Correlation of Intravascular Ultrasound Findings With Histopathological Analysis of Thrombus Aspirates in Patients With Very Late Drug-Eluting Stent Thrombosis
Background— Intravascular ultrasound of drug-eluting stent (DES) thrombosis (ST) reveals a high incidence of incomplete stent apposition (ISA) and vessel remodeling. Autopsy specimens of DES ST show delayed healing and hypersensitivity reactions. The present study sought to correlate histopathology...
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| Published in | Circulation (New York, N.Y.) Vol. 120; no. 5; pp. 391 - 399 |
|---|---|
| Main Authors | , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Hagerstown, MD
Lippincott Williams & Wilkins
04.08.2009
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| Subjects | |
| Online Access | Get full text |
| ISSN | 0009-7322 1524-4539 1524-4539 |
| DOI | 10.1161/CIRCULATIONAHA.109.854398 |
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| Abstract | Background—
Intravascular ultrasound of drug-eluting stent (DES) thrombosis (ST) reveals a high incidence of incomplete stent apposition (ISA) and vessel remodeling. Autopsy specimens of DES ST show delayed healing and hypersensitivity reactions. The present study sought to correlate histopathology of thrombus aspirates with intravascular ultrasound findings in patients with very late DES ST.
Methods and Results—
The study population consisted of 54 patients (28 patients with very late DES ST and 26 controls). Of 28 patients with very late DES ST, 10 patients (1020±283 days after implantation) with 11 ST segments (5 sirolimus-eluting stents, 5 paclitaxel-eluting stents, 1 zotarolimus-eluting stent) underwent both thrombus aspiration and intravascular ultrasound investigation. ISA was present in 73% of cases with an ISA cross-sectional area of 6.2±2.4 mm
2
and evidence of vessel remodeling (index, 1.6±0.3). Histopathological analysis showed pieces of fresh thrombus with inflammatory cell infiltrates (DES, 263±149 white blood cells per high-power field) and eosinophils (DES, 20±24 eosinophils per high-power field; sirolimus-eluting stents, 34±28; paclitaxel-eluting stents, 6±6;
P
for sirolimus-eluting stents versus paclitaxel-eluting stents=0.09). The mean number of eosinophils per high-power field was higher in specimens from very late DES ST (20±24) than in those from spontaneous acute myocardial infarction (7±10), early bare-metal stent ST (1±1), early DES ST (1±2), and late bare-metal stent ST (2±3;
P
from ANOVA=0.038). Eosinophil count correlated with ISA cross-sectional area, with an average increase of 5.4 eosinophils per high-power field per 1-mm
2
increase in ISA cross-sectional area.
Conclusions—
Very late DES thrombosis is associated with histopathological signs of inflammation and intravascular ultrasound evidence of vessel remodeling. Compared with other causes of myocardial infarction, eosinophilic infiltrates are more common in thrombi harvested from very late DES thrombosis, particularly in sirolimus-eluting stents, and correlate with the extent of stent malapposition. |
|---|---|
| AbstractList | Intravascular ultrasound of drug-eluting stent (DES) thrombosis (ST) reveals a high incidence of incomplete stent apposition (ISA) and vessel remodeling. Autopsy specimens of DES ST show delayed healing and hypersensitivity reactions. The present study sought to correlate histopathology of thrombus aspirates with intravascular ultrasound findings in patients with very late DES ST.
