eMedicine Specialties > Endocrinology > Metabolic Disorders

Hypercholesterolemia, Polygenic: Follow-up

Author: Elena Citkowitz, MD, PhD, FACP, Clinical Professor of Medicine, Yale University School of Medicine; Director, Cholesterol Management Center, Director, Cardiac Rehabilitation, Department of Medicine, Hospital of St Raphael
Coauthor(s): William L Isley, MD, Senior Associate Consultant, Associate Professor of Medicine, Division of Endocrinology, Diabetes, Metabolism, and Nutrition, Mayo Clinic of Rochester
Contributor Information and Disclosures

Updated: Nov 17, 2009

Follow-up

Deterrence/Prevention

  • Obviously, the adoption of a healthier lifestyle that included aerobic exercise and a low-fat diet would probably reduce the prevalence of obesity, hypercholesterolemia, and, ultimately, the risk of coronary heart disease (CHD). Hopefully, younger Americans will adopt these measures to reduce CHD events in the coming years.

Prognosis

  • The statin era has revolutionized the treatment of hypercholesterolemia. Coupled with the treatment of hypertension and the use of beta-blockers, angiotensin-converting enzyme inhibitors, and aspirin, the potential for reduction of CHD events in patients with known atherosclerosis is significant.
  • Cholesterol reduction is certainly useful as a CHD risk-reduction strategy and for primary prevention in individuals who are at high risk for CHD or other forms of atherosclerosis.

Patient Education

Miscellaneous

Medicolegal Pitfalls

  • High total cholesterol levels can be due to a very high high-density lipoprotein cholesterol (HDL-C) level, particularly in women. If the low-density lipoprotein cholesterol (LDL-C) level is not elevated, no treatment is needed.
  • Patients with marked hypertriglyceridemia (>1000 mg/dL) have very high cholesterol concentrations (300-600 mg/dL), but this situation is due to large numbers of chylomicrons and very low-density lipoprotein (VLDL), not LDL. Therefore, do not treat these patients with statins; treat them with agents that lower triglycerides (eg, fibrates, niacin, fish oils).
  • Obtain serum thyroid-stimulating hormone levels, liver function test results, creatinine values, and urinalysis results to help rule out secondary dyslipidemias.

