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Biomedical subjects

N J Stone

Publications and source records attributed to N J Stone.

At least 37 records · Page 2Linked to original sources
PubMed1994

Secondary causes of hyperlipidemia.

Secondary causes of hyperlipidemia are important to recognize. In fact, hyperlipidemia may be a clue to the presence of an underlying systemic disorder. It may greatly heighten the risk of atherosclerosis with a raised LDL-c, triglyceride-rich lipoprotein excess, and increased lipoprotein(a) as well as lowered HDL-c. The search for secondary causes may provide a clue as to why patients with primary lipid disorders suddenly develop worsening lipid profiles. The point is a crucial one because some acquired causes of hyperlipidemia, such as alcohol, estrogens, steroids, or pregnancy, when superimposed on a primary familial form of hypertriglyceridemia can result in a saturated removal system and a buildup of chylomicrons, which can lead to life-threatening pancreatitis. A convenient way to remember secondary causes is to think of the four D's of diet, drugs, disorders of metabolism, and diseases. Although diets rich in saturated fats and cholesterol are a common cause of the mild hypercholesterolemia seen in our society, alcohol excess and weight gain can explain much of the tendency toward hypertriglyceridemia. Interestingly anorexia nervosa has long been associated with severe but reversible hypercholesterolemia. Several classes of drugs need to be considered as common causes of altered lipid profiles. Glucocorticoids and estrogens elevate triglycerides and raise levels of HDL-c. Anabolic steroids taken orally markedly reduce levels of HDL-c in contrast to injectable testosterone, which does not adversely affect the LDL-to-HDL ratio. Oral contraceptives affect atherosclerotic risk depending on the kind and doses of progestin/estrogen. In those with an underlying primary hypertriglyceridemia and associated obesity, estrogenic medications can depress triglyceride removal mechanisms, leading to the chylomicronemia syndrome and pancreatitis. Antihypertensives have variable effects on lipids and lipoproteins. Although short-term thiazide usage raises cholesterol, triglycerides, and LDL-c, long-term usage is not necessarily associated with significant alterations in lipid levels. Alpha blockers may cause an increase in HDL-c, whereas beta blockers raise triglycerides and lower HDL-c. Sympatholytics, angiotensin converting enzyme inhibitors, and calcium channel blockers are essentially lipid neutral. Retinoids can be associated with increased LDL-to-HDL ratios and occasionally striking elevations in triglycerides. Cyclosporine raises LDL-c and lipoprotein(a). Classes of drugs that may raise HDL-c include cimetidine, antiepileptic drugs, and tamoxifen, but the effect may be seen primarily in women. Hypothyroidism is the most common secondary cause of hyperlipidemia after dietary causes are considered. A thyroxine and TSH level should be obtained on all new cases of clinically important hyperlipidemia.(ABSTRACT TRUNCATED AT 400 WORDS)

Humans↗
PubMed1994

Atherosclerotic plaque evolution in the descending thoracic aorta in familial hypercholesterolemic patients. A transesophageal echo study.

We explored the concept that transesophageal echocardiography can be used as a tool to detect, characterize, and study plaque morphology in the descending thoracic aorta. The pattern of atherosclerotic plaques in the descending thoracic aorta in familial hypercholesterolemic (FH) patients was evaluated. Additionally, evolution of plaque characteristics as a result of therapy was analyzed. In a randomized prospective protocol, eight FH patients (five men and three women, aged 23 to 65 years [mean +/- SD, 42 +/- 14 years]) receiving standard therapy (n = 3; baseline low-density lipoprotein [LDL] cholesterol, 222 +/- 71 mg/dL, mean +/- SD) or LDL apheresis (n = 5; baseline LDL cholesterol, 262 +/- 51 mg/dL) were studied. Baseline and follow-up (mean, 12 months) transesophageal echocardiographic studies were performed. Measurements obtained were atherosclerotic plaque area (PA), aortic wall area (WA), total arterial area (TAA), and plaque-to-wall area ratio (PWR). LDL cholesterol decreased in both groups. The greatest severity of plaque was detected at 30 to 35 cm from the incisors (approximately 15 to 20 cm from the aortic arch). The smallest plaques were present at the arch and more distal descending aorta. In the control group, TAA, PA, and PWR did not change significantly (P = NS versus baseline). In the LDL-apheresis group, TAA increased (P < .05 versus baseline), PA decreased in three of five patients (P = NS versus baseline), and PWR fell (P < .05 versus baseline).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Performance, mood, satisfaction, and task type in various work environments: a preliminary study.

