Hypercholesterolemia

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Hypercholesterolemia (literally: high blood cholesterol) is the presence of high levels of cholesterol in the blood. It is not a disease but a metabolic derangement that can be secondary to many diseases and can contribute to many forms of disease, most notably cardiovascular disease. It is closely related to the terms "hyperlipidemia" (elevated levels of lipids) and "hyperlipoproteinemia" (elevated levels of lipoproteins). Familial hypercholesterolemia is a rare genetic disorder that can occur in families, where sufferers cannot properly metabolise cholesterol.

Current Research

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For current research articles click - here

Signs and Symptoms

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Elevated cholesterol does not lead to specific symptoms unless it has been longstanding. Some types of hypercholesterolemia lead to specific physical findings: xanthoma (thickening of tendons due to accumulation of cholesterol), xanthelasma palpabrum (yellowish patches around the eyelids) and arcus senilis (white discoloration of the peripheral cornea).

Longstanding elevated hypercholesterolemia leads to accelerated atherosclerosis; this can express itself in a number of cardiovascular diseases:

• Angina pectoris, leading to PTCA or CABG
• Myocardial infarction (heart attack)
• Transient ischemic attacks (TIAs)
• Cerebrovascular accidents/Strokes
• Peripheral artery disease (PAD)

Diagnosis

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When measuring cholesterol, it is important to measure its subfractions before drawing a conclusion on the cause of the problem. The subfractions are LDL, HDL and VLDL. In the past, LDL and VLDL levels were rarely measured directly due to cost concerns. VLDL levels are reflected in the levels of triglycerides (generally about 45% of triglycerides is composed of VLDL). LDL was usually estimated as a calculated value from the other fractions (total cholesterol minus HDL and VLDL); this method is called the Friedewald calculation; specifically: LDL ~= Total Cholesterol - HDL - (0.2 x Triglycerides).

Less expensive (and less accurate) laboratory methods and the Friedewald calculation have long been utilized because of the complexity, labor and expense of the electrophoretic methods developed in the 1970s to identify the different lipoprotein particles which transport cholesterol in the blood. As of 1980, the original methods, developed by research work in the mid-1970s cost about $5K, US 1980 dollars, per blood sample/person.

With time, more advanced laboratory analyses have been developed which do measure LDL and VLDL particle sizes and levels, and at far lower cost. These have partly been developed and become more popular as a result of the increasing clinical trial evidence that intentionally changing cholesterol transport patterns, including to certain abnormal values compared to most adults, often has a dramatic effect on reducing, even partially reversing, the atherosclerotic process. With ongoing research and advances in laboratory methods, the prices for more sophisticated analyses have markedly decreased, to less than $100, US 2004, by some labs, and with simultaneous increases in the accuracy of measurement for some of the methods.

Screening

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Screening for a disease refers to testing for a disease, such as hypercholesterolemia, in a patients who have no signs or symptoms of the disease.

In patients without any other risk factors, moderate hypercholesterolemia is often not treated. According to Framingham Heart Study, people with an age greater than 50 years have no increased overall mortality with either high or low serum cholesterol levels. There is, however, a correlation between falling cholesterol levels over the first 14 years and mortality over the following 18 years (11% overall and 14% CVD death rate increase per 1 mg/dL per year drop in cholesterol levels). This, however, does not mean that a decrease in serum levels is dangerous, as there has not yet been a recorded heart attack in the study in a person with a total cholesterol below 150 mg/dL.

The U.S. Preventive Services Task Force (USPSTF) has evaluated screening for hypercholesterolemia.

Classification

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Fredrickson Classification

Classically, hypercholesterolemia was categorized by lipoprotein electrophoresis and the Fredrickson classification. Newer methods, such as "lipoprotein subclass analysis" have offered significant improvements in understanding the connection with atherosclerosis progression and clinical consequences.

If the hypercholesterolemia is hereditary (familial hypercholesterolemia), there is more often a family history of premature, earlier onset atherosclerosis, as well as familial occurrence of the signs mentioned above.

