Download The Year in Cardiology 2012: acute coronary syndromes

European Heart Journal Advance Access published January 2, 2013
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European Heart Journal
doi:10.1093/eurheartj/ehs462
The Year in Cardiology
The Year in Cardiology 2012: acute coronary
syndromes
Nick E.J. West*
Received 16 November 2012; accepted 6 December 2012
This paper was edited by Filippo Crea, Dipartimento di Scienze Cardiovascolari, Universita Cattolica Rome, Rome, Italy
Patients presenting with acute coronary syndromes (ACS) remain amongst the highest-risk of all acute medical admissions. Despite significant
reductions in morbidity and mortality via refinements in treatment methods in recent years, such individuals remain at a high risk of recurrent
ischaemic events and death. Whilst 2012 has brought a wealth of novel data in the field of ACS regarding diagnosis and both medical and
invasive management strategies, continued focus on this high-risk patient subset is necessary to further our understanding and improve
patient outcomes.
----------------------------------------------------------------------------------------------------------------------------------------------------------Keywords
Acute coronary syndromes † Antiplatelet therapies † PPCI † STEMI † NSTEMI † Guidelines † ECG †
Stem cell therapy † Coronary intervention † PCI † Microvascular obstruction
Introduction
There have been few recent years where the management of
acute coronary syndromes (ACS) has not been significantly
advanced in terms of novel therapies and treatment strategies. In
the last 12 months, new societal guidance has been published
from Europe and North America, and there have also been important ACS studies concerning non-invasive diagnostics, stent
type/choice, and adjunctive therapies designed to reduce infarct
size in percutaneous coronary intervention (PCI) for ACS. In
similar fashion to recent years, the area most published in and
most likely to alter practice concerns the choice and utilization
of antiplatelet/anticoagulant strategies for ACS patients managed
either medically or with an invasive/interventional strategy. This
review will seek to summarize the most important advances in
these areas over the last year.
Guideline updates
The ESC not only produced updated guidance on management of
STEMI1 in 2012, but also produced a third version of the Universal Definition of Myocardial Infarction.2 The former document
updates previous guidance from the ESC and contains important
new recommendations in key areas (Table 1): the importance of
early diagnosis is stressed, with first ECG in patients with suspected STEMI recommended within 10 min of first medical
contact (FMC) and primary percutaneous coronary intervention
(PPCI) for STEMI ideally within 90 min (rated ‘acceptable’ out
to a maximum of 120 min). Such strict criteria may have an
impact on more rural geographies where transit time to PPCI
centres is an issue, and with this in mind, the guidance highlights
the importance of collaborative networks to facilitate achievement of such targets. The guideline also emphasizes the importance of prompt assessment and management of atypical
presentations not always considered under the umbrella of
STEMI, including left bundle branch block (LBBB), paced
rhythms, and isolated ST-segment elevation in lead aVR, especially
when accompanied by symptoms consistent with myocardial ischaemia. Therapeutic hypothermia is now recommended for all
resuscitated patients with STEMI complicated by cardiac arrest
cases, with immediate coronary angiography with a view to
follow-on PPCI when the ECG demonstrates persistent
ST-segment elevation. Additionally, in the light of recently published studies and meta-analyses, including that of Kalesan
et al.,3 drug-eluting stents (DES) are now routinely preferred to
bare metal stents (BMS) in view of the reduced need for repeat
revascularization and the lack of previously perceived hazard for
stent thrombosis. The more potent antiplatelet agents prasugrel
* Corresponding author. Tel: +44 1480 364504, Fax: +44 1480 364799, Email: [email protected]; [email protected]
Published on behalf of the European Society of Cardiology. All rights reserved. & The Author 2013. For permissions please email: [email protected]
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Department of Interventional Cardiology, Papworth Hospital, Cambridge CB23 3RE, UK
Page 2 of 6
N.E.J. West
Table 1 Summary of new changes in ESC Guidelines
for the management of acute myocardial infarction in
patients presenting with ST-segment elevation1
New changes
Early diagnosis
First ECG within 10 min of FMC
Attention to atypical presentations (e.g. LBBB,
paced rhythm, ST elevation in aVR)
Cardiac arrest
Therapeutic hypothermia after successful
resuscitation
Immediate angiography and follow-on PCI for
resuscitated STEMI
Regional networks to deliver timely PPCI
All PPCI centres to be 24/7-capable
New time standards for FMC to PPCI (maximum
≤120 mins)
DES now preferred to BMS
Ticagrelor or prasugrel preferred to clopidogrel
DAPT to continue to 12 months ideally—
minimum 1 month for BMS, 6 months for DES
................................................................................
