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Biomedical subjects

H R Superko

Publications and source records attributed to H R Superko.

At least 19 recordsLinked to original sources
PubMed2000

Small, dense, low-density lipoprotein and atherosclerosis.

Disorders of low-density lipoprotein (LDL) and high- density lipoprotein (HDL) subclass distribution are more common contributors to coronary artery disease (CAD) than is elevated low-density lipoprotein cholesterol (LDLC). Recent research has emphasized the importance of LDL and HDL subclass distribution in patient management and response to treatments. Laboratory determination of LDL and HDL subclass distribution involves analytic ultracentrifugation or polyacrylalmide gradient gel electrophoresis. If subclass distribution is to be used for patient management, research quality control and standards are necessary in order to assure that the patient's values accurately reflect the metabolic disorder. The importance of this topic for patient care has been recognized by the medical insurance industry. Investigations employing electron beam computed tomography in asymptomatic individuals has revealed that 50% with established CAD have normal lipids by National Cholesterol Education Program (NCEP) criteria. However, a large proportion of other metabolic contributors to CAD are not revealed by routine blood tests.

Arteriosclerosis↗
PubMed2000

Garlic powder, effect on plasma lipids, postprandial lipemia, low-density lipoprotein particle size, high-density lipoprotein subclass distribution and lipoprotein(a).

OBJECTIVES: To test the hypothesis that a garlic supplement alters plasma lipoproteins, postprandial lipemia, low-density lipoprotein (LDL) size and high-density lipoprotein (HDL) subclass distribution differently in 50 moderately hypercholesterolemic subjects classified as LDL subclass pattern A or B. BACKGROUND: Garlic has been variably reported to reduce or not affect plasma cholesterol values. Low-density lipoprotein pattern B is a common inherited disorder of lipoprotein metabolism that has been shown to have a significantly greater response to several lipid lowering treatments including low fat diet when compared with LDL pattern A individuals. METHODS: A double blind, randomized, placebo controlled trial in an outpatient lipid research clinic was performed and included fifty moderately hypercholesterolemic subjects (mean LDL cholesterol = 166 +/- 22 mg/dl) classified as LDL subclass pattern A (predominantly large LDL, n = 22) or B (predominantly small LDL, n = 28). Following a two-month stabilization period, subjects were randomly assigned to a placebo or 300 mg three times a day of a standardized garlic tablet for three months. RESULTS: For all subjects, LDL pattern A and B subjects combined, garlic treatment for three months resulted in no significant change in total cholesterol, LDL cholesterol, HDL cholesterol, HDL subclass distribution, postprandial triglycerides, apolipoprotein B, lipoprotein (a) (Lp[a]), LDL peak particle diameter or LDL subclass distribution. There was no significant difference in response for the same parameters among subjects classified as LDL pattern A or B with the exception of significantly greater (p = 0.01) reduction in mean peak particle diameter in pattern A subjects treated with either garlic or placebo. There was no significant change in LDL subclass distribution. CONCLUSIONS: This investigation confirms that garlic therapy has no effect on major plasma lipoproteins and further, that it has no impact on HDL subclasses, Lp(a), apolipoprotein B, postprandial triglycerides or LDL subclass distribution. Garlic may have a greater effect on LDL particle diameter in LDL pattern A compared with pattern B subjects. This difference was not reflected in other plasma lipid measurements.

Biomarkers↗
PubMed1999

Small, dense low-density lipoprotein subclass pattern B: issues for the clinician.

A large portion of coronary artery disease (CAD) can be attributed to disorders of lipoprotein metabolism. However, these disorders are a complex interaction of genetic susceptibility and environmental interaction. The most common disorder of lipoprotein metabolism contributing to CAD is the Small, Dense Low-Density Lipoprotein Pattern B disorder, also known as the Atherogenic Lipoprotein Profile (ALP), which consists of multiple metabolic disorders. This disorder is an independent risk factor for CAD and in patients with established CAD, identifies a subgroup with a twofold greater rate of arteriographic progression compared with CAD patients without this disorder. Treatment of the disorder is specific to lifestyle and some pharmacologic agents. The most effective treatments are often the least expensive.