Secondary Causes

There are a number of secondary causes for high cholesterol:

• Diabetes mellitus and metabolic syndrome
• Kidney disease (nephrotic syndrome)
• Hypothyroidism
• Anorexia nervosa
• Zieve's syndrome
• Family history
• Diet: Saturated fat raises blood cholesterol levels. Although dietary cholesterol exerts some influence, the regulatory mechanism of the liver upon absorption of cholesterol decreases the effect of dietary cholesterol on total cholesterol levels. Thus it is mainly by limiting the amount of saturated fat in one's diet that helps lower total serum cholesterol.
• Weight. Being overweight is a definite risk factor for heart disease. It also tends to increase your cholesterol. Losing weight can help lower your LDL and total cholesterol levels, as well as raise your HDL and lower your triglyceride levels.
• Physical Activity. Lack of physical activity is a risk factor for heart disease. Regular physical activity can also help lower LDL (bad) cholesterol and raise HDL (good) cholesterol levels. It also helps you lose weight.

All three of these activities done together can have a positive effect on one's blood cholesterol level.

Dietary Influence

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While part of the circulating cholesterol originates from diet, and restricting cholesterol intake may reduce blood cholesterol levels, there are various other links between the dietary pattern and cholesterol levels. The American Heart Association also compiles a list of the acceptable/unacceptable foods for those who are diagnosed with hypercholesterolemia.

Carbohydrates

Evidence is accumulating that eating more carbohydrates - especially simpler, more refined carbohydrates - increases levels of triglycerides in the blood, lowers HDL, and may shift the LDL particle distribution pattern into unhealthy atherogenic patterns. Thus a low fat diet, which often means a higher carbohydrate intake, may actually be an unhealthy change.

Trans Fats

An increasing number of researchers are suggesting that a major dietary risk factor for cardiovascular diseases is trans fatty acids, not saturated fats, as had been suggested by the Framingham Heart Study, and in the US the FDA plans revised food labeling to include listing trans fat quantities, by 2007

Treatment

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Clinical Evidence has summarized treatment for both primary prevention and secondary prevention. Two factors to consider when choosing therapy are the patient's risk of coronary disease and their lipoprotein pattern.

Risk of coronary disease. To calculated the benefit of treatment, there are two online calculators that can estimate baseline risk. Combining the baseline risk with the relative risk reduction of a treatment can lead to the absolute risk reduction of number needed to treat. For example, one of the calculators projects that a patient had a 10% risk of coronary disease over ten years. As noted below, the relative risk reduction of a statin is 30%. Thus, after 4-7 years of treatment with a statin, a patient's risk will drop to 7%. This equates to an absolute risk reduction of 3%, or a number needed to treat of 33. Thirty three such patients must be treated for 4-7 years for one to benefit.

Lipoprotein patterns. (See hyperlipoproteinemia for details) The treatment depends on the type of hypercholesterolemia. Clinical trials, starting in the 1970s, have repeatedly and increasingly found that normal cholesterol values do not necessarily reflect healthy cholesterol values. This has increasingly lead to the newer concept of dyslipidemia, despite normo-cholesterolemia. Thus there has been increasing recognition of the importance of "lipoprotein subclass analysis" as an important approach to better understand and change the connection between cholesterol transport and atherosclerosis progression. Fredrickson Types IIa and IIb can be treated with diet, statins (most prominently rosuvastatin, atorvastatin, simvastatin, or pravastatin), cholesterol absorption inhibitors (ezetimibe), fibrates (gemfibrozil, bezafibrate, fenofibrate or ciprofibrate), vitamin B3 (nicotinic acid), bile acid sequestrants (colestipol, cholestyramine), LDL apheresis and in hereditary severe cases liver transplantation. The treatment is made more complex when elevated levels of asymmetric dimethylarginine (ADMA) are present in endothelial blood, since ADMA down-regulates the production of endothelial nitric oxide production and hence aggravates the extent of oxidized LDL.

Multiple clinical trials, each, by design, examining only one of multiple relevant issues, have increasingly examined the connection between these issues and atherosclerosis clinical consequences. Some of the better recent randomized human outcome trials include ASTEROID, ASCOT-LLA, REVERSAL, PROVE-IT, CARDS, Heart Protection Study, HOPE, PROGRESS, COPERNICUS, and especially a newer research approach utilizing a synthetically produced and IV administered human HDL, the Apo A-I Milano Trial.

