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==Overview==
==Overview==
The natural history and prognosis of patients with elevated LDL are directly related to the complications associated with [[dyslipidemia]]. The decreased affinity of small dense LDL particles for LDL receptors has been postulated to be the cause of atherogenic properties of small dense LDL.<ref name="pmid8994419">{{cite journal| author=Lamarche B, Tchernof A, Moorjani S, Cantin B, Dagenais GR, Lupien PJ et al.| title=Small, dense low-density lipoprotein particles as a predictor of the risk of ischemic heart disease in men. Prospective results from the Québec Cardiovascular Study. | journal=Circulation | year= 1997 | volume= 95 | issue= 1 | pages= 69-75 | pmid=8994419 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8994419 }} </ref> They are more prone to oxidation,<ref name="pmid1590824">{{cite journal| author=Tribble DL, Holl LG, Wood PD, Krauss RM| title=Variations in oxidative susceptibility among six low density lipoprotein subfractions of differing density and particle size. | journal=Atherosclerosis | year= 1992 | volume= 93 | issue= 3 | pages= 189-99 | pmid=1590824 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1590824 }} </ref> have higher affinity to vascular proteoglycans,<ref name="pmid9519339">{{cite journal| author=Chapman MJ, Guérin M, Bruckert E| title=Atherogenic, dense low-density lipoproteins. Pathophysiology and new therapeutic approaches. | journal=Eur Heart J | year= 1998 | volume= 19 Suppl A | issue= | pages= A24-30 | pmid=9519339 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9519339 }} </ref> and are preferentially phagocytosed by [[macrophage]]s via scanvenger proteins that promote [[atherosclerosis]].<ref name="pmid16357786">{{cite journal| author=Vergès B| title=New insight into the pathophysiology of lipid abnormalities in type 2 diabetes. | journal=Diabetes Metab | year= 2005 | volume= 31 | issue= 5 | pages= 429-39 | pmid=16357786 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16357786 }} </ref> Accordingly, high LDL concentrations are not only associated with the initiation of atherogenesis, but also with the gradual worsening of atherosclerosis.<ref name="pmid8994405">{{cite journal| author=Grundy SM| title=Small LDL, atherogenic dyslipidemia, and the metabolic syndrome. | journal=Circulation | year= 1997 | volume= 95 | issue= 1 | pages= 1-4 | pmid=8994405 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8994405 }} </ref> Patients with elevated plasma LDL who are left untreated often develop [[atherosclerosis]] and [[cardiovascular disease]] ([[CVD]]). More importantly, the risk of CVD further increases when dyslipidemia is associated with other cardiovascular risk factors, such as diabetes mellitus, hypertension, and low HDL, which are often concomitantly present among patients with dyslipidemia.<ref name="pmid8432214">{{cite journal| author=Stamler J, Vaccaro O, Neaton JD, Wentworth D| title=Diabetes, other risk factors, and 12-yr cardiovascular mortality for men screened in the Multiple Risk Factor Intervention Trial. | journal=Diabetes Care | year= 1993 | volume= 16 | issue= 2 | pages= 434-44 | pmid=8432214 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8432214 }} </ref><ref name="pmid7259370">{{cite journal| author=Gordon T, Kannel WB, Castelli WP, Dawber TR| title=Lipoproteins, cardiovascular disease, and death. The Framingham study. | journal=Arch Intern Med | year= 1981 | volume= 141 | issue= 9 | pages= 1128-31 | pmid=7259370 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=7259370 }} </ref>
 
 
The natural history and prognosis of patients with elevated LDL are directly related to the complications associated with [[dyslipidemia]]. High LDL concentrations are not only associated with the initiation of atherogenesis, but also with the gradual worsening of atherosclerosis.<ref name="pmid8994405">{{cite journal| author=Grundy SM| title=Small LDL, atherogenic dyslipidemia, and the metabolic syndrome. | journal=Circulation | year= 1997 | volume= 95 | issue= 1 | pages= 1-4 | pmid=8994405 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8994405 }} </ref> Patients with elevated plasma LDL who are left untreated often develop [[atherosclerosis]] and [[cardiovascular disease]] ([[CVD]]). More importantly, the risk of CVD further increases when dyslipidemia is associated with other cardiovascular risk factors, such as diabetes mellitus, hypertension, and low HDL, which are often concomitantly present among patients with dyslipidemia.<ref name="pmid8432214">{{cite journal| author=Stamler J, Vaccaro O, Neaton JD, Wentworth D| title=Diabetes, other risk factors, and 12-yr cardiovascular mortality for men screened in the Multiple Risk Factor Intervention Trial. | journal=Diabetes Care | year= 1993 | volume= 16 | issue= 2 | pages= 434-44 | pmid=8432214 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8432214 }} </ref><ref name="pmid7259370">{{cite journal| author=Gordon T, Kannel WB, Castelli WP, Dawber TR| title=Lipoproteins, cardiovascular disease, and death. The Framingham study. | journal=Arch Intern Med | year= 1981 | volume= 141 | issue= 9 | pages= 1128-31 | pmid=7259370 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=7259370 }} </ref>
 
