LIPOPROTEIN(A) AND CORONARY HEART-DISEASE

Elevated plasma or serum lipoprotein(a) (Lp(a)) levels have been assoc iated with premature coronary heart disease (CHD). Lp(a) levels can be assessed quantitatively by electrophoresis and quantitatively by immu noassays determining either total Lp(a) mass, apo(a) mass on Lp(a) pro tein mass, or by precipitation methods followed by measurement of Lp(a ) cholesterol. We prefer the latter method because it can be standardi zed. Electrophoretic methods can detect total Lp(a) values greater tha n or equal to 30 mg/dl. These values correspond to Lp(a) cholesterol v alues greater than or equal to 10 mg/dl. Such values are above the 75t h percentile and represent high risk values for CHD. Values above the 90th percentile for middle aged men and women in Framingham (n = 2678) are greater than or equal to 38 mg/dl for total Lp(a). About 16% of p atients with premature CHD (n = 321) have such values and have familia l Lp(a) excess. Lp(a) is atherogenic because it can be deposited in th e arterial wall, and it also can interfere with fibrinolysis. Multiple apo(a) isoforms have been found and are due to a variable number of k ringle 4 like repeats. Lower molecular weight apo(a) isoforms forms ar e associated with elevated Lp(a) values and are more frequent in CHD k indreds. Both Lp(a) levels and apo(a) isoforms are highly heritable in this Caucasian population. Lp(a) values can be decreased with niacin, and such therapy should be strongly considered in CHD patients with e levated Lp(a) levels (greater than or equal to 30 mg/dl) since niacin treatment has been shown to decrease CHD morbidity and mortality in un selected CHD patients.