Diet

On the other hand, and though less dramatic than the many cardiovascular procedures, some people, especially with newer and more sophisticated information, are changing their eating and especially food supplement patterns, many of the supplements still being prescription agents. Though generally not aware of the internal changes in their cholesterol transport patterns, recent trials have demonstrated increasing success with some of these strategies; see the LDL, HDL and IVUS sections.

Medications

Many primary physicians and heart specialists will initially prescribe medication in combination with diet and exercise. According to various resources, statins are the most commonly used and effective forms of medication for the treatment of high cholesterol. The U.S. Preventive Services Task Force (USPSTF) estimated that after 5 to 7 years of treatment, statins can reduce the risk of coronary heart disease events is decreased by approximately 30%. More recently, a meta-analysis reported an almost identical reduction of 29.2% in low risk patients treated for 4.3 years.

Alternative Medicine

A survey released in May 2004 by the National Center for Complementary and Alternative Medicine focused on who used complementary and alternative medicine (CAM), what was used, and why it was used in the United States by adults age 18 years and over during 2002. According to this survey, CAM was used to treat cholesterol by 1.1% of U.S. adults who used CAM during 2002. Consistent with previous studies, this study found that the majority of individuals (i.e., 54.9%) used CAM in conjunction with conventional medicine.

Clinical Practice Guidelines

Various clinical practice guidelines have addressed the treatment of hypercholesterolemia. The American College of Physicians has addressed hypercholesterolemia in patients with diabetes. Their recommendations are:

• Recommendation 1: Lipid-lowering therapy should be used for secondary prevention of cardiovascular mortality and morbidity for all patients (both men and women) with known coronary artery disease and type 2 diabetes.
• Recommendation 2: Statins should be used for primary prevention against macrovascular complications in patients (both men and women) with type 2 diabetes and other cardiovascular risk factors.
• Recommendation 3: Once lipid-lowering therapy is initiated, patients with type 2 diabetes mellitus should be taking at least moderate doses of a statin.
• Recommendation 4: For those patients with type 2 diabetes who are taking statins, routine monitoring of liver function tests or muscle enzymes is not recommended except in specific circumstances.

(adapted from Wikipedia, the free encyclopedia http://en.wikipedia.org/wiki/High_cholesterol)

Hyperlipidemia

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Hyperlipidemia, hyperlipoproteinemia or dyslipidemia is the presence of elevated or abnormal levels of lipids and/or lipoproteins in the blood. Lipids (fatty molecules) are transported in a protein capsule, and the density of the lipids and type of protein determines the fate of the particle and its influence on metabolism.

Lipid and lipoprotein abnormalities are extremely common in the general population, and are regarded as a highly modifiable risk factor for cardiovascular disease due to the influence of cholesterol, one of the most clinically relevant lipid substances, on atherosclerosis. In addition, some forms may predispose to acute pancreatitis.

Classification

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Hyperlipidemias are classified according to the Fredrickson classification which is based on the pattern of lipoproteins on electrophoresis or ultracentrifugation. It was later adopted by the World Health Organization (WHO). It does not directly account for HDL, and it does not distinguish among the different genes that may be partially responsible for some of these conditions. It remains a popular system of classification, but is considered dated by many.

Fredrickson Classification of Hyperlipidemias

Hyperlipoproteinemia	Synonyms	Problems	Labs Description	Treatment
Type I	Buerger-Gruetz syndrome, Primary hyperlipoproteinaemia, or Familial hyperchylomicronemia	Decreased lipoprotein lipase (LPL) or altered ApoC2	Elevated Chylomicrons	Diet Control
Type IIa	Polygenic hypercholesterolaemia or Familial hypercholesterolemia	LDL receptor deficiency	Elevated LDL only	Bile Acid Sequestrants, Statins, Nicotinic acid
Type IIb	Combined hyperlipidemia	Decreased LDL receptor and Increased ApoB	Elevated LDL and VLDL and Triglycerides	Statins, Nicotinic acid, Gemfibrozil
Type III	Familial Dysbetalipoproteinemia	Defect in ApoE synthesis	Increased IDL	Drug of choice: Gemfibrozil
Type IV	Endogenous Hyperlipemia	Increased VLDL production and Decreased elimination	Increased VLDL	Drug of choice: Nicotinic acid
Type V	Familial Hypertriglyceridemia	Increased VLDL production and Decreased LPL	Increased VLDL and Chylomicrons	Nicotinic acid, Gemfibrozil

