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gAccording to researchers, Saturday, at a scientific meeting, the use of a generic anti-inflammatory drug widely used to treat rheumatoid arthritis in people who have already had a heart attack or stroke brain did not allow better than placebo to prevent another cardiovascular event.
The trial, called the Cardiovascular Inflammation Reduction Test (CIRT) and sponsored by the National Heart, Lung, and Blood Institute, tested methotrexate in people who had previously had a heart attack or stroke in Canada. more than a diabetes or metabolic syndrome, which can lead to inflammation. . Methotrexate was an attractive option because people who took this relatively inexpensive oral medication to treat their rheumatoid arthritis also appeared to have lower heart disease rates. The study was published in the New England Journal of Medicine and presented at the meeting of the American Heart Association in Chicago.
While methotrexate may not have been successful in overcoming heart disease, preventative cardiologists call it a vote of confidence for a more precise interpretation of what is called the inflammatory hypothesis. First proposed 25 years ago by Dr. Paul Ridker of Brigham and Women's Hospital, the theory holds that inflammation causes atherosclerosis – the hardening and narrowing of the arteries that carry oxygen-rich blood to the heart – regardless of the "bad" cholesterol, which also clogs the coronary arteries. .
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Ridker recently led both the CIRT and another randomized clinical trial in parallel to test whether drugs known to interfere with the inflammation of other diseases could also reduce the risk of future heart attacks or strokes. Brain attacks in people at high risk of recurrence. In September, the first study, dubbed CANTOS (Canakinumab) and sponsored by Novartis, showed that Novartis drug, canakinumab, an injectable monoclonal antibody targeting a particular immune molecule, reduced the number of subsequent heart attacks by 15%. , stroke, or death in people with high inflammation as measured by C-reactive protein in the blood.
The CIRT trial was stopped in the spring, earlier than planned, because its data protection and control committee had concluded that the drug had no beneficial effect and that it was unlikely that the results would be better.
Dr. Robert Harrington, a cardiologist and chair of the Stanford Department of Medicine, a member of the CIRT safety committee, said on Wednesday that methotrexate results were disappointing but not surprising, as these patients – unlike patients with The CANTOS trial – levels of inflammation, perhaps because their diabetes or their metabolic syndrome were well controlled by the other medications that they were taking.
"I'm not sure you can say that CIRT has tested the inflammatory process in the same way as CANTOS," he said. "That's why CANTOS is so important, not so much for the drug itself as for the step forward that is improving outcomes for patients if we inhibit specific inflammatory pathways."
The drug used in the CANTOS trial, canakinumab, has not been approved by the Food and Drug Administration for heart patients. It is taken by people with juvenile idiopathic arthritis and other auto-inflammatory diseases; monthly injections cost $ 200,000 a year. In the CANTOS trial, some serious side effects, including fatal infections, were observed. In the CIRT trial on methotrexate, some patients had liver problems and the rate of non-basal skin cancer was higher.
For Ridker, canakinumab is only a proof of principle and indicates a specific inflammatory pathway in which the innate immune molecule, interleukin-1 beta, is a target of choice. C-reactive protein is also found in this pathway, and detection of its levels in a blood test indicates inflammation.
"I do not think we still have the perfect medicine for that," Ridker said. "I consider the CIRT trial to be a very informative negative control. One study showed that the reduction of interleukin-1 beta and CRP clearly resulted in a substantial reduction in heart attacks and strokes. The other study now indicates that if you give an anti-inflammatory that does not change this way, you will not benefit. "
Dr. Erin Donnelly Michos, Assistant Director of Preventive Cardiology at the Ciccarone Center for the Prevention of Heart Disease at Johns Hopkins University, also believes that the way forward is important.
"We need to target inflammation in the direct causal pathway, which seems to come from IL-1B, rather than targeting another marker of the inflammatory medium that might not be a direct causal factor," he says. said Michos, who has not been involved in studying, said Thursday.
Michos is hoping for another generic anti-inflammatory drug currently being tested in cardiac patients: gout treatment, colchicine. This inexpensive drug targets adhesion molecules in an inflammatory pathway similar to the beta pathway of interleukin-1. The results of this test are expected next year.
Whether colchicine or a new drug eventually controls inflammation, preventive cardiologists recommend that patients already taking drugs lower LDL cholesterol and reduce herbal diet.
Ridker believes a new drug may take 10 to 15 years to reach patients, but he is more optimistic after CIRT and CANTOS.
"When you think of drug development and finally make my patients understand, when you have a very good idea of the way forward, you can really start focusing your efforts," he said.
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