Arteriosclerosis↗
PubMed1999

Long-term blood cholesterol-lowering effects of a dietary fiber supplement.

BACKGROUND: The study evaluated the blood cholesterol-lowering effects of a dietary supplement of water-soluble fibers (guar gum, pectin) and mostly non-water-soluble fibers (soy fiber, pea fiber, corn bran) in subjects with mild to moderate hypercholesterolemia (LDL cholesterol, 3.37-4.92 mmol/L). METHODS: After stabilization for 9 weeks on a National Cholesterol Education Program Step 1 Diet, subjects were randomly assigned to receive 20 g/d of the fiber supplement (n = 87) or matching placebo (n = 82) for 15 weeks and then receive the fiber supplement for 36 weeks. The efficacy analyses included the 125 subjects (58 fiber; 67 placebo) who were treatment and diet compliant. One hundred two (52 fiber; 50 placebo) completed the 15-week comparative phase. Of these subjects 85 (45 fiber; 40 placebo) elected to continue in the 36-week noncomparative extension phase. RESULTS: The mean decreases during the 15-week period for LDL cholesterol (LDL-C), total cholesterol (TC), and LDL-C/HDL-C ratio were greater (P < 0.001) in the fiber group. The mean changes from pre-treatment values in LDL-C, TC, and LDL-C/HDL-C ratio for subjects in the fiber group were -0.51 mmol/L (-12.1%), -0.53 mmol/L (-8.5%), and -0.30 (-9.4%), respectively. The corresponding changes in the placebo group were -0.05 mmol/L (-1.3%), -0.05 mmol/L (-0.8%), and 0.05 (1.5%), respectively. The fiber supplement had no significant effects (P > 0.05) on HDL cholesterol (HDL-C), triglyceride, iron, ferritin, or vitamin A or E levels. Similar effects were seen over the subsequent 36-week noncomparative part of the study. CONCLUSIONS: The fiber supplement provided significant and sustained reductions in LDL-C without reducing HDL-C or increasing triglycerides over the 51-week treatment period.

Adolescent↗
PubMed1998

Did grandma give you heart disease? The new battle against coronary artery disease.

Atherosclerosis/coronary artery disease (CAD) is largely a result of genetically linked dyslipidemias that can often be identified in clinical practice. Expression of these genetic traits is highly individual and can be affected by environmental factors such as diet and exercise. By understanding the heterogeneity of CAD, it becomes clear that all patients cannot be optimally managed with the same therapeutic regimen. Whereas elevated low-density lipoprotein (LDL) cholesterol is strongly correlated with CAD risk, reduction of LDL cholesterol alone is not an adequate strategy in many cases. Patients with the small, dense LDL of the atherogenic lipoprotein profile (pattern B) experience a 3-fold increased risk of CAD, and pattern B is also correlated with the development of type 2 diabetes. Likewise, elevated lipoprotein(a) increases atherosclerotic risk, particularly in the presence of other risk factors, and is predictive of CAD risk in both women and men. Recent data show that the routine lipid profile--total cholesterol, triglycerides, LDL cholesterol, and high-density lipoprotein (HDL) cholesterol--does not detect the most common inherited dyslipidemias. Newer, more sophisticated tests, such as gradient gel electrophoresis, can detect disease-relevant lipidemic details, e.g., LDL subclass pattern, LDL particle diameter, and LDL subregions. Although these testing procedures are more expensive, their cost must be weighed against the potential lifelong cost of sometimes expensive drug treatment that may be avoided based on the results of such tests. Thus, by attending to the implications of family history, the interactions of genetic, metabolic, and environmental factors, and utilizing more targeted testing procedures, physicians can match the patient's disorder with specifically effective therapy while maintaining a cost-effective approach to disease management.