We investigated the influence of windows on performance, mood, and satisfaction for different task types. Forty students worked computational or managerial tasks in offices with or without windows. Contrary to expectation, windowed offices did not effect higher performance, positive mood, or satisfaction. Actually, students felt slightly more confident (p < .10) and more in control (p < .01) in the windowless condition, suggesting a need for privacy to reduce evaluation apprehension. How windows affect performance, mood, and satisfaction remains unclear.

Adult↗
PubMed1990

Diet, lipids, and coronary heart disease.

This review has highlighted some of the experimental studies in animals and humans that have shown an important link between dietary change and atherosclerosis. This relationship was further supported by population studies showing a key role for saturated fat intake in the determination of serum cholesterol level and the prediction of CHD. Recent data linking dietary cholesterol independent of serum cholesterol level to the prediction of CHD were discussed as well. Various components of the diet and their effects on lipid and lipoproteins were reviewed. The chief factors in the diet which raise cholesterol and low-density lipoprotein cholesterol (LDL-c) are dietary cholesterol, saturated fat, and excess calories leading to obesity. Dietary factors useful in lowering cholesterol and low-density lipoprotein cholesterol include monounsaturated fats, polyunsaturated fats, and dietary fiber, which can be substituted for saturated fats. The usefulness of a special class of polyunsaturated oil, the omega-3 fatty acids, in both lowering triglyceride levels and preventing thrombosis was also discussed. Although alcohol raises the HDL-c level, it is not clear that its use offers protection against CHD, and its risks clearly outweigh its advantages in this regard. Regular aerobic exercise is recommended as a healthier alternative to raising high-density lipoprotein cholesterol. Also discussed was postprandial lipemia, which may prove to be another indicator of risk of CHD. Finally, the recent NCEP dietary guidelines were discussed along with practical suggestions as to their implementation.

Animals↗
PubMed1988

Controlling cholesterol levels through diet.

High blood cholesterol levels are a major risk factor for coronary artery disease. Recent studies have shown that a cholesterol-lowering diet has a principal role in reducing coronary events in humans. A diet low in saturated fat and cholesterol is recommended for patients with a cholesterol level of more than 240 mg/dl or a level of between 200 and 239 mg/dl plus other risk factors. Measurement of low-density lipoprotein and high-density lipoprotein cholesterol levels provides a baseline value by which to gauge progress. Periodic assessment by the physician will give an indication of patient compliance. For patients who do not achieve desired goals within six months, drug therapy may be necessary.

Cholesterol↗
PubMed1985

Secondary prevention and lipid lowering: results and implications.

In a secondary prevention trial conducted by the National Heart, Lung, and Blood Institute, the effect of lipid lowering by drug intervention on the progression of existing coronary artery disease (CAD) was evaluated in type II hyperlipidemic patients. This first randomized, secondary prevention trial compared the effect of cholestyramine and diet with that of placebo and diet in 143 patients over a 5-year period. End points evaluated were progression or regression of CAD, as demonstrated by angiographic changes compared with baseline angiograms. The cholestyramine-treated group demonstrated a significant reduction in total cholesterol and in low-density lipoprotein cholesterol (LDL) levels as compared with placebo, and an 8% increase in high-density lipoprotein cholesterol (HDL). A statistically significant result supporting the use of cholestyramine treatment was found in one category of CAD progression.

Angiocardiography↗
PubMed1984

Effects of therapy with cholestyramine on progression of coronary arteriosclerosis: results of the NHLBI Type II Coronary Intervention Study.

