Heart fatty acid binding protein in comb

Available online at www.sciencedirect.com

Journal of Electrocardiology 44 (2011) 432 – 438
www.jecgonline.com

Heart fatty acid–binding protein in combination with the
80-lead body surface potential map improves early detection of acute
myocardial infarction in patients who are cardiac troponin T–negative
at presentation☆,☆☆
Michael J. Daly, MB, MRCP, a Conor J. McCann, MD, MRCP, a Colum G. Owens, MD, MRCP, a
Mark T. Harbinson, MD, FRCP, b Jennifer A. Adgey, MD, FRCP, FACC a,⁎
b

Abstract

a
The Heart Centre, Royal Victoria Hospital, Belfast, Northern Ireland, UK
Centre for Vision and Vascular Sciences, Queen's University, Belfast, Northern Ireland, UK
Received 1 December 2010

Of patients who present with ischemic-type chest pain and a negative cardiac troponin T (cTnT) at first

medical contact, there are patients at a very early stage of infarction. The aim of this research was to assess
heart fatty acid–binding protein (H-FABP), a novel marker of myocyte necrosis, in combination with the
80-lead body surface potential map (BSPM) in the early diagnosis of acute myocardial infarction (AMI).
Methods: In this prospective study, consecutive patients presenting with acute ischemic-type chest
pain between 2003 and 2006 were enrolled. At first medical contact, blood was sampled for cTnT
and H-FABP; in addition, a 12-lead electrocardiogram (ECG) and BSPM were recorded. A second
cTnT was sampled 12 hours or more after presentation. Peak cTnT 0.03 μg/L or higher diagnosed
AMI. Elevated H-FABP was 5 ng/mL or higher. A cardiologist blinded to both the clinical details
and 12-lead ECG interpreted the BSPM.
Results: Enrolled were 407 patients (age 62 ± 13 years; 70% men). Of these 407, 180 had cTnT less
than 0.03 μg/L at presentation. Acute myocardial infarction occurred in 52 (29%) of 180 patients. Of
these 180 patients, 27 had ST-segment elevation (STE) on ECG, 104 had STE on BSPM (sensitivity,
88%; specificity, 55%), and 95 (53%) had H-FABP elevation. The proportion with elevated H-FABP
was higher in the AMI group compared with non-AMI group (P b .001). Body surface potential map
STE was significantly associated with H-FABP elevation (P b .001). Of those with initial cTnT less
than 0.03 μg/L, the c-statistic for the receiver operating characteristic curve distinguishing AMI from
non-AMI using H-FABP alone was 0.644 (95% confidence interval [CI], 0.521-0.771), using BSPM
alone was 0.716 (95% CI, 0.638-0.793), and using the combination of BSPM and H-FABP was
0.812 (95% CI, 0.747-0.876; P b .001).
Conclusion: In patients with acute ischemic-type chest pain who have a normal cTnT at presentation,

the combination of H-FABP and BSPM at first assessment identifies those with early AMI (c-statistic,
0.812; P b .001), thus allowing earlier triage to reperfusion therapy and secondary prevention.
© 2011 Elsevier Inc. All rights reserved.

☆

Financial support: Dr. Michael J. Daly is supported by The Heart
Trust Fund (Royal Victoria Hospital), 9B Castle Street, Comber,
Newtownards Northern Ireland BT23 5DY.
☆☆
Relationship with Industry/Conflict of Interest: None.
⁎ Corresponding author. The Heart Centre, Royal Victoria Hospital,
Grosvenor Road, Belfast, Northern Ireland BT12 6BA, UK.
E-mail address: jennifer.adgey@belfasttrust.hscni.net
0022-0736/$ – see front matter © 2011 Elsevier Inc. All rights reserved.
doi:10.1016/j.jelectrocard.2011.03.001

Introduction
In patients presenting with ischemic-type chest pain, early
diagnosis of acute myocardial infarction (AMI) ensures prompt

triage to urgent revascularization. Current guidelines require a
positive serum level of cardiac troponin for AMI diagnosis.1
However, because of its large molecular size, cardiac troponin

