Elevated Lp(a) Levels Correlate with Severe and Multiple Coronary Artery Stenotic Lesions (original) (raw)
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LP(a) phenotypes and levels in angiographically proven coronary heart disease patients and controls
Indian Journal of Clinical Biochemistry, 1998
Lipoprotein Lp(a) excess has been identified as a powerful predictor of premature atherosclerotic vascular diseases. To evaluate this in a North-Indian population, 130 CAD patients and 130 controls were analyzed. The size of the apo(a) phenotypic isoforms was inversely proportional to Lp(a) concentrations. The mean concentration of Lp(a) in the CAD patients was 42±34 mg/dl whereas in the normal subjects it was much lower, 27±27 mg/dl. 157 subjects out of the total 260 subjects showed plasma levels of >20mg/dl. The frequency of high Lp(a) levels was much higher in patients(73%) than controls (43%). These data suggest (1) that there is heterogeneity of the Lp(a) polymorphism, (2) Higher Lp(a) levels were found in patients than in the controls, (3) Patients showed 1.5 fold increase in Lp(a) levels as compared to the controls. We conclude that low molecular weight apo(a) isoforms are significantly associated with increased risk of CAD in the North-Indian population.
High Level of Lipoprotein (a) is a Strong Predictor for Progression of Coronary Artery Disease
Journal of Atherosclerosis and Thrombosis, 1998
Elevated levels of serum lipoprotein(a)[Lp(a)] are reported to be associated with risk of atherosclerosis and thrombosis. Little is known about the influence of Lp(a) on the progression of coronary artery disease. We evaluated the association of serum Lp(a) and the longterm changes of angiographic severity in patients who underwent repeated coronary angiography at intervals of more than 2 years. We evaluated 70 patients, and divided them into 3 groups by angiographic findings. Median Lp(a) concentration was significantly higher in the progression group (N = 36) than in the no-change group (N = 23) or the regression group (N =11) (32.4 vs 22, 19.3 mg/dl, p < 0.05). Furthermore, the progression group had more patients whose Lp(a) levels were greater than 30 mg/dl (p = 0.006), while in the regression group all patients were under 30 mg/dl. Stepwise logistic regression analysis for progression of lesions showed that Lp(a) 30 mg/dl remainedsignificant, giving an estimated odds ratio (OR) of 2.46 (p = 0.005). In the subgroup analysis, OR in patients with mild lesions was reduced to 2.05 (p < 0.05) while in patients with severe lesions OR was increased to 3.39 (p = 0.003). The serum Lp(a) level has a close correlation with angiographic progression, and may be an important predictor for progression.
Clinical Cardiology, 1995
Lipoprotein (a) [Lp(a)] concentrations were determined in 365 patients undergoing coronary angiography for stable angina (n = 159), unstable angina (n = 99), recent myocardial infarction (n = 43, and nonischetnic heart disease (cardiomyopathy or valvular disease, n = 62, non-IHD). Mean k SD and median Lp(a) concentrations in stable angina (29.9 f 29.2; 22 mddl) did not differ from those in non-IHD (26.9 f 26.3; 17), but were significantly lower than in patients with unstable angina (52.7 k 36.6; 58) and myocardial infarction (44.8 f 36.4; 34) (p < 0.01). Coronary angiography revealed that 261 patients, including 4 patients in the non-IHD group, had significant (250%) coronary lesions. Lp(a) was higher in patients with (41 ? 35; 32) than in those without (28 f 27; 19) angiographic evidence of significant coronary stenosis (p < 0.05) and showed a weak univariate correlation with the angiographic index (Total Score) of the severity of the disease (r = 0.106; p < 0.05). However, in the subgroup of303 patients with stable/unstable angina or myocardial infarction, Lp(a) was predictive neither of angiographic presence nor of seventy of coronary disease. Patients were then ranked according to the Total Score values. Among patients with comparable angiographic severity of coronary artery disease, Lp(a) appeared to be remarkably higher in patients with acute ischemic syndromes (unstable angina, myocardial infarction) than in patients with stable angina. In conclusion, Lp(a) was roughly twice as high in acute (unstable angina, myocardial infarction) than in chronic (stable angina) ischemic syndromes, but there was no difference between chronic stable angina and non-IHD. Serum level determination of Lp(a) made a poor contribution in predicting the extent of coronary artery disease.
