J Forensic Sci, November 2013, Vol. 58, No. 6 doi: 10.1111/1556-4029.12285 Available online at: onlinelibrary.wiley.com
PAPER PATHOLOGY/BIOLOGY Erik Mont,1 M.D.; Nathaniel Cresswell,2 M.S.; and Allen Burke,3 M.D.
Pathologic Findings of Coronary Stents: A Comparison of Sudden Coronary Death Versus Non-cardiac Death
ABSTRACT: There are few histologic studies of intracoronary stents found at autopsy. We studied histologic findings of 87 intracoronary
stents from 45 autopsy hearts. There were 40 patients with chronically implanted stents and five shorter than 30 days. Of five patients with recent stent placement, the cause of death was related to the stent (in-stent thrombosis) in one case. Of the 40 patients with chronic stents, there were 16 sudden coronary deaths and 24 noncoronary deaths (controls). There were no late stent thromboses in the coronary deaths. In the coronary deaths, 26% of stents showed restenosis versus 11% in controls (p = 0.1). The rate of healed infarcts and cardiomegaly was similar in the coronary and noncoronary groups, and acute thrombi in native arteries were seen only in three hearts in the coronary group. We conclude that the cause of death is rarely impacted by in-stent findings at autopsy, especially in chronically implanted stents.
KEYWORDS: forensic science, stent implantation, coronary death, noncoronary death Since balloon angioplasty was adapted to the treatment of coronary artery disease in the late 1970s (1), the technique has gained widespread acceptance. However, vascular recoil may lead to periprocedural coronary occlusion and myocardial infarction, and there is a high rate of restenosis after successful revascularization (2,3). Scaffolding using a metallic mesh or stent was developed to prevent restenosis after angioplasty. The introduction of stent implantation into clinical practice has dramatically changed treatment of obstructive coronary artery disease (4,5). The indication for stent implantation has been widened substantially and has become the new standard angioplasty procedure (6,7). In-stent restenosis (ISR) is a major complication that was initially encountered with the widespread use of bare-metal stents (BMS) (8,9). Although coating of stents with polymers that elute a drug has dramatically reduced the rates of restenosis compared with BMS (10), a low rate of ISR after drug-eluting stents (DES) still exists, and its prevalence is not negligible because the population treated with DES is large. The histopathologic evaluation of ISR is hindered by the presence of the metal mesh. Several studies have described ISR using plastic embedding techniques (11–13). Paraffin-embedded histologic evaluation, which is far more widespread in use, is very labor-intensive for stents and requires either microdissection with specialized techniques, or electrolysis. There are few pathologic studies using these techniques in autopsies. The purpose of
1
Nova Scotia Medical Examiner Office, 5670 Spring Garder Road, Suite 701, Halifax Nova Scotia, Canada B3J 1H7. 2 Georgetown University Hospital, 3800 Reservoir Rd., Washington, DC 20007. 3 University of Maryland Medical System, 22 S. Greene St., Baltimore, MD 21201. Received 5 May 2012; and in revised form 1 Aug. 2012; accepted 5 Aug. 2012.
1542
this present study is to evaluate the impact of histologic stent evaluation in paraffin-embedded sections of coronary and noncoronary deaths, and its impact on determining the mechanism of death. Materials and Methods Forty-five cases with a documented history of stent implantation were prospectively studied from a medical examiner’s office. Hearts were dissected in a standard fashion, to document the presence of native coronary disease, cardiomegaly, and healed infarcts. The number of native vessels with >75% luminal area narrowing was noted, as was the presence of acute thrombi. Stented arteries were radiographed and decalcified. Stents were removed either after longitudinal microdissection with tungsten carbide scissors or by electrolysis (14). For the scissors technique, each stent was cut into 3 mm lengths at the proximal and distal segments by circumferentially cutting through stent struts, and then wires excised under a dissecting microscope. The central area was cut through longitudinally with the scissors exposing the lumen and media. The electrolysis technique was performed as previously described (14). Briefly, the stented portion of the artery was carefully dissected free of adventitial tissue. A silver wire was looped around the proximal portion of the stent, between struts. The wire was connected to the positive end of an electrophoresis unit (cathode). The current was adjusted such that visible electrolysis of the stent occurred after placing an anode wire from the anode of the unit into the solution. The stent was held in place until complete dissolution of the metal occurred. Sections were embedded and processed in paraffin. In-stent area and neointimal area were determined morphometrically (IPLab Spectrum®, Ontario, NY). In-stent restenosis was defined as a stent lumen cross-sectional area stenosis of ≥75% (equivalent to © 2013 American Academy of Forensic Sciences
MONT ET AL.