M.J. Daly et al. / Journal of Electrocardiology 44 (2011) 432–438

T (cTnT) does not peak until 6 to 12 hours after symptom
onset.2 In addition, the 12-lead electrocardiogram (ECG) has
only 50% sensitivity for AMI diagnosis.3,4 However, body
surface potential mapping (BSPM) using 80-lead ECG has
been shown to be more sensitive for detection of ST-segment
elevation myocardial infarction (STEMI) than 12-lead ECG
(67%-76% vs 45%-60%, respectively),5,6 particularly in the
high right anterior, posterior, and right ventricular territories.5,7
Heart-type fatty acid–binding protein (H-FABP), a small
cytoplasmic molecule, has been suggested as an early
biomarker for evolving AMI, as it has high diagnostic
sensitivity in the first few hours after symptom onset.8
Several studies in various clinical settings have reported
favorable diagnostic results.9-14 In addition, H-FABP has

been shown to predict long-term mortality in patients with
acute coronary syndrome15 and identifies those troponinnegative patients who are at high risk for death.15-18
Thus, we hypothesized that the combination of H-FABP
and BSPM assessment at presentation would improve the
early diagnosis of AMI in patients with ischemic-type chest
pain who are cTnT negative.

433

2. Twelve-lead ECG and BSPM at first medical contact
(BSPM recorded within 15 minutes of 12-lead ECG)
3. Blood sampled for H-FABP (Hycult Biotech, Uden,
The Netherlands) and creatinine (estimated glomerular
filtration rate) at first medical contact
4. Blood sampled for cTnT (Roche Diagnostics,
Rotkreuz, Switzerland) initially and at 12 hours or
more post symptom onset
Patients were excluded from analysis if they had been
transferred from another ward or hospital for tertiary care (n =
118); had improper timing or collection of initial blood sample

(n = 20); had received fibrinolytic therapy or anticoagulant
before the 12-lead ECG, BSPM, or initial blood sample (n =
59); had ECG confounders, that is, left bundle-branch block
(n = 14), right bundle-branch block (n = 6), left ventricular
hypertrophy (n = 9), digitalis therapy (n = 2), or ventricular
pacing (n = 7); or had greater than 15 minutes between
recording of initial 12-lead ECG and BSPM (n = 22) (Fig. 1).
Demographic data and established risk factors for
coronary artery disease were also collected.

Methods

Twelve-lead ECG analysis

Study population

A 12-lead ECG was recorded at first medical contact (25
mm/s and 10 mm/mV). ST-segment alteration was measured
at the J point for ST-segment elevation (STE) and 80
milliseconds after the J point for ST-segment depression

(STD) using the preceding TP segment as a baseline19 by 2
cardiologists who were blinded to all other clinical data. STsegment elevation myocardial infarction was defined using
the Minnesota criteria 9-220 as greater than or equal to 0.1

Over a 3-year period (2003-2006), we recruited prospectively all patients (n = 664) admitted to the coronary care unit
who fulfilled the following criteria:
1. Typical ischemic-type chest discomfort occurring at rest
and of greater than or equal to 20 minutes of duration

Fig. 1. Overview of methodology to obtain study population.

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M.J. Daly et al. / Journal of Electrocardiology 44 (2011) 432–438

mV STE in 1 or more of leads I, II, III, aVL, aVF, V5, V6 or
greater than or equal to 0.2 mV STE in 1 or more of leads V1
to V4. ST-segment depression (STD) was defined as greater
than or equal to 0.05 mV in any lead, and T wave inversion
(TWI) was greater than or equal to 0.1 mV but was not

assessed in leads III or V1.
BSPM analysis
The BSPM was recorded with a flexible plastic anterior and
posterior electrode harness and a portable recording unit
(Heartscape Technologies, Inc, Bangor, N. Ireland). The
anterior harness contains 64 electrodes, including 3 proximal
bipolar limb leads (Mason-Likar position) and a posterior
harness with 16 electrodes. This lead configuration enables the
recording of 77 unipolar ECG signals with respect to the Wilson
central terminal. During the interpretation process, the electrodes are defined to represent anterior, lateral, inferior, high right
anterior, right ventricular, and posterior epicardial regions.5,6
Harness application takes 3 to 4 minutes.7 Body surface
potential mapping was recorded over 5 to 10 seconds at a
sampling rate of 1 kHz and a bandwidth of 0.05 to 100 Hz7
and transferred into digital format for core laboratory
analysis. The 80-lead BSPMs were uploaded and displayed
on an IBM compatible computer running PRIME analysis
software (Heartscape Technologies, Inc., Bangor, N.

