Fatty deposits in arteries (atheroma) account for the most deaths in America, as well as in the rest of the western world. The most common manifestation of atheroma is coronary artery disease (CAD), the cause of heart attacks and angina. But when such deposits occur in the main neck arteries, the carotids, the result is all too often a stroke. Strokes can be transient or minor but they also commonly cripple, disable, or kill. In fact, stroke is the 4th leading cause of death in the U.S., accounting for 130,000 in 2010. Anything that can reduce fatty buildup in the carotid arteries should reduce the toll of strokes.
A new study published in the journal Arteriosclerosis, Thrombosis and Vascular Biology studied the effect of long-term lipid-lowering drugs (LLD) on measurements of fatty deposits in the carotids among almost 3,000 Norwegian men and women over the course of 13 years. The patients studied had their burden of arterial fat measured via ultrasound at the outset of the study (baseline) and again 13 years later, while being treated with LLD (mostly statin drugs). Four-hundred forty-three (about 15 percent) of the patients were on LLD; at baseline they had the highest risk of vascular disease, manifested by higher blood pressure, lipid levels, male gender and older age. At the study's conclusion, it was found that progression of fatty deposition in the carotids was significantly slower in those on LLD than in the 85 percent of the study group not on LLD, or on intermittent LLD. This assessment was made based on a parameter called the CIMT: carotid intima-media thickness, a measure of the arterial wall's thickness due to fatty accumulation. There was a dose-response observed as well, with those on daily LLD having more reduction in progression of atheroma than those on intermittent doses, and these having less progression than those on no LLD at all.
ACSH's Dr. Gilbert Ross noted, "This might be a precursor to a very important study, since measurements like these are called 'surrogate markers,' meaning they are believed to foretell actual health outcomes but are not themselves outcomes. In other words, it is highly logical and evidence-based to believe that fatty deposition in the key neck arteries is an important cause of stroke, and to slow its progress would mean reducing the occurrence of strokes. But it is not the same as actually measuring the number of strokes (or heart attacks, etc.) among those on LLD as compared to those not on such therapies. That is the study that I hope is being done. In heart attack prevention, we do know that those with a history of heart disease are best treated with LLDs to ward off recurrences. But the issue is not so clear for those who have risk factors only but no history of an event. We can say the same about stroke, and I look forward to a study of actual stroke outcomes on, and off, LLDs."