The study population consisted of 54 patients (28 patients with very late DES ST and 26 controls). Of 28 patients with very late DES ST, 10 patients (1020+/-283 days after implantation) with 11 ST segments (5 sirolimus-eluting stents, 5 paclitaxel-eluting stents, 1 zotarolimus-eluting stent) underwent both thrombus aspiration and intravascular ultrasound investigation. ISA was present in 73% of cases with an ISA cross-sectional area of 6.2+/-2.4 mm(2) and evidence of vessel remodeling (index, 1.6+/-0.3). Histopathological analysis showed pieces of fresh thrombus with inflammatory cell infiltrates (DES, 263+/-149 white blood cells per high-power field) and eosinophils (DES, 20+/-24 eosinophils per high-power field; sirolimus-eluting stents, 34+/-28; paclitaxel-eluting stents, 6+/-6; P for sirolimus-eluting stents versus paclitaxel-eluting stents=0.09). The mean number of eosinophils per high-power field was higher in specimens from very late DES ST (20+/-24) than in those from spontaneous acute myocardial infarction (7+/-10), early bare-metal stent ST (1+/-1), early DES ST (1+/-2), and late bare-metal stent ST (2+/-3; P from ANOVA=0.038). Eosinophil count correlated with ISA cross-sectional area, with an average increase of 5.4 eosinophils per high-power field per 1-mm(2) increase in ISA cross-sectional area.
Very late DES thrombosis is associated with histopathological signs of inflammation and intravascular ultrasound evidence of vessel remodeling. Compared with other causes of myocardial infarction, eosinophilic infiltrates are more common in thrombi harvested from very late DES thrombosis, particularly in sirolimus-eluting stents, and correlate with the extent of stent malapposition. Intravascular ultrasound of drug-eluting stent (DES) thrombosis (ST) reveals a high incidence of incomplete stent apposition (ISA) and vessel remodeling. Autopsy specimens of DES ST show delayed healing and hypersensitivity reactions. The present study sought to correlate histopathology of thrombus aspirates with intravascular ultrasound findings in patients with very late DES ST.BACKGROUNDIntravascular ultrasound of drug-eluting stent (DES) thrombosis (ST) reveals a high incidence of incomplete stent apposition (ISA) and vessel remodeling. Autopsy specimens of DES ST show delayed healing and hypersensitivity reactions. The present study sought to correlate histopathology of thrombus aspirates with intravascular ultrasound findings in patients with very late DES ST.The study population consisted of 54 patients (28 patients with very late DES ST and 26 controls). Of 28 patients with very late DES ST, 10 patients (1020+/-283 days after implantation) with 11 ST segments (5 sirolimus-eluting stents, 5 paclitaxel-eluting stents, 1 zotarolimus-eluting stent) underwent both thrombus aspiration and intravascular ultrasound investigation. ISA was present in 73% of cases with an ISA cross-sectional area of 6.2+/-2.4 mm(2) and evidence of vessel remodeling (index, 1.6+/-0.3). Histopathological analysis showed pieces of fresh thrombus with inflammatory cell infiltrates (DES, 263+/-149 white blood cells per high-power field) and eosinophils (DES, 20+/-24 eosinophils per high-power field; sirolimus-eluting stents, 34+/-28; paclitaxel-eluting stents, 6+/-6; P for sirolimus-eluting stents versus paclitaxel-eluting stents=0.09). The mean number of eosinophils per high-power field was higher in specimens from very late DES ST (20+/-24) than in those from spontaneous acute myocardial infarction (7+/-10), early bare-metal stent ST (1+/-1), early DES ST (1+/-2), and late bare-metal stent ST (2+/-3; P from ANOVA=0.038). Eosinophil count correlated with ISA cross-sectional area, with an average increase of 5.4 eosinophils per high-power field per 1-mm(2) increase in ISA cross-sectional area.METHODS AND RESULTSThe study population