Lipoprotein Lp(a). A risk factor for myocardial infarction.

Abstract

The aim of this study was to test plasma lipoprotein Lp(a) and other lipkj and lipoprotein levels for association with the Incidence of myocardial Infarction. Total plasma cholesterol, trlglycerides, low density lipoprotein (LDL) cholesterol, high density lipoprotein (HDL) cholesterol, and Lp(a) were measured In 1486 men at the age of 18 years. In addition, the Broca Index (a measure of relative body weight) and other data were recorded. The sample was divided Into probands whose mothers or fathers suffered a myocardial Infarction (case group, n=52) and Into probands whose parents had no myocardial Infarction (control group, n = 1434). In the case group, 32% had Lp(a) plasma concentrations greater than 25 mg/dl, but only 13.4% of the control group had this level of concentration, a highly significant difference (p<0.01). In addition, there was a statistically significant difference In the ratio of LDL cholesterol/HDL cholesterol (p<0.05) and the Broca Index (p<0.01) between cases and controls. The parents of the case group were significantly older than the parents of the control group; however, when a control group was matched for parents' age, the result* were similar. These data suggest that parents of male children with Lp(a) plasma concentrations greater than 25 mg/dl have a 2.5-fold higher Incidence of myocardial Infarction. Considering the familial aggregation of elevated Lp(a) levels, we conclude that increased levels of this lipoprotein may be a significant risk factor for myocardial infarction. (Arteriosclerosis 8:398-401, July/August 1988) A ccording to current concepts, increased plasma concentrations of atherogenic lipoproteins play an important role in the development of atherosclerosis leading to premature myocardial infarction (Ml) and stroke. This has been shown in many case-control studies.1 ' 23 The results from prospective studies are scarce and, in most instances, they include only the measurements of lipids and lipoprotein lipids, 4 ' 5 despite the fact that individual lipoprotein levels seem to be of greater predictive value in the assessment of atherosclerosis risk.36 -8 One particular fraction, which is important in that respect, is Lp(a), a lipoprotein that is inherited as a quantitative genetic trait (reviewed by Kostner 10 ). Albers et al. 11 demonstrated that plasma Lp(a) levels were not correlated with apolipoprotein B levels. We have shown in previous reports 12 that I-P(a) is synthesized independently of other cholesterol ester-rich apo B-containing lipoproteins. Furthermore, the rate of Lp(a) synthesis is the determinant of plasma Lp(a) concentration, 13 which may vary considerably among individuals and may range from <1 to >150 mg/dl. Lp(a) catabolism, on the other hand, proceeds via routes that resemble those of LDL. Parts of this study were submitted for presentation at the 60th Scientific Sessions of the American Heart Association.Address for reprints: Dr. Gerald Hoefler, Kennedy Institute for Handicapped Children, 707 North Broadway, Baltimore, MD 21205.Received November 3...

Glutamine/histidine polymorphism in apo A-IV affects plasma concentrations of lipoprotein(a) and fibrin split products in coronary heart disease patients.

“…Remarkably, in apo A-FVcases (%) 49 In apo A-IV-1/2 heterozygotes, the relative frequency of Lp(a) >20 mg/dl was decreased by a factor of 2.25 compared with apo A-IV-1/1 homozygotes (15% versus 33.8%, p<0.03, x 2 test). When one considers a threshold value of 30 mg/dl, which has been suggested by other investigators, 50 the difference between apo A-IV-1/2 heterozygotes and apo A-IV-1/1 homozygotes amounted to a factor of 3.5 (7.5% versus 26%,/?<0.02, X 2 test). Although the differences were not significant, it is noteworthy that in a converse manner the mean concentrations of LDL cholesterol and apo B and the concentrations of HDL cholesterol and apo A-I showed opposite trends in apo A-IV-1/2 heterozygotes and apo A-IV-1/1 homozygotes and differed by 3-5% ( Table 2).…”

Lp(a) in hypertensive patients

“…diseases such as CHD [24][25][26][27][28][29][30][31] and the re-stenosis of corMany studies have shown clearly that high concenonary bypass [32][33][34][35] but are also considered an indetrations of low-density lipoproteins (LDL-C), Apolipendent risk factor for these pathologies. poprotein B (Apo B) and total cholesterol (TC) Up to now there is very little information on Lp(a) accompanied by low concentrations of high-density in hypertensive patients available in the literature, lipoproteins (HDL-C) and Apoprotein AI (Apo AI) and any results published are contrasting.…”

The assembly of lipoprotein Lp(a)

“…Despite intensive work in numerous laboratories, the physiological role of Lp(a) remains elusive. Concerning the pathophysiology of Lp(a), there are numerous reports that an elevated plasma concentration of Lp(a) (above 25-30 mg dL ÿ 1 ) is strongly associated with myocardial infarction, peripheral vascular diseases and stroke [5][6][7][8][9][10][11]. In addition, Lp(a) is considered to be a prothrombotic lipoprotein [12].…”