Hyperlipoproteinemia Type I

This very rare form (also known as Buerger-Gruetz syndrome, primary hyperlipoproteinaemia, or familial hyperchylomicronemia) is due to a deficiency of lipoprotein lipase (LPL) or altered apolipoprotein C2, resulting in elevated chylomicrons, the particles that transfer fatty acids from the digestive tract to the liver. Its prevalence is 0.1% of the population.

Hyperlipoproteinemia Type II

Hyperlipoproteinemia type II, by far the most common form, is further classified into type IIa and type IIb, depending mainly on whether there is elevation in the triglyceride level in addition to LDL cholesterol.

Type IIa

This may be sporadic (due to dietary factors), polygenic, or truly familial as a result of a mutation either in the LDL receptor gene on chromosome 19 (0.2% of the population) or the ApoB gene (0.2%). The familial form is characterized by tendon xanthoma, xanthelasma and premature cardiovascular disease.

Type IIb

The high VLDL levels are due to overproduction of substrates, including triglycerides, acetyl CoA, and an increase in B-100 synthesis. They may also be caused by the decreased clearance of LDL. Prevalence in the population is 10%.

• Familial combined hyperlipoproteinemia (FCH)
• Secondary combined hyperlipoproteinemia (usually in the context of metabolic syndrome, for which it is a diagnostic criterium)

Treatment

While dietary modification is the initial approach, many patients require treatment with statins (HMG-CoA reductase inhibitors) to reduce cardiovascular risk. If the triglyceride level is markedly raised, fibrates may be preferable due to their beneficial effects. Combination treatment of statins and fibrates, while highly effective, causes a markedly increased risk of myopathy and rhabdomyolysis and is therefore only done under close supervision. Other agents commonly added to statins are ezetimibe, nicotinic acid and bile acid sequestrants. There is some evidence for benefit of plant sterol-containing products and ω3-fatty acids

Hyperlipoproteinemia Type III

This form is due to high chylomicrons and IDL (intermediate density lipoprotein). Also known as broad beta disease or dysbetalipoproteinemia, the most common cause for this form is the presence of ApoE E2/E2 genotype. It is due to cholesterol-rich VLDL (β-VLDL). Prevalence is 0.02% of the population.

Hyperlipoproteinemia Type IV

This form is due to high triglycerides. It is also known as hypertriglyceridemia (or pure hypertriglyceridemia). Pr evalence is 1% of the population.

Hyperlipoproteinemia Type V

This type is very similar to type I, but with high VLDL in addition to chylomicrons.

Unclassified Forms

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Non-classified forms are extremely rare:

• Hypo-alpha lipoproteinemia
• Hypo-beta lipoproteinemia (prevalence 0.01-0.1%)

(adapted from Wikipedia, the free encyclopedia http://en.wikipedia.org/wiki/Hyperlipidemia)

Findings From Current Research

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Non-Traditional Markers of Atherosclerosis Potentiate the Risk of Coronary Heart Disease in Patients with Type 2 Diabetes and Metabolic Syndrome.

Authors: Bianchi C, Penno G, Malloggi L, Barontini R, Corfini M, Giovannitti MG, Di Cianni G, Del Prato S, Miccoli R.

Department of Endocrinology and Metabolism, Section of Diabetes and Metabolic Disease, University of Pisa, Ospedale Cisanello, Via Paradisa 2, 56126 Pisa, Italy.

