Crestor adds no benefit in heart study

AstraZeneca has been dealt a fresh blow with the news that its blockbuster cholesterol drug Crestor (rosuvastatin) does not significantly improve the prognosis of patients with optimised heart failure because it cannot reverse or prevent heart deterioration. 

New research shows that treating patients with optimised heart failure with statins, such as Corona, alongside their regular treatment does not significantly improve their prognosis.

The Anglo-Swedish pharma company had hoped that Crestor would be the first statin to offer additional benefits in the treatment of heart failure. This would have enabled the company to extend Crestor's patent, and added significant value to the drug. 

The main US patent for Crestor does not expire until 2016 and it was recently extended by four years under the provisions of the Patent Term Restoration Act. However, five generic companies filed manufacturing applications in August 2007 to make forms of Crestor.  

The study, Controlled Rosuvastatin Multinational Study in Heart Failure (Corona), showed that patients taking 10mg Crestor experienced an 8 per cent reduction in the combined primary endpoint of cardiovascular death or myocardial infarction or stroke, which was not statistically significant.

"We added a highly effective statin on top of an optimal treatment regimen. Our findings suggest the major cause of death in these patients was likely not to be related to atherosclerotic events, where benefit with statins in non-heart failure patients has been demonstrated, but instead may have been caused by the deterioration of failing heart muscle damaged beyond repair. CORONA underscores the need for early intervention in the progression of atherosclerosis to prevent one of its worst consequences, heart failure." 

"The CORONA results represent a major advancement in medical research and understanding of patients with advanced heart failure, they clearly differ from patients without heart failure in their response to statin treatment" said lead investigator Prof. John Kjekshus, Department of Cardiology, Rikshospitalet University Hospital, Oslo, Norway.