 
The decreased affinity of small dense LDL particles for LDL receptors has been postulated to be the cause of atherogenic properties of these small dense LDL particles<ref name="pmid8994419">{{cite journal| author=Lamarche B, Tchernof A, Moorjani S, Cantin B, Dagenais GR, Lupien PJ et al.| title=Small, dense low-density lipoprotein particles as a predictor of the risk of ischemic heart disease in men. Prospective results from the Québec Cardiovascular Study. | journal=Circulation | year= 1997 | volume= 95 | issue= 1 | pages= 69-75 | pmid=8994419 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8994419 }} </ref> They are more prone to oxidation,<ref name="pmid1590824">{{cite journal| author=Tribble DL, Holl LG, Wood PD, Krauss RM| title=Variations in oxidative susceptibility among six low density lipoprotein subfractions of differing density and particle size. | journal=Atherosclerosis | year= 1992 | volume= 93 | issue= 3 | pages= 189-99 | pmid=1590824 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1590824 }} </ref> have higher affinity to vascular proteoglycans,<ref name="pmid9519339">{{cite journal| author=Chapman MJ, Guérin M, Bruckert E| title=Atherogenic, dense low-density lipoproteins. Pathophysiology and new therapeutic approaches. | journal=Eur Heart J | year= 1998 | volume= 19 Suppl A | issue= | pages= A24-30 | pmid=9519339 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9519339 }} </ref> and are preferentially phagocytosed by [[macrophage]]s via scanvenger proteins that promote [[atherosclerosis]].<ref name="pmid16357786">{{cite journal| author=Vergès B| title=New insight into the pathophysiology of lipid abnormalities in type 2 diabetes. | journal=Diabetes Metab | year= 2005 | volume= 31 | issue= 5 | pages= 429-39 | pmid=16357786 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16357786 }} </ref>  
===Coronary artery disease===
===Coronary artery disease===
*Dyslipidemia caused by elevated LDL is a major risk factor for coronary artery disease (CAD) and often regarded as a prerequisite.<ref name="pmid21160056">{{cite journal| author=Roger VL, Go AS, Lloyd-Jones DM, Adams RJ, Berry JD, Brown TM et al.| title=Heart disease and stroke statistics--2011 update: a report from the American Heart Association. | journal=Circulation | year= 2011 | volume= 123 | issue= 4 | pages= e18-e209 | pmid=21160056 | doi=10.1161/CIR.0b013e3182009701 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21160056  }} </ref>  
*Dyslipidemia caused by elevated LDL is a major risk factor for coronary artery disease (CAD) and often regarded as a prerequisite.<ref name="pmid21160056">{{cite journal| author=Roger VL, Go AS, Lloyd-Jones DM, Adams RJ, Berry JD, Brown TM et al.| title=Heart disease and stroke statistics--2011 update: a report from the American Heart Association. | journal=Circulation | year= 2011 | volume= 123 | issue= 4 | pages= e18-e209 | pmid=21160056 | doi=10.1161/CIR.0b013e3182009701 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21160056  }} </ref>  
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*The majority of patients with elevated LDL have other components of the metabolic syndrome, such as hypertriglyceridemia, hypertension, and insulin resistance.<ref name="pmid16628021">{{cite journal| author=Solano MP, Goldberg RB| title=Management of dyslipidemia in diabetes. | journal=Cardiol Rev | year= 2006 | volume= 14 | issue= 3 | pages= 125-35 | pmid=16628021 | doi=10.1097/01.crd.0000188034.76283.5e | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16628021  }} </ref>
*The majority of patients with elevated LDL have other components of the metabolic syndrome, such as hypertriglyceridemia, hypertension, and insulin resistance.<ref name="pmid16628021">{{cite journal| author=Solano MP, Goldberg RB| title=Management of dyslipidemia in diabetes. | journal=Cardiol Rev | year= 2006 | volume= 14 | issue= 3 | pages= 125-35 | pmid=16628021 | doi=10.1097/01.crd.0000188034.76283.5e | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16628021  }} </ref>
===Stroke===
*The association between elevated LDL and stroke has been observed, but the association has not been as strongly established as in the case of coronary artery disease.<ref name="pmid7968073">{{cite journal| author=| title=Randomised trial of cholesterol lowering in 4444 patients with coronary heart disease: the Scandinavian Simvastatin Survival Study (4S) | journal=Lancet | year= 1994 | volume= 344 | issue= 8934 | pages= 1383-9 | pmid=7968073 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=7968073  }} </ref>
*Nonetheless, statin therapy is important in cerebrovascular events, especially among patients with other manifestations of atherosclerosis, namely coronary artery disease. Statin therapy may significantly reduce the rate of ischemic stroke by approximately 20-30%.<ref name="pmid7968073">{{cite journal| author=| title=Randomised trial of cholesterol lowering in 4444 patients with coronary heart disease: the Scandinavian Simvastatin Survival Study (4S) | journal=Lancet | year= 1994 | volume= 344 | issue= 8934 | pages= 1383-9 | pmid=7968073 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=7968073  }} </ref><ref name="pmid9841303">{{cite journal| author=| title=Prevention of cardiovascular events and death with pravastatin in patients with coronary heart disease and a broad range of initial cholesterol levels. The Long-Term Intervention with Pravastatin in Ischaemic Disease (LIPID) Study Group. | journal=N Engl J Med | year= 1998 | volume= 339 | issue= 19 | pages= 1349-57 | pmid=9841303 | doi=10.1056/NEJM199811053391902 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9841303  }} </ref>
*The true relation between elevated LDL levels and ischemic stroke as a complication is yet to be delineated.
===Carotid artery atherosclerosis===
*Elevated LDL is the primary risk factor for the initiation and development of carotid artery atherosclerosis.
*A reduction of LDL concentrations by at least 25% is associated with a significant reduction in the radiographic progression of carotid atherosclerosis


