AstraZeneca PLC
01 September 2003
NEW DATA DEMONSTRATES CLEAR BENEFITS OF ATACAND(R) IN TREATMENT OF SYMPTOMATIC
HEART FAILURE
Atacand(R), the only Angiotensin Receptor Blocker to reduce cardiovascular death
and hospitalisation in chronic heart failure when given together with
conventional therapy
AstraZeneca announced today that data presented at the European Society of
Cardiology annual meeting demonstrated Atacand(R) (candesartan cilexetil)
reduces both cardiovascular deaths as well as hospital admissions for heart
failure, across a broad spectrum of patients with chronic heart failure.
Atacand is the only Angiotensin Receptor Blocker (ARB) to increase survival in
chronic heart failure patients with left ventricular dysfunction, whether or not
they are taking an ACE-inhibitor.
'This new data differentiates Atacand from other ARBs and provides AstraZeneca
with a unique opportunity to make the benefits of the drug available to a wider
population of patients with chronic heart failure' said Gunnar Olsson,
AstraZeneca's Vice President Cardiovascular Therapy Area
The Candesartan in Heart failure - Assessment of Reduction in Mortality and
morbidity (CHARM) Programme, which recruited 7,601 patients, is the largest ever
trial programme conducted in heart failure with an AT1-receptor blocker.
Patients with classic symptomatic chronic heart failure - depressed left
ventricular (LV) systolic function (Left Ventricular Ejection Fraction (LVEF) <
40 per cent), were randomised into one of two studies - either an ACE-inhibitor
intolerant population (CHARM-Alternative), or the population treated with
ACE-inhibitors (CHARM-Added). In addition, patients with preserved LV systolic
function (LVEF> 40 per cent) were also randomised in a third study (CHARM
Preserved). All patients received either Atacand or placebo.
Atacand showed an overall 23 per cent reduction (p<0.0004) in risk of a
cardiovascular(CV) death or hospitalisation for chronic heart failure(CHF) in
patients who were not taking ACE inhibitors due to previous intolerance. This
is comparable to the benefit seen in heart failure studies using ACE-inhibitors
alone.
In patients that were prescribed conventional therapy for chronic heart failure
including an ACE inhibitor, Atacand demonstrated additional mortality and
morbidity benefits. Atacand produced an additional reduction in the risk of
cardiovascular death or hospitalisation for chronic heart failure of 15 per cent
(p=0.011) when compared to conventional treatment alone. Importantly, Atacand
demonstrated this efficacy, along with a high level of tolerability, when taken
as part of triple combination therapy that included an ACE-inhibitor and
beta-blocker - standard treatments in patients with chronic heart failure.
The CHARM Programme also included the largest completed trial in chronic heart
failure patients with preserved left ventricular function, patients for whom
little evidence based treatment guidance presently exist. The primary endpoint
of cardiovascular death or hospitalisations for chronic heart failure showed a
trend, 11 per cent risk reduction in favour of Atacand (p=0.118), consistent
with the significant findings seen in the other two studies. The total number
of hospitalisations for CHF was significantly lower in the Atacand group (402 v
566). There was also a significant 40 per cent reduction in the number of
patients diagnosed with new onset diabetes (47 v. 77; p=0.005).
Pooled analysis of the three studies showed that Atacand provided a significant
reduction in cardiovascular death and also demonstrated a positive trend in the
overall reduction in all cause mortality approaching statistical significance (p
=0.055). Interestingly, it also demonstrated a significant 22 per cent
reduction in onset of new diabetes, with 163 new cases of diabetes on Atacand
compared with 202 on placebo.
Regulatory filings in the US and Europe based on the outcomes of the CHARM
programme are anticipated during Q1 2004. Atacand, currently licensed for the
treatment of hypertension, had sales of $569m worldwide in 2002. The CHARM
study is due to be published in The Lancet on 6 September 2003.
-Ends-
September 1, 2003
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This information is provided by RNS
The company news service from the London Stock Exchange
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