HDL (Good), LDL (Bad) Cholesterol and Triglycerides | American Heart Association
In a subset of patients in both the highest triglyceride (> mg/dl) and lowest HDL-C Relationships between lipoproteins and cardiovascular events were. The American Heart Association explains LDL cholesterol, HDL cholesterol, triglycerides, Two types of lipoproteins carry cholesterol to and from cells. One is A healthy HDL cholesterol level may protect against heart attack and stroke. Over 50% of people with “normal cholesterol” still develop heart attacks. Why? Lipoproteins, not cholesterol, cause heart disease. Lipoproteins are the carriers.
The half-life of Lp a in the circulation is about 3 to 4 days Rader et al. Ethnicity is a factor, with those of Asian and African origin averaging the highest concentrations. Within ethnic groups, individual elevation of Lp a is directly associated with increased risk of cardiovascular diseases Sandholzer et al.
Lp a is usually unaffected by factors like age, blood pressure, and total cholesterol. Similarity between lipoprotein a and plasminogen The structure of Lp a is similar to plasminogen, a naturally occurring glycoprotein that participates in dissolving of clots that form in the bloodstream, and tissue plasminogen activator tPA. Lp a competes with plasminogen for its binding site, leading to reduced fibrinolysis Loscalzo et al.
Also because Lp a stimulates secretion of PAI-1 it leads to thrombogenesis. In addition, because of LDL cholesterol content, Lp a contributes to atherosclerosis Schreiner et al. Correlation between apolipoprotein size and Lp a concentration There is a general inverse correlation between the size of the apo a isoform and the Lp a plasma concentration Bowden et al. The plasma concentration of Lp a is unaffected by many physiological, pharmacological, and environmental factors that affect the levels of other plasma lipoproteins Albers et al.
Lipoprotein(a). What is lipoprotein(a) and why is it important?
A genetic determination of plasma Lp a levels was strongly suggested due to this lack of environmental and physiological influences. Consistent with this formulation, early genetic studies suggested that the presence of Lp a in plasma was inherited as a single autosomal dominant trait Berg and Mohr, ; Iselius et al. Plasma Lp a concentrations vary fold between individuals and represent a continuous quantitative genetic trait with a skewed distribution in Caucasian populations Utermann, A study was conducted by Lackner et al.
It was found that within a given family, sibling pairs with identical apo a genotypes tended to have very similar plasma Lp a levels Lackner et al. However, individuals with the same apo a genotypes who were members of different families often had significantly different plasma concentrations of Lp a. Taken together, these observations suggest that the apo a gene is the major determinant of plasma Lp a levels and that cis-acting DNA sequences at or near the apo a locus, other than the number of kringle 4 repeats, contribute importantly to plasma Lp a concentrations Boerwinkle et al.
Variation in the hypervariable apo a gene on chromosome 6q2. Furthermore, the size of the apo a glycoprotein varies in individuals and this size is inversely correlated with the plasma level of Lp a.
The reason for the inverse correlation between the size of the apo a gene and level of plasma Lp a is not known, but a variation of length within the kringle 4-encoding region of the apo a gene may account for a greater proportion of the inter-individual variation in plasma Lp a concentrations. Also, the number of kringle 4 repeats in the gene may not have a direct effect on plasma Lp a concentration Boerwinkle et al. A study conducted on apo a gene of mamorset monkeys showed a plasma Lp a concentration of a very wide range of over a fold, but only one apo a isoform Guo et al.
This may be explained by the differences in the composition of kringle 4 sequence of apo a genes in which individuals may have same sizes of apo a alleles but different plasma Lp a concentrations.
Role of oxidation in atherogenesis Oxidative stress, especially LDL oxidation has been suggested for almost three decades as the most probable aetiology of atherosclerosis Steinbrecher et al.
Markers of LDL oxidation in plasma, particularly circulating oxidized LDL and auto-antibodies against oxidized LDL, could be used to assess the development of atherosclerosis in patients Carmena et al. Circulating oxidized LDL is additive to the global risk score based on age, sex, total and HDL cholesterol, diabetes mellitus, hypertension, and smoking as a useful marker for identifying persons at risk for CAD Holvoet et al. This conclusion supports the concept that oxidatively modified LDL may play a major role in development of atherosclerosis Hulthe and Fagerberg, It has been proposed that, because of the antigenic properties of oxidized LDL, the anti-oxidized LDL antibody titer could represent a useful index of in vivo LDL oxidation.