BACKGROUND AND AIMS: The aims of this study were to establish the prevalence of metabolic syndrome (MS), in type 2 diabetes mellitus (DM), according to National Cholesterol Education Program Adult Treatment Panel III (NCEP ATP III) criteria, and to assess the association of MS with other cardiovascular (CV) risk factors in these patients. METHODS AND RESULTS: A cross-sectional study was conducted in 1610 patients with type 2 DM. Glycated hemoglobin A1c (HbA1c), total cholesterol, low-density lipoprotein cholesterol (LDL-C) and high-density lipoprotein cholesterol (HDL-C), uric acid, fibrinogen, creatinine, and albumin/creatinine ratios were measured. The risk of coronary heart disease (CHD) was calculated using the UKPDS Risk Engine. Seventy percent of the diabetic population met the criteria for MS; central obesity and hypertension were the most common criteria. Subjects with MS had higher levels of HbA1c, LDL-C, non-HDL-C, uric acid, and fibrinogen compared to patients without MS. Similarly, microalbuminuria and a high triglyceride (Tg)/HDL-C ratio (a marker of small LDL-C) occurred more frequently in patients with MS. When patients with no history of CHD events were considered, mean CHD risk was greater in those with, than those without, MS. CONCLUSIONS: MS is highly prevalent in type 2 DM and is commonly associated with non-traditional CV risk factors. The diagnosis of MS seems to confer additional CHD risk in patients with type 2 diabetes.

Journal: Nutr Metab Cardiovasc Dis. 2007 Apr 7;
Adapted from PubMed; click here to access full journal article.

Tobacco Use and Plasma Lipid-Lipoprotein Profile in Adolescents.

Authors: Guedes DP, Guedes JE, Barbosa DS, Oliveira JA.

Universidade Estadual de Londrina, Parana.

OBJECTIVE: To analyze the impact of tobacco use on plasma lipid lipoprotein profile in representative sample of adolescents. METHODS: A sample of 452 subjects (246 girls and 206 boys) 15 to 18 years old were included in the study. Each participant completed a structured and self-administered questionnaire concerning tobacco use. Plasma lipid-lipoprotein concentrations were measured by standard procedures. Differences between mean values were evaluated by analysis of covariance, controlling for saturated fat and cholesterol intake. Odds ratio was used to estimate the relative risk of the smokers being classified with an undesirable level of a plasma lipidlipoprotein parameter. RESULTS: The proportion of smokers was 20.9% for boys and 15.4% for girls. The average consumption of cigarettes per day was 9.2 ± 4.7 for boys and 5.6 ± 3.1 for girls. When compared with non-smokers, boy and girl smokers showed a significantly higher serum levels of total cholesterol, LDL-cholesterol, triglycerides and apolipoprotein B100, and significantly lower serum levels of HDL-cholesterol. Adolescent smokers tended to show a two-fold higher risk of altered lipid-lipoprotein levels than non-smokers. CONCLUSION: The present data could imply that intervention promoting a healthy lifestyle, including non smoking, should start at an early age to prevent or delay development of atherosclerotic lesions and ultimately to minimize the appearance of premature coronary heart disease in adults.

Journal: Rev Assoc Med Bras. 2007 Feb;53(1):59-63.
Adapted from PubMed; click here to access full journal article.

Hypertriglyceridemia: Its Etiology, Effects and Treatment.

Authors: Yuan G, Al-Shali KZ, Hegele RA.

Schulich School of Medicine and Dentistry, University of Western Ontario, London, Ont.

Elevated plasma triglyceride concentration is a common biochemical finding, but the evidence for the benefit of treating this lipid disturbance remains less robust than that for treating elevated low-density lipoprotein-cholesterol. Part of the difficulty in the provision of specific recommendations has been the frequent coexistence of elevated triglycerides with other conditions that affect cardiovascular disease risk, such as depressed high-density lipoprotein-cholesterol, obesity, metabolic syndrome, proinflammatory and prothrombotic biomarkers, and type 2 diabetes. Recent investigations of outcomes of cardiovascular disease when medications are used to reduce triglyceride levels suggest that, although a net benefit probably exists, both relative and absolute risk reductions seem underwhelming when compared with the benefit of reducing low-density lipoprotein-cholesterol levels with treatment. However, the totality of evidence suggests that elevated triglyceride levels likely contribute independently to increased risk of cardiovascular disease, although there is no consensus about appropriate target levels. Furthermore, severe hypertriglyceridemia is associated with an increased risk of acute pancreatitis, irrespective of its effect on risk of cardiovascular disease. We review the causes and classification of elevated triglyceride levels, the clinical manifestations of primary hypertriglyceridemia and the management of patients with elevated triglyceride levels.

