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Biomedical subjects

H R Superko

Publications and source records attributed to H R Superko.

At least 55 records · Page 3Linked to original sources
PubMed1991

The effect of apolipoprotein E isoform difference on postprandial lipoprotein in patients matched for triglycerides, LDL-cholesterol, and HDL-cholesterol.

The postprandial response to three test meals provided during a single day was investigated in subjects with either the apo E3/3 phenotype (n = 8), or the apo E4/3 phenotype (n = 4), who had LDL-C greater than 160 mg/dl. Vitamin A (60,000 U/m2) was ingested with the first meal and retinyl palmitate determined four hours later. Triglyceride and total cholesterol concentration were determined on whole plasma and total cholesterol and free cholesterol determined following single spin ultracentrifugation (d less than 1.006 g/ml) and dextran precipitation of the d greater than 1.006 fraction to separate apoprotein-B containing lipoproteins. Fasting values revealed significantly lower HDL-cholesterol ester (p less than 0.03) and HDL3-cholesterol ester (p less than 0.03) and significantly greater HDL-free cholesterol (p less than 0.03) and HDL3-free cholesterol (p less than 0.02) in subjects with the E4/3 phenotype. Four hour postprandial HDL and HDL3 cholesterol ester increased significantly more (p less than 0.05) in E4/3 patients and HDL and HDL3 free cholesterol decreased significantly more (p less than 0.05) in E4/3 subjects. Eight-hour postprandial change values maintained the significant HDL3-cholesterol ester and free cholesterol difference, and, revealed a significantly greater triglyceride rich lipoprotein cholesterol ester reduction (p less than 0.01) in the E4/3 group. Individuals with the apolipoprotein E4/3 phenotype reveal significant differences in postprandial lipemia compared to individuals with the E3/3 phenotype, and, postprandial lipemia following multiple meals reveals differences not apparent from responses to a single meal.

Apolipoproteins E↗
PubMed1991

Exercise training, serum lipids, and lipoprotein particles: is there a change threshold?

The role of lipoprotein manipulation in the treatment of atherosclerosis is well established. Improvement in lipoprotein cholesterol concentrations and subclass distribution through exercise training is often advised prior to pharmacologic intervention. As with other therapeutic interventions, dose must be stipulated to the patient. The dose of exercise training required to induce beneficial lipoprotein changes is unclear. This issue is further complicated by the potential effect of exercise training on lipoprotein subclass distribution (LDL I, LDL II, LDL III, LDL IV, HDL2a, HDL2b, HDL3a, HDL3b, HDL3c), enzymes, apoproteins, and transfer proteins and by the changes in diet and body composition that often accompany exercise training. These changes may be responsible for all or part of the lipoprotein change attributed to exercise. From available data, it appears that a threshold of approximately 15 miles.wk(-1) of jogging may be required to induce beneficial change.

Arteriosclerosis↗
PubMed1990

Lipoprotein and hepatic lipase activity and high-density lipoprotein subclasses after cardiac transplantation.

Atherosclerosis is the leading obstacle to long-term survival in cardiac transplant patients. Increases in plasma triglycerides and lipoprotein cholesterol levels occur after transplantation that may contribute to transplant atherosclerosis. The etiology of this increase is unclear. We investigated the interaction of immunosuppressive medications with plasma triglycerides, low-density lipoprotein (LDL) cholesterol, high-density lipoprotein (HDL) cholesterol, the HDL subclasses HDL2 and HDL3 cholesterol, and hepatic and lipoprotein lipase activity in 72 consecutive cardiac transplant patients compared to 51 healthy control subjects. In the transplantation group, greater concentrations of plasma triglyceride (80%, p less than 0.001), LDL cholesterol (16%, p less than 0.005) and hepatic lipase activity (100%, p less than 0.001) were noted, whereas lipoprotein lipase activity was noted to be significantly lower (124%, p less than 0.001). No difference was detected in HDL, HDL2, or HDL3 cholesterol. Cyclosporine dose was significantly associated with hepatic lipase activity (r = 0.33, p less than 0.02) and inversely associated with lipoprotein lipase activity (r = -0.28, p less than 0.05). Lipoprotein lipase activity after transplantation correlated inversely with triglycerides (r = -0.36, p less than 0.002) and positively with HDL cholesterol (r = 0.23, p less than 0.05) and HDL2 cholesterol (r = 0.29, p less than 0.05). Hepatic lipase activity correlated inversely with LDL cholesterol (r = -0.21, p less than 0.08). In multiple regression analysis, cyclosporine dose was the major source of variation in hepatic lipase activity.