Ireland).5 All 80 leads were manually checked; and those

of unacceptable quality, that is, where noise or movement
artifact disallowed recognition of QRST variables, were
marked and substituted using linear grid interpolation. Any
BSPM with greater than 6 leads requiring interpolation were
disregarded, and these patients were excluded from
analysis.6 Printouts were obtained from the processed
BSPM of the 80-lead ECG and a color-contour map
displaying the amount of STE at the J point (ST0 isopotential
map) (Fig. 2). The result of the PRIME diagnostic algorithm
was noted. Using the 80-lead BSPM and color-contour map,
a single cardiologist familiar with BSPM interpretation and
blinded to the clinical details, 12-lead ECG, and PRIME
diagnostic algorithm result coded the BSPM as AMI or nonAMI. The STE measured from the ST0 point was defined by
the following thresholds: anterior greater than or equal to 0.2
mV elevation, lateral/inferior/high right anterior/right ventricular greater than or equal to 0.1 mV elevation, and
posterior greater than or equal to 0.05 mV elevation.6
Diagnosis
Acute myocardial infarction diagnosis was made when
peak cTnT was 0.03 μg/L or higher. Heart-type fatty
acid–binding protein elevation was defined as 5 ng/mL or

higher.21,22

Fig. 2. Patient with cTnT less than 0.03 μg/L at presentation, anterior TWI on 12-lead ECG, and H-FABP elevation. Body surface potential mapping performed
within 15 minutes of 12-lead ECG shows inferior territory STE. Peak cTnT of 2.24 μg/L confirms AMI diagnosis.

M.J. Daly et al. / Journal of Electrocardiology 44 (2011) 432–438

Statistical analysis
Data are presented as mean ± SD. Group comparisons were
tested using the unpaired t test and χ2 test. Sensitivity and
specificity of the various diagnostic methods were calculated
by comparing the prediction of AMI against peak cTnT 0.03
μg/L or higher. Overall, performance of the various diagnostic
methods by receiver operating characteristic curve analysis
was assessed, with area under the curve (c-statistic) greater
than 0.75 taken as a good performance. Statistical analysis was
performed using SPSS version 17.0 for Windows (SPSS Inc,
Chicago, IL). P b .05 was taken as statistically significant. The
Northern Ireland Research Ethics Committee granted ethical
approval for this research before commencement. All patients

gave informed consent at the time of enrollment.

Results
Baseline characteristics
Four hundred seven patients with ischemic-type chest
pain at rest (70% men; mean ± SD age, 62 ± 13 years) were
included in this study. Of these, 180 (44%) had initial cTnT
less than 0.03 μg/L. Demographic characteristics are
summarized in Table 1. Hyperlipidemia (P b .001), cigarette
smoking (P b .05), and family history of ischemic heart
disease (P b .05) differed significantly between groups, that
is, were more prevalent in those with initial cTnT less than
0.03 μg/L compared with those with initial cTnT 0.03 μg/L
or higher. Furthermore, history of angina (P b .05), AMI, or
percutaneous coronary intervention (PCI) (P b .001) was
Table 1
Baseline demographic characteristics
All patients Initial cTnT Initial cTnT P
(n = 407), b0.03 μg/L ≥0.03 μg/L
n (%)

(n = 180), (n = 227),
n (%)
n (%)
Age (y)
Male sex
Time from symptom onset
to first medical contact
(min) (median [IQR])
Risk factors
Hyperlipidemia
Cigarette smoking
Hypertension
Family history IHD
Diabetes mellitus
eGFR b30 mL/h
Cardiac history
Previous angina
Previous AMI
Previous PCI
Previous CABG
Any (angina/AMI/
PCI/CABG)
AMI
Peak cTnT (≥0.03 μg/L)

