Hypertriglyceridemia (HTG) is among the most common dyslipidemias seen in clinical practice. Studies in recent years have demonstrated a causal relationship between triglyceride-rich lipoproteins (TRL) and cardiovascular disease (CVD). This is primarily due to enhanced atherogenicity of cholesterol-enriched remnants, the metabolic byproducts of TRLs. Other factors influencing atherogenicity of TRLs include apolipoprotein CIII–directed proinflammatory signaling pathways and triglyceride enrichment of low-density lipoprotein that results in overabundance of small dense atherogenic particles within a prooxidative milieu that serves as the gateway for unregulated incorporation by vascular wall macrophages. HTG is caused by familial and metabolic disorders as well as selected medications that impair TRL hydrolysis.