keith a a fox edinburgh centre for cardiovascular science new markers of myocardial damage in acs...
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Keith A A Fox
Edinburgh Centre for Cardiovascular Science
New Markers of Myocardial New Markers of Myocardial Damage in ACSDamage in ACS
BCIS Risk Stratification in ACS: Jan 2004BCIS Risk Stratification in ACS: Jan 2004
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• Why do we need new markers?
• How good is existing risk stratification?
Acute Coronary Syndrome
• Improve clinical risk stratificationImprove clinical risk stratification• Guide current treatment optionsGuide current treatment options• Identify systemic & plaque inflammationIdentify systemic & plaque inflammation• New targets for therapyNew targets for therapy
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Clinical suspicion of ACS
Physical examination, ECG monitoring, Blood samples
No persistentST-Segment elevation
No persistentST-Segment elevation
Heparin (LMWH or UFH), ASA,Clopidogrel, Betablockers, Nitrates
Heparin (LMWH or UFH), ASA,Clopidogrel, Betablockers, Nitrates
New ESC guidelines
Twice negativeTwice negative
Stress testStress testCor. angiographyCor. angiography
Low riskLow risk
PositivePositive
Second troponin measurementSecond troponin measurement
Gp2b/3a
Cor. Angiography
Gp2b/3a
Cor. Angiography
High riskHigh risk
PCI, CABG or medical management
Depending upon clinical and angiographic features
How do we resolve How do we resolve the interface?the interface?
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• 64 yr male• 45 min ischaemic pain• No sig prior history• HR 115min BP 138/86• 2mm ST depression II, III,
AVF• Killip class 1• Creatinine 108mol/L• No complications• 10 hr trop T 3.5ng/ml
• 64 yr female• 45 min ischaemic pain • No sig prior history• HR 108min BP 138/86• 2mm ST elevation II, III,
AVF• Killip class 1• Creatinine 50mol/L• No complications• 10 hr trop T 6.4ng/ml
Who is at greater risk of death Who is at greater risk of death and, high or low risk?and, high or low risk?
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• 64 yr male• 45 min ischaemic pain• No sig prior history• HR 115min BP 138/86• 2mm ST depression II, III,
AVF• Killip class 1• Creatinine 108mol/L• No complications• 10 hr trop T 3.5ng/ml
• 64 yr female• 45 min ischaemic pain • No sig prior history• HR 108min BP 138/86• 2mm ST elevation II, III,
AVF• Killip class 1• Creatinine 50mol/L• No complications• 10 hr trop T 6.4ng/ml
Who is at greater risk of Who is at greater risk of death?death?
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• 64 yr male• 2mm ST depression II, III,
AVF. HR 115min• 10hr trop T 3.5ng/ml• Creatinine 108mol/L
• 64 yr female • 2mm ST elevation II, III,
AVF, HR 108min• 10hr trop 6.4ng/ml• Creatinine 50mol/L
9.0% death 5.0% death
In-hospital:
6 months:
16% death 11% death
Who is at greater risk of Who is at greater risk of death?death?
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GRACE Risk ModelGRACE Risk Model
Variables
• Age (continuous)
• Killip class
• Blood pressure
• ST deviation
• Cardiac arrest
• Creatinine
• Elevated CK-MB or Tn
• Heart rate
Variables
• Age (continuous)
• Killip class
• Blood pressure
• ST deviation
• Cardiac arrest
• Creatinine
• Elevated CK-MB or Tn
• Heart rate
Archives Int Med 2003
KAAFox ESC2003
www.umassmed.edu/outcomes/grace
Derived in 21 688 patients: 1046 in-hospital deaths, 711 post
discharge deathsValidated in GUSTO IIb 12142
C-index = 0.84 death (in-hosp),
C-index = 0.82 death (6 months)
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GRACE: Model CalibrationGRACE: Model Calibration
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The frequency of death The frequency of death by tertile of GRACE risk scoreby tertile of GRACE risk score
0.71.51.1
3.6
6.7
13.7
0
10
Death (in-hospital) Death (admission to 6months)
Pat
ien
ts (
%)
Lowest tertile (n = 4011)
Middle tertile (n = 4013)
Highest tertile (n = 4025)
P <0.0001 P <0.0001
All ACS patients
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Does the frequency of intervention Does the frequency of intervention relate to the risk of the patients?relate to the risk of the patients?
