The ECG in acute coronary syndromes: new tricks from an

Document technical information

Format pdf
Size 119.7 kB
First found May 22, 2018

Document content analysis

Category Also themed
not defined
no text concepts found





Downloaded from on May 5, 2017 - Published by
The ECG in acute coronary syndromes: new tricks from an
old dog
H S Gurm, E J Topol
Heart 2005;91:851–853. doi: 10.1136/hrt.2004.047258
The ECG remains the pre-eminent test for myocardial
ischaemia, directing therapeutic management and
prognostic stratification.
cute coronary syndrome (ACS) is a broad,
clinically defined, ‘‘umbrella’’ term that
encompasses patients presenting with
ischaemic discomfort who have evidence of
myonecrosis or are felt to be at high risk of
myonecrosis in the immediate future. The ECG
changes associated with myocardial infarction
were recognised as early as 1917 and allowed for
the first time the ante-mortem recognition of
coronary occlusion. The dynamic ST changes
associated with angina were recognised nearly a
decade later and since then the ECG has become
an integral part of the work up of a patient with
chest pain.1 Now patients with ACS are, for the
most part, dichotomised by whether significant
ST elevation is present or not. On the basis of
serial enzymatic measurements, patients without
ST elevation can subsequently be categorised to
have unstable angina or non-ST elevation myocardial infarction (NSTEMI). In this article we
will attempt to review recent advances that
expand on the role of ECG in ACS.
See end of article for
authors’ affiliations
Correspondence to:
Eric J Topol,
MD, Department of
Cardiovascular Medicine,
Cleveland Clinic
Foundation, Cleveland,
OH 44195 USA; [email protected]
ST elevation myocardial infarction (STEMI), also
known as ‘‘current of injury’’, is defined by the
occurrence of new or presumed new ST elevation
in two or more contiguous leads that is > 0.2 mV
in leads V1, V2, and V3 and . 0.1 mV in other
leads or the occurrence of new onset left bundle
branch block.2 These patients usually have
ongoing occlusion of an epicardial coronary
artery and require consideration for immediate
reperfusion therapy.
An ECG not only helps in establishing the
diagnosis of STEMI but also provides valuable
information on infarct location, success or failure
of reperfusion, as well as prognosis.3 Arterial
occlusion at particular anatomical sites is associated with specific ECG patterns and imparts
correspondingly varying degrees of short or long
term mortality hazard.4 The majority of patients
with ST elevation MI have ST depression in
reciprocal leads. This finding appears to be
associated with an increased hazard of adverse
long term outcome, at least in some series.5 6
While the utility of ECG in screening for
epicardial coronary arterial occlusion has been
long recognised, the ECG provides accretive
information on the integrity of the microcirculation, the significance of which has been only
recently recognised.
Impaired myocardial microperfusion has been
shown to be a major predictor of adverse
outcome in patients undergoing reperfusion
therapy.7 Complete resolution of ST changes
has emerged as a simple yet robust marker of
microvascular perfusion with the degree of ST
resolution being strongly correlated with myocardial blush grade on angiography.8 Numerous
groups have demonstrated a poor short and long
term outcome in patients that have persistent ST
elevation despite successful restoration of TIMI
(thrombolysis in myocardial infarction) grade 3
flow in the infarct related artery by mechanical
or pharmacological means.9–14 Cura and colleagues recently reported the results of RESTART
(resolution of ST segment after reperfusion
therapy), a substudy of the GUSTO (global use
of strategies to open occluded coronary arteries)
V trial.15 In this prospective study of 1764
patients randomised to full dose reteplase or
half dose reteplase and abciximab, patients with
. 70% ST resolution at 60 minutes had a 30 day
mortality of 2.1%, those with partial resolution
(30–70%) 5.2%, those with no ST resolution
5.5%, while those with worsening ST elevation
had a mortality of 8.1%. Persistent ST segment
elevation may be a more sensitive marker of
impaired microcirculation with at least one study
demonstrating worst outcome in those with both
poor myocardial blush and persistent ST elevation, the best outcome in those with resolution of
both, and an intermediate outcome in those with
normal blush but persistent ST elevation.16
Furthermore, compared with myocardial blush,
normalisation of ST segment is a better predictor
of early recovery of left ventricular function.