62 ± 13
60 ± 13
285 (70)
140 (78)
74 (45, 94) 75 (44, 96)

62 ± 12
NS
145 (64)
.063
70 (40, 102) NS

322 (79)
278 (68)
232 (57)
230 (57)
77 (19)
18 (4)

163 (91)
141 (78)
108 (60)
128 (71)
26 (14)
5 (3)

159 (70)
137 (60)
124 (55)
102 (45)
51 (22)
13 (6)

b.001
b.05
NS
b.05
NS
NS

199 (49)
160 (39)
106 (26)
49 (12)
232 (57)

99 (55)
90 (50)
65 (36)
27 (15)
121 (67)

100 (44)
70 (31)
41 (18)
22 (10)
111 (49)

.048
b.001
b.001
NS
b.001

279 (69)

52 (29)

227 (100)

–

Results expressed as n (%), mean ± SD, and median (interquartile range). NS
indicates nonsignificant; IQR, interquartile range; IHD, ischemic heart
disease; eGFR, estimated glomerular filtration rate; CABG, coronary artery
bypass grafting.

435

more frequently encountered in those with initial cTnT less
than 0.03 μg/L.
AMI diagnosis
Of those with initial cTnT less than 0.03 μg/L, 52 (29%) of
180 patients had AMI diagnosis, that is, peak cTnT 0.03 μg/L
or higher at greater than or equal to 12 hours postsymptoms.
Univariate analysis of the various diagnostic methods studied
is summarized in Table 2. Using the 12-lead ECG, STEMI
using Minnesota 9-2 criteria occurred in 27 patients and had a
sensitivity of 38%, specificity of 95%, positive predictive
value of 74%, and negative predictive value of 79% for AMI
diagnosis. ST-segment depression in 2 or more contiguous
leads occurred in 54 patients and had a sensitivity of 58%,
specificity of 81%, positive predictive value of 56%, and
negative predictive value of 83%. T wave inversion in 2 or
more contiguous leads occurred in 28 patients and had a
sensitivity of 27%, specificity of 89%, positive predictive
value of 50%, and negative predictive value of 75%; and the
combination of both STD and TWI in 2 or more contiguous
leads had a sensitivity of 33%, specificity of 98%, positive
predictive value of 85%, and negative predictive value of
78% for AMI diagnosis. In addition, STEMI (Minnesota 9-2
criteria) with STD greater than or equal to 0.05 mV and TWI
greater than or equal to 0.1 mV in 2 or more contiguous leads
occurred in 18 patients and had a sensitivity of 29%,
specificity of 98%, positive predictive value of 83%, and
negative predictive value of 77% for AMI diagnosis.
Using BSPM, STE was detected in 100 patients using the
PRIME diagnostic algorithm, having a sensitivity of 85%,
specificity of 56%, positive predictive value of 44%, and
negative predictive value of 90% for AMI diagnosis. On
physician's analysis of BSPM, STE was detected in 104
patients, resulting in a sensitivity of 88%, specificity of 55%,
positive predictive value of 44%, and negative predictive
value of 92% for AMI diagnosis.
Heart-type fatty acid–binding protein elevation occurred in
95 patients. In those with AMI, a significant proportion had
H-FABP elevation (81%; P b .001), that is, sensitivity of 81%,
specificity of 59%, positive predictive value of 44%, and
negative predictive value of 88% for the diagnosis. Furthermore, H-FABP elevation was significantly associated with the
detection of STE on BSPM (P b .001). In this study, 15 (14%)
of 109 of those with no Minnesota STE, STD, or TWI on initial
12-lead ECG had AMI. Of these 15 patients, all had either
BSPM STE or H-FABP elevation, with 12 (80%) having both.
Receiver operating characteristic curve analysis
Receiver operating characteristic curves were constructed
to assess the ability of H-FABP elevation, BSPM STE, and
various 12-lead ECG abnormalities to predict AMI in those
with initial cTnT less than 0.03 μg/L (Fig. 3). Heart-type fatty
acid–binding protein elevation had c-statistic 0.644 (95%
confidence interval [CI], 0.521-0.771; P = .045) for AMI
diagnosis. Using BSPM, the c-statistic for AMI diagnosis
using only physician's diagnosis of STE on BSPM was 0.716
(95% CI, 0.638-0.793; P = .034); and using only PRIME
algorithm, diagnosis of STE was 0.708 (95% CI, 0.628-0.784;