===Renovascular disease===
===Renovascular disease===
Line 21: Line 36:
*Oxidation of high concentrations of LDL, along with an increasein local and systemic oxidative stress, promotes the generation of reactive oxygen species (ROS) that cause vasoconstriction and worsen renal ischemia.<ref name="pmid17210599">{{cite journal| author=Meier P, Rossert J, Plouin PF, Burnier M| title=Atherosclerotic renovascular disease: beyond the renal artery stenosis. | journal=Nephrol Dial Transplant | year= 2007 | volume= 22 | issue= 4 | pages= 1002-6 | pmid=17210599 | doi=10.1093/ndt/gfl784 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17210599  }} </ref>
*Oxidation of high concentrations of LDL, along with an increasein local and systemic oxidative stress, promotes the generation of reactive oxygen species (ROS) that cause vasoconstriction and worsen renal ischemia.<ref name="pmid17210599">{{cite journal| author=Meier P, Rossert J, Plouin PF, Burnier M| title=Atherosclerotic renovascular disease: beyond the renal artery stenosis. | journal=Nephrol Dial Transplant | year= 2007 | volume= 22 | issue= 4 | pages= 1002-6 | pmid=17210599 | doi=10.1093/ndt/gfl784 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17210599  }} </ref>
*Emerging evidence currently favors the pharmacologic management of dyslipidemia for the treatment of renal artery stenosis compared to angioplasty.<ref name="pmid22279335">{{cite journal| author=Annigeri RA| title=Medical therapy is best for atherosclerotic renal artery stenosis: Arguments for. | journal=Indian J Nephrol | year= 2012 | volume= 22 | issue= 1 | pages= 1-4 | pmid=22279335 | doi=10.4103/0971-4065.91177 | pmc=PMC3263056 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22279335  }} </ref>
*Emerging evidence currently favors the pharmacologic management of dyslipidemia for the treatment of renal artery stenosis compared to angioplasty.<ref name="pmid22279335">{{cite journal| author=Annigeri RA| title=Medical therapy is best for atherosclerotic renal artery stenosis: Arguments for. | journal=Indian J Nephrol | year= 2012 | volume= 22 | issue= 1 | pages= 1-4 | pmid=22279335 | doi=10.4103/0971-4065.91177 | pmc=PMC3263056 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22279335  }} </ref>
===Stroke===
*The association between elevated LDL and stroke has been observed, but the association has not been as strongly established as in the case of coronary artery disease.<ref name="pmid7968073">{{cite journal| author=| title=Randomised trial of cholesterol lowering in 4444 patients with coronary heart disease: the Scandinavian Simvastatin Survival Study (4S) | journal=Lancet | year= 1994 | volume= 344 | issue= 8934 | pages= 1383-9 | pmid=7968073 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=7968073  }} </ref>
*Nonetheless, statin therapy is important in cerebrovascular events, especially among patients with other manifestations of atherosclerosis, namely coronary artery disease. Statin therapy may significantly reduce the rate of ischemic stroke by approximately 20-30%.<ref name="pmid7968073">{{cite journal| author=| title=Randomised trial of cholesterol lowering in 4444 patients with coronary heart disease: the Scandinavian Simvastatin Survival Study (4S) | journal=Lancet | year= 1994 | volume= 344 | issue= 8934 | pages= 1383-9 | pmid=7968073 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=7968073  }} </ref><ref name="pmid9841303">{{cite journal| author=| title=Prevention of cardiovascular events and death with pravastatin in patients with coronary heart disease and a broad range of initial cholesterol levels. The Long-Term Intervention with Pravastatin in Ischaemic Disease (LIPID) Study Group. | journal=N Engl J Med | year= 1998 | volume= 339 | issue= 19 | pages= 1349-57 | pmid=9841303 | doi=10.1056/NEJM199811053391902 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9841303  }} </ref>
*The true relation between elevated LDL levels and ischemic stroke as a complication is yet to be delineated.


