heparin before and warfarin sodium (Coumadin) and aspirin after stent placement. Most patients also received dipyridamole and lovastatin during the follow-up period. Compliance with medications was confirmed by telephone conversation with each patient. Six (32%) of the 19 stented arteries showed evidence of coronary artery aneurysm, defined as expansion of the lumen outside the margins of the stent. None of the patients in the control group (who did not receive steroids or colchicine) developed aneurysm. This pattern of altered vascular healing in stented coronary segments appears to be due to the addition of multiple anti-inflammatory drugs rather than to stent presence alone. This observation demonstrates the possibility of medical impairment of normal vascular remodeling after acute injury and stent placement, which may be of benefit in designing future trials on restenosis.

Intra-vascular glucocorticoid metabolism as a modulator of vascular structure and function

“…Dexamethasone reduces cholesterol ester accumulation in the aorta [133], and glucocorticoids (dexamethasone, hydrocortisone) inhibit neointimal lesion formation in rats [134,135], rabbits [136][137][138] and dogs [139] (with a few contradictory reports [140,141]). Clinical trials in humans, by contrast, have proved disappointing (with notable exceptions [130]): methylprednisolone did not inhibit restenosis after coronary angioplasty [142] or stent implantation [143], whilst the combination of a glucocor-570 P. W. F. Hadoke et al Intra-vascular glucocorticoid metabolism ticoid with colchicine increased the risk of coronary aneurysm following stent placement [144]. Discrepancies between clinical studies and animal models could be attributed to species differences or, more probably, to methodological variation (e.g.…”

Coronary Artery Aneurysms: A Review of the Epidemiology, Pathophysiology, Diagnosis, and Treatment

“…First, DESs are primed with various cytotoxic antirestenosis drugs, which are known to suppress smooth muscle and endothelial cell proliferation, thus preventing restenosis (44–46). However, this antiproliferative nature of DES has been shown to increase the risk of CAAs via mechanisms of delayed neointimal healing and reendotheliazation (44, 45, 47).…”

Therapeutic manipulation of glucocorticoid metabolism in cardiovascular disease

“…No reduction in the incidence of restenosis (Reimers et al, 1998) Stent Dex Increased Aneurysm (Rab et al,1991) No effect (Stone et al, 1989) No effect (Pepine et al, 1990) Oral Methylprednisolone (1 g) No effect (Lee et al, 1999)…”