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M.J. Daly et al. / Journal of Electrocardiology 44 (2011) 432–438

Table 2
Univariate analysis of initial 12-lead ECG, BSPM, and H-FABP in the 180 patients with initial cTnT less than 0.03 μg/L
Patients with cTnT b0.03 μg/L
With and without AMI
(n = 180; 52 with AMI, 128 without AMI)
n (%)
12-lead ECG
STEMI (Minnesota 9-2 criteria)
STD ≥0.05 mV in ≥2 CL
TWI ≥0.1 mV in ≥2 CL
STEMI (Minnesota 9-2 criteria) and
STD ≥0.05 mV in ≥2 CL
STD ≥0.05 mV and TWI ≥0.1 mV in ≥2CL
STEMI (Minnesota 9-2 criteria) and
STD ≥0.05 mV and TWI ≥0.1 mV in ≥2 CL
BSPM STE
PRIME diagnostic algorithm
Physician's interpretation
H-FABP elevation (≥5 ng/mL)
H-FABP elevation (≥5 ng/mL) and
STEMI (Minnesota 9-2 criteria)
STD ≥0.05 mV in ≥2 CL
TWI ≥0.1 mV in ≥2 CL
STEMI (Minnesota 9-2 criteria) and
STD ≥0.05 mV in ≥2 CL
STD ≥0.05 mV and TWI ≥0.1 mV in ≥2 CL
STEMI (Minnesota 9-2 criteria) and STD ≥0.05 mV
and TWI ≥0.1 mV in ≥2 CL
BSPM STE using PRIME diagnostic algorithm
BSPM STE using physician's interpretation

With AMI
(n = 52)

c-Statistic

Sensitivity

Specificity

PPV

NPV

n

(15)
(30)
(16)
(11)

38%
58%
27%
35%

95%
81%
89%
98%

74%
56%
50%
90%

79%
83%
75%
79%

20
30
14
18

0.540
0.582
0.518
0.542

20 (11)
18 (10)

33%
29%

98%
98%

85%
83%

78%
77%

17
15

0.534
0.529

100 (56)
104 (58)
95 (53)

85%
88%
81%

56%
55%
59%

44%
44%
44%

90%
92%
88%

44
46
42

0.708
0.716
0.644

35%
46%
15%
29%

97%
77%
86%
97%

82%
44%
31%
79%

78%
78%
71%
77%

18
24
8
15

0.538
0.578
0.480
0.522

13 (7)
17 (9)

12%
27%

95%
98%

46%
82%

72%
77%

6
14

0.488
0.521

89 (49)
88 (49)

73%
77%

60%
63%

43%
45%

85%
87%

38
40

0.807
0.812

27
54
28
20

22
54
26
19

(12)
(30)
(14)
(11)

CL indicates contiguous leads; NPV, negative predictive value; PPV, positive predictive value.

P = .037). Using the 12-lead ECG, STEMI defined by
Minnesota 9-2 criteria had c-statistic of 0.540 (95% CI, 0.4600.611; P = .088); STD in 2 or more contiguous leads, 0.582
(95% CI, 0.510-0.651; P = .073); TWI in 2 or more contiguous
leads, 0.518 (95% CI, 0.447-0.592; P = .096); and the

combination of both STD and TWI in 2 or more contiguous
leads, 0.534 (95% CI, 0.468-0.606; P = .090).
The combination of H-FABP elevation and all 12-lead
ECG abnormalities and BSPM criteria in AMI diagnosis is
summarized in Table 2. The physician's diagnosis of STE on

Fig. 3. Receiver operating characteristics for diagnostic modalities listed in Table 2.