===Peripheral arterial disease===
===Peripheral arterial disease===

Revision as of 04:14, 29 September 2014

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Rim Halaby, M.D. [2]

Overview

The natural history and prognosis of patients with elevated LDL are directly related to the complications associated with dyslipidemia. High LDL concentrations are not only associated with the initiation of atherogenesis, but also with the gradual worsening of atherosclerosis.[1] Patients with elevated plasma LDL who are left untreated often develop atherosclerosis and cardiovascular disease (CVD). More importantly, the risk of CVD further increases when dyslipidemia is associated with other cardiovascular risk factors, such as diabetes mellitus, hypertension, and low HDL, which are often concomitantly present among patients with dyslipidemia.[2][3]


The decreased affinity of small dense LDL particles for LDL receptors has been postulated to be the cause of atherogenic properties of these small dense LDL particles[4] They are more prone to oxidation,[5] have higher affinity to vascular proteoglycans,[6] and are preferentially phagocytosed by macrophages via scanvenger proteins that promote atherosclerosis.[7]

Coronary artery disease

  • Dyslipidemia caused by elevated LDL is a major risk factor for coronary artery disease (CAD) and often regarded as a prerequisite.[8]
  • There is a direct association between cardiovascular death and duration of elevated plasma LDL levels.[9]
  • An increase of LDL by 10 mg/dL is associated with a 12% increase in CVD risk in both genders.
  • Accumulating evidence has proved the role of elevated LDL in the development of atherosclerosis and has demonstrated that lowering LDL attributes to significant reductions (30-37%) in CAD.[10]

Diabetes mellitus and insulin resistance

  • Elevated concentrations of small dense LDL is often observed among patients before development of insulin resistance.[11]
  • The majority of patients with elevated LDL have other components of the metabolic syndrome, such as hypertriglyceridemia, hypertension, and insulin resistance.[11]

Stroke

  • The association between elevated LDL and stroke has been observed, but the association has not been as strongly established as in the case of coronary artery disease.[12]
  • Nonetheless, statin therapy is important in cerebrovascular events, especially among patients with other manifestations of atherosclerosis, namely coronary artery disease. Statin therapy may significantly reduce the rate of ischemic stroke by approximately 20-30%.[12][13]
  • The true relation between elevated LDL levels and ischemic stroke as a complication is yet to be delineated.

Carotid artery atherosclerosis

  • Elevated LDL is the primary risk factor for the initiation and development of carotid artery atherosclerosis.
  • A reduction of LDL concentrations by at least 25% is associated with a significant reduction in the radiographic progression of carotid atherosclerosis

Renovascular disease

  • Elevations of LDL is hypothesized to be the major initiator of renovascular injury associated with renal artery stenosis.[14]
  • Oxidation of high concentrations of LDL, along with an increasein local and systemic oxidative stress, promotes the generation of reactive oxygen species (ROS) that cause vasoconstriction and worsen renal ischemia.[15]
  • Emerging evidence currently favors the pharmacologic management of dyslipidemia for the treatment of renal artery stenosis compared to angioplasty.[14]

Peripheral arterial disease

  • Elevated LDL is a risk factor for the development of peripheral arterial disease (PAD) and contributes to its progression and other manifestations of CVD.
  • The aggressive management of atherosclerosis is a primary goal in the management of PAD, given the abundance of data to suggest that LDL normalization improves femoral arterial atherosclerosis and alters the natural history of PAD.