a stent lumen diameter stenosis of ≥50%) (15). No restenosis was defined as a stent lumen area stenosis of ≤75% (equivalent to a stent lumen diameter stenosis of ≤50%). Thrombosis and fibrin deposition were documented in each case. Medial injury was defined as ≥1 stent struts present through the media into the adventitia. The underlying plaque type was defined as fibrous plaque with smooth muscle cells, with or without calcification; pathologic intimal thickening, with or without calcification; and fibroatheroma, with or without calcification. The neointimal plaque was similarly classified. The cause of death was classified as coronary or noncoronary. Coronary deaths were all sudden. Noncoronary death was further categorized as unnatural or natural. Morphologic substrates for arrhythmias (subendocardial or healed infarcts, increased heart TABLE 1––Case characteristics.
All patients (n = 45) Acutely stented patients (n = 5) Chronic stented patients (n = 40)
Men: women Age, years, at death, mean SD
Number of stents, total
37: 8 59 13; 64 13 4:1 69 13; 54
87 12*
33:7 58 13; 66 13
75*
*Two chronically implanted stents were found in the acutely stented patients; therefore, the total number of acute implants was 10, and chronic implants 77.
.
CORONARY ARTERY STENTS AT FORENSIC AUTOPSY
1543
weight, and left ventricular hypertrophy) were recorded in each case. Statistics were performed using JMP software; SAS Institute, Cory, NC. Comparison of two means was performed using Student’s t-test and of multiple categories was performed using ANOVA means table with Fisher’s post hoc testing. Results There were total of 87 intracoronary stents, 85 were in native arteries, and two in vein grafts, from 45 autopsy hearts (Table 1). There were 37 men (59 13 years) and eight women (64 13 years). 53 stents were microdissected (Fig. 1), 32 stents were successfully dissolved (Fig. 2); two were microdissected after unsuccessful electrolysis. Of five patients with recent stent placement, 75% of the stented area (restenosis). The arrow points to the higher magnification of the strut perforating the media (see F, below). (D) There is total occlusion of the stented area by organized thrombus. (E) A higher magnification of the stent struts shows the interface between the neointimal (left) and the media (center). The adventitial collagen is at the left. There are giant cells surrounding the upper portion of the strut (arrow). (F) A higher magnification of a stent strut in C. The stent is entirely outside the media and resides in the adventitia.
stents, two chronically implanted stents, one each in two patients. Neither of these stents showed restenosis or thrombosis. Of the 40 patients with only chronic stents, causes of death were unnatural (16), sudden coronary death (n = 13), natural noncoronary (n = 8), and nonsudden coronary deaths (n = 3) (Table 3). The rate of healed infarcts and cardiomegaly was higher in the coronary deaths as compared to the noncoronary deaths, but the difference was not significant (Table 4). There were three acute thrombi in the nonstented coronary arteries in the coronary deaths, and none in the noncoronary deaths (Table 4). There were 31 stents in the 16 sudden and nonsudden coronary deaths and 44 stents in the 24 noncoronary deaths (Table 5). There was a moderate increase in restenosis with medial injury (Table 5). In the coronary deaths, there were 8 of
32 = 1 with restenosis (26%) versus 5 of 45 in the noncoronary deaths (11%, p = 0.1); mean percent stenosis was 45% versus 35%, respectively (p = 0.1) (Table 6). There were five in-stent total occlusions in the coronary deaths and three in the noncoronary deaths (p = 0.5) (Fig. 3) (Table 6). Eleven of 48 chronic drug-eluting stents showed peristrut fibrin and incomplete healing; this finding was seen in one BMS (Table 7). There was a similar rate of restenosis dependent on the underlying plaque type (Table 8). The neointimal plaque was composed of fibrous tissue with smooth muscle cells in the majority of cases (Table 9); there were few in-stent fibroatheromas. Chronic total in-stent occlusions were most frequently fibrous plaques, with equal numbers of fibrocalcific total occlusions and organized thrombi (Fig. 2D, Table 5). One patient
MONT ET AL.
.