Autoantibodies against oxidized LDL have been reported to be associated with atherosclerosis, but existing reports are still conflicting. There is a strong cross-reactivity between autoantibodies against oxidized LDL and anticardiolipin antibodies, which have been positively associated with CHD Erkkila et al.
Relationship between insulin resistance, diabetes, and small, dense LDL Cardiovascular heart disease risk is usually significantly increased when elevated levels of small, dense LDL accompanied by hypertriglyceridemia, reduced HDL-cholesterol levels, abdominal obesity, and insulin resistance.
Sensitivity to insulin in diabetic and non-diabetic individuals was assessed using nuclear magnetic resonance NMR spectroscopy. Insulin resistance had profound effects on lipoprotein size and an increase in serum triglycerides. In type 2 diabetes, these alterations could be attributed primarily to the underlying insulin resistance.
LDL & HDL: Good & Bad Cholesterol | posavski-obzor.info
These changes in the NMR lipoprotein subclass profile predictably increased the risk of cardiovascular disease but were not fully apparent in the conventional lipid profile Garvey et al.
This effect was related in part to the correction of lipoprotein abnormalities. Compared with placebo, fenofibrate treatment significantly increased LDL particle size and HDL cholesterol and decreased plasma total cholesterol, LDL cholesterol, and triglyceride concentrations. The final LDL particle size was inversely correlated with the increase in percentage diameter stenosis Vakkilainen et al.
Dyslipoproteinaemia Dyslipoproteinaemia is a term broadly used for derangement in lipid and lipoprotein metabolism, which may either be hyperlipoproteinaemia or hypolipoproteinaemia. Dyslipoproteinaemias are generally classified as familial primary or acquired secondary. This chapter discusses hyperlipoproteinaemia with its close relevance to development of cardiovascular diseases.
Primary hyperlipoproteinaemias are of genetic origin and may be due to a mutation in a receptor protein which presents as inborn errors of lipid metabolism, and includes common hypercholesterolemia, combined familiar hyperlipidemia, familiar hypercholesterolemia, familiar hypertriglyceridemia, VLDL remnants hyperlipidemia and primary chylomicronaemia Garmendia, They divided primary hyperlipoproteinaemias into four types and details are show in Table 3 below.
The secondary hyperlipoproteinemias also mimic primary types and may present with similar symptoms. Secondary dyslipoproteinaemias are usually due to other underlying causes that lead to alterations in plasma lipid and lipoprotein metabolism, including hypothyroidism, diabetes mellitus, nephrotic syndrome, chronic biliary obstruction, renal insufficiency. Some drugs modify lipid metabolism and these include alcohol, beta-adrenergic blockers, diuretics, progestagens, corticosteroids Garmendia, Treatment of the underlying cause or discontinuation of offending drug may resolve the dyslipoproteinaemia.
Lipid and lipoprotein abnormalities are common observations and are regarded as modifiable risk factors for development of cardiovascular diseases.
Lipoproteins and Cardiovascular Diseases
According to a statement from the EAS; … the evidence clearly supports Lp a as a priority for reducing cardiovascular risk, beyond that associated with LDL-C.
Clinicians should consider screening statin-treated patients with recurrent heart disease, in addition to those considered at moderate to high risk of heart disease.
What Is Lp a? Lipoproteins are the particles that transport cholesterol and triglycerides in the blood stream. Lipoproteins are composed of proteins apolipoproteinsphospholipids, triglycerides and cholesterol. The lipoproteins vary in the major lipoprotein present and the relative contents of the different lipid components.
Lp a is a lipoprotein rich in cholesterol. It as assumed that Lp a is produced by liver cells. However, the pathways for the clearance of this substance are not clearly understood. Plasma levels of Lp a rise shortly after birth and the levels appear to become consistent within a few months. In adults, plasma levels of Lp a vary widely, ranging from 0.
The levels are similar in men and women. A meta-analysis of prospective studies provided evidence of a link between Lp a and coronary artery disease. Studies on patients with familial hypercholesterolemia have provided additional evidence. Studies have indicated that the association between Lp a and CVD is without a threshold, and does not depend on high levels of LDL or non-HDL cholesterolor the presence of other cardiovascular risk factors.
Lp a and LDL penetrate the inner layer of the arterial wall and accumulate together at sites for atherosclerotic plaque formation. FurthermoreLp a transports oxidized phospholipids whose plasma levels are strongly correlated with the severity of coronary artery disease.
Interestingly, these Lp a associated oxidized phospholipids possess pro-inflammatory activity.