consisted of 54 patients (28 patients with very late DES ST and 26 controls). Of 28 patients with very late DES ST, 10 patients (1020+/-283 days after implantation) with 11 ST segments (5 sirolimus-eluting stents, 5 paclitaxel-eluting stents, 1 zotarolimus-eluting stent) underwent both thrombus aspiration and intravascular ultrasound investigation. ISA was present in 73% of cases with an ISA cross-sectional area of 6.2+/-2.4 mm(2) and evidence of vessel remodeling (index, 1.6+/-0.3). Histopathological analysis showed pieces of fresh thrombus with inflammatory cell infiltrates (DES, 263+/-149 white blood cells per high-power field) and eosinophils (DES, 20+/-24 eosinophils per high-power field; sirolimus-eluting stents, 34+/-28; paclitaxel-eluting stents, 6+/-6; P for sirolimus-eluting stents versus paclitaxel-eluting stents=0.09). The mean number of eosinophils per high-power field was higher in specimens from very late DES ST (20+/-24) than in those from spontaneous acute myocardial infarction (7+/-10), early bare-metal stent ST (1+/-1), early DES ST (1+/-2), and late bare-metal stent ST (2+/-3; P from ANOVA=0.038). Eosinophil count correlated with ISA cross-sectional area, with an average increase of 5.4 eosinophils per high-power field per 1-mm(2) increase in ISA cross-sectional area.Very late DES thrombosis is associated with histopathological signs of inflammation and intravascular ultrasound evidence of vessel remodeling. Compared with other causes of myocardial infarction, eosinophilic infiltrates are more common in thrombi harvested from very late DES thrombosis, particularly in sirolimus-eluting stents, and correlate with the extent of stent malapposition.CONCLUSIONSVery late DES thrombosis is associated with histopathological signs of inflammation and intravascular ultrasound evidence of vessel remodeling. Compared with other causes of myocardial infarction, eosinophilic infiltrates are more common in thrombi harvested from very late DES thrombosis, particularly in sirolimus-eluting stents, and correlate with the extent of stent malapposition. Background— Intravascular ultrasound of drug-eluting stent (DES) thrombosis (ST) reveals a high incidence of incomplete stent apposition (ISA) and vessel remodeling. Autopsy specimens of DES ST show delayed healing and hypersensitivity reactions. The present study sought to correlate histopathology of thrombus aspirates with intravascular ultrasound findings in patients with very late DES ST. Methods and Results— The study population consisted of 54 patients (28 patients with very late DES ST and 26 controls). Of 28 patients with very late DES ST, 10 patients (1020±283 days after implantation) with 11 ST segments (5 sirolimus-eluting stents, 5 paclitaxel-eluting stents, 1 zotarolimus-eluting stent) underwent both thrombus aspiration and intravascular ultrasound investigation. ISA was present in 73% of cases with an ISA cross-sectional area of 6.2±2.4 mm 2 and evidence of vessel remodeling (index, 1.6±0.3). Histopathological analysis showed pieces of fresh thrombus with inflammatory cell infiltrates (DES, 263±149 white blood cells per high-power field) and eosinophils (DES, 20±24 eosinophils per high-power field; sirolimus-eluting stents, 34±28; paclitaxel-eluting stents, 6±6; P for sirolimus-eluting stents versus paclitaxel-eluting stents=0.09). The mean number of eosinophils per high-power field was higher in specimens from very late DES ST (20±24) than in those from spontaneous acute myocardial infarction (7±10), early bare-metal stent ST (1±1), early DES ST (1±2), and late bare-metal stent ST (2±3; P from ANOVA=0.038). Eosinophil count correlated with ISA cross-sectional area, with an average increase of 5.4 eosinophils per high-power field per 1-mm 2 increase in ISA cross-sectional area. Conclusions— Very late DES thrombosis is associated with histopathological signs of inflammation and intravascular ultrasound evidence of vessel remodeling. Compared with other causes of myocardial infarction, eosinophilic infiltrates are more common in thrombi harvested from very late DES thrombosis, particularly in sirolimus-eluting stents, and correlate with the extent of stent malapposition. |