Special Concerns

  • Therapeutic controversies
    • Post hoc analysis of some studies (eg, Cholesterol and Recurrent Events, West of Scotland Coronary Prevention Study14 ) has been interpreted to indicate the presence of a lower limit for LDL-C, and, beyond this level, lowering the LDL-C is no longer beneficial. Similar analyses of other studies (eg, Scandinavian Simvastatin Survival Study,12,13 Air Force/Texas Coronary Atherosclerosis Prevention Study15 ) have failed to indicate an LDL-C therapeutic threshold.
    • The Medical Research Council/British Heart Foundation Heart Protection Study enrolled subjects at high risk for CHD and total cholesterol (not LDL-C) concentrations greater than 135 mg/dL. CHD event reduction was observed in the total patient population and in the subgroup with the lowest tertile of LDL-C.
    • The completed Pravastatin or Atorvastatin Evaluation and Infection Therapy trial showed CHD event reduction when postacute coronary syndrome patients were treated with atorvastatin at 80 mg/d (LDL-C level at treatment was approximately 62 mg/dL) compared with pravastatin at 40 mg/d (LDL-C level at treatment was approximately 95 mg/dL). The study was plagued by high dropout (approximately one third of subjects in both groups at 2 y), and the fact that liver function test abnormalities (transaminase levels >3 times the upper limit normal) were common. The number needed to treat to prevent a CHD event was 26, and the number needed to treat to potentially harm (transaminases >3 times the upper limit normal) was 45.
    • The Post Coronary Artery Bypass Graft Trial showed less progression of the disease in bypass grafts with attainment of an LDL-C value of approximately 95 mg/dL (achieved with lovastatin) compared with less aggressive treatment, with an LDL-C value of approximately 135 mg/dL.28
    • The Reversal of Atherosclerosis with Aggressive Lipid Lowering trial showed minimal regression of atherosclerosis in CHD subjects treated with 80 mg of atorvastatin for 18 months compared with minimal progression in CHD subjects treated with 40 mg of pravastatin.
    • The Atorvastatin versus Revascularization Treatment trial showed no difference in CHD events in patients treated to achieve an LDL-C level of approximately 77 mg/dL compared with patients with an LDL-C level of approximately 115 mg/dL who had angioplasty.17
    • The Treating to New Targets Study showed a reduction in cardiovascular events, but not mortality, in patients with stable CHD who were given atorvastatin 80 mg/d compared with atorvastatin 10 mg/d (LDL-C 77 mg/dL vs 101 mg/dL). Persistent transaminase elevations were 6 times as common in the former group.
    • Because the epidemiologic data suggest a curvilinear relationship between LDL-C values and CHD events, an LDL-C level below which no benefit may accrue is probable; however, that actual level is unknown. The National Cholesterol Education Program (NCEP) guidelines probably provide an adequate estimate of an appropriate LDL-C target, except perhaps in patients with diabetes. 
    • The author believes that lower targets (<70 mg/dL) may be reasonable in patients who can be treated with low-to-moderate dose statin. However, the author feels that the risk/benefit ratio for high-dose statin (atorvastatin 80 mg/d is what has been tested so far) across the board to try to achieve an LDL-C level of less than 70 mg/dL (many patients will not achieve this level despite this therapy) is not yet proven definitely to be acceptable and achieve extra added benefit. The question of achieving lower LDL-C values with combination therapy (statin plus ezetimibe), in terms of showing further CHD risk reduction, remains unanswered at this point.
    • Whether patients with low HDL-C and high LDL-C values should use a drug (eg, niacin) to raise their HDL-C levels, in addition to using a drug to lower LDL-C levels, is questionable. The HDL Atherosclerosis Treatment Study showed positive effects of low-dose (10 mg) simvastatin and niacin on angiographic measures. However, no outcome studies have been performed with more conventionally used doses of statins. Statins often raise HDL-C levels a small amount. Some statin trials show a marked diminution of increased CHD risk in patients treated with statins who have lower HDL-C levels compared with individuals with higher HDL-C levels. The results of the Veterans Affairs HDL Intervention Trial may not be applicable to patients with high baseline LDL-C concentrations.
  • Patients with mixed dyslipidemias
    • Patients with insulin resistance and those with type 2 diabetes mellitus are likely to have mild-to-moderate triglyceride elevations.
    • Whether lipid therapy beyond statins is beneficial is debatable, although combination therapy with statins plus niacin or fibrates improves lipid parameters. Such therapy clearly increases the potential for adverse effects. The author believes that most patients should be treated with monotherapy. If a fibrate is given with a statin, fenofibrate is probably safer than gemfibrozil.