CORONARY ARTERY STENTS AT FORENSIC AUTOPSY
1545
TABLE 2––Case findings, acutely implanted stents. Age, sex Source
Duration
Indication for stent placement
Artery, stent type
1 day
Acute MI,
79 Male
6h
Acute MI
56 Male
8h
Unstable angina; Rotoblader for severe calcification
59 Male
28 days
Stable angina
82 Male
9 days
Acute STEMI
LAD Cypher X 2* Multi-Link RX 9 1 RCA Xience 9 2* LAD/left main Xience (3)* LOM1 Taxus† LAD Cypher‡ LAD Liberte/ Express
54 Female
Stent findings
Cause of death
Occlusive thrombus
In-stent thrombosis, acute
Medial dissection distal to stent
Acute MI
Medial laceration with epicardial hemorrhage
Perforation of right ventricle by pacer wire with hemopericardium
Medial dissection, extensive
Acute plaque rupture, circumflex artery, with acute infarction AMI with acute renal failure, ARDS, sepsis
Patent
*Overlapping. † Patent Multi-Link RX in right coronary, placed years prior. ‡ Patent Cypher stent placed 1 year prior in circumflex proximal to acute native thrombus.
FIG. 3––Spectrum of restenosis. (A) 54-year-old female, with acute stent implantation, acute thrombosis in stent. The stent was removed by the scissor technique. (B) 67-year-old male, with chronic stent implantation, no in-stent restenosis. The stent was removed by electrolysis. (C) 50-year-old male with chronic stent implantation and restenosis by intimal fibrous thickening. Stent removed by scissor technique. (D) 50-year-old male with chronic stent implantation, organized thrombosis in stent, removed by scissor technique. Note medial injury at multiple strut sites (arrows).
with a remote history of coronary stenting died with subarachnoid hemorrhage after placement of a cerebral stent for a middle cerebral artery aneurysm. Histologic examination of the stented portion demonstrated perforation of the artery at the stented site. Discussion This present study demonstrates that evaluation of stents is valuable in acute (75% narrowing Number of hearts with stents showing medial injury Stent fractures Number of stents with total occlusions Mean in-stent narrowing, % SE
Coronary deaths (n = 16 hearts, 31 stents)
Noncoronary deaths (n = 24 hearts, 44 stents)
p
0 9/22 4.2 0.4
1* 18/26 3.5 0.4
0.3 0.2
8/31 (26%)
5/44 (11%)
0.1
5/16 (31%)
2/24 (8%)
0.09
3/31 5/31 (16%)
1/44 3/44 (7%)
0.7 0.2
45 5
36 4
0.1
*
SVG graft, organizing.
TABLE 4––Cardiac and native artery findings, chronic stent placement. TABLE 7––Presence of peristrut fibrin and giant cells.
Coronary deaths (n = 16)
Noncoronary deaths (n = 24)
p
31 (1.9)
44 (1.8)
0.9
3 3 0: 0 1: 1 (6%) 2: 4 (25%) 3: 11 (69%) 1 75% 58%
4 0 0: 2 (8%) 1: 3 (13%) 2: 7 (29%) 3: 12 (50%) 0 65% 53%
0.8 0.06 0.2
631 162 89%
545 146 67%
0.2 0.2
Numbers of stents (total, mean per heart) Prior CABG Acute coronary thrombi Numbers of stenotic arteries (>75% narrowed) Acute myocardial infarcts Presence of healed infarct Presence of transmural healed infarct Mean heart weight Presence of cardiomegaly
0.5 0.6 0.8
TABLE 5––In-stent restenosis measurements, 75 chronically implanted stents from 40 hearts.
n
Neointimal area, mm2 mean SD
Vessel LM ostium 1 LAD–LD 35 LCX–OM 12 RCA 24 SVG 3 Type 27 BMS1 48 DES2 Overlapping No 63 Yes 12 Malposition/media injury Absent 65 Present 10
5.9 4.0 2.2 3.9 6.4
2.6 0.9 2.0 2.4
% narrowing mean SD 80 41 25 41 55
25 26 36 18
% with restenosis 1 4 1 6 1
(100%) (11%) (8%) (25%) (33%)
3.2 1.4 4.3 2.9
41 27 39 28
5 (19%) 8 (17%)
3.7 4.6 4.6 3.1
41 30 33 27
12 (19%) 1 (8%)
3.4 1.9 6.0 3.1*
45 15 62 25
15 (27%) 6 (60%)†
Multi-Link 11 (Penta 6; Vision 5); Driver (4); AVE GFX (2); NIR (3); Palmaz Schatz (3); unknown (1). Taxus (21); Endeavor (17); Cypher (7); RX Achieve (3). *
PAPER PATHOLOGY/BIOLOGY Erik Mont,1 M.D.; Nathaniel Cresswell,2 M.S.; and Allen Burke,3 M.D.