Adult↗
PubMed1989

Drug therapy and the prevention of atherosclerosis in humans.

The results of the World Health Organization Cooperative Trial, the Coronary Drug Project, the Coronary Primary Prevention Trial and the Helsinki Heart Study indicate that clinical expression of coronary artery disease can be delayed with pharmacologic modification of plasma lipoproteins. Change in coronary artery disease can be semiquantitated by repeat arteriograms. Three randomized clinical trials indicate that rate of progression of atherosclerosis, as defined by arteriography, can be reduced, and existing lumen obstruction decreased. Tendon xanthomas occur in hypercholesterolemia, and reduction in xanthoma size with drug therapy suggests an improved atherosclerotic disease state. The clinician has a variety of pharmacologic therapies available. The role of bile acid-binding resins, fibric acid derivatives, hydroxymethylglutaryl coenzyme A reductase inhibitors, nicotinic acid and antioxidants is each unique. Understanding the role of lipoproteins in atherosclerosis will help in selecting the most appropriate therapy for each individual patient. Medications not designed for their lipoprotein effects can significantly alter lipoproteins. Medications, such as nonselective beta blockers, can alter low-density lipoprotein (LDL) subclass distribution with no change in LDL cholesterol content. Such changes may eradicate part of the beneficial cardiovascular effect of beta blockade therapy. In the future, therapeutic choices may depend in part on lipoprotein abnormalities such as lipoprotein (a), apolipoprotein E isoforms, hyperapobetalipoproteinemia, LDL.

Clinical Trials as Topic↗
PubMed1989

Effect of alpha- and selective beta-blockade for hypertension control on plasma lipoproteins, apoproteins, lipoprotein subclasses, and postprandial lipemia.

Fourteen male patients (mean age +/- SD, 52 +/- 11 years) with a history of hypertension (systolic blood pressure, 148 +/- 10 mm Hg; diastolic blood pressure, 99 +/- 2 mm Hg) were enrolled in a cross-over trial of prazosin and atenolol, with a minimum of eight weeks of treatment with each drug. Measures of lipoprotein metabolism included levels of: total plasma cholesterol, triglycerides, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, and high-density lipoprotein2 cholesterol. Lipoprotein mass was measured by analytical ultracentrifugation in low-density to very low-density lipoprotein flotation rate intervals of 0 to 12, 12 to 20, and 20 to 400, and high-density lipoprotein flotation rate intervals of 0 to 3.5 and 3.5 to 9.0. Apolipoproteins A1 and B, postheparin lipoprotein and hepatic lipase activities, and magnitude of postprandial lipemia also were determined. Mass of intermediate-density lipoproteins (flotation rate, 12 to 20) was significantly lower (p = 0.05) following prazosin therapy compared with atenolol therapy. Other lipid parameters, including triglycerides and low- and high-density lipoprotein cholesterol, were not significantly different for the two drug treatments.

Apoproteins↗
PubMed1988

Changes in plasma lipids and lipoproteins in overweight men during weight loss through dieting as compared with exercise.