Indeed, in a small study, failure to resolve ST
segment was closely related to defects on
myocardial contrast echocardiography.10 The
demographic factors that predispose to persistent
Abbreviations: ACS, acute coronary syndromes; CABG,
coronary artery bypass graft surgery; FRISC-II, fast
revascularization during instability in coronary artery
disease; GUSTO, global use of strategies to open
occluded coronary arteries; NSTEMI, non-ST elevation
myocardial infarction; PARAGON-B, platelet IIb/IIIa
antagonism for the reduction of acute coronary syndrome
events in a global organization network; PCI,
percutaneous coronary intervention; RESTART, resolution
of ST segment after reperfusion therapy; RITA 3,
randomized intervention trial of unstable angina; STEMI,
ST elevation myocardial infarction; TACTICS-TIMI-18,
treat angina with Aggrastat and determine cost of therapy
with an invasive or conservative strategy; TIMI,
thrombolysis in myocardial infarction
Downloaded from on May 5, 2017 - Published by
ST segment elevation remain somewhat ambiguous, but
include older age and low systolic blood pressure at
presentation,17 anterior myocardial infarction,15 as well as
prolonged time to reperfusion.18 Given its universal availability, simplicity and proven superiority to angiographic
measures, the ECG continues to be the platinum standard for
assessing adequacy of myocardial reperfusion in STEMI.
The ECG at presentation in NSTEMI ACS not only helps
differentiate it from STEMI but the nature of ST changes
itself provides key diagnostic and prognostic clues. Savonitto
and colleagues divided 12 142 patients with ACS enrolled in
GUSTO-IIb trial into those with T wave inversion (22%), ST
elevation (28%), ST depression (35%), and a combination of
ST elevation and depression (15%).19 Patients with T wave
inversion were most likely to have angiographically normal
coronary arteries (19%) while those with ST depression were
more likely to have three vessel disease (36%). One month
mortality showed a gradient with the lowest incidence in
those with only T wave changes (1.7%), intermediate in those
with ST elevation (5.1%) or only depression (5.1%), and
worst in those with both elevation and depression (6.6%).
Further similar trends in six month mortality were observed
with the mortality rate being 3.4% in those with T wave
changes, 6.8% in those with ST elevation, 8.9% in those with
ST depression, and 9.1% in those with both ST depression
and elevation. These mortality associations remained significant after adjusting for elevated creatine kinase (CK) MB
and for other variables that were predictors of 30 day
mortality. Similarly, Kaul and colleagues demonstrated the
severity of ST depression (. 2 mm in two contiguous leads)
to be associated with an almost 6–10 fold hazard of one year
While these early studies established a role for using the
ECG in risk stratification in NSTEMI ACS, the parallel
development and validation of troponin as a marker of
myonecrosis and prognosis required retesting this hypothesis
in a more contemporary setting. Kaul and colleagues
evaluated the six month outcome among 959 patients
enrolled in the troponin T substudy of the PARAGON-B
(platelet IIb/IIIa antagonism for the reduction of acute
coronary syndrome events in a global organization network)
trial and demonstrated the complementary value of troponin
status and quantitative ST depression.21
The next paradigm shift in management of NSTEMI ACS
was the validation of an early invasive strategy on a
background of potent antiplatelet treatment. It was soon
recognised that the presenting ECG continued to provide
additional prognostic information. Retrospective data from
the FRISC-II (fast revascularization during instability in
coronary artery disease) trial demonstrated that the benefit of
early revascularisation was proportional to the degree of ST
deviation with an almost halving of the risk of death and
myocardial infarction among those with the most extensive
ST changes. This association appeared independent of age,
sex, or troponin status.22 In another analysis from the same
study the benefit of early revascularisation was most
pronounced in those with both ST depression and troponin
elevation, intermediate in those with only one of the two
factors, and uncertain in those with neither.23 The discrepant
outcome between T wave inversion and ST depression was
confirmed even in a cohort treated with early invasive
therapy. In a Swiss study of 1450 patients, the in-house
mortality was 4% with ST depression, 2% with no ECG
changes, and 0.2% in those with T wave inversions. Similar
trends were seen in long term mortality.24 However, the other
two pivotal trials of early invasive therapy in ACS, TACTICSTIMI-1825 (treat angina with Aggrastat and determine cost of
therapy with an invasive or conservative strategy) and
RITA 326 (randomized intervention trial of unstable angina)
failed to demonstrate any difference in the effectiveness of
early invasive strategy across different categories of ECG
In the current issue of Heart, Kaul and colleagues27 report
their findings from over 11 000 patients enrolled in GUSTOIIb and PARAGON A and B trials. They found that
revascularisation (although not randomised) was associated
with an increased survival benefit only in patients with ST
depression > 1 mm. Their findings are concordant with
those from FRISC-II, but given the divergent findings from
TACTICS-TIMI-18 and RITA-3, it will be premature to limit
early invasive treatment to patients with ST depression only.
