Which of the many so called “risk factors” correlated with Coronary Heart Disease (CHD) actually cause disease? According to Dr. Sekar Kathiresan, genetic discoveries are proving crucial to disentangling cause from correlation. Dr. Kathiresan will present the session “Is There Anything More to CHD Risk than LDL Cholesterol?” on Thursday, October 23, 2014 at the 9th Annual CMHC.
“Our work to date,” he said, “suggests that there are three lipid fractions that show evidence in terms of a causal relationship: LDL; lipoprotein(a); and triglyceride-rich lipoproteins (TRLs). In contrast, although low levels of HDL are correlated with CHD risk, low HDL levels do not represent a causal relationship.”
“The good news,” Dr. Kathiresan continued, “is that there is something beyond LDL. Naturally occurring genetic mutations in four different genes alter triglycerides and CHD risk. In a recent study, it was found lifelong lower levels of APOC3 caused by a genetic mutation led to a 50% reduced risk of CHD… We’re in an interesting phase, where there’s a resurgence of interest in TRLs. The challenge over the next few years will be in proving that reducing TRLs will not only lower triglycerides but also the risk of CHD.”
The Role of Inflammation
In their Thursday morning keynote address, Drs. Peter Libby and Paul Ridker will also address CHD risk factors beyond lipids by presenting their research on the role of inflammation in the pathophysiology of atherosclerosis and the impact anti-inflammatory therapies under investigation may have on reducing cardiovascular event rates. “The magnitude of independent risk associated with inflammation is at least as large, if not larger, than that of blood pressure and cholesterol,” said Dr. Paul Ridker.
View CMHC highlights – visit CMHC Rewind for featured presentations from the 2014 CMHC.