We studied separately the influence of two methods for losing fat weight on the levels of plasma lipids and lipoproteins in overweight sedentary men--decreasing energy intake without increasing exercise (diet), and increasing energy expenditure without altering energy intake (exercise, primarily running)--in a one-year randomized controlled trial. As compared with controls (n = 42), dieters (n = 42) had significant loss of total body weight (-7.8 +/- 0.9 kg [mean +/- SE]), fat weight (-5.6 +/- 0.8 kg), and lean (non-fat) weight (-2.1 +/- 0.5 kg) (P less than 0.001 for each variable), and exercisers (n = 47) had significant loss of total body weight (-4.6 +/- 0.8 kg) and fat weight (-3.8 +/- 0.7 kg) (P less than 0.001 for both variables) but not lean weight (-0.7 +/- 0.4 kg). Fat-weight loss did not differ significantly between dieters and exercisers. All subjects were discouraged from altering their diet composition; however, dieters and exercisers had slight reductions in the percentage of kilojoules derived from fat. As compared with the control group, both weight-loss groups had significant increases (P less than 0.01) in plasma concentrations of high-density lipoprotein (HDL) cholesterol (diet vs. exercise, 0.13 +/- 0.03 vs. 0.12 +/- 0.03 mmol per liter), HDL2 cholesterol (0.07 +/- 0.02 vs. 0.07 +/- 0.02 mmol per liter), and HDL3 cholesterol (0.07 +/- 0.02 vs. 0.06 +/- 0.02 mmol per liter) and significant decreases (P less than 0.05) in triglyceride levels (diet vs. exercise, -0.35 +/- 0.14 vs. -0.24 +/- 0.12 mmol per liter). Levels of total and low-density lipoprotein cholesterol were not significantly changed, relative to values in controls. None of these changes were significantly different between dieters and exercisers. Thus, we conclude that fat loss through dieting or exercising produces comparable and favorable changes in plasma lipoprotein concentrations.

Adult↗
PubMed1988

Effects of solid and liquid guar gum on plasma cholesterol and triglyceride concentrations in moderate hypercholesterolemia.

Guar gum is a dietary fiber reported to decrease plasma cholesterol concentration. This study investigated the effect of guar therapy in 50 men with moderately elevated plasma cholesterol who were randomized to an 8-week study of guar therapy. Three forms of guar gum were used: a medium viscosity solid or liquid form, a high viscosity liquid form or placebo. When the medium viscosity guar therapy groups were combined, 4 weeks of therapy were shown to result in a substantial reduction in total and low density lipoprotein (LDL) cholesterol of 25 mg/dl and 23 mg/dl (p = 0.035 and 0.12), respectively. The high viscosity guar group had a reduction in total cholesterol and LDL cholesterol of 37 and 30 mg/dl, respectively (p less than 0.003 and p less than 0.02). Following 8 weeks of therapy, a return toward baseline values was observed. No significant changes were demonstrated in blood chemistries, triglyceride values, total high density lipoprotein (HDL) cholesterol or the HDL2 fraction of HDL cholesterol. The effect of the solid and liquid forms of guar on plasma cholesterol reduction was similar. This study shows that a nonpharmacologic dietary additive reduces plasma total and LDL cholesterol.

Cholesterol↗
PubMed1988

Blood cholesterol treatment attitudes of community physicians: a major problem.

Blood cholesterol treatment attitudes of community physicians are an important component of the NIH recommendation to reduce blood cholesterol. To determine current blood cholesterol treatment attitudes, a survey of 2413 multispecialty Northern California physicians was conducted. A total of 793 physicians responded. Results show that treatment habits among medical specialties are similar with a tendency for lower initial treatment levels in the subspecialties of endocrinology and cardiology. No specialty or subspecialty group indicated an aggressive plasma lipid treatment attitude. The findings include the following: Mean values at which physicians reported treating hypercholesterolemia with medication (312 +/- 44 mg/dl) exceed the NIH definition of "high risk." Younger physicians treated hypercholesterolemia with diet at significantly lower blood cholesterol levels than did older colleagues (p = 0.04). Physicians exposed to the CPPT-LRC investigation did not show a difference in treatment attitudes with regard to blood cholesterol levels when compared to physicians without such an experience. The type of lipid-lowering medication used differs significantly among medical specialties and subspecialties. Physicians lack confidence in the precision of laboratory measurement of plasma lipids. Physician treatment attitudes require substantial change if the NIH cholesterol consensus conference goals are to be achieved.

Adult↗
PubMed1987

The role of exercise training in the therapy of hyperlipoproteinemia.

Exercise therapy is a valid therapeutic modality in patients with hyperlipoproteinemia (HLP). In combination with appropriate dietary modification, it can be a powerful therapeutic tool and may allow a reduction in hyperlipidemic medication doses. Improved triglyceride values and lipoprotein profiles can be obtained. The dose of therapy is an important aspect of exercise prescription, as it is in any medical therapy. The amount and type of exercise required to achieve therapeutic lipid changes in patients with HLPs deserves further attention.