24.9
6.1
22.5
7.5
29.430.2
22.8
5.9
17.5
0
10
20
30
PCI CABG PCI/CABG
Pat
ien
ts (
%)
Lowest tertile (n = 4011)
Middle tertile (n = 4013)
Highest tertile (n = 4025)
P <0.0001 P <0.0001p=0.007
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• Key systemic markers
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0
5
10
15
20
25
0 30 60 90 120 150 1800
5
10
15
20
25
0 30 60 90 120 150 180
CAPTURE: Event rate in % (Death, AMI)CAPTURE: Event rate in % (Death, AMI)
Follow-up (days)
CRP > 10 mg/LCRP > 10 mg/L
CRP < 10 mg/LCRP < 10 mg/L
OR 1.92; P=0.003
Heeschen, Hamm et.al., JACC 2000Heeschen, Hamm et.al., JACC 2000
• CRP…cause or consequence?CRP…cause or consequence?
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Lindahl. NEJM 2000; 343:1139Lindahl. NEJM 2000; 343:1139
0022446688
10101212141416161818
C-reactive proteinC-reactive protein>10mg/L>10mg/L
C-reactive proteinC-reactive protein10mg/L10mg/L
<0.06<0.06
0.06-0.590.06-0.59
0.60.6
3434
105105
170170
207207
262262
139139
Trop
onin
T
Trop
onin
T (µ
g/L)
(µg/L
)
Death
fro
m C
ard
iac C
au
ses
Death
fro
m C
ard
iac C
au
ses (
%)
(%)
FRISC Study
Death from Cardiac Cause at 2 years: Influence Death from Cardiac Cause at 2 years: Influence of C-R Protein & Troponin T levels at 24 Hoursof C-R Protein & Troponin T levels at 24 Hours
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Noninvasive< 5ng/L
>= 5 ng/L
012345
6
7
8
91-
year
mo
rtal
ity
%
833
295
FRISC II 1-year mortality: IL-6 levels
at entry in the noninvasive vs invasive groups
Invasive
820
315
P=0.006
P< 0.001
IL-6
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• Angiographic score & CRP only weakly correlated but both predict outcome
CRP and Extent of CAD Predict CRP and Extent of CAD Predict OutcomeOutcome
JACC 2002: 39; 632-7JACC 2002: 39; 632-7
• Contribution of CRP to risk is especially marked in patients with minor angiographic stenoses
• CRP may reflect disease activity rather than extent of obstructive atheroma
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• Subtle markers of myocardial dysfunction…Subtle markers of myocardial dysfunction…
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De Lemos JA, et al. NEJM. 2001.
