Lipoprotein (a) is an LDL particle with an inherited apoprotein (a) variant attached. Potential physiologic mechanisms to explain the role of Lp(a) in cardiovascular disease involve the structural similarity of apoprotein (a) to plasminogen, a fibrinolytic proenzyme.

Clinical Implications:

Lp(a) has been linked to the promotion of both early and advanced stage atherosclerosis. Elevated Lp(a) (>=30 mg/dL) is associated with increased coagulation and a three to five-fold increased incidence of cardiovascular disease (CVD). An elevated level of Lp(a) is an independent risk factor for CVD. When in combination with other abnormal disease markers, the associated risk increases further. Lp(a) is inherited in a dominant fashion.

Treatment considerations:

• Common first-line pharmacological considerations:
  • Nicotinic acid - therapeutic response may be gradual and delayed
  • Niaspan^® 2,000 mg/d may decrease Lp(a) by approximately 24%
  • IR Niacin 3,000 mg/d may decrease Lp(a) by approximately 36%
• Additional pharmacological considerations:
  • Estrogen may decrease Lp(a) 20-30% (possible effect)
  • Fenofibrates (limited effect)
• Consider that statins may elevate Lp(a) in some patients
• Lifestyle has no impact on Lp(a)
• Aggressively treat all associated atherogenic lipoprotein abnormalities

For more information and detailed references, please refer to our Clinical Implications Reference Manual.