Death

  • The Framingham study demonstrated that elevated LDL is associated with non-CAD-death among both genders.[3]

References

  1. Grundy SM (1997). "Small LDL, atherogenic dyslipidemia, and the metabolic syndrome". Circulation. 95 (1): 1–4. PMID 8994405.
  2. Stamler J, Vaccaro O, Neaton JD, Wentworth D (1993). "Diabetes, other risk factors, and 12-yr cardiovascular mortality for men screened in the Multiple Risk Factor Intervention Trial". Diabetes Care. 16 (2): 434–44. PMID 8432214.
  3. 3.0 3.1 Gordon T, Kannel WB, Castelli WP, Dawber TR (1981). "Lipoproteins, cardiovascular disease, and death. The Framingham study". Arch Intern Med. 141 (9): 1128–31. PMID 7259370.
  4. Lamarche B, Tchernof A, Moorjani S, Cantin B, Dagenais GR, Lupien PJ; et al. (1997). "Small, dense low-density lipoprotein particles as a predictor of the risk of ischemic heart disease in men. Prospective results from the Québec Cardiovascular Study". Circulation. 95 (1): 69–75. PMID 8994419.
  5. Tribble DL, Holl LG, Wood PD, Krauss RM (1992). "Variations in oxidative susceptibility among six low density lipoprotein subfractions of differing density and particle size". Atherosclerosis. 93 (3): 189–99. PMID 1590824.
  6. Chapman MJ, Guérin M, Bruckert E (1998). "Atherogenic, dense low-density lipoproteins. Pathophysiology and new therapeutic approaches". Eur Heart J. 19 Suppl A: A24–30. PMID 9519339.
  7. Vergès B (2005). "New insight into the pathophysiology of lipid abnormalities in type 2 diabetes". Diabetes Metab. 31 (5): 429–39. PMID 16357786.
  8. Roger VL, Go AS, Lloyd-Jones DM, Adams RJ, Berry JD, Brown TM; et al. (2011). "Heart disease and stroke statistics--2011 update: a report from the American Heart Association". Circulation. 123 (4): e18–e209. doi:10.1161/CIR.0b013e3182009701. PMID 21160056.
  9. Rader DJ, Cohen J, Hobbs HH (2003). "Monogenic hypercholesterolemia: new insights in pathogenesis and treatment". J Clin Invest. 111 (12): 1795–803. doi:10.1172/JCI18925. PMC 161432. PMID 12813012.
  10. Sharma SB, Garg S (2012). "Small dense LDL: risk factor for coronary artery disease (CAD) and its therapeutic modulation". Indian J Biochem Biophys. 49 (2): 77–85. PMID 22650003.
  11. 11.0 11.1 Solano MP, Goldberg RB (2006). "Management of dyslipidemia in diabetes". Cardiol Rev. 14 (3): 125–35. doi:10.1097/01.crd.0000188034.76283.5e. PMID 16628021.
  12. 12.0 12.1 "Randomised trial of cholesterol lowering in 4444 patients with coronary heart disease: the Scandinavian Simvastatin Survival Study (4S)". Lancet. 344 (8934): 1383–9. 1994. PMID 7968073.
  13. "Prevention of cardiovascular events and death with pravastatin in patients with coronary heart disease and a broad range of initial cholesterol levels. The Long-Term Intervention with Pravastatin in Ischaemic Disease (LIPID) Study Group". N Engl J Med. 339 (19): 1349–57. 1998. doi:10.1056/NEJM199811053391902. PMID 9841303.
  14. 14.0 14.1 Annigeri RA (2012). "Medical therapy is best for atherosclerotic renal artery stenosis: Arguments for". Indian J Nephrol. 22 (1): 1–4. doi:10.4103/0971-4065.91177. PMC 3263056. PMID 22279335.
  15. Meier P, Rossert J, Plouin PF, Burnier M (2007). "Atherosclerotic renovascular disease: beyond the renal artery stenosis". Nephrol Dial Transplant. 22 (4): 1002–6. doi:10.1093/ndt/gfl784. PMID 17210599.



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