Lipoprotein (a) as a predictor of coronary heart disease: the PRIME Study
Atherosclerosis, 2002
The association of an elevated level of lipoprotein (a) (Lp(a)) with the development of coronary heart disease (CHD) remains controversial. Lp(a) was investigated as a CHD risk factor in the PRIME Study, a prospective cohort study which included 9133 French and Northern Irish men aged 50-59 at entry, without a history of CHD and not on hypolipidaemic drugs. During a follow-up of 5 years, 288 subjects experienced at least one CHD event (myocardial infarction (MI), coronary death, angina pectoris). Lp(a) was measured by immunoassay in all subjects on fresh plasma obtained at entry. Traditional cardiovascular risk factors such as low-density lipoproteins (LDL)-cholesterol, HDL-cholesterol, triglycerides, the presence of diabetes, hypertension or smoking were determined. Logistic regression analysis was used to evaluate Lp(a) level as a CHD risk factor after controlling for the other risk factors. In addition, its possible interaction with LDL- and HDL-cholesterol levels was investigated. Lp(a) appeared a significant risk factor (P&amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt;0.0006) in the whole cohort without between-population interaction, even if the association was not statistically significant in the Belfast sample. The relative risk (RR) of CHD events in subjects with Lp(a) levels in the highest quartile was 1.5 times that of subjects in the lowest quartile (RR: 1.56; 95% confidence intervals (CIs): 1.10-2.21). A high Lp(a) level was a risk for MI, coronary death and angina pectoris. A significant interaction term between Lp(a) and LDL-cholesterol levels, however, was found. The relative CHD risk associated with a Lp(a) level &amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;gt; or =33 mg/dl in comparison with Lp(a) &amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt;33 mg/dl increasing gradually from 0.82 (95% CI: 0.28-2.44) in men with LDL-cholesterol in the lowest quartile (&amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt;121 mg/dl) to 1.58 (95% CI: 1.06-2.40) in the highest quartile (&amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;gt;163 mg/dl). In conclusion, Lp(a) increased the risk for MI and angina pectoris, especially in men with a high LDL-cholesterol level. This study which analyzed Lp(a) level using a measurement independent of apolipoprotein (a) size on fresh plasma, has confirmed utility of Lp(a) as a predictor of CHD.
Journal of Biosciences and Medicines, 2015
Atherosclerosis is the most important contributor to increasing burden of coronary artery disease (CAD). Growing evidence suggests that the ratios of Apo B/Apo A-I and Lp(a) are better indexes for risk assessment of CAD. Elevated plasma levels of lipoprotein(a) in humans represent a major inherited risk factor for atherosclerosis. Thus, a study was performed to determine the association betwwen serum Apo B, Apo A-I, and lipoprotein(a) levels, and severity of CAD in patients with CAD confirmed on coronary angiography findings. An analytical case control study was carried out with 85 patients (58 males and 27 females) 40 -60 years of age confirmed as having CAD on coronary angiography and 85 age and sex matched healthy volunteers as controls. Serum samples were analyzed for Apo A-1 LDL, Apo B, Apo A-I, and lipoprotein(a) concentration and the severity of CAD was assessed using coronary angiography scoring method. Patients with CAD had significantly high serum LDL-C, Apo B and Lp(a) levels compared to control subjects. However, serum Apo A-I level did not show a significant difference between two groups. Subjects with a positive family history of CAD with increased serum Lp(a) ≥ 17.3 mg/dL have high risk for development of CAD. Present study suggests that serum Lp(a) cut-off value of 17.3 mg/dL may be an important predictor in ruling out major vessel disease and luminal narrowing by atheroma.
