ESC Congress 2017 In Review – Focus on CAD&ACS - 18

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The results of the PEGASUS-TIMI 54 trial provided evidence of the longer-term accrual of benefits from DAPT
using 60 mg ticagrelor twice daily [Bonaca MP et al. N
Engl J Med. 2015], with comparable relative risk benefit
for diabetic and nondiabetic patients [Bhatt DL et al.
J Am Coll Cardiol. 2016]. The results from the ongoing
THEMIS trial [NCT01991795] will specifically address the
effects of long-term DAPT involving ticagrelor in 19,000
patients with diabetes at high risk for CV events.
In patients who have experienced an MI, long-term
DAPT appears beneficial in terms of reduced CV death,
MI, or stroke, with an increase in major bleeding [Udell JA
et al. Eur Heart J. 2016. The 2017 ESC Focused Update on
DAPT in Coronary Artery Disease [Valgimigli M et al. Eur
Heart J. 2017] provides the following recommendations
concerning the duration of therapy (Table 1).
Table 1. DAPT Duration in ACS Patients Treated With PCI
Recommendations

Class

Level

In patients with ACS who have tolerated DAPT without a
bleeding complication, continuation of DAPT for longer
than 12 months may be considered.

IIb

In patients with MI and high ischaemic risk who have tolerated DAPT without a bleeding complication, ticagrelor
60 mg BID for longer than 12 months on top of aspirin
may be preferred over clopidogrel or prasugrel.

IIb

ACS, acute coronary syndrome; DAPT, dual antiplatelet therapy; MI, myocardial
infarction.
Adapted from Valgimigli M et al. 2017 ESC focused update on dual antiplatelet
therapy in coronary artery disease developed in collaboration with EACTS. Eur
Heart J. 2017.

The main considerations regarding the optimal duration of DAPT is summarised in Table 2 [Eisen A, Bhatt
DL. Nat Rev Cardiol. 2015].
Table2. Factors Regarding the Optimal Duration of DAPT
≤ 12 Months DAPT

Patient-related factors

≥ 12 Months DAPT

Patients with stable CAD

Patients with ACS

Patients with bleeding
history
Patients with high risk of
bleeding

Patients with diabetes
Patients with renal
dysfunction
Patients with CHF
Patents with previous ST
Patients with PAD

Anatomy-related factors

Short lesion
Single vessel disease

Stent-related factors

Second generation DES

Long lesion
Small vessel
Bifurcation lesion
Complex anatomy
Left main coronary artery
First generation DES
Long stent
Multiple stents

ACS, acute coronary syndrome; CAD, coronary artery disease; CHF, chronic
heart failure; DAPT, dual antiplatelet therapy; DES, drug-eluting stent; PAD,
peripheral artery disease.

October 2017

Non-vitamin K Antagonist Oral Coagulation
Post STEMI
Dan Atar, MD, Oslo University Hospital Ullevål, Oslo,
Norway, discussed non-vitamin K antagonist oral
coagulation (NOAC) therapy following STEMI. The persistent elevation of thrombin up to a year following an
ACS event creates an environment favouring formation
of coronary artery thrombi [Ardissino D et al. Blood.
2003]. Warfarin- and aspirin-mediated anticoagulation
have long been known to be protective following MI
[Hurlen M et al. N Engl J Med. 2002; Andreotti F et al.
Eur Heart J. 2006].
More recent studies have explored the efficacy
of NOACs. The APPRAISE-2 randomised controlled
trial of twice-daily apixaban plus antiplatelet therapy
documented increased major bleeds compared with
antiplatelet therapy alone without a significant reduction
in recurrent ischaemic events in high-risk patients
following an ACS [Alexander JH et al. N Engl J Med. 2011].
Likewise, increased bleeding and other complications
were also observed with dabigatran in the RE-DEEM
randomised controlled trial [Oldgren J et al. Eur Heart J.
2011] and with rivaroxaban in ATLAS ACS-TIMI 46 [Mega
JL et al. Lancet. 2009]. However, a breakthrough was
reached when using very low doses of Rivaroxaban in
the Phase 3 ATLAS-TIMI 51 study [Mega JL et al. N Engl
J Med. 2012]. In this population post ACS, rivaroxaban
2.5 mg BID on top of antiplatelet therapy (mostly aspirin
and clopidogrel) led to a reduction in stent thrombosis,
CV death, MI, or stroke as well as, notably, in all-cause
mortality during the 24-month study period. This strong
evidence has given rise to a recommendation in the 2012
ESC STEMI guideline, reinforced in the 2017 ESC STEMI
guideline (Table 3) [Ibanez B et al. Eur Heart J. 2017].
Interestingly, at the same time of the ATLAS-II trial,
strong evidence from the TRITON-TIMI 38 study using
prasugrel instead of clopidogrel and the PLATO trial
using ticagrelor instead of clopidogrel emerged supporting a more aggressive platelet inhibition. As discussed earlier in this article, the pertinent recommendations in the STEMI guidelines are strongly in favour
of ticagrelor and prasugrel, diminishing the utility of
low-dose rivaroxaban, since the ATLAS-II trial did not
test these two newer antiplatelet agents. Hence, for
now, according to Dr Atar, there has been limited clinical utility of oral anticoagulation following STEMI. The
just-released findings of the COMPASS trial [Eikelboom
JW et al. N Engl J Med. 2017] could inform treatment
recommendations post STEMI, but are valid only in
patients with stable CAD and hence not in the acute
phase.

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