In the National Heart, Lung and Blood Institute Type II Coronary Intervention Study, patients with Type II hyperlipoproteinemia and coronary artery disease (CAD) were placed on a low-fat, low-cholesterol diet and then were randomly allocated to receive either 6 g cholestyramine four times daily or placebo. This double-blind study evaluated the effects of cholestyramine on the progression of CAD as assessed by angiography. Diet alone reduced the low-density lipoprotein cholesterol 6% in both groups. After randomization, low-density lipoprotein cholesterol decreased another 5% in the placebo group and 26% in the cholestyramine-treated group. Coronary angiography was performed in 116 patients before and after 5 years of treatment. CAD progressed in 49% (28 of 57) of the placebo-treated patients vs 32% (19 of 59) of the cholestyramine-treated patients (p less than .05). When only definite progression was considered, 35% (20 of 57) of the placebo-treated patients vs 25% (15 of 59) of the cholestyramine-treated patients exhibited definite progression; the difference was not statistically significant. However, when this analysis was performed with adjustment for baseline inequalities of risk factors, effect of treatment was more pronounced. Of lesions causing 50% or greater stenosis at baseline, 33% of placebo-treated and 12% of cholestyramine-treated patients manifested lesion progression (p less than .05). Similar analyses with other end points (percent of baseline lesions that progressed, lesions that progressed to occlusion, lesions that regressed, size of lesion change, and all cardiovascular end points) all favored the cholestyramine-treated group, but were not statistically significant. Thus, although the sample size does not allow a definitive conclusion to be drawn, this study suggests that cholestyramine treatment retards the rate of progression of CAD in patients with Type II hyperlipoproteinemia.

Adult↗
PubMed1984

The influence of changes in lipid values induced by cholestyramine and diet on progression of coronary artery disease: results of NHLBI Type II Coronary Intervention Study.

The National Heart, Lung and Blood Institute Type II Coronary Intervention Study, a double-blind, placebo-controlled trial, evaluated the efficacy of reduction in cholesterol levels induced by cholestyramine on progression of coronary artery disease (CAD). The rate of CAD progression in patients treated with cholestyramine plus diet was compared with that of patients treated with placebo plus diet. CAD progression was defined angiographically. Significant decrease in total cholesterol (TC) and low-density lipoprotein cholesterol (LDLc) and increases in high-density lipoprotein cholesterol (HDLc), as well as in HDLc/TC and HDLc/LDLc ratios, were observed with cholestyramine. HDLc change was due to increase in HDL2A and HDL2B. When the relationship between CAD progression and lipid changes was examined independent of specific treatment group, a significant inverse relationship was found between progression at 5 years and the combination of an increase in HDLc and a decrease in LDLc; changes in HDLc/TC and HDLc/LDLc were the best predictors of CAD change. While the testing of these relationships independent of treatment group was not part of the initial study design, the trends were observed in both the placebo-treated and cholestyramine-treated groups. Moreover, with multivariate analysis, the effect of cholestyramine treatment on CAD progression was eliminated by adding changes in HDLc/TC to the regression model. These findings support the hypothesis that increases in HDLc and decreases in TC (or LDLc) can prevent or delay CAD progression.

Adult↗
PubMed1982

Reliability of assessing change with sequential coronary angiography.

Data are presented from a study evaluating the reliability of sequential angiography in estimating changes in coronary lesions. Three panels of three expert angiographers each read on two separate, independent occasions 18 sets of paired angiograms taken 24 months apart. All readers were blinded to the temporal sequence of the films, clinical data, and ventriculography information. The need for simultaneous viewing and reading of the two films, for training sessions, and for allowance to be made for apparent differences arising from boundary definitions prior to final analysis was demonstrated. Under stringent conditions (determination of change based on agreement of at least two out of three panels of physicians) it was possible to ascertain change in coronary atherosclerosis from sequential sets of coronary angiograms with good reliability. However, single-panel readings yielded an unacceptable overestimate of the number of patients with lesion changes.

Coronary Angiography↗
PubMed1982

National Heart, Lung, and Blood Institute type II Coronary Intervention Study: design, methods, and baseline characteristics.

The Type II Coronary Intervention Study (Type II Study) is a double-blind, randomized, placebo-controlled clinical trial conducted by the Division of Intramural Research of the National Heart, Lung, and Blood Institute of Bethesda, Maryland. The study was designed to evaluate the 5-year treatment effect of cholestyramine on low density lipoprotein (LDL) cholesterol and on lesions in the coronary arteries. One hundred forty-three patients with Type II hyperlipoproteinemia (elevated LDL cholesterol) and coronary artery disease (CAD) were entered into the study between 1972 and 1976. Patients were stratified by sex and extent of coronary disease as defined angiographically and were randomly allocated to a daily dosage of 24 g cholestyramine and diet (treatment group) or placebo and diet (control group). Changes in the coronary arteries were evaluated by sequential coronary angiography carried out before and after five years of treatment. This report describes the trial design and baseline characteristics of the study patients.

Adult↗