on September 22, 2003
Circulation. 2003
Published online before print September 22, 2003, doi: 10.1161/01.CIR.0000091115.05480.B0
Published online before print September 22, 2003, doi: 10.1161/01.CIR.0000091115.05480.B0
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Submitted on March 28, 2003
From the Department of Cardiovascular Pathology, Armed Forces Institute of Pathology, Washington, DC. * To whom correspondence should be addressed. E-mail: Virmani{at}afip.osd.mil.
Background--Coronary stent deployment is associated with a low incidence of acute thrombosis. However, late stent thrombosis (LST) has likely been underrecognized clinically, and pathological descriptions are lacking. Methods and Results--LST was defined as an acute thrombus within a stent that had been in place Conclusions--LST is a potentially fatal complication of coronary stenting. Stenting across branch ostia, disruption of adjacent vulnerable plaques, radiation therapy, and extensive plaque prolapse can precipitate LST. Impaired intimal healing (ie, the failure to form a complete neointimal layer over stent struts) extends the window during which stents are prone to thrombosis.
Revised on July 21, 2003
Accepted on July 22, 2003
Pathological Mechanisms of Fatal Late Coronary Stent Thrombosis in Humans
Andrew Farb MD,
30 days. Cases of LST were selected from a registry of human coronary stents submitted for analysis. Thirteen cases of LST (9 men, 4 women) were identified. The mean duration from implantation to thrombosis was 3.6±3.5 months (range, 1 to 11.9 months). The causes of death were sudden cardiac death (n=10), acute myocardial infarction (n=2), and heart failure (n=1). The pathological mechanisms of LST were as follows: (1) stenting across ostia of major arterial branches (5 cases); (2) exposure to radiation therapy (3 cases); (3) plaque disruption in the nonstented arterial segment within 2 mm of the stent margin (2 cases); (4) stenting of markedly necrotic, lipid-rich plaques with extensive plaque prolapse (2 cases); and (5) diffuse in-stent restenosis (1 case). Twelve cases demonstrated a failure to form a completely healed neointimal layer overlying stent struts. Underlying in-stent restenosis was present in only 4 (31%) of 13 cases.
Key words: thrombosis • stents • restenosis • coronary disease
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