| Author | Neidhart, Michel Nakazawa, Gaku Windecker, Stephan Billinger, Michael Eshtehardi, Parham Jüni, Peter Virmani, Renu Vogel, Rolf Cook, Stéphane Wenaweser, Peter Togni, Mario Ladich, Elena Gay, Steffen Seiler, Christian Meier, Bernhard Pichler, Werner J. |
| Author_xml | – sequence: 1 givenname: Stéphane surname: Cook fullname: Cook, Stéphane organization: From the Department of Cardiology, Bern University Hospital, Bern, Switzerland (S.C., P.E., R.V., M.T., P.W., M.B., C.S., B.M., S.W.); CVPath Institute Inc, Gaithersburg, Md (E.L., G.N., R.V.); World Health Organization Collaborating Center for Molecular Biology and Novel Therapeutic Strategies for Rheumatic Diseases, University Hospital Zürich, Zürich, Switzerland (M.N., S.G.); Institute of Social and Preventive Medicine, University of Bern, Bern, Switzerland (P.J.); and Division of Allergology – sequence: 2 givenname: Elena surname: Ladich fullname: Ladich, Elena organization: From the Department of Cardiology, Bern University Hospital, Bern, Switzerland (S.C., P.E., R.V., M.T., P.W., M.B., C.S., B.M., S.W.); CVPath Institute Inc, Gaithersburg, Md (E.L., G.N., R.V.); World Health Organization Collaborating Center for Molecular Biology and Novel Therapeutic Strategies for Rheumatic Diseases, University Hospital Zürich, Zürich, Switzerland (M.N., S.G.); Institute of Social and Preventive Medicine, University of Bern, Bern, Switzerland (P.J.); and Division of Allergology – sequence: 3 givenname: Gaku surname: Nakazawa fullname: Nakazawa, Gaku organization: From the Department of Cardiology, Bern University Hospital, Bern, Switzerland (S.C., P.E., R.V., M.T., P.W., M.B., C.S., B.M., S.W.); CVPath Institute Inc, Gaithersburg, Md (E.L., G.N., R.V.); World Health Organization Collaborating Center for Molecular Biology and Novel Therapeutic Strategies for Rheumatic Diseases, University Hospital Zürich, Zürich, Switzerland (M.N., S.G.); Institute of Social and Preventive Medicine, University of Bern, Bern, Switzerland (P.J.); and Division of Allergology – sequence: 4 givenname: Parham surname: Eshtehardi fullname: Eshtehardi, Parham organization: From the Department of Cardiology, Bern University Hospital, Bern, Switzerland (S.C., P.E., R.V., M.T., P.W., M.B., C.S., B.M., S.W.); CVPath Institute Inc, Gaithersburg, Md (E.L., G.N., R.V.); World Health Organization Collaborating Center for Molecular Biology and Novel Therapeutic Strategies for Rheumatic Diseases, University Hospital Zürich, Zürich, Switzerland (M.N., S.G.); Institute of Social and Preventive Medicine, University of Bern, Bern, Switzerland (P.J.); and Division of Allergology – sequence: 5 givenname: Michel surname: Neidhart fullname: Neidhart, Michel organization: From the Department of Cardiology, Bern University Hospital, Bern, Switzerland (S.C., P.E., R.V., M.T., P.W., M.B., C.S., B.M., S.W.); CVPath Institute Inc, Gaithersburg, Md (E.L., G.N., R.V.); World Health Organization Collaborating Center for Molecular Biology and Novel Therapeutic Strategies for Rheumatic Diseases, University Hospital Zürich, Zürich, Switzerland (M.N., S.G.); Institute of Social and Preventive Medicine, University of Bern, Bern, Switzerland (P.J.); and Division of Allergology – sequence: 6 givenname: Rolf surname: Vogel fullname: Vogel, Rolf organization: From the Department of Cardiology, Bern University Hospital, Bern, Switzerland (S.C., P.E., R.V., M.T., P.W., M.B., C.S., B.M., S.W.); CVPath Institute Inc, Gaithersburg, Md (E.L., G.N., R.V.); World Health