ESC Congress 2017 In Review -- Main Edition - 15B

with angina without obstructive CAD.12 Dr Pepine commented that it is time for a paradigm change.
It is important to delineate the biologic mechanisms underlying the pathophysiology of angina, with
an emphasis on a cellular basis. According to Luís H.
Gowdak, MD, PhD, Heart Institute, São Paulo, Brazil,
the cardiac cell is the common victim of myocardial
ischaemia, regardless of the underlying mechanism.
He reviewed the mechanisms of myocardial ischaemia
stemming from atherosclerotic disease, vasospastic disease, and microvascular dysfunction.13
Dr Gowdak presented 4 scenarios to illustrate the
management of angina at the cardiac cell level. For a
patient with angina who cannot tolerate ß-blockers,
trimetazidine has similar efficacy to propranolol.14 A
patient on ß-blockers who still has angina could benefit
from the addition of trimetazidine, which significantly
reduces angina episodes.15 By increasing the supply of
adenine triphosphate (ATP), trimetazidine complements
the action of ß-blockers, which decrease cardiac ATP
demand.
Trimetazidine given before elective percutaneous coronary intervention (PCI) for angina protects the cardiac
cells during PCI and for 24 hours after by reducing troponin release; CV events are also decreased after 3 years of
treatment (Figure 2).16-19
Figure 2. Trimetazidine as Adjunctive Therapy to PCI

n = 266 patients

Circulating cTnl (ng/mL)

***

PCI

***

6
***

4
2
0

P = .032
10.8

43.5%

***

n = 635 patients

6.1

2
0

Time (h)

Number of MACCEs

cTnI, cardiac troponin I; MACCEs, major cardiac and cerebrovascular events.
Reproduced from Bonello L, Sbragia P, Amabile N. Protective effect of an acute
oral loading dose of trimetazidine on myocardial injury following percutaneous coronary intervention. Heart. 93:703-707. With permission from the BMJ
Publishing Group.
Reproduced from Chen J, Zhou S, Jin J, et al. Chronic treatment with trimetazidine after discharge reduces the incidence of restenosis in patients who
received coronary stent implantation: a 1-year prospective follow-up study. Int
J Cardiol. 2014;174:634-639. With permission from Elsevier.

Valentin Fuster, MD, PhD, Icahn School of Medicine
at Mount Sinai, New York, New York, USA, pointed out
that microvascular disease, rather than epicardial coronary artery disease, is the cause of angina in many
patients with diabetes. Thus, revascularisation may not
be the best option for therapy in this population. In the
FREEDOM trial, many patients with diabetes and multivessel disease treated with CABG versus PCI still had
angina at 60 months and returned for repeat revascularisation.22
The BARI and COURAGE studies showed that patients
who underwent CABG or PCI had similar outcomes as
those treated with OMT. Among diabetic patients in the
BARI-2D, COURAGE, and FREEDOM trials, only 20%, 19%,
and 20%, respectively, achieved all risk factor reduction
targets with OMT at 1 year.23
Data from a study comparing the impact of adherence to OMT on outcomes in patients who underwent
CABG vs PCI showed that compliance with OMT was
a more powerful predictor of major adverse cardiac
event-free survival than choice of intervention .24
Studies of polypills show that they lead to better
adherence in patients with stable CAD.25 Implementation
of a polypill strategy should lead to better clinical outcomes and overall costs.
Guiseppe M.C. Rosano, MD, PhD, St. George's University
Medical School, London, United Kingdom, noted that 35%
of patients with stable CAD have angina or ischaemia or
both.26 Reduction of heart rate in patients with CAD is
important because high heart rate is associated with a
worse prognosis.27 A large proportion of patients, even
when treated with ß-blockers, have a high heart rate.
According to Dr Rosano, the paradigm needs to shift from
heart rate as a threshold to heart rate as a target.
The anti-ischaemic effect of ivabradine per beat of
heart rate reduction is almost double that of atenolol
and it has an additive anti-ischaemic effect in patients
already on ß-blockers (Figure 3).28,29
Figure 3. Additive Anti-Ischaemic Effect of Ivabradine in Patients
Already on ß-Blockers
Change in ETT criteria* at 4 months
60

P < .001

P < .001
Ivabradine + atenolol
Placebo + atenolol
* Evaluated at trough of drug

50
40

P < .001

activity

P < .001

30
20

For a patient with stable angina and left ventricular (LV) dysfunction on OMT, addition of trimetazidine
improves ATP production by as much as 33%, inducing
partial recovery of LV function, which translates into
better survival after 2 years' treatment.20,21

10
0

Total exercise
duration

Time to limiting
angina

Time to angina Time to 1-mm STonset
segment depression

ETT, exercise tolerance test.
Adapted from Tardif JC et al. Eur Heart J. 2009;30:540-8.

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