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Acute Coronary Syndromes
Figure 1: Multimarker Strategy for Incremental Risk Stratification in Acute Coronary Syndromes
A
%
)
C
%
)
1 year ( 1 year (
Death Death
30 25
170
211
25
20
56
62
39
20 67
15
15
35
51
41
37
14
10
10
38
24
28 25
30
14
11
22
5
22
>1,869
5
11 17
>1,869
669–1,869 6 13 669–1,869
10
10
0
9
237–669
2
13
8
0
237–669
2≤51 >9.62 10
51–66 3.96–9.62≤237 ≥237
Creatine
66–84
>84
NT-proBNP CRP
1.84–3.96
NT-proBNP
≤1.84
clearance (ml/min) quartiles (ng/l) quartiles (mg/l) quartiles (ng/l)
B D
)
ar (
%
)
ar (
%
Death 1 ye Death 1 ye
25 30
168
153
25
20
92
52
79
20
15
50
15
15
44
42
38
10
34
35
38
24
10
24
5
13
17 27
16
18
>1,869
5 16
>1,869
17
3
19
669–1,869
8
16
669–1,869
0
3
10
237–669
0 6
8 237–669
>0.47
15
>79 9
0.12–0.47 68–79 ≥237≥237
CRP
0.01–0.12
0.01
NT-proBNP Heart rate
60–68
NT-proBNP
≤60≤
quartiles (mg/l) quartiles (ng/l) (beats/min) quartiles (ng/l)
Data from the Global Utilization of STrategies to Open occluded arteries (GUSTO)-IV Acute Coronary Syndrome (ACS) study showing mortality at one-year follow-up among strata of patients,
according to quartiles of N-terminal prohormone brain natriuretic peptide (NT-proBNP) and quartiles of creatinine clearance (A), troponin T (B), C-reactive protein (CRP) (C) and heart rate (D).
Source: James SK et al., 2003
46
with permission.
those with a negative troponin.
31
Data from community hospital B-type Natriuretic Peptide
settings suggest that mortality in troponin-positive subjects may be B-type natriuretic peptide (BNP) and its amino terminal fragment
closer to eight-fold higher than for those with negative troponin.
29
(NT-proBNP) are predominantly synthesised in the ventricular
There is an almost linear relationship between troponin level and myocardium and released into the circulation in response
risk of mortality or re-infarction, with stepwise increases in to myocardial stretch resulting from pressure or volume overload.
mortality rates observed for increasing levels of troponin.
28,30–32
Secretion of both peptides is increased during myocardial ischaemia
or infarction and circulating plasma levels reflect the extent of
Elevated troponin levels play an important role in guiding therapy in myocardial damage, correlating inversely with left ventricle (LV)
ACS. Treatment with low-molecular-weight heparin was associated ejection fraction.
39,42,43
Elevated BNP or NT-proBNP levels in ACS are
with lower rates of death, MI or need for urgent re-vascularisation among the most powerful markers of outcome in ACS and are
in troponin-positive but not in troponin-negative subjects.
33,34
associated with increased risk of mortality or heart-failure events
Benefit from glycoprotein (GP) IIb/IIIa inhibitors as an adjunct to independent of clinical risk factors, LV ejection fraction and troponin
either medical therapy or an invasive strategy for ACS is limited to level.
18,42–44
Elevation of NT-proBNP levels may also identify subjects
subjects with elevated troponin.
35–37
Findings from the Fast who will benefit from an early invasive strategy.
38
Revascularisation during Instability in Coronary artery disease
(FRISC) II and Treat Angina with aggrastat and determine Cost of High-sensitivity C-reactive Protein
Therapy with Invasive or Conservative Strategy – Thrombolysis In MI Inflammatory mechanisms play an important role in atherosclerosis
(TACTICS–TIMI) 18 trials demonstrated that the benefit of an early and may contribute to plaque disruption associated with ACS.
5
invasive strategy for ACS was seen in subjects with elevated C-reactive protein (CRP) is a non-specific acute-phase reactant;
troponin, but not in those with normal troponin.
38–41
whether it has a pathogenic role in ACS is unclear, but recent
76 EUROPEAN CARDIOLOGY
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