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Biomedical subjects

N J Stone

Publications and source records attributed to N J Stone.

At least 19 recordsLinked to original sources
PubMed2000

The Gruppo Italiano per lo Studio della Sopravvivenza nell'Infarto Miocardio (GISSI)-Prevenzione Trial on fish oil and vitamin E supplementation in myocardial infarction survivors.

A recent large-scale, open-label, randomized, controlled trial in 11, 324 myocardial infarction (MI) survivors has shown low-dose fish oil, but not vitamin E, to reduce significantly the cumulative rate of all-cause death, nonfatal MI, and nonfatal stroke. Neither intervention significantly reduced the other primary endpoint, the cumulate rate of cardiovascular death, nonfatal MI, and nonfatal stroke. Analysis of secondary endpoints indicated that the benefits of the 875 mg fish oil capsules containing 850 to 882 mg eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) as ethyl esters was in reducing mortality and not in a reduction of nonfatal MI. It was a safe intervention. The internal validity and external validity of the data was examined and the findings placed in clinical perspective. Important questions remain about the benefits of increased plant sources of n-3 polyunsaturated fatty acids (PUFA) for those who cannot obtain or consume fish. Also the benefits of diet versus fish oil supplementation haven't been determined precisely. Although it seems reasonable to increase sources of n-3 PUFA in the diet for those at high risk of coronary heart disease, current data do not support a policy of promoting fish oil capsules for secondary prevention of coronary heart disease.

Dietary Supplements↗
PubMed2000

Effects of dietary modification and treatment of obesity. Emphasis on improving vascular outcomes.

This article has considered a vast literature attesting to the efficacy of dietary intervention on risk factors and on vascular outcomes. Rather than rely solely on pharmacotherapy to improve risk factors and vascular outcomes, physicians, nurses, dietitians, pharmacists, and medical providers should emphasize the benefits of a well-balanced, nutritionally sound dietary program. It should be low in SFA; controlled in calories to avoid (or reduce) obesity; and rich in fruits, vegetables, whole-grain products, and good sources of protein. Emphasis on foods rich in n-3 fatty acids shows promise for reducing cardiovascular outcomes. Further studies using these and antioxidants are eagerly awaited.

Diet, Fat-Restricted↗
PubMed1998

Month-to-month variability of lipids, lipoproteins, and apolipoproteins and the impact of acute infection in adolescents.

OBJECTIVE: To assess month-to-month variability of total cholesterol, triglycerides, high-density lipoprotein-cholesterol (HDL-C), calculated low-density lipoprotein-cholesterol (LDL-C), apolipoprotein A1, apolipoprotein B, and lipoprotein (a), as well as factors that could influence variability, including recent acute infection in an adolescent population. METHODS: Sixty-three high school students had fasting lipids and lipoproteins measured at 4 separate times during the school year and another venipuncture 3 to 7 days after recovery from an acute infection. Erythrocyte sedimentation rate was also measured. Coefficients of variation were calculated for each study variable. The influence of recent infection on variability was assessed. RESULTS: The 50th and 95th percentiles, respectively, for the coefficient of variation for each variable were as follows: total cholesterol, 7.3% and 13.6%; triglycerides, 22% and 47.3%; HDL-C, 7.9% and 16.8%; LDL-C, 12.1% and 25%; apolipoprotein A1, 6.3% and 15.2%; apolipoprotein B, 9.5% and 17.2%; and lipoprotein (a), 19.3% and 40%. Recent infection significantly lowered HDL-C (4 mg/dL; P < .0001) and apolipoprotein A1 (7 mg/dL; P < .005). CONCLUSIONS: Clinicians evaluating lipids and lipoproteins serially should expect significant visit-to-visit variation in triglycerides and calculated LDL-C values. Assessment of HDL-C and apolipoprotein A1 should not be done within 2 weeks of an acute infection. Apolipoproteins B and A1 have slightly less variability than their respective lipoprotein cholesterol values (LDL-C and HDL-C).

Acute Disease↗
PubMed1996

Lipid management: current diet and drug treatment options.

Diet and drug therapy are two of the principal approaches to lipid management. The aim of both is to reduce low-density-lipoprotein (LDL) cholesterol to goal levels established by the National Cholesterol Education Program Expert Panel in its second report, based on a patient's short-term risk of a coronary event. In prescribing diet therapy, it is important to determine patients' willingness to initiate and adhere to dietary modifications, their skill at reading nutritional labels, adapting recipes, and ordering "heart-healthy" foods when eating out. Diet therapy should be directed at modifying dietary factors known to adversely influence blood cholesterol-saturated fats, cholesterol, and obesity. Diet therapy (with exercise) is not always adequate. High risk individuals with no overt coronary artery disease but with >/=2 risk factors, as well as patients with coronary artery disease, are potential candidates for drug therapy, depending on their LDL cholesterol levels. The "statins" are the drug of choice for patients with coronary disease and elevated LDL cholesterol or familial LDL-cholesterol abnormalities. These drugs increase high-density-lipoprotein (HDL) cholesterol and reduce LDL cholesterol, coronary artery disease, and total mortality. Bile acid resins lower LDL cholesterol and are often used to augment the effects of the statins and niacin. Niacin is particularly useful in the management of patients with combined hyperlipidemia and low HDL cholesterol levels. Gemfibrozil is effective in familial dysbetalipoproteinemia and is the drug of choice for patients with severely elevated serum triglycerides.

Diet↗
PubMed1996

The clinical and economic significance of atherosclerosis.

The clinical and economic impact of cardiovascular disease is tremendous. Of the four major cardiovascular diseases, coronary artery disease caused by atherosclerosis is the leading cause of death in the United States. It is also a major cause of morbidity. The cost of treating heart disease continues to spiral, from $128 billion in 1994 to an estimated $151 billion in 1996. Studies have shown that treating risk factors for coronary disease--e.g., cigarette smoking, physical inactivity, and elevated low-density-lipoprotein cholesterol and blood-pressure levels--can significantly reduce mortality and improve clinical outcomes. Studies have also shown that risk-factor reduction results in cost savings. Today's challenge is to effectively incorporate risk-reduction strategies into daily clinical practice and reduce the personal and societal burden of cardiovascular disease.

Coronary Artery Disease↗
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↗