Logistics
Procedural
issues
Post-procedure
Hospital discharge after 72 h post-PPCI for
low-risk patients
Mandatory assessment of LV function after acute
phase
Assessment of ischaemia for patients with residual
untreated multivessel disease
and ticagrelor are also preferred to clopidogrel for all STEMI
cases, with duration of dual antiplatelet therapy (DAPT) ideally
for 1 year, but reduced to a strict minimum of 6 months for
patients receiving DES.
Accompanying and integral to such guidance was the Third
Universal Definition of Myocardial Infarction,2 published simultaneously with the STEMI guidance. This guideline endorses cardiac
troponin as the biomarker of choice to detect myocardial necrosis,
with spontaneously occurring myocardial infarction (MI) defined as
an elevation above the 99th percentile upper reference value for
the specific assay used. There is further development and clarification of MI in different settings to allow standardization across trials
and registries, in particular after revascularization procedures: after
CABG with normal baseline troponin, MI is defined as a rise to a
value 10 times greater than baseline in the first 48 h, and a rise to
5 times greater than 99th percentile upper reference after PCI in
patients with a normal baseline level (or a 20% rise when troponin
is elevated and stable or falling pre-procedure).
The ACCF/AHA also produced updated guidance on the management of unstable angina/non-STEMI:4 angiography with a view
to revascularization is now recommended within 12 –24 h of presentation, with DAPT pre-loading prior to PCI procedures also now
advocated. Ticagrelor and prasugrel are cited as acceptable alternatives to clopidogrel, and the maintenance dose of aspirin recommended for the majority of cases has finally fallen to 81 mg daily.
Although there remain some differences in nuance between
North American and European practices, this guideline broadly
brings about transatlantic agreement in most areas for the first
time.
Identification and appropriate triage of patients presenting to
emergency departments with acute chest pain remains a difficult
dilemma: many are low-risk and have a non-cardiac origin, but a
significant minority with coronary artery disease may not be
picked up on clinical grounds even when accompanied by appropriate tests, including ECG and biomarker estimation used in conjunction with a clinical risk score (e.g. GRACE, TIMI). As endorsed
in ESC guidance,1 there has been increasing interest in non-typical
ECG patterns for the diagnosis of STEMI; although LBBB is an
accepted surrogate, Widimsky et al.5 retrospectively analysed
6742 patients admitted to hospital with acute MI and found that
in patients presenting with right bundle branch block, a blocked
epicardial vessel was more common (51.7 vs. 39.4%; P , 0.001)
and incidence of both shock and mortality comparable with
LBBB (14.3 vs. 13.1%; P ¼ NS; and 15.8 vs. 15.4%; P ¼ NS, respectively). In a similar vein, Wong et al.6 demonstrated the importance
of ST-elevation in lead aVR, often viewed as indicative of left main
stem occlusion, betokening increased mortality in patients presenting with both inferior and anterior infarction.
Perhaps the most important data regarding the ECG in 2012
were also the most simple: Antoni et al.7 highlighted a powerful
and very simple method of risk stratification; they found that
heart rate measured on a 12-lead ECG at discharge after PPCI is
a strong and independent predictor of mortality at 1 and 4 years
of follow-up (Figure 1). Patients with a discharge heart rate of
≥70 b.p.m. had a two-fold higher mortality at both follow-up
time points, with every increase of 5 b.p.m. in heart rate equating
to a 29% increase in mortality at 1 year and 24% at 5 years. These
findings have important implications for the optimization of patient
therapies after MI (including the use of rate-limiting agents such as
beta-blockers, calcium channel-blockers, and ivabradine), although
large randomized trials are needed to confirm that interventions to
reduce heart rate will replicate the benefits observed in this study.
Two important studies concerning the use of coronary computed tomographic angiography as a triage tool for suspected
ACS were published this year;8,9 the findings are discussed fully
in another review in this series, but in essence, while improving
the efficiency of the emergency department, the studies suggest
no cost improvement and an additional hazard for radiation exposure without clear clinical outcome benefit, suggesting that such a
strategy has little data to support it at the present time.
Antiplatelet and anticoagulant
therapies
As in preceding years, the major area of interest in ACS and ACS
PCI in 2012 has been the further refinement of optimal antiplatelet/anticoagulant regimens; as mortality and adverse event rates fall
year-on-year for ACS patients whether they are managed medically or invasively, the focus on the balance between prevention of
ischaemic events and avoidance of bleeding sharpens ever more.
One agent potentially fulfilling some of these requirements is
the factor Xa inhibitor rivaroxaban; in the previous ATLAS
ACS-TIMI 46 phase 2 study, patients with a recent ACS receiving
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Field
Risk stratification
The Year in Cardiology 2012
Page 3 of 6
rivaroxaban had improved outcomes with a dose-dependent increase in bleeding compared with placebo when used in addition
to standard therapies. The ATLAS ACS 2-TIMI 5110 study therefore randomized 15 526 patients with a recent ACS to receive
low doses of 2.5 or 5 mg rivaroxaban twice daily or placebo.