Apoproteins↗
PubMed1986

High-density lipoprotein cholesterol measurements. A help or hindrance in practical clinical medicine?

Often, plasma high-density lipoprotein cholesterol (HDLC) measurements lack sufficient accuracy to be of practical use in an individual clinical setting. Recent clinical investigations have demonstrated the strong predictive value of HDLC concentration for future coronary events and rate of progression of angiographically assessed coronary atherosclerosis. Clinical demand for HDLC measurements by clinicians has increased after the announcements of these results. The ability of clinical laboratories to assess HDLC values accurately, so that they may be applied on an individual basis, may be lacking, and enhanced accuracy should be encouraged.

Cholesterol↗
PubMed1985

Coronary heart disease and risk factor modification. Is there a threshold?

Modification of coronary heart disease risk factors may play an important role in the control and alteration of the atherosclerotic process. The amount of modification necessary to obtain beneficial results is a controversial issue. Review of epidemiologic studies and recent arteriographic investigations allows for the approach to the issue of threshold levels of modification that may be required prior to obtaining some benefit. Serum lipoproteins appear to play a central role in the atherosclerotic risk factor relationship. On the basis of current evidence, clinical aims are suggested for coronary heart disease risk factor modification in order to assist in obtaining optimal health goals.

Adult↗
PubMed1985

Modification of plasma cholesterol through exercise. Rationale and recommendations.

Until relatively recently, clinical information regarding plasma lipoproteins and their association with human atherosclerosis had been based on epidemiologic evidence obtained from cross-sectional studies or prospective studies that used clinical events as end points. Authorities have cautioned against the interpretation of these results to imply that drug therapy be used to alter the high-density lipoprotein (HDL) fraction of total cholesterol. Several recent investigations strongly suggest that decreasing the low-density lipoprotein fraction of total cholesterol and increasing the HDL fraction may alter the progression of atherosclerosis. Appropriate exercise may be a viable tool to assist in elevating plasma HDL levels.

Adult↗
PubMed1985

Associations of resting heart rate with concentrations of lipoprotein subfractions in sedentary men.

In major prospective studies it has been reported that high heart rate at rest predicts the development of coronary heart disease (CHD) or cardiovascular disease (CVD) in men, but the mechanisms producing these relationships are unknown. Since lipoprotein levels contribute strongly to the risk of CHD and CVD, we examined the relationship of resting heart rate to plasma concentrations of high-density (HDL), low-density (LDL), and very low-density (VLDL) lipoproteins, apolipoprotein (apo) A-I and A-II, and serum concentrations of lipoprotein subfractions in 81 men to determine if atherogenic lipoproteins could potentially induce the reported association of heart rate with development of CHD or CVD. The significant (p less than or equal to .05) Spearman's correlations for resting heart rate vs HDL2 mass (rs = -.24), HDL3 mass (rs = -.40), HDL cholesterol (rs = -.36), apo A-I (rs = -.29), triglycerides (rs = .31), VLDL cholesterol (rs = .24), VLDL mass (rs = .27), and LDL mass of Sof 0-7 subfraction (rs = .30) lend support to our hypothesis of lipoprotein-induced relationships of CHD with heart rate. The correlations for resting heart rate vs triglycerides, HDL cholesterol, HDL3 mass, VLDL mass, and LDL mass of Sof 0-7 subfraction remain significant when adjusted for adiposity, age, smoking habits, diet, and physical fitness as measured by maximum aerobic power (VO2 max) or submaximal heart rate during a graded exercise test.

Age Factors↗
PubMed1984

Dairy product consumption.

In the announcement of the 1985 winter schedule of the Gordon Research Conferences (5 Oct., p. 77), the dates for the conference "Multiple Opiate Receptors" (on p. 79) were incorrectly given. The conference will be held in February, not January. The days of the month were correct.

Adult↗
PubMed1984

Effects of ozone inhalation during exercise in selected patients with heart disease.

