Serum Lp(a) lipoprotein concentration is not associated with clinical and angiographic outcome five years after coronary artery bypass graft surgery (original) (raw)
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BMC Cardiovascular Disorders, 2016
Background: Lipoprotein(a) (Lp(a)) excess is an independent risk factor of coronary artery disease (CAD) and have shown wide ethnic variations. Further, lipid parameters used in the assessment and management of risk factors for CAD may not reflect accurately the disease or severity if the patients are on pharmacological interventions when compared to Lp(a). Lp(a) levels of Sri Lankan CAD patients awaiting coronary artery bypass graft are not documented. Methods: A cross sectional study was carried out with patients (n = 102) awaiting coronary artery bypass graft at a tertiary healthcare institution in Sri Lanka. Lp(a) was determined by immunoturbidimetric method (Konelab 20XT) and information on risk factors collected using a standardized questionnaire. The severity of CAD was determined by Gensini score. Lipid parameters and pharmacological treatment data were obtained from the Medical Records. Data were analysed using independent sample t-test, Pearson and Spearman tests respectively. Results: Total cholesterol (TC), LDL cholesterol (LDLc) and HDL cholesterol (HDLc) of the total study sample (average ± SD) were, 150 ± 36 mg/dL, 92 ± 36 mg/dL and 34 ± 9 mg/dL respectively with no significant difference irrespective of being on pharmacological treatment or not. All lipid parameters were significantly high (p < 0.05) in females. The average Lp(a) was 50 ± 38 (SD) mg/dL with no significant difference in males or females independent of being on treatment (50 ± 39 mg/dL) or not (49 ± 39 mg/dL) and above the cut off value (30 mg/dL). Conclusions: Despite pharmacological interventions 27 % of the study population had high LDLc and majority low HDLc. Mean Lp(a) was in excess irrespective of risk factors or being on treatment or not and is confirmed as an independent, potential marker for assessing the susceptibility for CAD especially in those with other intermediate risk factors but considered non-hyperlipidemic by conventional methods.
Lipoprotein(a) Changes during and after Coronary Artery Bypass Grafting: An Epiphenomenon?
Annals of Clinical Biochemistry: International Journal of Laboratory Medicine, 1998
The lipoprotein(a) (Lp(a)) time course during and after coronary artery bypass grafting was examined in 20 caucasoid patients, in relation to the time courses of serum cholesterol and serum triglycerides. Samples were taken at eight different time points. Baseline geometric means (SD) for Lp(a), cholesterol and triglycerides were 115 (336) mg/L, 5.73 (1.10) mmol/L and 1.73 (1.21) mmol/L, respectively. Up to 10 min after cardiopulmonary bypass (CPB) and after correction for haemodilution, no observable effect of CPB on serum concentrations of Lp(a) could be demonstrated, whereas serum concentrations of total cholesterol and triglycerides showed a progressive and significant decline. Ten minutes after stopping CPB geometric means for cholesterol and triglyceride were 3.90 (0.82) and 0.90 (0.58) mmol/L, respectively. At the third post-operative day geometric Lp(a) and cholesterol means decreased to 62 (90) mg/L and 2.97 (0.84) mmol/L, respectively, while triglycerides went up. It is co...