Organization Collaborating Center for Molecular Biology and Novel Therapeutic Strategies for Rheumatic Diseases, University Hospital Zürich, Zürich, Switzerland (M.N., S.G.); Institute of Social and Preventive Medicine, University of Bern, Bern, Switzerland (P.J.); and Division of Allergology – sequence: 7 givenname: Mario surname: Togni fullname: Togni, Mario organization: From the Department of Cardiology, Bern University Hospital, Bern, Switzerland (S.C., P.E., R.V., M.T., P.W., M.B., C.S., B.M., S.W.); CVPath Institute Inc, Gaithersburg, Md (E.L., G.N., R.V.); World Health Organization Collaborating Center for Molecular Biology and Novel Therapeutic Strategies for Rheumatic Diseases, University Hospital Zürich, Zürich, Switzerland (M.N., S.G.); Institute of Social and Preventive Medicine, University of Bern, Bern, Switzerland (P.J.); and Division of Allergology – sequence: 8 givenname: Peter surname: Wenaweser fullname: Wenaweser, Peter organization: From the Department of Cardiology, Bern University Hospital, Bern, Switzerland (S.C., P.E., R.V., M.T., P.W., M.B., C.S., B.M., S.W.); CVPath Institute Inc, Gaithersburg, Md (E.L., G.N., R.V.); World Health Organization Collaborating Center for Molecular Biology and Novel Therapeutic Strategies for Rheumatic Diseases, University Hospital Zürich, Zürich, Switzerland (M.N., S.G.); Institute of Social and Preventive Medicine, University of Bern, Bern, Switzerland (P.J.); and Division of Allergology – sequence: 9 givenname: Michael surname: Billinger fullname: Billinger, Michael organization: From the Department of Cardiology, Bern University Hospital, Bern, Switzerland (S.C., P.E., R.V., M.T., P.W., M.B., C.S., B.M., S.W.); CVPath Institute Inc, Gaithersburg, Md (E.L., G.N., R.V.); World Health Organization Collaborating Center for Molecular Biology and Novel Therapeutic Strategies for Rheumatic Diseases, University Hospital Zürich, Zürich, Switzerland (M.N., S.G.); Institute of Social and Preventive Medicine, University of Bern, Bern, Switzerland (P.J.); and Division of Allergology – sequence: 10 givenname: Christian surname: Seiler fullname: Seiler, Christian organization: From the Department of Cardiology, Bern University Hospital, Bern, Switzerland (S.C., P.E., R.V., M.T., P.W., M.B., C.S., B.M., S.W.); CVPath Institute Inc, Gaithersburg, Md (E.L., G.N., R.V.); World Health Organization Collaborating Center for Molecular Biology and Novel Therapeutic Strategies for Rheumatic Diseases, University Hospital Zürich, Zürich, Switzerland (M.N., S.G.); Institute of Social and Preventive Medicine, University of Bern, Bern, Switzerland (P.J.); and Division of Allergology – sequence: 11 givenname: Steffen surname: Gay fullname: Gay, Steffen organization: From the Department of Cardiology, Bern University Hospital, Bern, Switzerland (S.C., P.E., R.V., M.T., P.W., M.B., C.S., B.M., S.W.); CVPath Institute Inc, Gaithersburg, Md (E.L., G.N., R.V.); World Health Organization Collaborating Center for Molecular Biology and Novel Therapeutic Strategies for Rheumatic Diseases, University Hospital Zürich, Zürich, Switzerland (M.N., S.G.); Institute of Social and Preventive Medicine, University of Bern, Bern, Switzerland (P.J.); and Division of Allergology – sequence: 12 givenname: Bernhard surname: Meier fullname: Meier, Bernhard organization: From the Department of Cardiology, Bern University Hospital, Bern, Switzerland (S.C., P.E., R.V., M.T., P.W., M.B., C.S., B.M., S.W.); CVPath Institute Inc, Gaithersburg, Md (E.L., G.N., R.V.); World Health Organization Collaborating Center for Molecular Biology and Novel Therapeutic Strategies for Rheumatic Diseases, University Hospital Zürich, Zürich, Switzerland (M.N., S.G.); Institute of Social and Preventive Medicine, University of Bern, Bern, Switzerland (P.J.); and Division of Allergology – sequence: 13 givenname: Werner