    • A potentially more benign nutraceutical is fish oil. The omega-3 fatty acids eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) lower triglyceride levels if at least 3 g/d is administered. Unfortunately, many preparations contain large amounts of fish oil that is not DHA or EPA. These preparations just supply fat, with little positive effect on the lipid profile. The author always insists on personally examining the fish oil bottle that his patients use to ensure that such patients will benefit from this therapy.
  • Women who are postmenopausal
    • Although epidemiologic studies have suggested that estrogen therapy is associated with better lipid profiles and lower CHD risk, recent intervention trials with estrogen have generated considerable controversy.
    • Currently, therapy with estrogens plus progestins is considered potentially harmful long-term therapy in postmenopausal women. This drug combination may still be useful for short-term therapy soon after menopause for vasomotor symptoms in women with an intact uterus.
    • In women who do not have a uterus, therapy with estrogen alone is of no proven benefit for CHD prevention.
    • Statin therapy, rather than estrogens, should be used for primary lipid modification and for CHD prevention in women who are postmenopausal, particularly in women with atherosclerosis. 
  • Patients with diabetes
    • The post hoc analysis of the Scandinavian Simvastatin Survival Study trial in patients with type 2 diabetes mellitus showed dramatic event reduction in patients who received simvastatin. Unfortunately, this trial did not include patients with high triglyceride levels, which is a common lipid abnormality in persons with type 2 diabetes mellitus.12,13
    • The Medical Research Council/British Heart Foundation Heart Protection Study (of simvastatin 40 mg/d) showed a similar reduction in CHD event rates in patients with type 2 diabetes mellitus compared with patients without diabetes.13
    • Epidemiologic work suggests that patients with diabetes who have not had a previous known myocardial infarction may be at the same risk for CHD events and mortality as patients with diabetes who have not had a previous known myocardial infarction, compared with patients without diabetes who have had a previous coronary event. These data led the American Diabetes Association to advocate an LDL-C level of less than 100 mg/dL for patients with diabetes. American Diabetes Association treatment based on LDL-C levels is as follows:
      • Medical nutrition therapy
        • Patients without coronary heart disease, peripheral vascular disease, or cardiovascular disease and an LDL-C level of greater than 100 mg/dL: Goal level of LDL-C is less than 100 mg/dL (<70 mg/dL is considered an option).
        • Patients with coronary heart disease, peripheral vascular disease, or cardiovascular disease and an LDL-C level higher than 100 mg/dL: Goal level of LDL-C is less than 100 mg/dL (<70 mg/dL is considered an option).
      • Drug treatment
        • Patients without coronary heart disease, peripheral vascular disease, or cardiovascular disease and an LDL-C level higher than 130 mg/dL: Goal level of LDL-C is less than 100 mg/dL. Additionally, for patients with diabetes who have multiple CHD risk factors (eg, low HDL-C level, hypertension, smoking, family history of cardiovascular disease, microalbuminuria or proteinuria), most authorities recommend drug therapy for LDL-C levels of 100-130 mg/dL. Age and sex are not risk factors because women and men have equal CHD risk.
        • Patients with CHD, peripheral vascular disease, or cardiovascular disease and an LDL-C level of greater than 100 mg/dL: Goal level of LDL-C is less than 100 mg/dL (goal of <70 mg/dL is an option).
    • The NCEP ATP III now considers diabetes mellitus a CHD risk equivalent, with the same LDL-C goal (<100 mg/dL, or if considered appropriate, <70 mg/dL) as patients with known CHD. 
  • Risk of myopathy
    • With statin monotherapy, the risk of myopathy is low and is increased with the concomitant use of fibrates, niacin, macrolides, protease inhibitors, and imidazoles. The fibrate effect appears to relate to inhibition of glucuronidation of statins, rather than an effect on cytochrome P450 metabolism, because it is observed with all statins.
    • Routine CK monitoring has no proven value in the prevention of myopathy. Because muscle aches are common, even in placebo-treated patients, a check of serum CK values, once the patient has myalgias, may be helpful. Many patients with myalgias have CK values within the reference range.
    • Sometimes, changing the statin is necessary to eliminate the problem. Anecdotal reports suggest that coenzyme Q supplements in patients with muscle aches and CK values within the reference range may reduce myalgias.
    • Reports suggest that histologic myopathy may occur in the absence of CK elevations. Whether this is a widespread phenomenon is debatable.
 