Further, they note a difference in percutaneous coronary
intervention (PCI) and coronary artery bypass graft surgery
(CABG) use across the ST continuum, with a fall in PCI rate
and a rise in CABG rates with worsening ST depression. This
is likely a reflection of the increased incidence of three vessel
disease and left main artery disease in patients with greater
ST depression. The international differences in clinical
practice noted by the authors are in line with previously
reported variation in cardiovascular practice, with the more
aggressive approach in USA being validated by the recent
clinical trials. However, these differences predate the validation of an invasive strategy and hence it would be more
relevant to study current international practice patterns to
assess if there has been a commensurate change in use of
invasive strategy globally.
Despite these limitations, the authors are to be commended for continuing the focus on the tool that has had
immeasurable impact on the field of cardiology. The ECG was
the first clinical tool that allowed assessment of myocardial
ischaemia and despite multiple paradigm shifts in the
management of ACS, it continues to be the pre-eminent test
directing therapeutic management and prognostic stratification.
Authors’ affiliations
H S Gurm, E J Topol, The Department of Cardiovascular Medicine, The
Cleveland Clinic Foundation, Cleveland, Ohio, USA
We have no relevant competing interests to disclose with regard to this
1 Fye WB. A history of the origin, evolution, and impact of electrocardiography.
Am J Cardiol 1994;73:937–49.
2 Alpert JS, Thygesen K, Antman E, et al. Myocardial infarction redefined—a
consensus document of the joint European Society of Cardiology/American
College of Cardiology committee for the redefinition of myocardial infarction.
J Am Coll Cardiol 2000;36:959–69.
3 Zimetbaum PJ, Josephson ME. Use of the electrocardiogram in acute
myocardial infarction. N Engl J Med 2003;348:933–40.
4 Topol E, Van de Werf F. Acute myocardial infarction; early diagnosis and
management. In: Topol E, eds. Textbook of cardiovascular medicine, 2nd ed.
Philadelphia: Lippincott Williams and Wilkins, 2002:385–419.
5 Krone RJ, Greenberg H, Dwyer EM Jr, et al. Long-term prognostic significance
of ST segment depression during acute myocardial infarction. The multicenter
diltiazem postinfarction trial research group. J Am Coll Cardiol
6 Birnbaum Y, Herz I, Sclarovsky S, et al. Prognostic significance of precordial
ST segment depression on admission electrocardiogram in patients with
inferior wall myocardial infarction. J Am Coll Cardiol 1996;28:313–8.
7 Ito H, Maruyama A, Iwakura K, et al. Clinical implications of the ‘no
reflow’ phenomenon. A predictor of complications and left ventricular
remodeling in reperfused anterior wall myocardial infarction. Circulation
8 van’t Hof AW, Liem A, Suryapranata H, et al. Angiographic assessment of
myocardial reperfusion in patients treated with primary angioplasty for acute
myocardial infarction: myocardial blush grade. Zwolle myocardial infarction
study group. Circulation 1998;97:2302–6.
9 van’t Hof AW, Liem A, de Boer MJ, et al. Clinical value of 12-lead
electrocardiogram after successful reperfusion therapy for acute myocardial
infarction. Zwolle myocardial infarction study group. Lancet
Downloaded from on May 5, 2017 - Published by
10 Lepper W, Sieswerda GT, Vanoverschelde JL, et al. Predictive value of
markers of myocardial reperfusion in acute myocardial infarction for followup left ventricular function. Am J Cardiol 2001;88:1358–63.
11 Matetzky S, Freimark D, Chouraqui P, et al. The distinction between coronary
and myocardial reperfusion after thrombolytic therapy by clinical markers of
reperfusion. J Am Coll Cardiol 1998;32:1326–30.
12 Matetzky S, Novikov M, Gruberg L, et al. The significance of persistent ST
elevation versus early resolution of ST segment elevation after primary PTCA.
J Am Coll Cardiol 1999;34:1932–8.
13 Schroder K, Wegscheider K, Zeymer U, et al. Extent of ST-segment deviation
in a single electrocardiogram lead 90 min after thrombolysis as a predictor of
medium-term mortality in acute myocardial infarction. Lancet
14 Stone GW, Peterson MA, Lansky AJ, et al. Impact of normalized myocardial
perfusion after successful angioplasty in acute myocardial infarction. J Am
Coll Cardiol 2002;39:591–7.
15 Cura FA, Roffi M, Pasca N, et al. ST-segment resolution 60 minutes after
combination treatment of abciximab with reteplase or reteplase alone for
acute myocardial infarction (30-day mortality results from the resolution of STsegment after reperfusion therapy substudy). Am J Cardiol 2004;94:859–63.