J. surname: Pichler fullname: Pichler, Werner J. organization: From the Department of Cardiology, Bern University Hospital, Bern, Switzerland (S.C., P.E., R.V., M.T., P.W., M.B., C.S., B.M., S.W.); CVPath Institute Inc, Gaithersburg, Md (E.L., G.N., R.V.); World Health Organization Collaborating Center for Molecular Biology and Novel Therapeutic Strategies for Rheumatic Diseases, University Hospital Zürich, Zürich, Switzerland (M.N., S.G.); Institute of Social and Preventive Medicine, University of Bern, Bern, Switzerland (P.J.); and Division of Allergology – sequence: 14 givenname: Peter surname: Jüni fullname: Jüni, Peter organization: From the Department of Cardiology, Bern University Hospital, Bern, Switzerland (S.C., P.E., R.V., M.T., P.W., M.B., C.S., B.M., S.W.); CVPath Institute Inc, Gaithersburg, Md (E.L., G.N., R.V.); World Health Organization Collaborating Center for Molecular Biology and Novel Therapeutic Strategies for Rheumatic Diseases, University Hospital Zürich, Zürich, Switzerland (M.N., S.G.); Institute of Social and Preventive Medicine, University of Bern, Bern, Switzerland (P.J.); and Division of Allergology – sequence: 15 givenname: Renu surname: Virmani fullname: Virmani, Renu organization: From the Department of Cardiology, Bern University Hospital, Bern, Switzerland (S.C., P.E., R.V., M.T., P.W., M.B., C.S., B.M., S.W.); CVPath Institute Inc, Gaithersburg, Md (E.L., G.N., R.V.); World Health Organization Collaborating Center for Molecular Biology and Novel Therapeutic Strategies for Rheumatic Diseases, University Hospital Zürich, Zürich, Switzerland (M.N., S.G.); Institute of Social and Preventive Medicine, University of Bern, Bern, Switzerland (P.J.); and Division of Allergology – sequence: 16 givenname: Stephan surname: Windecker fullname: Windecker, Stephan organization: From the Department of Cardiology, Bern University Hospital, Bern, Switzerland (S.C., P.E., R.V., M.T., P.W., M.B., C.S., B.M., S.W.); CVPath Institute Inc, Gaithersburg, Md (E.L., G.N., R.V.); World Health Organization Collaborating Center for Molecular Biology and Novel Therapeutic Strategies for Rheumatic Diseases, University Hospital Zürich, Zürich, Switzerland (M.N., S.G.); Institute of Social and Preventive Medicine, University of Bern, Bern, Switzerland (P.J.); and Division of Allergology |
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Intravascular ultrasound of drug-eluting stent (DES) thrombosis (ST) reveals a high incidence of incomplete stent apposition (ISA) and vessel... Intravascular ultrasound of drug-eluting stent (DES) thrombosis (ST) reveals a high incidence of incomplete stent apposition (ISA) and vessel remodeling.... |
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| SubjectTerms | Aged Angioplasty, Balloon, Coronary Biological and medical sciences Biomarkers - metabolism Blood and lymphatic vessels Cardiology. Vascular system Coronary Artery Disease - therapy Coronary Thrombosis - diagnostic imaging Coronary Thrombosis - immunology Coronary Thrombosis - pathology Coronary Vessels - diagnostic imaging Coronary Vessels - immunology Coronary Vessels - pathology Diseases of the cardiovascular system Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous Drug-Eluting Stents - adverse effects Eosinophils - pathology Female Humans Male Medical sciences Middle Aged Radiotherapy. Instrumental treatment. Physiotherapy. Reeducation. Rehabilitation, orthophony, crenotherapy. Diet therapy and various other treatments (general aspects) Thrombectomy Ultrasonography, Interventional Vasculitis - diagnostic imaging Vasculitis - etiology Vasculitis - pathology |
| Title | Correlation of Intravascular Ultrasound Findings With Histopathological Analysis of Thrombus Aspirates in Patients With Very Late Drug-Eluting Stent Thrombosis |
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