The previous positive findings were reproduced with a reduction
in the composite endpoint of cardiovascular death, MI, or stroke
(HR 0.84; 95% CI 0.74–0.96; P ¼ 0.008). However, there was
more non-fatal bleeding with rivaroxaban overall, particularly at
the higher dose. The 2.5 mg twice-daily dose had fewer fatal bleeding events than the 5 mg twice-daily regimen (0.1 vs. 0.4%; P ¼
0.04) and resulted in lower cardiovascular and all-cause mortality
(2.7 vs. 4.1%; P ¼ 0.002 and 2.9 vs. 4.5%; P ¼ 0.002, respectively).
It would therefore appear that rivaroxaban may be a useful adjunct
to currently available therapies, especially when targeted at
patients with low potential for bleeding.
Previous studies have demonstrated that platelet inhibition can
be improved by either increasing dose or switching to more
potent antiplatelet agents, but whether this results in improved
clinical outcomes remains to be seen. The TRIGGER-PCI study11
(presented in 2011 but published in 2012) aimed to investigate
whether switching patients with residual high platelet reactivity
on clopidogrel after elective PCI with DES to prasugrel would
improve outcomes; the study was stopped early owing to a low
incidence of the primary endpoint (death/MI at 6 months) with
no difference between clopidogrel- and prasugrel-treated groups
(total of 1 single event) despite increased platelet inhibition. The
larger scale TRILOGY-ACS study12 randomized 7243 patients
with unstable angina or NSTEMI not undergoing revascularization
to prasugrel or clopidogrel. There was no difference between the
groups in terms of the primary endpoint (cardiovascular death/MI/
stroke) and no change in bleeding events either. These two studies
underscore the fact that current DAPT regimens are both efficacious and safe; that said, some patients clearly are at risk of
either recurrent ischaemic events and/or bleeding, and perhaps
the way forward should be to attempt to seek alternative triage
methods to identify the individuals at highest risk of further
events and alter therapies accordingly.
In terms of pharmacology delivered in the catheterization laboratory/PCI setting, the direct thrombin inhibitor bivalirudin has
already shown promise in reducing bleeding events without sacrificing anti-ischaemic efficacy in PPCI for STEMI, resulting in widespread endorsement in societal guidance. A pooled analysis
of the ACUITY and ISAR-REACT 4 studies13 examined 3798
NSTEMI cases undergoing PCI randomized to receive either bivalirudin or heparin plus a glycoprotein IIb/IIIa inhibitor (GPI). The
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Figure 1 Kaplan– Meier time-to-event plots for heart rate at discharge divided by quartiles and all-cause mortality (A and C) and cardiovascular mortality (B and D) at 1-year (A and B) and 4-year (C and D) follow-up, demonstrating relationship between discharge heart rate and
mortality after PPCI for STEMI. Modified from Antoni et al.9
Page 4 of 6
composite efficacy endpoint of death, recurrent MI, or urgent
target vessel revascularization (TVR) was no different between
groups (OR 1.04; 95% CI 0.85– 1.27; P ¼ 0.69) but major bleeding
was significantly reduced with bivalirudin treatment (OR 0.54, 95%
CI 0.40–0.72; P , 0.001). However, whether such results would
be replicated with state-of-the-art management including universal
DAPT pre-loading and high rates of transradial intervention (respectively, improving event reduction and bleeding risks) has yet
to be determined.
Microvascular obstruction during PCI for ACS/STEMI is associated
with increased infarct size and adverse prognosis; its pathophysiology is thought to be a combination of mechanical distal embolization of thrombus and plaque constituents during PCI coupled
with enhanced constriction/hyperreactivity of the distal vascular
bed. Three studies in 2012 in the setting of PPCI for STEMI have
therefore sought to reduce distal embolization: in the INFUSE-AMI
trial,14 452 patients presenting within the first 4 h of an anterior
STEMI were randomized in a 2 × 2 factorial design to receive
either manual aspiration thrombectomy or no thrombectomy
and intracoronary bolus abciximab delivered via the ClearWay
catheter (Atrium Medical, Hudson, NH, USA) or no abciximab;
all patients received bivalirudin as standard therapy. Manual
thrombectomy did not affect infarct size assessed by cardiac magnetic resonance imaging (MRI) at 30 days, but bolus intracoronary
abciximab did [median infarct mass 18.7 g (IQR 7.4 –31.3 g) vs.