Angioplasty, Balloon, Coronary↗
PubMed1998

Effectiveness of once-nightly dosing of extended-release niacin alone and in combination for hypercholesterolemia.

We performed a multicenter, open-label study to determine the long-term safety and efficacy of a new extended-release once-a-night niacin preparation, Niaspan, in the treatment of hypercholesterolemia. Niaspan, 0.5 to 3.0 g once a night at bedtime, was used alone or in combination with a statin (inhibitor of hydroxymethylglutaryl coenzyme A reductase), a bile acid sequestrant, or both. Patients included 269 hypercholesterolemic male and female adults enrolled in a 96-week study, and 230 additional adults for whom short-term safety data were available. The dosages of Niaspan attained by 269 patients were 1,000 mg (95% of patients), 1,500 mg (86%), and 2,000 mg (65%). After 48 weeks of treatment, Niaspan alone (median dose 2,000 mg) reduced low-density lipaprotein (LDL) cholesterol (18%), apolipoprotein B (15%), total cholesterol (11%), triglycerides (24%), and lipoprotein(a) (36%), and increased high-density lipoprotein (HDL) cholesterol (29%). Niaspan plus a statin lowered LDL cholesterol (32%), apolipoprotein B (26%), total cholesterol (23%), triglycerides (30%), and lipoprotein(a) (19%), and increased HDL cholesterol (26%). Reversible elevations of aspartate aminotransferase or alanine aminotransferase more than twice the normal range occurred in 2.6% of patients. One patient discontinued Niaspan because of transaminase elevations. Intolerance to flushing, leading to discontinuation of Niaspan, occurred in 4.8% of patients. The overall rate of discontinuance due to flushing in this study combined with 2 previous randomized trials was 7.3%. In the long-term treatment of hypercholesterolemia, Niaspan produced favorable changes in LDL and HDL cholesterol, triglycerides, and lipoprotein(a). Adverse hepatic effects were minor and occurred at rates similar to those reported for statin therapy.

Adult↗
PubMed1998

Equivalent efficacy of a time-release form of niacin (Niaspan) given once-a-night versus plain niacin in the management of hyperlipidemia.

This study compared the efficacy and safety of a once-a-night, time-release niacin formulation, Niaspan (Kos Pharmaceuticals, Miami Lakes, FL), with plain niacin and placebo for the treatment of primary hypercholesterolemia. The study was conducted in nine academic lipid research clinics in a randomized, double-blind design. Niaspan 1.5 g at bedtime was compared with plain niacin 1.5 g/d after 8 weeks and 3.0 g/d after 16 weeks in divided doses and with placebo. A total of 223 hypercholesterolemic adult men and women participated. Compared with placebo at 8 weeks, Niaspan versus plain niacin at 1.5 g/d showed comparable efficacy, comparably lowering total cholesterol (C) (8%/8%), triglycerides (16%/18%), low-density lipoprotein (LDL)-C (12%/12%), apolipoprotein (apo B) (12%/12%), apo E (9%/7%), and lipoprotein(a) [Lp(a)] (15%/11%), and raising high-density lipoprotein (HDL)-C (20%/17%), HDL2-C (37%/33%), HDL3-C (17%/16%), and apo A-I (8%/6%) (P < or = .05 in all instances). After 16 weeks, the Niaspan effect on LDL-C and triglyceride was unchanged while the plain niacin effect approximately doubled. At equal doses of 1.5 g/d of Niapan versus plain niacin, respectively, AST increased 5.0% versus 4.8% (difference not significant [NS]), fasting plasma glucose increased 4.8% versus 4.5% (NS), and uric acid concentrations increased less, 6% versus 16% (P=.0001). Flushing events were more frequent with plain niacin versus Niaspan (1,905 v 576, P < .001). Flushing severity was slightly greater with Niaspan, but still well tolerated. In conclusion, Niaspan 1.5 g hour of sleep (hs) has comparable efficacy, a lower incidence of flushing, a lesser uric acid rise, and an equivalent hepatic enzyme effect than 500 mg thrice-daily plain niacin in hyperlipidemic subjects. Niaspan may be an equivalent or better alternative to plain niacin at moderate doses in the management of hyperlipidemia.