Bangladesh Journal of Medical Science, 2016
Background: In 2020 there were estimated to be 25 million deaths each year from cardiovascular disease; most of them being coronary heart disease. Traditional risk factors such as smoking, hypertension, diabetes, dyslipidemia reported to affect only 50% of the prevalence and degree of coronary heart disease. It pushes a lot of research on non-traditional risk factors one of which is lipoprotein (a). Levels of Lp (a) also reflects the degree of severity and is associated with the number of coronary arteries involved. The purpose of this study was to determine the relationship of Lp (a) level with the complexity of coronary artery lesion. Methods: This was a cross-sectional study. Subjects were male and women patients aged between 20 to 60 years who underwent coronary angiography for theirs STEMI, NSTEMI, unstable angina pectoris, and stable angina pectoris. Correlation between elevated Lp (a) with the complexity of coronary artery lesion was performed by Pearson test. If the distribution was abnormal we used Spearman test. Result: Number of samples was 64 subjects (49 men and 15 women). The result showed a significant positive correlation between Lp (a) level and complexity of coronary vessel lesion that counted by SYNTAX score (p 0,004) even though the coefficient correlation is weak (r 0, 33). Conclusion: The higher Lp (a) level shows bigger SYNTAX score which means the coronary vessel lesion more complex.
Molecular and Cellular Biochemistry, 2020
Calcific aortic valve disease (CAVD) is a common cardiovascular disorder of high social significance. This study aimed to identify independent predictors of hemodynamic progression of CAVD. The relationship between some risk factors, including the rs10455872 polymorphism in the intron 25 of the lipoprotein(a) [Lp(a)] coding region and the plasma Lp(a) concentration, and CAVD severity were prospectively examined in 114 patients. Age (p = 0.023), smoking (p = 0.038), lack of obesity (p = 0.005), triglyceride levels (p = 0.039), and plasma Lp(a) (p < 0.0001) levels were found to be significant determinants of stenosis progression. The rs10455872 polymorphism; however, was not found to be a significant factor for neither the stenosis severity (p = 0.773) nor for plasma Lp(a) levels (p = 0.617). We established a highly significant Lp(a) cutoff concentration (21.2 mg/dL) distinguishing the aortic valve calcification without stenosis from the significant stenosis. Plasma Lp(a) concentration was the only independent predictor of disease progression (p < 0.0001). Moreover, patients with plasma levels of Lp(a) ≥ 21.2 mg/dL were 55 times more likely to develop aortic valve stenosis. We conclude that Lp(a) concentration may prove valuable for more reliable identification of patients at risk of accelerated CAVD development. Future studies are desirable to determine whether plasma Lp(a) levels could be used as a potential biomarker for aortic stenosis progression.
Apolipoprotein(a) phenotypes predict the severity of coronary artery stenosis
Clinical and investigative medicine. Médecine clinique et experimentale, 2002
Studies on the impact of elevated levels of lipoprotein(a) (Lp[a]) or apolipoprotein(a) (apo[a]) on the development of coronary artery disease have given controversial results. The relationship between apo(a) phenotypes and coronary artery stenosis remains unclear. Lipid profiles, and apo(a) levels and phenotypes were analyzed in 225 patients who underwent elective coronary angiography. Coronary artery stenosis, as indicated by angiography, was estimated by a newly devised minimal lesion (ML) grading system. Relationships between lipoprotein variables and coronary artery stenosis were examined by linear and logistic regression models. On the basis of ML score, patients with larger apo(a) phenotypes (S3, S3a or S4) had a lower rate of coronary artery stenosis (68%-76%) than those with smaller phenotypes (S1, S1a, S2 or S2a - 79%-95%). The odds of coronary artery stenosis in patients with smaller apo(a) phenotypes were significantly different from those of patients with larger phenoty...