High density lipoprotein natural history, complications and prognosis: Difference between revisions
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==Chronic Kidney Disease== | |||
==Carcinoma== | ==Carcinoma== | ||
Revision as of 23:45, 20 September 2013
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High Density Lipoprotein Microchapters |
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Diagnosis |
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Treatment |
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Clinical Trials |
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Case Studies |
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High density lipoprotein natural history, complications and prognosis On the Web |
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aarti Narayan, M.B.B.S [2]; Raviteja Guddeti, M.B.B.S. [3]; Vendhan Ramanujam M.B.B.S [4]
Overview
The plasma levels of HDL are inversely proportional to the development of coronary artery disease (CAD) making HDL a negative cardiac risk factor.[1] Low serum HDL-cholesterol can be an isolated abnormality or can be associated with hypercholesterolemia. Patients with premature coronary artery disease, defined as CAD in men less than 55 to 60 years of age and women less than 65 years of age, have a primary reduction in HDL-cholesterol. Studies have shown that low HDL risk is independent of the risk attributed to elevated LDL-cholesterol (low density lipoprotein) in the serum. Findings from large scale prospective studies indicate that for every 1 mg/dL rise in serum HDL levels the risk of CAD reduces by 2% to 3% in men and women respectively.
Cardiovascular Risk
The Framingham Heart Study has shown that the risk of myocardial infarction increases by about 25% for every 5 mg/dL decrement in serum HDL-cholesterol below median values for both men and women.[2] According to the study the relative risk of death due to cardiovascular and coronary artery disease for men in the first HDL-C quintile (less than 35 mg/dL) as compared to the top quintile (greater than 54 mg/dL) is 3.6 and 4.1 respectively and for women the corresponding values were 1.6 and 3.1, comparing the bottom HDL-C quintile (less than 45 mg/dl) to the top quintile (greater than 69 mg/dl).
Studies have shown that in patients with known coronary artery disease HDL-C levels are predictive of coronary events over a broad range of LDL-C levels. The LIPID (Long-Term Intervention with Pravastatin in Ischemic Disease) trial[3] and the CARE (Cholesterol and Recurrent Events) trial[4] have shown that reduced serum HDL-C levels strongly predicted acute coronary events in patients with LDL-C less than 125 mg/dL compared to those with levels above 125 mg/dL. There was a significant reduction in the event rate in patients with LDL-C <125 mg/dL for every 10 mg/dL rise in HDL-C compared to those with LDL-C levels more than 125 mg/dL. A similar relationship between the levels of HDL-C and LDL-C was also shown in the Treating to New Targets (TNT) trial.[5]
Meta-analysis of 23 studies in the Asia-Pacific region showed that isolated low HDl-C, defined as <40 mg/dL in men and <50 mg/dL in women, is associated with an increased risk of cardiovascular events. But Mendelian randomization analyses failed to establish HDL-C as a causative factor for increased cardiovascular risk.
Genetic studies have shown that two polymorphisms in phospholipid transfer protein are associated with a lower cardiovascular risk and elevate concentrations of cholesterol depleted HDL in the serum. MESA (Multi-ethnic Study of Atherosclerosis) cohort, a multi-ethnic study, evaluated nearly 6000 individuals without known coronary artery disease who were not taking lipid lowering drugs to evaluate independent associations of high-density lipoprotein cholesterol (HDL-C) and particle (HDL-P) concentrations with carotid intima-media thickness (cIMT) and incident coronary artery disease (CAD). The result of this study was a persistently significant inverse relationship between HDL-P but not HDL-C and CAD risk.[6]
Cholesterylester Transfer Protein
Cholesteryl ester transfer protein (CETP) (also called plasma lipid transfer protein) is a plasma protein that facilitates the transport of cholesteryl esters and triglycerides between the lipoproteins. It collects triglycerides from very low density or low density lipoproteins (VLDL or LDL) and exchanges them for cholesteryl esters from high density lipoproteins (and vice versa). Most of the time, however, CETP does a homoexchange- trading a triglyceride for a triglyceride or a cholesteryl ester for a cholesteryl ester. Numerous case control studies have shown that elevated CETP levels were associated with increased CAD risk in patients with elevated triglyceride (TG) levels and decreased risk in those with low TG levels. Mutation I405V (Isoleucine for Valine substitution at codon 405) has been shown to be associated with reduced activity of CETP of increased levels of HDL-C in the plasma, but the consistency of this finding has not been proved in all studies.[7][8]
CAD in Pediatric Population
Premature CAD
CAD in Elderly
CAD in Women
CAD in AIDS
CAD in GH Deficiency
Post-CAD Treatment
CAD in Experimental Models
Post-Procedure
Congestive Heart Failure
Atrial Fibrillation
Chronic Kidney Disease
Carcinoma
Cirrhosis
Dementia
Kawasaki Disease
Sepsis
Stroke
References
- ↑ Rajagopal G, Suresh V, Sachan A (2012). "High-density lipoprotein cholesterol: How High". Indian J Endocrinol Metab. 16 (Suppl 2): S236–8. doi:10.4103/2230-8210.104048. PMC 3603035. PMID 23565387. Unknown parameter
|month=ignored (help) - ↑ Wilson PW, Abbott RD, Castelli WP (1988). "High density lipoprotein cholesterol and mortality. The Framingham Heart Study". Arteriosclerosis. 8 (6): 737–41. PMID 3196218.
- ↑ Simes RJ, Marschner IC, Hunt D; et al. (2002). "Relationship between lipid levels and clinical outcomes in the Long-term Intervention with Pravastatin in Ischemic Disease (LIPID) Trial: to what extent is the reduction in coronary events with pravastatin explained by on-study lipid levels?". Circulation. 105 (10): 1162–9. PMID 11889008. Unknown parameter
|month=ignored (help) - ↑ Pfeffer MA, Sacks FM, Moyé LA; et al. (1995). "Cholesterol and Recurrent Events: a secondary prevention trial for normolipidemic patients. CARE Investigators". Am. J. Cardiol. 76 (9): 98C–106C. PMID 7572695. Unknown parameter
|month=ignored (help) - ↑ Waters DD (2009). "Clinical insights from the Treating to New Targets trial". Prog Cardiovasc Dis. 51 (6): 487–502. doi:10.1016/j.pcad.2009.01.001. PMID 19410683.
- ↑ Mackey RH, Greenland P, Goff DC, Lloyd-Jones D, Sibley CT, Mora S (2012). "High-density lipoprotein cholesterol and particle concentrations, carotid atherosclerosis, and coronary events: MESA (multi-ethnic study of atherosclerosis)". J. Am. Coll. Cardiol. 60 (6): 508–16. doi:10.1016/j.jacc.2012.03.060. PMC 3411890. PMID 22796256. Unknown parameter
|month=ignored (help) - ↑ Darabi M, Abolfathi AA, Noori M; et al. (2009). "Cholesteryl ester transfer protein I405V polymorphism influences apolipoprotein A-I response to a change in dietary fatty acid composition". Horm. Metab. Res. 41 (7): 554–8. doi:10.1055/s-0029-1192034. PMID 19242900. Unknown parameter
|month=ignored (help) - ↑ Rejeb J, Omezzine A, Boumaiza I; et al. (2012). "Four polymorphisms of cholesteryl ester transfer protein gene and coronary stenosis in a Tunisian population". J Cardiovasc Med (Hagerstown). 13 (9): 546–53. doi:10.2459/JCM.0b013e3283569b24. PMID 22854712. Unknown parameter
|month=ignored (help)