Double-Blind Method↗
PubMed1997

Effect of fluvastatin on low-density lipoprotein peak particle diameter.

The effect of fluvastatin on low-density lipoprotein (LDL) particle diameter was investigated in 42 hypercholesterolemic patients. Fluvastatin reduced LDL cholesterol significantly but had no effect on LDL particle diameter; it also had no differential effect on patients classified as LDL pattern A (large LDL), pattern B (small LDL), or I (intermediate LDL).

Analysis of Variance↗
PubMed1997

The new thinking on lipids and coronary artery disease.

Detection and treatment of high blood cholesterol has significantly reduced cardiovascular events. However, most individuals with coronary artery disease do not have hypercholesterolemia. Atherosclerosis is a complex interaction of inherited susceptibility and environmental issues that combine to create an atherogenic milieu. Appropriate diagnosis and treatment of patients with coronary artery disease can be of significant benefit, but if treatment is not individualized to the patient's individual metabolic abnormality, many patients will receive little to no benefit despite improved lipid profiles.

Cholesterol↗
PubMed1996

Cost-effective treatment of coronary artery disease--the new imperative.

Large lipid-lowering clinical trials have demonstrated a significant reduction in cardiovascular events and the need for cardiovascular procedures. These clinical and point trials used relatively weak treatment modalities, and when the cost savings of the reduced number of events is balanced against the estimated cost of treatment, the average difference is approximately $1,500 per patient per year. Arteriographic trials have used similar or more aggressive lipoprotein therapy over shorter periods of time. Estimates of cost savings from reduced clinical events balanced against the cost of treatment in these studies indicate a wide spectrum of estimated patient costs. These estimates range between a cost of $2,273 per patient per year to a cost savings of (-)$901 per patient per year. Extrapolation to the United States population with coronary artery disease (CAD) suggests that greater than one billion dollars per year could be saved if patients with CAD received similar treatment and responded in a similar manner.

Cholesterol, HDL↗
PubMed1996

What can we learn about dense low density lipoprotein and lipoprotein particles from clinical trials?

The small LDL pattern B trait, and triglyceride rich lipoproteins, have now been established as major coronary heart disease risk factors and have been associated with its severity. The presence of these disorders identifies a patient subgroup which is at substantial coronary artery disease risk but also exhibits the best arteriographic response to treatment. Most lipid-lowering treatments have a differential effect in LDL subclass pattern A patients compared with those with pattern B that helps explain the differential arteriographic response seen in clinical trials.

Clinical Trials as Topic↗
PubMed1995

New aspects of risk factors for the development of atherosclerosis, including small low-density lipoprotein, homocyst(e)ine, and lipoprotein(a).

The risk factors for coronary artery disease have been expanded in recent years to include several clinically significant metabolic disorders. The small, dense low-density lipoprotein trait is one of the most common inherited coronary artery disease risk factors and recent reports describe the clinical use of low-density lipoprotein phenotyping for coronary artery disease risk determination, and for treatment in patients with established disease. Apolipoprotein E isoforms play a role in diet responsiveness and may explain approximately 12% of cases of myocardial infarction. Hypoalphalipoproteinemia appears to be a spectrum of overlapping disorders and is difficult to treat. Low-density lipoprotein oxidation may be affected by dietary sources of oxidized fat, and a recent antioxidation trial reported negative results. In the past year, homocyst(e)inemia was reported to play a significant role in coronary artery disease risk prediction and lipoprotein(a) phenotypes appear to clarify the risk of lipoprotein(a).

Coronary Artery Disease↗