M.J. Daly et al. / Journal of Electrocardiology 44 (2011) 432–438

BSPM in combination with H-FABP elevation has c-statistic
0.812 (95% CI, 0.747-0.876), which is significantly better
than that obtained through combination of H-FABP and any
12-lead ECG criteria for AMI diagnosis in those with initial
cTnT less than 0.03 μg/L (P b .001). Importantly, there is a
trend toward a significant difference between the c-statistic
for H-FABP alone and BSPM alone (P = .053) and a highly
significant difference between the c-statistic for the combinations of BSPM STE and H-FABP elevation and both HFABP alone (P b .001) and BSPM STE alone (P b .001).

Discussion
The major findings of this study on the early diagnosis of
AMI in patients with chest pain, who have cTnT less than
0.03 μg/L at presentation, using H-FABP and BSPM at first
medical contact can be summarized as follows: (1) H-FABP
greater than or equal to 5 ng/mL has a sensitivity of 81% and
specificity of 59% for AMI diagnosis (c-statistic, 0.644); (2)
STE occurred in 58% patients using BSPM, compared with
15% patients using the 12-lead ECG, resulting in sensitivity
of 88% and specificity of 55% for AMI diagnosis (c-statistic,
0.716); and (3) the combination of H-FABP elevation and
BSPM STE improved AMI diagnosis (c-statistic, 0.812).
The appropriate triage of patients with suspected AMI
depends on the availability of results from sensitive diagnostic
tests. The 12-lead ECG is the cornerstone in the initial
evaluation of patients with chest pain and is especially crucial
in the diagnosis of STEMI. In patients with STE on initial 12lead ECG, the diagnosis of AMI is easily and rapidly
established. However, 40% or more of patients with a final
diagnosis of AMI have a nondiagnostic 12-lead ECG on
admission23; and therefore, the initial 12-lead ECG has poor
sensitivity for AMI diagnosis when STE is not present.20,24-27
It is also severely limited in its detection of right-sided, high
right anterior, lateral, and posterior myocardial infarctions.24
Furthermore, in 60% to 70% of patients admitted to hospital
with chest pain, the suspicion of AMI will ultimately be
dismissed because of lack of diagnostic ECG changes and
negative biochemical tests.23 As a consequence, patients with
STEMI that are not identified on the initial 12-lead ECG have
been shown to have a poor prognosis,28 in part, because of
delayed invasive strategies.24
In an effort to improve AMI diagnosis at presentation,
McCann et al12 have shown initial H-FABP in unselected
patients with ischemic-type chest pain to have c-statistic of
0.740 (P b .001) for AMI diagnosis, improving to 0.770 (P b
.001) when restricted to those admitted less than 4 hours
from symptom onset. In addition, Haltern et al29 have shown
H-FABP greater than 7.3 ng/mL to have a sensitivity of 71%
and specificity of 65% for AMI diagnosis (c-statistic, 0.710),
with improved sensitivity in 49 consecutive patients
admitted less than 4 hours from onset of ischemic-type
chest pain (sensitivity, 86%; c-statistic, 0.760). In our study
of unselected patients with ischemic-type chest pain who
have cTnT less than 0.03 μg/L at presentation, H-FABP
greater than or equal to 5 ng/mL had sensitivity of 81%,
specificity of 59%, positive predictive value of 44%,