Although epidemiologic evidence suggests that patients with heart and lung disease are more vulnerable to the acute toxic effects of photochemical air pollution, no laboratory studies have been reported in patients with coronary heart disease. In the present investigation, six male volunteers, ages 46 to 64 years, with clinically documented coronary heart disease and a well-defined symptomatic angina pectoris threshold, served as subjects. Each patient was exposed on three 40-minute occasions to either filtered air or ozone at concentrations of 0.20 or 0.30 parts per million (ppm), while walking on a treadmill at workloads simulating their regularly prescribed exercise training regimen. Results of standard pulmonary function tests and periodic observations of exercise ventilation, respiratory metabolism, electrocardiographic changes, hemodynamic response, and clinical signs and symptoms were recorded. Analysis of variance revealed that none of the patients' physiologic responses to ozone exposure were statistically significant. Furthermore, neither onset of angina pain or ischemic changes were related to ozone exposure in a dose-dependent fashion. Hence, the patients not only failed to exhibit any unexpected cardiovascular strain while exposed to ozone during exercise, but also evidenced no significant pulmonary function impairment or exercise ventilatory pattern alteration, as has been observed in clinically normal subjects exercising at similar ozone concentration levels. This apparent incongruity may be due to the fact that acute ozone toxicity is more closely related to the total amount of ozone inhaled, which is a function of pulmonary ventilation volume and exposure time, as well as ozone concentration. In the patients with angina, symptom-limited exercise tolerance resulted in a lower total amount of ozone inhaled than that observed to effect ozone toxicity in clinically normal subjects who exercised at greater intensities and for longer durations. Patients with angina appear to be no more susceptible to ozone toxicity than are clinically normal subjects at the effective doses imposed. However, had the patients exercised longer, they might well have evidenced pulmonary function impairment and/or cardiovascular strain. Hence, caution is advised in generalizing these observations to other conditions and patient groups.

Angina Pectoris↗
PubMedDate not supplied

A review of combined hyperlipidaemia and its treatment with fenofibrate.

Approximately 15% of myocardial infarction survivors less than 60 years of age have a plasma lipid abnormality defined as combined hyperlipidaemia. Patients with this condition are at substantial risk for future cardiovascular events. Combined hyperlipidaemia involves elevations in both plasma triglycerides and low-density lipoprotein (LDL) cholesterol and may share similarities with hyperapolipoproteinaemia, LDL-pattern B and the small LDL-pattern. Treatment is directed at reduction of LDL-cholesterol and plasma triglyceride values. Nicotinic acid and the fibric acid derivatives are useful therapeutic agents. Fenofibrate is a fibric acid derivative that lowers both triglycerides and LDL-cholesterol in combined hyperlipidaemia. In combined hyperlipidaemia, fenofibrate has been shown to reduce significantly plasma triglycerides by approximately 40%, LDL-cholesterol by 6%, and to increase high-density lipoprotein cholesterol by 15%. Apoproteins are favourably altered with increases in apoprotein-A, decreases in apoprotein-E and inconsistent decreases in apoprotein-B. Fenofibrate is well tolerated with primarily dermatological side-effects.

Fenofibrate↗
PubMedDate not supplied

Current and future trends in therapy for dyslipidemias.

OBJECTIVE: To characterize the atherogenic lipoprotein profile and discuss its implications in terms of treatment. METHODS: Findings from large clinical trials and personal series of patients are reviewed, and the effectiveness of various interventions is assessed. A cost analysis of management of patients with dyslipidemias is offered. RESULTS: The dyslipidemia associated with non-insulin-dependent diabetes mellitus (NIDDM) is similar to low-density lipoprotein (LDL) pattern B. This atherosclerosis susceptibility trait--which typically consists of a preponderance of small dense LDL particles, intermediate-density lipoprotein, slightly increased triglycerides, and inappropriately low high-density lipoprotein type 2-- tends to precede the actual diagnosis of NIDDM and to identify a group with increased risk for cardiovascular events. It also usually signifies a group with good responses to treatment, including arteriographic evidence of regression of coronary artery disease. In general, niacin and fibrates are superior to statins for treatment of patients with LDL pattern B. Lipid management has been proved to be a cost-effective treatment strategy. CONCLUSION: Therapeutic options that lower triglyceride-rich lipoproteins and small dense LDL should be recommended in patients with NIDDM.

Journal Article↗