Journal: CMAJ. 2007 Apr 10;176(8):1113-20.
Adapted from PubMed; click here to access full journal article.

National Cholesterol Education Program and International Diabetes Federation definitions of metabolic syndrome in the prediction of diabetes. Results from the FIrenze-Bagno A Ripoli study.

Authors: Mannucci E, Monami M, Cresci B, Pala L, Bardini G, Petracca MG, Dicembrini I, Pasqua A, Buiatti E, Rotella CM.

Diabetes Section, Geriatric Unit, Department of Critical Care, University of Florence, Florence, Italy.

Background: The International Diabetes Federation (IDF) proposed to modify the diagnostic criteria for metabolic syndrome (MS) previously issued by the National Cholesterol Education Program (NCEP). Aim of the present investigation is to compare the predictive value for diabetes of NCEP and IDF definitions of MS in a large sample of predominantly Caucasian subjects. Methods: A prospective observational study was performed on a cohort study (n = 3096) enrolled in a diabetes-screening programme, the FIrenze-Bagno A Ripoli study. All subjects with fasting glucose >126 mg/dl and/or post-load glucose >/=200 mg/dl (5.7%) were excluded from the present analysis. Follow-up of each subject was continued until diagnosis of diabetes, death or until 31 December 2005. Mean follow-up was 27.7 +/- 11.3 months. Results: Among subjects enrolled, 13.7 and 25.2% were affected by MS using NCEP and IDF criteria respectively. During follow-up, 38 new cases of diabetes were diagnosed, with a yearly incidence rate of 0.5%. The relative risk for diabetes in subjects with MS was 10.10 [5.13; 20.00] and 7.87 [3.70; 16.7] using NCEP and IDF definitions respectively. After adjustment for age, sex, fasting glucose and waist circumference, NCEP-defined MS, but not IDF-, was significantly associated with incident diabetes (hazard ratio, 95% CI: 2.41 [1.01; 5.95] and 2.05 [0.80; 5.29] respectively). Conclusions: Although the reasons for the proposed changes in diagnostic criteria for MS are easily understandable, the newer IDF definition, while increasing estimates of prevalence of the syndrome, reduces the effectiveness of MS in identifying subjects at risk for diabetes. Further research is needed before the previous NCEP criteria are abandoned.

Journal: Diabetes Obes Metab. 2007 Apr 5;
Adapted from PubMed; click here to access full journal article.

Rate of Progression of Coronary Atherosclerotic Plaque in Women.

Authors: Nicholls SJ, Wolski K, Sipahi I, Schoenhagen P, Crowe T, Kapadia SR, Hazen SL, Tuzcu EM, Nissen SE.

Department of Cardiovascular Medicine, Cleveland Clinic Foundation, Cleveland, Ohio 44195, USA. nichols1@ccf.org

OBJECTIVES: The purpose of this study was to determine the relationship between gender and the extent of coronary atherosclerosis assessed by intravascular ultrasound (IVUS) and its rate of progression in subjects treated with established medical therapies. BACKGROUND: It is uncertain whether the pathophysiology of coronary artery disease (CAD) differs between genders. METHODS: A systematic analysis was performed of 978 subjects who participated in serial studies of atheroma progression. Genders were compared with regard to the extent of coronary atheroma at baseline and subsequent change in response to use of established medical therapies. RESULTS: Women were more likely to have a history of hypertension and higher levels of body mass index, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, triglycerides, C-reactive protein, and systolic and diastolic blood pressure. Despite this, women had less plaque in terms of percent atheroma volume (PAV) (33.9 +/- 10.2% vs. 37.8 +/- 10.3%, p < 0.001) and total atheroma volume (TAV) (148.7 +/- 66.6 mm3 vs. 194.7 +/- 84.3 mm3, p < 0.001). With medical therapy, the rate of change of PAV (0.7 +/- 0.6% vs. 0.7 +/- 0.5%, p = 0.92) and TAV (-2.3 +/- 3.2 mm3 vs. -1.9 +/- 2.9 mm3, p = 0.84) did not differ between genders. In the setting of intensive risk factor modification, there was no significant difference between genders with regard to the rates of plaque progression or regression. CONCLUSIONS: Despite the presence of more risk factors, the extent of atheroma in women with angiographic CAD is less than in men in subjects participating in clinical trials that employed serial assessments with IVUS. The finding that the rate of plaque progression or regression does not differ between genders in the setting of intensive risk factor modification supports the use of established medical therapies in women with CAD.