More on Hypercholesterolemia, Polygenic

Overview: Hypercholesterolemia, Polygenic
Differential Diagnoses & Workup: Hypercholesterolemia, Polygenic
Treatment & Medication: Hypercholesterolemia, Polygenic
Follow-up: Hypercholesterolemia, Polygenic
Multimedia: Hypercholesterolemia, Polygenic
References
Further Reading
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References

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Further Reading

Related eMedicine topics:
 High HDL Cholesterol (Hyperalphalipoproteinemia)
Hypercholesterolemia, Familial
Hypoglycemia [Emergency Medicine]
Hypoglycemia [Endocrinology]
Hypoglycemia [Pediatrics: General Medicine]
Renal Vein Thrombosis [Radiology]
Renal Vein Thrombosis [Vascular Surgery]

Clinical guidelines:
 Ezetimibe for the treatment of primary (heterozygous-familial and non-familial) hypercholesterolaemia.
National Institute for Health and Clinical Excellence (NICE) - National Government Agency [Non-U.S.]. 2007 Nov. 30 pages. NGC:006202

Cardiometabolic risk management in primary care.
Qatif Primary Health Care - National Government Agency [Non-U.S.].  2008. Various pagings. NGC:006689 

Diagnosis and treatment of childhood hypercholesterolaemia.
Finnish Medical Society Duodecim - Professional Association.  2004 Jun 14 (revised 2007 Feb 13). Various pagings. NGC:005813

Clinical trials:
Pediatric Study to Evaluate the Efficacy and Safety of Ezetimibe Monotherapy in Children With Primary Hypercholesterolemia (Study P05522)

Efficacy and Safety Study of Pitavastatin Compared to atoRvastatin in Type 2 dIabeTes Mellitus With Hypercholesterolemia (ESPRIT)

Combination Treatment With Green Tea Extract and Statins in Patients With Hypercholesterolemia (GTE-Stat)

Evaluation of Ezetimibe and Atorvastatin Coadministration Versus Atorvastatin or Rosuvastatin Monotherapy in Japanese Patients With Hypercholesterolemia (Study P06027)

Treatment of HDL to Reduce the Incidence of Vascular Events HPS2-THRIVE

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Keywords

polygenic hypercholesterolemia, hypercholesterolemia, hyperlipidemia, cholesterol level, high cholesterol, cholesterol lowering foods, familial hypercholesterolemia, nonfamilial hypercholesterolemia, non-familial hypercholesterolemia cholesterol, statins, statin therapy, simvastatin, pravastatin, atorvastatin, coronary heart disease, CHD, atherothrombotic stroke, atherosclerosis, heart disease

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Contributor Information and Disclosures

Author

Elena Citkowitz, MD, PhD, FACP, Clinical Professor of Medicine, Yale University School of Medicine; Director, Cholesterol Management Center, Director, Cardiac Rehabilitation, Department of Medicine, Hospital of St Raphael
Elena Citkowitz, MD, PhD, FACP is a member of the following medical societies: American College of Physicians, American Heart Association, National Lipid Association, and Sigma Xi
Disclosure: Nothing to disclose.

Coauthor(s)

William L Isley, MD, Senior Associate Consultant, Associate Professor of Medicine, Division of Endocrinology, Diabetes, Metabolism, and Nutrition, Mayo Clinic of Rochester
William L Isley, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, American Diabetes Association, American Federation for Medical Research, Endocrine Society, and Phi Beta Kappa
Disclosure: Nothing to disclose.

Medical Editor

Steven R Gambert, MD, MACP, Chairman, Department of Medicine, Physician-in-Chief, Sinai Hospital of Baltimore; Professor of Medicine, Program Director, Internal Medicine Program, Johns Hopkins University School of Medicine
Steven R Gambert, MD, MACP is a member of the following medical societies: Alpha Omega Alpha, American College of Physician Executives, American College of Physicians, American Geriatrics Society, Association of Professors of Medicine, Endocrine Society, and Gerontological Society of America
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Yoram Shenker, MD, Chief of Endocrinology Section, Veterans Affairs Medical Center of Madison; Interim Chief, Associate Professor, Department of Internal Medicine, Section of Endocrinology, Diabetes and Metabolism, University of Wisconsin at Madison
Yoram Shenker, MD is a member of the following medical societies: American Heart Association, Central Society for Clinical Research, and Endocrine Society
Disclosure: Nothing to disclose.

CME Editor

Mark Cooper, MBBS, PhD, FRACP, Head, Diabetes & Metabolism Division, Baker Heart Research Institute, Professor of Medicine, Monash University
Disclosure: Nothing to disclose.

Chief Editor

George T Griffing, MD, Professor of Medicine, St Louis University School of Medicine
George T Griffing, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Medical Practice Executives, American College of Physician Executives, American College of Physicians, American Diabetes Association, American Federation for Medical Research, American Heart Association, Central Society for Clinical Research, Endocrine Society, International Society for Clinical Densitometry, and Southern Society for Clinical Investigation
Disclosure: Nothing to disclose.

 
 
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