Pathologic Findings of Coronary Stents: A Comparison of Sudden Coronary Death Versus Non-cardiac Death
ABSTRACT: There are few histologic studies of intracoronary stents found at autopsy. We studied histologic findings of 87 intracoronary
stents from 45 autopsy hearts. There were 40 patients with chronically implanted stents and five shorter than 30 days. Of five patients with recent stent placement, the cause of death was related to the stent (in-stent thrombosis) in one case. Of the 40 patients with chronic stents, there were 16 sudden coronary deaths and 24 noncoronary deaths (controls). There were no late stent thromboses in the coronary deaths. In the coronary deaths, 26% of stents showed restenosis versus 11% in controls (p = 0.1). The rate of healed infarcts and cardiomegaly was similar in the coronary and noncoronary groups, and acute thrombi in native arteries were seen only in three hearts in the coronary group. We conclude that the cause of death is rarely impacted by in-stent findings at autopsy, especially in chronically implanted stents.
KEYWORDS: forensic science, stent implantation, coronary death, noncoronary death Since balloon angioplasty was adapted to the treatment of coronary artery disease in the late 1970s (1), the technique has gained widespread acceptance. However, vascular recoil may lead to periprocedural coronary occlusion and myocardial infarction, and there is a high rate of restenosis after successful revascularization (2,3). Scaffolding using a metallic mesh or stent was developed to prevent restenosis after angioplasty. The introduction of stent implantation into clinical practice has dramatically changed treatment of obstructive coronary artery disease (4,5). The indication for stent implantation has been widened substantially and has become the new standard angioplasty procedure (6,7). In-stent restenosis (ISR) is a major complication that was initially encountered with the widespread use of bare-metal stents (BMS) (8,9). Although coating of stents with polymers that elute a drug has dramatically reduced the rates of restenosis compared with BMS (10), a low rate of ISR after drug-eluting stents (DES) still exists, and its prevalence is not negligible because the population treated with DES is large. The histopathologic evaluation of ISR is hindered by the presence of the metal mesh. Several studies have described ISR using plastic embedding techniques (11–13). Paraffin-embedded histologic evaluation, which is far more widespread in use, is very labor-intensive for stents and requires either microdissection with specialized techniques, or electrolysis. There are few pathologic studies using these techniques in autopsies. The purpose of
1
Nova Scotia Medical Examiner Office, 5670 Spring Garder Road, Suite 701, Halifax Nova Scotia, Canada B3J 1H7. 2 Georgetown University Hospital, 3800 Reservoir Rd., Washington, DC 20007. 3 University of Maryland Medical System, 22 S. Greene St., Baltimore, MD 21201. Received 5 May 2012; and in revised form 1 Aug. 2012; accepted 5 Aug. 2012.
1542
this present study is to evaluate the impact of histologic stent evaluation in paraffin-embedded sections of coronary and noncoronary deaths, and its impact on determining the mechanism of death. Materials and Methods Forty-five cases with a documented history of stent implantation were prospectively studied from a medical examiner’s office. Hearts were dissected in a standard fashion, to document the presence of native coronary disease, cardiomegaly, and healed infarcts. The number of native vessels with >75% luminal area narrowing was noted, as was the presence of acute thrombi. Stented arteries were radiographed and decalcified. Stents were removed either after longitudinal microdissection with tungsten carbide scissors or by electrolysis (14). For the scissors technique, each stent was cut into 3 mm lengths at the proximal and distal segments by circumferentially cutting through stent struts, and then wires excised under a dissecting microscope. The central area was cut through longitudinally with the scissors exposing the lumen and media. The electrolysis technique was performed as previously described (14). Briefly, the stented portion of the artery was carefully dissected free of adventitial tissue. A silver wire was looped around the proximal portion of the stent, between struts. The wire was connected to the positive end of an electrophoresis unit (cathode). The current was adjusted such that visible electrolysis of the stent occurred after placing an anode wire from the anode of the unit into the solution. The stent was held in place until complete dissolution of the metal occurred. Sections were embedded and processed in paraffin. In-stent area and neointimal area were determined morphometrically (IPLab Spectrum®, Ontario, NY). In-stent restenosis was defined as a stent lumen cross-sectional area stenosis of ≥75% (equivalent to © 2013 American Academy of Forensic Sciences
MONT ET AL.
