Opinion about treating triglycerides
Cardiovasc Diabetol. 2014 Dec 4;13(1):159. [Epub ahead of print]
Hypertriglyceridemia: a too long unfairly neglected major cardiovascular risk factor.
Abstract
The
existence of an independent association between elevated triglyceride
(TG) levels, cardiovascular (CV) risk and mortality has been largely
controversial. The main difficulty in isolating the effect of
hypertriglyceridemia on CV risk is the fact that elevated triglyceride
levels are commonly associated with concomitant changes in high density
lipoprotein (HDL), low density lipoprotein (LDL) and other lipoproteins.
As a result of this problem and in disregard of the real biological
role of TG, its significance as a plausible therapeutic target was
unfoundedly underestimated for many years. However, taking
epidemiological data together, both moderate and severe
hypertriglyceridaemia are associated with a substantially increased long
term total mortality and CV risk. Plasma TG levels partially reflect
the concentration of the triglyceride-carrying lipoproteins (TRL): very
low density lipoprotein (VLDL), chylomicrons and their remnants.
Furthermore, hypertriglyceridemia commonly leads to reduction in HDL and
increase in atherogenic small dense LDL levels. TG may also stimulate
atherogenesis by mechanisms, such excessive free fatty acids (FFA)
release, production of proinflammatory cytokines, fibrinogen,
coagulation factors and impairment of fibrinolysis. Genetic studies
strongly support hypertriglyceridemia and high concentrations of TRL as
causal risk factors for CV disease. The most common forms of
hypertriglyceridemia are related to overweight and sedentary life style,
which in turn lead to insulin resistance, metabolic syndrome (MS) and
type 2 diabetes mellitus (T2DM). Intensive lifestyle therapy is the main
initial treatment of hypertriglyceridemia. Statins are a cornerstone of
the modern lipids-modifying therapy. If the primary goal is to lower TG
levels, fibrates (bezafibrate and fenofibrate for monotherapy, and in
combination with statin; gemfibrozil only for monotherapy) could be the
preferable drugs. Also ezetimibe has mild positive effects in lowering
TG. Initial experience with en ezetimibe/fibrates combination seems
promising. The recently released IMPROVE-IT Trial is the first to prove
that adding a non-statin drug (ezetimibe) to a statin lowers the risk of
future CV events. In conclusion, the classical clinical paradigm of
lipids-modifying treatment should be changed and high TG should be
recognized as an important target for therapy in their own right.
Hypertriglyceridemia should be treated.