16 Poli A, Fetiveau R, Vandoni P, et al. Integrated analysis of myocardial blush
and ST-segment elevation recovery after successful primary angioplasty: realtime grading of microvascular reperfusion and prediction of early and late
recovery of left ventricular function. Circulation 2002;106:313–8.
17 Claeys MJ, Bosmans J, Veenstra L, et al. Determinants and prognostic
implications of persistent ST-segment elevation after primary angioplasty for
acute myocardial infarction: importance of microvascular reperfusion injury
on clinical outcome. Circulation 1999;99:1972–7.
18 De Luca G, van’t Hof AW, de Boer MJ, et al. Time-to-treatment significantly
affects the extent of ST-segment resolution and myocardial blush in patients
with acute myocardial infarction treated by primary angioplasty. Eur Heart J
19 Savonitto S, Ardissino D, Granger CB, et al. Prognostic value of the admission
electrocardiogram in acute coronary syndromes. JAMA 1999;281:707–13.
20 Kaul P, Fu Y, Chang WC, et al. Prognostic value of ST segment depression in
acute coronary syndromes: insights from PARAGON-A applied to GUSTOIIb. PARAGON-A and GUSTO IIb investigators. Platelet IIb/IIIa antagonism
for the reduction of acute global organization network. J Am Coll Cardiol
21 Kaul P, Newby LK, Fu Y, et al. Troponin T and quantitative ST-segment
depression offer complementary prognostic information in the risk
stratification of acute coronary syndrome patients. J Am Coll Cardiol
22 Holmvang L, Clemmensen P, Lindahl B, et al. Quantitative analysis of the
admission electrocardiogram identifies patients with unstable coronary artery
disease who benefit the most from early invasive treatment. J Am Coll Cardiol
23 Diderholm E, Andren B, Frostfeldt G, et al. The prognostic and therapeutic
implications of increased troponin T levels and ST depression in unstable
coronary artery disease: the FRISC II invasive troponin T electrocardiogram
substudy. Am Heart J 2002;143:760–7.
24 Mueller C, Neumann FJ, Perach W, et al. Prognostic value of the admission
electrocardiogram in patients with unstable angina/non-ST-segment elevation
myocardial infarction treated with very early revascularization. Am J Med
25 Cannon CP, Weintraub WS, Demopoulos LA, et al. Comparison of early
invasive and conservative strategies in patients with unstable coronary
syndromes treated with the glycoprotein IIb/IIIa inhibitor tirofiban. N Engl J Med
26 Fox KA, Poole-Wilson PA, Henderson RA, et al. Interventional versus
conservative treatment for patients with unstable angina or non-ST-elevation
myocardial infarction: the British Heart Foundation RITA 3 randomised
trial. Randomized intervention trial of unstable angina. Lancet
27 Kaul P, Newby LK, Fu Y, et al. Relation between baseline risk and treatment
decisions in non-ST elevation acute coronary syndromes: an examination of
international practice patterns. Heart 2005;91:876–81.
IMAGES IN CARDIOLOGY . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
doi: 10.1136/hrt.2004.052142
‘‘Sea anemones’’ on a degenerated bicuspid aortic valve
72 year old man was operated on for a severely stenotic
(gradient 120 mm Hg) congenitally bicuspid aortic
valve. The valve was replaced by a prosthetic valve
and the resected leaflets were stored in formalin for routine
pathologic analysis. Under formalin two beautiful sea
anemone-like glistening white papillary tumours unfolded
at the valvar surface, with all the features of papillary
fibroelastomas (panels B and C). The tumours measured
5 mm and 9 mm, respectively.
When the valve leaflets were taken out of the formalin
container, the fibroelastomas collapsed like sea anemones do
at low tide (panel A, arrow); an image which corresponded
with the aspect of the valves at the time of surgery.
A C van der Wal
J J Kloek
[email protected]
(A) Overview of resected valve tissue. Photo is of a ‘‘dry specimen’’. Arrow indicates collapsed fibroelastomas. (B) Detail of leaflet with unfolded
fibroelastomas. Photo is of a wet specimen (placed in water). (C) Histology of fibroelastoma showing cell-poor, elastin-rich (black) papillary structures
(elastic van Gieson stain 624).
Downloaded from on May 5, 2017 - Published by
''Sea anemones'' on a degenerated bicuspid
aortic valve
A C van der Wal and J J Kloek
Heart 2005 91: 853
doi: 10.1136/hrt.2004.052142
Updated information and services can be found at:
These include:
Email alerting
Receive free email alerts when new articles cite this article. Sign up in the
box at the top right corner of the online article.
To request permissions go to:
To order reprints go to:
To subscribe to BMJ go to:

Report this document