The American Journal of Cardiology, 2015
Cardiovascular risk remains uncertain in patients with cardiovascular disease (CVD) despite achieving target lipid levels. Serum levels of lipoprotein (a) [Lp(a)] can be risk factors for adverse events. Aim of this study was to determine the role of Lp(a) as a residual risk factor in patients who achieve target lipid levels by the time of treatment by percutaneous coronary intervention (PCI). A total of 3,508 patients were treated by PCI between 1997 and 2011 at our institution. Among them, we analyzed consecutive 569 patients who achieved target lipid levels of low density lipoprotein cholesterol (LDL-C) < 100 mg/dL, high density lipoprotein cholesterol (HDL-C) ≥ 40 mg/dL and triglycerides <150 mg/dL at PCI. Eligible 411 patients were assigned to groups according to Lp(a) levels of ≥ 30 mg/dL [high Lp(a)] (n=119) or < 30 mg/dL [low Lp(a)] (n=292). The primary outcome was a composite of all-cause death and acute coronary syndrome (ACS). The median follow-up period was 4.7 years. Cumulative event-free survival was significantly worse for the group with high Lp(a) than with low Lp(a) group (P = 0.04). Multivariable analysis selected a high Lp(a) level as an independent predictor of primary outcomes (hazard ratio [HR], 1.68; 95% confidence interval [95%CI],1.03-2.70; p=0.04). In conclusion, A high Lp(a) value (≥30 mg/dL) could be associated with a poor prognosis after PCI even for patients who achieved target lipid levels.
Lipid Control before CABG and Its Association with In-Hospital Mortality
Iranian Red Crescent medical journal, 2011
Controlling risk factors such as dyslipidemia in patients with coronary artery disease, including candidates for coronary artery bypass grafting (CABG), is of great importance and has serious effects on CABG morbidity and mortality. The aim of this study was to evaluate lipid serum levels, comprising TG, LDL, and HDL, before CABG and their relation with in-hospital outcome. The clinical profiles of 3,593 patients in the hospital cardiac surgery databank who underwent isolated CABG between April 2006 and April 2008 were reviewed. Three components of lipid profile, including TG, LDL, and HDL serum levels, were checked at the time of hospitalization in all the patients. Lipid control was evaluated according to the published guidelines. The mean LDL, HDL, and TG serum levels were 103.4±48.5, 40.9±16, and 168±87 mg/dl, respectively. Additionally, 487 (13.6%) patients had entire TG, LDL, and HDL serum levels within the acceptable range and in 668 (18.6%) patients, all of these components ...
Atherosclerosis, 1999
The reported results (The Post Coronary Artery Bypass Graft Trial Investigators. The effect of aggressive lowering of low-density lipoprotein cholesterol levels and low-dose anticoagulation on obstructive changes in saphenous-vein coronary-artery bypass grafts. New Engl J Med 1997;336:153-162) of the Post Coronary Artery Bypass Graft (Post CABG) trial have shown that aggressive lowering was more effective than moderate lowering of low density lipoprotein (LDL) cholesterol in reducing the progression of atherosclerosis in saphenous-vein grafts (27 vs. 39%; PB 0.001); low dose warfarin had no effect on the progression of atherosclerosis. The present report describes the effect of long-term (an average of 4.3 years) aggressive treatment with high (40-80 mg/day) and moderate treatment with low (2.5-5 mg/day) doses of lovastatin on lipids, apolipoproteins (apo) and apoAand apoB-containing lipoprotein families. To achieve the target LDL-cholesterol levels (60 -85 mg/dl for aggressive group and 134-140 mg/dl for moderate group), cholestyramine (8 g/day) was given to 25% of subjects on aggressive and 5% of subjects on moderate treatment. Although with both treatment strategies there were significant decreases (P B 0.001) in the levels of total cholesterol, LDL-cholesterol, apoB, LDL-apoB and cholesterol-rich Lp-B family, percent changes in the levels of these variables were greater in the aggressive-than in the moderate-treatment groups. These treatments had only marginal effects in increasing the levels of high density lipoprotein cholesterol, apoA-I and Lp-A-I and Lp-A-I:A-II families. The long-term aggressive treatment exerted no effect on the concentrations of triglycerides, apoC-III, apoC-III in VLDL +LDL and triglyceride-rich Lp-B c families. Neither treatment affected the levels of Lp(a). The potentially modifying influence of warfarin and apoE phenotypes on lovastatin-induced changes in lipoprotein variables was found to be of little significance. It is likely that the beneficial effect of lovastatin in reducing the progression of atherosclerosis in grafts is mediated through its specific lowering effect on cholesterol-rich Lp-B particles.
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.