Journal: J Am Coll Cardiol. 2007 Apr 10;49(14):1546-51. Epub 2007 Mar 26.
Adapted from PubMed; click here to access full journal article.

Impact of Telephonic Interventions on Glycosylated Hemoglobin and Low-Density Lipoprotein Cholesterol Testing.

Authors: Coberley C, Hamar B, Gandy B, Orr P, Coberley S, McGinnis M, Hudson L, Forman S, Shurney D, Pope J.

Center for Health Research, 3841 Green Hills Village Dr, Ste 300, Nashville, TN 37215. E-mail: carter.coberley@healthways.com.

OBJECTIVES: To determine whether diabetes disease management (DM) programs are able to improve adherence to glycosylated hemoglobin (A1C) and low-density lipoprotein cholesterol (LDL-C) clinical testing in a nonadherent population and to quantify the efficacy of telephonic interventions in improving clinical testing rates. STUDY DESIGN: Retrospective, observational cohort study before and after DM program implementation. METHODS: A baseline cohort of members with diabetes (n = 5640) was identified from among large-scale diabetes DM programs administered for 13 geographically diverse health plans. Members were defined by nonadherence at baseline to A1C and/or LDL-C testing, grouped together based on how long they had participated in the program, divided retrospectively into telephonically contacted and uncontacted groups, and analyzed in the subsequent 12-month implementation period for testing rates. Subgroups defined by disease burden at baseline and frequency of telephonic interactions were analyzed to determine achievement of guideline-based A1C and LDL-C testing rates. RESULTS: Participation in diabetes DM programs was associated with improved A1C and LDL-C testing rates in previously nonadherent members. Calling nonadherent members improved A1C testing by 30.2% and LDL-C testing by 10.9% compared with testing rates for members who were not called. Members with high disease burden benefited even more from the diabetes intervention. Frequency of telephonic contacts with nonadherent individuals demonstrated a linear relationship with improved rates of adherence to A1C and LDL-C testing guidelines, and markedly improved testing rates compared with a not-called group. CONCLUSION: Telephonic interventions as part of comprehensive DM programs are associated with improved disease-monitoring testing.

Journal: Am J Manag Care. 2007 Apr;13(4):188-92.
Adapted from PubMed; click here to access full journal article.

Combined Diet and Exercise Intervention in the Workplace: Effect on Cardiovascular Disease Risk Factors.

Authors: White K, Jacques PH.

Bird Health Center, Western Carolina University, Cullowhee, NC, USA.

This study assessed the effectiveness of a 12-week pilot employee wellness program in reducing risk factors for coronary heart disease. Fifty university employees with at least one cardiovascular disease risk factor participated in the program. Interventions focused on diet, exercise, and monthly workshops. Pre- and post-intervention measurements included weight, body composition, blood pressure, total cholesterol, low-density lipoprotein (LDL) cholesterol, high-density lipoprotein (HDL) cholesterol, total cholesterol/HDL cholesterol ratio, triglycerides, and blood sugar. Twenty-five employees had post-intervention measurements. A survey was administered to assess adherence. The correlation between adherence and improvement in cardiovascular disease risk factors was also tested. Significant differences were observed between pre- and post-intervention measurements of total cholesterol, LDL cholesterol, total cholesterol/HDL cholesterol ratio, triglycerides, and weight. A significant correlation existed between self-reported level of participation in the diet aspect of the program and improvement in LDL levels. This multi-component, 12-week pilot employee wellness program was effective in reducing cardiovascular disease risk.

Journal: AAOHN J. 2007 Mar;55(3):109-14.
Adapted from PubMed; click here to access full journal article.