437

negative predictive value of 88%, and c-statistic of 0.644
(P = .045) for AMI diagnosis (Table 2 and Fig. 3). In
assessing the prognostic role of H-FABP, Viswanathan
et al18 have shown an initial titer greater than 6.48 μg/L to
have clear prognostic value in those with cTnI less than 0.05
μg/L at presentation, that is, adjusted hazard ratio 3.12 (P =
.03) for death or myocardial infarction at 1 year.
High-sensitivity cardiac troponin assays are now currently
available, which detect cardiac troponin in excess of the 99th
percentile, assuring impressive sensitivity and specificity for
AMI.30,31 A recent comparison of highly sensitive cTnT
(TnThs) and H-FABP in the early identification of AMI in
patients with acute coronary syndrome conducted by Kurz
et al30 found no significant difference in the diagnostic
ability of either biomarker at presentation, that is, c-statistic
0.817 vs 0.808, respectively (P = .991). In contrast to our
study, all patients in the study of Kurz et al30 with baseline
ECG STEMI (n = 263) were excluded. Kurz et al conclude
that TnThs has a performance comparable with that of
H-FABP at presentation. Ilva et al31 studied 293 patients
with acute chest pain, 187 (63.8%) of whom had an
initial TnIhs less than 0.03 μg/L. Although the
diagnostic performance of TnIhs was again comparable
with H-FABP, death or recurrent AMI at 6 months
occurred in 21.4% of those with initial TnIhs less than
0.03 μg/L and H-FABP greater than 10.4 μg/L, in
comparison with only 6.9% of those with normal levels
of both biomarkers at presentation.30
Regarding early ECG diagnosis of AMI, Owens et al5
have shown BSPM to have a sensitivity of 76%, specificity of
92%, and c-statistic of 0.84 for AMI diagnosis in consecutive
patients presenting with acute ischemic-type chest pain at rest
(n = 755). Furthermore, the improvement in sensitivity over
the 12-lead ECG (sensitivity, 68%) was shown to be mainly
due to detection of STE in the high right anterior, posterior,
and right ventricular territories in this study.5 In the Optimal
Cardiovascular Diagnostic Evaluation Enabling Faster Treatment of Myocardial Infarction (OCCULT-MI) trial, BSPM
was shown once again to provide an incremental 27.5%
increase in STEMI detection vs the 12-lead ECG.24 In our
study of 52 patients with AMI and cTnT less than 0.03 μg/L
initially, 20 (38%) of 52 had STEMI on 12-lead ECG; and 46
(88%) of 52 patients had STE on BSPM (Table 2). This
improvement in STE detection is due to STE occurring in
leads beyond the territory of the 12-lead ECG. However, the
recording of the BSPM 15 minutes or less after the 12-lead
ECG in our patients potentially favored the BSPM as a
diagnostic modality. In addition, 12-lead ECG diagnosis of
AMI in those with factors confounding the interpretation of
the ST-segment, for example, left bundle-branch block, right
bundle-branch block, left ventricular hypertrophy, and
digitalis therapy, remains a challenge. As these patients
were excluded from analysis in our study, we cannot indicate
whether H-FABP would improve AMI diagnosis in them.
In the OCCULT-MI trial, STE on BSPM was associated
with increased risk of death or myocardial infarction at 30
days (odds ratio, 3.4) in those without initial 12-lead ECG
STEMI.24 In addition, H-FABP elevation is independently
established as a poor prognostic indicator.18 In our study,

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H-FABP elevation was significantly associated with STE on
BSPM, that is, of those with H-FABP elevation, 88 (93%) of
95 patients had STE on BSPM beyond the territory of the 12lead ECG (P b .001). Furthermore, in those patients with
AMI and the absence of Minnesota STE, STD, or TWI on
initial 12-lead ECG, 80% had both BSPM STE and H-FABP
elevation. As such, early BSPM and H-FABP assessment can
identify patients with AMI who might otherwise have
delayed diagnosis or be discharged from the emergency
department. In addition, as shown in the OCCULT-MI trial,
patients with STEMI identified on BSPM only are treated
with significantly delayed or conservative invasive strategies;
yet they have angiographic and clinical adverse outcomes
similar to those of patients with 12-lead ECG STEMI.24

Conclusion
In this study, the combination of H-FABP and BSPM
STE improves early diagnosis of AMI in those with chest
pain who are cTnT negative at presentation. Both BSPM
STE in patients without 12-lead ECG STEMI24 and H-FABP
elevation18 have independently been shown to be poor
prognostic indicators for death or recurrent myocardial
infarction. In this study, early BSPM and H-FABP
assessment in those with ischemic-type chest pain who are
cTnT negative have the potential to identify an important
group of high-risk patients at an earlier time point, facilitate
more timely revascularization, and reduce mortality.
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