a stent lumen diameter stenosis of ≥50%) (15). No restenosis was defined as a stent lumen area stenosis of ≤75% (equivalent to a stent lumen diameter stenosis of ≤50%). Thrombosis and fibrin deposition were documented in each case. Medial injury was defined as ≥1 stent struts present through the media into the adventitia. The underlying plaque type was defined as fibrous plaque with smooth muscle cells, with or without calcification; pathologic intimal thickening, with or without calcification; and fibroatheroma, with or without calcification. The neointimal plaque was similarly classified. The cause of death was classified as coronary or noncoronary. Coronary deaths were all sudden. Noncoronary death was further categorized as unnatural or natural. Morphologic substrates for arrhythmias (subendocardial or healed infarcts, increased heart TABLE 1––Case characteristics.
All patients (n = 45) Acutely stented patients (n = 5) Chronic stented patients (n = 40)
Men: women Age, years, at death, mean SD
Number of stents, total
37: 8 59 13; 64 13 4:1 69 13; 54
87 12*
33:7 58 13; 66 13
75*
*Two chronically implanted stents were found in the acutely stented patients; therefore, the total number of acute implants was 10, and chronic implants 77.
.
CORONARY ARTERY STENTS AT FORENSIC AUTOPSY
1543
weight, and left ventricular hypertrophy) were recorded in each case. Statistics were performed using JMP software; SAS Institute, Cory, NC. Comparison of two means was performed using Student’s t-test and of multiple categories was performed using ANOVA means table with Fisher’s post hoc testing. Results There were total of 87 intracoronary stents, 85 were in native arteries, and two in vein grafts, from 45 autopsy hearts (Table 1). There were 37 men (59 13 years) and eight women (64 13 years). 53 stents were microdissected (Fig. 1), 32 stents were successfully dissolved (Fig. 2); two were microdissected after unsuccessful electrolysis. Of five patients with recent stent placement, 75% of the stented area (restenosis). The arrow points to the higher magnification of the strut perforating the media (see F, below). (D) There is total occlusion of the stented area by organized thrombus. (E) A higher magnification of the stent struts shows the interface between the neointimal (left) and the media (center). The adventitial collagen is at the left. There are giant cells surrounding the upper portion of the strut (arrow). (F) A higher magnification of a stent strut in C. The stent is entirely outside the media and resides in the adventitia.
stents, two chronically implanted stents, one each in two patients. Neither of these stents showed restenosis or thrombosis. Of the 40 patients with only chronic stents, causes of death were unnatural (16), sudden coronary death (n = 13), natural noncoronary (n = 8), and nonsudden coronary deaths (n = 3) (Table 3). The rate of healed infarcts and cardiomegaly was higher in the coronary deaths as compared to the noncoronary deaths, but the difference was not significant (Table 4). There were three acute thrombi in the nonstented coronary arteries in the coronary deaths, and none in the noncoronary deaths (Table 4). There were 31 stents in the 16 sudden and nonsudden coronary deaths and 44 stents in the 24 noncoronary deaths (Table 5). There was a moderate increase in restenosis with medial injury (Table 5). In the coronary deaths, there were 8 of
32 = 1 with restenosis (26%) versus 5 of 45 in the noncoronary deaths (11%, p = 0.1); mean percent stenosis was 45% versus 35%, respectively (p = 0.1) (Table 6). There were five in-stent total occlusions in the coronary deaths and three in the noncoronary deaths (p = 0.5) (Fig. 3) (Table 6). Eleven of 48 chronic drug-eluting stents showed peristrut fibrin and incomplete healing; this finding was seen in one BMS (Table 7). There was a similar rate of restenosis dependent on the underlying plaque type (Table 8). The neointimal plaque was composed of fibrous tissue with smooth muscle cells in the majority of cases (Table 9); there were few in-stent fibroatheromas. Chronic total in-stent occlusions were most frequently fibrous plaques, with equal numbers of fibrocalcific total occlusions and organized thrombi (Fig. 2D, Table 5). One patient
MONT ET AL.
.
