ESC Congress 2017 In Review -- Main Edition - 16

Late-Breaking Clinical Trials

Patients were a mean age of 61 years; most were
men. About 24% were smokers and 40% were diabetic. Median LDL cholesterol was ~82 mg/dL and hsCRP
was 4.1 mg/L. More than 93% of patients were on lipid
lowering therapy; 80% were taking a renin-angiotensin
inhibitor, and 95% an oral antithrombotic. Most (80%)
had undergone prior coronary interventions.
Canakinumab decreased hsCRP in a dose-dependent
manner, but had no effect on LDL-C or HDL-C, and only a
4-5% increase in triglycerides (Figure 1).

(Figure 2). The effect was also significant for the 300mg group (HR 0.86; P = .0314); however, the P-value did
not meet the prespecified threshold for significance. No
significant effect was observed for the 50-mg group (HR,
0.93; P = .30).
The 150-mg group met multiplicity adjusted thresholds
for formal statistical significance for both the primary and
secondary CV endpoints.
Figure 2. Primary Endpoint With Canakinumab, 150 mg vs Placebo

Figure 1. CANTOS: Dose-dependent Effects on Inflammatory Biomarkers
and Lipids (48 Months)
Canakinumab
50 mg

Canakinumab
150 mg

Cumulative Incidence of
Primary Endpoint (%)

Placebo

Canakinumab
300 mg

A High-Sensitivity C-Reactive Protein Level
10

Percent Change From Baseline

0

HR, 0.85 (95% CI, 0.74-0.98)
P = .021

80

20

Placebo
Canakinumab, 150 mg

15
10

60

5
40
0

0

1

2

3

4

5

20

-10

0

-20

0

2

1

-30

-50
-60

0

3

6

9

12

24

36

48

36

48

Months

B LDL Cholesterol Level
10
0
-10

Years

3

5

4

From The New England Journal of Medicine, Ridker PM et al, Antiinflammatory
Therapy with Canakinumab for Atherosclerotic Disease, EPub 27 August 2017.
Copyright © 2017 Massachusetts Medical Society. Reprinted with permission
from Massachusetts Medical Society.

-40

-70

Percent Change
From Baseline

25
100

0

3

6

9

12

24

The 150-mg dose of canakinumab was also associated
with significant (P = .005) reductions in the key secondary CV endpoint (the components of the primary endpoint plus hospitalisation for unstable angina that led to
urgent revascularisation; Figure 3).

Months

Figure 3. Key Secondary Endpoint With Canakinumab, 150 mg vs
Placebo

10
0
-10

0

3

6

9

12

24

36

48

Months

Percent Change
From Baseline

D Triglyceride Level
10
0
-10

25

HR, 0.83 (95% CI, 0.73-0.95)
P = .005

20

Placebo
Canakinumab, 150 mg

100

0

3

6

9

12

24

36

48

Cumulative Incidence of
Secondary Endpoint (%)

Percent Change
From Baseline

C HDL Cholesterol Level

80

15
10

60

5
40
0

0

1

2

3

4

5

20

Months

0

HDL, high-density lipoprotein; hsCRP, high-sensitivity C-reactive protein; LDL,
low-density lipoprotein.
From The New England Journal of Medicine, Ridker PM et al, Antiinflammatory
Therapy with Canakinumab for Atherosclerotic Disease, EPub 27 August 2017.
Copyright © 2017 Massachusetts Medical Society. Reprinted with permission
from Massachusetts Medical Society.

When given SC every 3 months canakinumab, at a
median follow-up of 3.7 years, had a significant effect
for the primary endpoint of MACE (nonfatal MI, nonfatal
stroke, or CV death) was observed in the 150-mg group

16

October 2017

0

1

2

Years

3

4

5

From The New England Journal of Medicine, Ridker PM et al, Antiinflammatory
Therapy with Canakinumab for Atherosclerotic Disease, EPub 27 August 2017.
Copyright © 2017 Massachusetts Medical Society. Reprinted with permission
from Massachusetts Medical Society.

In addition to the primary and secondary endpoints,
there were consistent and significant HR reductions in
MI, unstable angina leading to urgent revascularisation,
and any coronary revascularisation for the 150 mg dose
(all P ≤ .02). There was no significant effect on stroke

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