24.0 g (IQR 12.1–34.2 g); P ¼ 0.03]. Although these are encouraging findings, the lack of a comparator with conventionally delivered intravenous abciximab is a potential concern, especially
given the negative findings of the much larger AIDA-STEMI
study15 (n ¼ 2065) that examined intracoronary vs. intravenous
abciximab. Just as the overall study failed to show any improvement in hard clinical endpoints, the AIDA-STEMI MRI substudy16
(n ¼ 795) failed to show any improvement in infarct size or reperfusion injury. The third and perhaps most novel strategy to reduce
infarct size was the use of a BMS covered on its outer surface with
a mesh micronet designed to trap and hold potentially friable material that might embolize distally at the time of PCI. The MASTER
study17 randomized 433 STEMI patients to PPCI with conventional
BMS or DES at the operator’s discretion vs. the novel MGuard
stent (InspireMD, Tel Aviv, Israel); the primary endpoint of complete ST-segment resolution was significantly better in patients receiving MGuard (57.85 vs. 44.7%; P ¼ 0.008), as was the
achievement of TIMI grade 3 flow in the treated vessel (91.7 vs.
82.9%; P ¼ 0.006); however, median ST-segment resolution did
not differ between treatment groups, myocardial blush grade was
no different, and safety outcomes at 30 days (death, adverse
events) as well as overall MRI-determined infarct mass were also
similar. Clearly, longer term data in a numerically larger cohort
will be required to confirm these findings before wider uptake
of this technology, especially given the potential for higher TVR
rates that may accrue with a BMS platform when compared with
current-generation DES (as now endorsed for PPCI in ESC
guidance).
Although most attempts to reduce infarct size/increase myocardial salvage during STEMI have focused on pharmacological or PCIbased changes in techniques such as those listed earlier, other
mechanisms have been investigated but these have similarly failed
to show evidence of substantial improvements in outcome,
perhaps indicating that PCI safety and efficacy are approaching
their zenith. Like ischaemic pre-conditioning, post-conditioning
(further episodes of repeated reversible ischaemia during early
reperfusion) remains an area of interest, and has been shown to
reduce infarct size by enzymatic criteria, although MRI-based
studies are conflicting. A meta-analysis by Zhou et al.18 seemed
Figure 2 Comparison of study endpoints for reduction in infarct size in STEMI. Study endpoints listed on the x-axis. STR, ST-segment resolution; TIMI 3, thrombolysis in myocardial infarction grade 3 antegrade flow; MBG 2/3, myocardial blush grade 2/3.
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Coronary intervention and
cardioprotection in acute
coronary syndromes
N.E.J. West
Page 5 of 6
The Year in Cardiology 2012
Cell therapies in AMI
As an alternative to protecting the myocardium against damage
either in the setting of MI or during PCI, there has been increasing
interest in regenerative methods aimed at repairing the myocardium with cell-based therapies. Although stem cell therapies
have held much promise, the two studies related to ACS presented
in the dedicated late-breaking trials session at the AHA were disappointing. The Swiss-AMI study20 randomized 200 STEMI patients
after PPCI to placebo, early (5– 7 days) or late (3–4 weeks) intracoronary infusion of autologous bone marrow-derived mononuclear cells (BMCs). Neither infusion approach affected the
primary endpoint, LVEF, nor the secondary endpoints of LV
volume, scar size, and regional function indices at 4 months. Similarly, the NHLBI-sponsored TIME trial21 randomized 120 patients
with LV dysfunction after PPCI to receive placebo or intracoronary
autologous BMCs at either 3 or 7 days post-MI. Again, there was
no effect on recovery of global or regional LV function at
6 months. Both studies had been designed to investigate the
time criticality of stem cell delivery post-MI, which has been
demonstrated in previous trials. However, although event rates
were no different between treatment and placebo groups in
these studies, Kang et al.22 have shown that, utilizing a strategy of
G-CSF administration to stimulate and mobilize peripheral blood
stem cells subsequently infused into the infarct-related artery,
a composite of major adverse events (driven predominantly by reduction in TVR) was reduced in patients receiving active treatment
5 years after MI, despite the fact that LV function indices were
no different at 2 years. Clearly, such a result is intriguing and
further investigations in the cell therapy field may yet yield novel
therapeutic strategies for patients with LV damage after ACS.
Summary
Although 2012 has again brought interesting and novel data in the
field of ACS, many studies have reported negative or equivalent
results: patient-tailored DAPT strategies have proved largely disappointing in improving outcomes, and interventional modifications,
including a variety of methods to improve cardiac protection
during ACS PCI and cell therapies to mitigate against
infarct-induced LV remodelling and dysfunction, seem not to be
able to clearly improve outcomes except by surrogate measures.
These data perhaps underline the fact that recent advances in
PCI equipment, peri-procedural pharmacology, technique, and
safety, as well as convergence of national guidance, are leading to
the point where even in the highest risk patients such as those presenting with ACS, small improvements may be difficult to discern
despite large well-designed and -conducted studies.
Conflict of interest: The author received consultancy and
lecture fees from Daiichi-Sankyo, Boston Scientific, Abbott Vascular, Medtronic, and Plaquetec Ltd.
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