Lipoprotein(a) as a marker of coronary artery disease and its association with dietary fat.

OBJECTIVE: The main objectives of the study were to evaluate the effect of dietary fat on plasma lipoprotein(a) [Lp(a)] levels and to study the potential of Lp(a) as a more reliable marker for CAD compared to other lipids and lipoproteins. METHODS: Twenty CAD patients and 20 healthy controls were recruited for the study. Their fasting plasma Lp(a) levels and complete lipid profile were assayed. The fat intake was calculated using 24 hours dietary recall method. The patients and controls were each divided into two subgroups: Group A consuming dietary fat > 30% and Group B consuming dietary fat < or = 30% of the total kilo-calories/day. RESULTS: Results indicated that plasma Lp(a), total serum cholesterol (TC), tryglyceride (TG), low density lipoprotein cholesterol (LDL-C), high density lipoprotein cholesterol (HDL-C) and LDL-C/HDL-C ratio of CAD patients were significantly higher than the controls. High fat intake was found to be associated with higher plasma Lp(a) levels (p<0.05) in patients only. No significant correlation was found between Lp(a) levels and other conventional lipoproteins. CONCLUSION: The lack of correlation between Lp(a) and other lipoproteins indicates its potential as an independent risk factor for CAD. High fat intake led to higher plasma Lp(a) levels in patients; hence it would be worthwhile to evaluate the effect of quality and quantity of fat intake on plasma Lp(a) levels in a larger sample size.

Serum levels of lipoprotein (a) and other lipids in angiographically defined coronary artery disease patients and healthy blood bank donors.

Lipoprotein (a) (Lp(a)) and other lipid values have been correlated with angiographically defined [table: see text] coronary artery disease. To study this relationship in Indian patients, plasma levels of Lipoprotein (a) and other lipids were assessed in 74 patients undergoing Coronary arteriography and also in 53 age and sex matched healthy male blood bank donors who served as controls. Total cholesterol (mg/dl) (211 +/- 56 vs 186 +/- 43; p < 0.001), low density lipoprotein Cholesterol (mg/dl) (117 +/- 40 vs 88 +/- 29; p > 0.001) and low density lipoprotein/high density lipoprotein cholesterol ratio (2.6 +/- 0.8 vs 2.2 +/- 0.9; p < .001) were significantly higher in patients than controls. High density lipoprotein-cholesterol (mg/dl) (43.5 +/- 6 vs 42.1 +/- 7; p-ns) very low density lipoprotein-cholesterol (mg/dl) (49.7 +/- 17 vs 56.1 +/- 25; p-ns) and triglycerides (mg/dl) (155 +/- 101 vs 167 +/- 88; p-ns) were not statistically different in two groups. Lipoprotein (a) levels showed highly skewed distribution. Patients (n = 74) showed almost five fold higher lipoprotein (a) levels (mg/dl) as compared to controls (n = 53) [105 +/- 565 vs 23 +/- 76]. Patients with very high lipoprotein (a) levels [values of more than 40 mg/dl] (n = 18) had high density lipoprotein cholesterol and total cholesterol significantly lower than rest of the patient group. [high density lipoprotein cholesterol (mg/dl) 41.00 +/- 3.7 vs 44 +/- 6.4; p < 0.01 and total cholesterol (mg/dl) 192 +/- 34 vs 217 +/- 53; p < 0.05].

Apolipoprotein(a) polymorphism and its association with plasma lipoprotein(a) levels: a north Indian study.

Elevated levels of lipoprotein(a) has been regarded as an independent risk factor for coronary, peripheral and cerebral atherosclerosis. The enormous intra-personal variation in the plasma concentration of lipoprotein(a) is almost entirely controlled by the apolipoprotein(a) i.e. gene locus on the chromosome 6q 26-27. The apolipoprotein(a) molecule is highly polymorphic and is known to exist in multiple, genetically determined isoforms. These polymorphisms may be responsible for difference in promoter activity, variable size of apolipoprotein(a) and thereby variation in plasma lipoprotein(a) concentration. We studied the effect of two types of polymorphisms, (i) variation in length of the pentanucleotide repeat in the 5' flanking region starting -1373 bp upstream of AUG codon, and (ii) the Kringle-4 type 2 size polymorphism, on plasma lipoprotein(a) levels in North Indian population. The study group consisted of 88 angiographically assessed male coronary artery disease patients (age range 30-70 years) and 83 age- and sex-matched healthy controls. The pentanucleotide repeat polymorphism was analysed using polymerase chain reaction. In all, 8/11 pentanucleotide repeat isoforms were observed. Using SDS-agarose gel electrophoresis and immunoblotting isoforms having 12-50 Kringle-4 type 2 repeats were detected. Our study indicates a strong association of elevated plasma lipoprotein(a) concentration with coronary artery disease. An inverse correlation was seen between lipoprotein concentration and isoform size for both the pentanucleotide repeat polymorphism and the Kringle-4 type 2 polymorphisms; statistically significant difference (p = 0.001) was, however, observed only for the later.

Interrelationship between angiographically defined coronary artery disease, plasma insulin levels and lipids in Indian patients.

We investigated the interrelationship between plasma insulin levels, various lipoproteins and coronary artery disease. No significant differences were observed on comparing patients with controls for plasma insulin, high density lipoprotein cholesterol, fasting blood sugar levels and triglyceride levels. However patients showed significantly higher levels of total cholesterol and low density lipoprotein cholesterol compared with controls. No significant differences were observed on comparing patients of multivessel disease with single vessel disease in serum insulin or various lipid subfractions. In addition, there was no correlation between serum insulin quartiles and various biochemical parameters. In conclusion, in this cross-sectional study plasma insulin levels failed to show any significant association with severity and extent of coronary artery disease. Further there was no correlation of various lipid parameters with insulin quartiles.

Effect of alcohol on serum lipids & lipoproteins in male drinkers.

The evaluation of the effect of moderate and high doses of ethanol on the serum levels of triglyceride (TG), total cholesterol (TC), cholesterol content of very low density lipoprotein (VLDL), low density lipoprotein (LDL), high density lipoprotein (HDL), HDL2, HDL3 subfractions and apoproteins: apo-AI and apo-B was undertaken in 45 (25 controls, 10 moderate and 10 high dose drinkers) healthy males. The results of this preliminary study showed a significant rise in total HDL-cholesterol and apo-AI levels of alcoholics of both the groups. Out of the two subfractions, HDL2 appeared to be induced more. Increased levels of atherogenic lipids (TG, VLDL-chol., LDL-chol. and apo-B) were found in high as well as moderate drinkers. Our results suggest that the benefit of alcohol intake need to be weighed carefully against its considerable risks.