00
22
44
1010
66
88
00 5050 100100 150150 200200 250250 300300
Mor
talit
y (%
) (
%)
Days after randomization
1st quartile
2nd quartile
3rd quartile
P<0.001
4th quartile
P<0.01
OPUS-TIMI 16 (n=2523)
BNP in Acute Coronary SyndromeBNP in Acute Coronary Syndrome
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0
20
40
60
> 0.01 ug/l < 0.01 ug/L
< 401
401-1653
> 1653
Troponin T
NT-proBNP (pg/ml)
Death(%)
T. Jernberg et al. JACC 2002
Interaction of Troponin T Interaction of Troponin T and N Terminal pro BNPand N Terminal pro BNP
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VULNERABLE CORONARY ARTERY PLAQUE
Macrophages:CD68 and actinCollagen
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VULNERABLE CORONARY ARTERY PLAQUE
Macrophages:CD68 and actinCollagen
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Altered growth factor production tissuetissueinjuryinjury
Lipid coreLipid-ladenmacrophages
Plaque formation and progression - inflammatory events
Excessive/uncontrolled adhesion Excessive/uncontrolled adhesion
Altered differentiation/Altered differentiation/apoptotic programmes apoptotic programmes
Failed clearance of Failed clearance of apoptotic cells apoptotic cells
matrix matrix metalloproteinases metalloproteinases
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markers of inflammationmarkers of inflammation
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Adhesion moleculesE-selectin, ICAM-1, VCAM-1
Permeability
Apoptosis
Leukocyte chemoattractants(MCP-1, IL-8, PDGF, MC-SF)
Procoagulant activity(tissue factor)
Cytokines(TNF, FAS,CD40L)
NOET-1
markers of inflammationmarkers of inflammation
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CD40 on platelets in type I DM vs. controlsCD40 on platelets in type I DM vs. controls
P<0.001
% p
ositi
ve p
late
lets
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Role of monocyte-platelet adhesionRole of monocyte-platelet adhesion
• Monocytes may act as a “sump” for activated platelets.• Bound platelets modulate monocyte adhesion• Influence monocyte signal transduction
P-selectin
PSGL-1Signaltransduction
monocyteplatelet
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Pro-inflammatory effects of Pro-inflammatory effects of platelet-monocyte bindingplatelet-monocyte binding
Proinflammatory Cytokines
Cell Adhesion Molecule Expression
Tissue FactorChemokines
(IL-8, MCP-1)
0
5
10
15
20
25
Non-cardiacchest pain
Unstable Angina MI
per
cen
tag
e p
late
let-
mo
no
cyte
bin
din
g
Cation independent adhesion( EDTA 10mM)
Sarma et al Circ 2002: 105; 2166-71Sarma et al Circ 2002: 105; 2166-71
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Glycoprotein IIb/IIIa does not mediate Glycoprotein IIb/IIIa does not mediate monocyte-platelet interactionmonocyte-platelet interaction
monoclonal antibody
abciximab does not block monocyte-platelet interaction.
BUT, platelet P-selectin and monocyte PSGL-1 mediate adhesion.
0
10
20
30
40
50
60
70
80
90C
on
tro
l
ED
TA
PS
GL
1
P-s
ele
ctin
abc
ixim
ab
perc
ent
bind
ing
Sarma et al Circ 2002: 105; 2166-71Sarma et al Circ 2002: 105; 2166-71
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• Markers of protection?Markers of protection?
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Adhesion moleculesE-selectin, ICAM-1, VCAM-1
Permeability
Apoptosis
Leukocyte chemoattractants(MCP-1, IL-8, PDGF, MC-SF)
Procoagulant activity(tissue factor)
Cytokines(TNF, FAS,CD40L etc.)
NOET-1
markers of inflammationmarkers of inflammation
TT
TT
TTIL-10IL-10
TTIL-10IL-10
IL-10IL-10
IL-10IL-10
TTIL-10IL-10
TThepatocytehepatocytegrowth factorgrowth factor
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Prognostic significance of Prognostic significance of HGF serum levels in ACSHGF serum levels in ACS
65432100
De
ath
, MI (
%)
20
10
6-month follow-up
P<0.0001 for the trend among the quartiles
> 6.8 µg/L4.7 – 6.8 µg/L
2.5 – 4.7 µg/L
< 2.5 µg/L
C. Heeschen et al.
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Proposed strategy for resolving Proposed strategy for resolving intermediate or uncertain riskintermediate or uncertain risk
Clinical syndrome of non-ST elevation ACSTroponin elevation,ST depression,or other high risk features
AngioYes +
AngioTIMI risk score > 4or GRACE risk of death > 4%? Elevated NT proBNP, hsCRP, PLGF, CD40L
no
Yes +
no
Perfusion scan or stress echoor other stress test Angio
Yes +
Non-invasive management
no
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JAMAJAMA 2000;284:831-32 2000;284:831-32
It’s never too late….It’s never too late….