CORONARY ARTERY STENTS AT FORENSIC AUTOPSY
1545
TABLE 2––Case findings, acutely implanted stents. Age, sex Source
Duration
Indication for stent placement
Artery, stent type
1 day
Acute MI,
79 Male
6h
Acute MI
56 Male
8h
Unstable angina; Rotoblader for severe calcification
59 Male
28 days
Stable angina
82 Male
9 days
Acute STEMI
LAD Cypher X 2* Multi-Link RX 9 1 RCA Xience 9 2* LAD/left main Xience (3)* LOM1 Taxus† LAD Cypher‡ LAD Liberte/ Express
54 Female
Stent findings
Cause of death
Occlusive thrombus
In-stent thrombosis, acute
Medial dissection distal to stent
Acute MI
Medial laceration with epicardial hemorrhage
Perforation of right ventricle by pacer wire with hemopericardium
Medial dissection, extensive
Acute plaque rupture, circumflex artery, with acute infarction AMI with acute renal failure, ARDS, sepsis
Patent
*Overlapping. † Patent Multi-Link RX in right coronary, placed years prior. ‡ Patent Cypher stent placed 1 year prior in circumflex proximal to acute native thrombus.
FIG. 3––Spectrum of restenosis. (A) 54-year-old female, with acute stent implantation, acute thrombosis in stent. The stent was removed by the scissor technique. (B) 67-year-old male, with chronic stent implantation, no in-stent restenosis. The stent was removed by electrolysis. (C) 50-year-old male with chronic stent implantation and restenosis by intimal fibrous thickening. Stent removed by scissor technique. (D) 50-year-old male with chronic stent implantation, organized thrombosis in stent, removed by scissor technique. Note medial injury at multiple strut sites (arrows).
with a remote history of coronary stenting died with subarachnoid hemorrhage after placement of a cerebral stent for a middle cerebral artery aneurysm. Histologic examination of the stented portion demonstrated perforation of the artery at the stented site. Discussion This present study demonstrates that evaluation of stents is valuable in acute (75% narrowing Number of hearts with stents showing medial injury Stent fractures Number of stents with total occlusions Mean in-stent narrowing, % SE
Coronary deaths (n = 16 hearts, 31 stents)
Noncoronary deaths (n = 24 hearts, 44 stents)
p
0 9/22 4.2 0.4
1* 18/26 3.5 0.4
0.3 0.2
8/31 (26%)
5/44 (11%)
0.1
5/16 (31%)
2/24 (8%)
0.09
3/31 5/31 (16%)
1/44 3/44 (7%)
0.7 0.2
45 5
36 4
0.1
*
SVG graft, organizing.
TABLE 4––Cardiac and native artery findings, chronic stent placement. TABLE 7––Presence of peristrut fibrin and giant cells.
Coronary deaths (n = 16)
Noncoronary deaths (n = 24)
p
31 (1.9)
44 (1.8)
0.9
3 3 0: 0 1: 1 (6%) 2: 4 (25%) 3: 11 (69%) 1 75% 58%
4 0 0: 2 (8%) 1: 3 (13%) 2: 7 (29%) 3: 12 (50%) 0 65% 53%
0.8 0.06 0.2
631 162 89%
545 146 67%
0.2 0.2
Numbers of stents (total, mean per heart) Prior CABG Acute coronary thrombi Numbers of stenotic arteries (>75% narrowed) Acute myocardial infarcts Presence of healed infarct Presence of transmural healed infarct Mean heart weight Presence of cardiomegaly
0.5 0.6 0.8
TABLE 5––In-stent restenosis measurements, 75 chronically implanted stents from 40 hearts.
n
Neointimal area, mm2 mean SD
Vessel LM ostium 1 LAD–LD 35 LCX–OM 12 RCA 24 SVG 3 Type 27 BMS1 48 DES2 Overlapping No 63 Yes 12 Malposition/media injury Absent 65 Present 10
5.9 4.0 2.2 3.9 6.4
2.6 0.9 2.0 2.4
% narrowing mean SD 80 41 25 41 55
25 26 36 18
% with restenosis 1 4 1 6 1
(100%) (11%) (8%) (25%) (33%)
3.2 1.4 4.3 2.9
41 27 39 28
5 (19%) 8 (17%)
3.7 4.6 4.6 3.1
41 30 33 27
12 (19%) 1 (8%)
3.4 1.9 6.0 3.1*
45 15 62 25
15 (27%) 6 (60%)†
Multi-Link 11 (Penta 6; Vision 5); Driver (4); AVE GFX (2); NIR (3); Palmaz Schatz (3); unknown (1). Taxus (21); Endeavor (17); Cypher (7); RX Achieve (3). *
