It has been recognised for decades that the hardening of arteries (or atherosclerosis), the cause of heart attacks and strokes, has the hallmarks of an inflammatory response.
Atherosclerosis, have many of the chief ‘dramatis personae’ of a severe inflammatory response, including infiltration by inflammatory cells and ongoing destruction of tissue.
Moreover individuals who have high levels of inflammatory markers in the serum (measured by CRP) have a higher risk of having heart attacks or strokes.
The logical therapeutic approach therefore is to treat atherosclerosis like we treat other inflammatory conditions, like rheumatoid arthritis.
However, and this has been a huge puzzle in the area of cardiovascular medicine, in-spite of decades of trying to show that this is an effective way of preventing disease the trials have failed.
Until last week, the results of CANTOS trial appeared in the New England Journal of Medicine: Antiinflammatory Therapy with Canakinumab for Atherosclerotic Disease, that show that one injection every three months of a drug, Canakinumab, that inhibits a chief component of the inflammatory response (interleukin-1) prevents heart attacks and strokes.
This is a major breakthrough that will provide a new armamentarium for physicians treating high risk patients (ie. with high levels of CRP), and certainly lead to a host of new trials to fine tune the way the drug, and its derivatives will be used.
But more than that, this discovery firmly puts inflammation at the center of the causation of cardiovascular disease in adults, and reaffirms the need to keep in check other sites of inflammation (such as seen in periodontitis) that are also associated with increased cardiovascular risk.