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Miller et al Miller et al JAMAJAMA 2000;284:831-32 2000;284:831-32
““Horemkenesi was a foreman of Horemkenesi was a foreman of craftsmen excavating and decorating craftsmen excavating and decorating the tombs of the pharohs of the 20th the tombs of the pharohs of the 20th
dynasty (c 1050 BC) at Thebes…”dynasty (c 1050 BC) at Thebes…”
““He was also a priest of Amun, and his He was also a priest of Amun, and his responsibilities required frequent journeys of responsibilities required frequent journeys of several miles in the desert.”several miles in the desert.”
““Forensic study of his mummy indicates that at Forensic study of his mummy indicates that at about age 60 years he fell face downward in the about age 60 years he fell face downward in the sand and was heavily infested with carrion sand and was heavily infested with carrion beetles before mummification, suggesting beetles before mummification, suggesting sudden cardiac death.”sudden cardiac death.”
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Miller et al Miller et al JAMAJAMA 2000;284:831-32 2000;284:831-32
MethodsMethods dessicated tissues from Horemkenesi’s dessicated tissues from Horemkenesi’s
abdomen extracted for myofibrillar proteins abdomen extracted for myofibrillar proteins reconstituted with TnI-negative human reconstituted with TnI-negative human serasera
modern positive controls (spleens from modern positive controls (spleens from subjects who died of acute MI) and negative subjects who died of acute MI) and negative controls (tissues from subjects who died of controls (tissues from subjects who died of other causes) were mummified for 40 other causes) were mummified for 40 daysdayslevel of TnI measured level of TnI measured
MethodsMethods dessicated tissues from Horemkenesi’s dessicated tissues from Horemkenesi’s
abdomen extracted for myofibrillar proteins abdomen extracted for myofibrillar proteins reconstituted with TnI-negative human reconstituted with TnI-negative human serasera
modern positive controls (spleens from modern positive controls (spleens from subjects who died of acute MI) and negative subjects who died of acute MI) and negative controls (tissues from subjects who died of controls (tissues from subjects who died of other causes) were mummified for 40 other causes) were mummified for 40 daysdayslevel of TnI measured level of TnI measured
Evidence of MI With Cardiac Evidence of MI With Cardiac Troponin in Mummified TissueTroponin in Mummified Tissue
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Miller et al Miller et al JAMAJAMA 2000;284:831-32 2000;284:831-32
Evidence of MI With Cardiac Evidence of MI With Cardiac Troponin in Mummified Troponin in Mummified
TissueTissue
cTnI (ng/g)cTnI (ng/g)
HoremkenesiHoremkenesi
12.3-22.212.3-22.2
Modern MI Modern MI MummiesMummies
1.3-3.71.3-3.7
Modern Non-MI Modern Non-MI MummiesMummies
0.7-0.90.7-0.9
“…“…our data suggest that myocardial death can our data suggest that myocardial death can be diagnosed several thousand years after the be diagnosed several thousand years after the
event…”event…”
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It’s never It’s never too late to too late to diagnose diagnose
MI!MI!
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New Royal Infirmary and Research InstituteUniversity of Edinburgh
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New Royal Infirmary and Research InstituteUniversity of Edinburgh
Cardiovascular Research EdinburghCardiovascular Research EdinburghCVRU:CVRU: KAA Fox, DE Newby,RA Riemersma KAA Fox, DE Newby,RA Riemersma
Inflammation:Inflammation: I Dransfield, J Sarma I Dransfield, J Sarma
Molecular cardiology: Molecular cardiology: JR Seckl, BR WalkerJR Seckl, BR Walker
Endothelial Biology:Endothelial Biology: DJ Webb, S Maxwell, I Megson DJ Webb, S Maxwell, I Megson
Molecular Physiology:Molecular Physiology: JJ Mullins, A Bagnall JJ Mullins, A Bagnall
Cardiovascular Imaging:Cardiovascular Imaging: WN McDicken, P Hoskins WN McDicken, P Hoskins