Although coronary heart disease (CHD) is currently the leading cause of death among American Indians, information on the prevalence of CHD and its association with known cardiovascular risk factors is limited. The Strong Heart Study was initiated in 1988 to quantify cardiovascular disease and its risk factors among three geographically diverse groups of American Indians. Members of 13 Indian communities in Arizona, Oklahoma, and South and North Dakota between 45 and 74 years of age underwent a physical examination that included medical history; an electrocardiogram; anthropometric and blood pressure measurements; an oral glucose tolerance test; and measurements of fasting plasma lipoproteins, fibrinogen, insulin, hemoglobin A1c, and urinary albumin. Prevalence rates of definite myocardial infarction and definite CHD were higher in men than in women at all three centers (p < 0.0001) and higher in those with diabetes mellitus (p = 0.002 in men and p = 0.0003 in women). Diabetes was associated with relatively higher prevalence rates of myocardial infarction (diabetic:nondiabetic prevalence ratio = 3.8 vs. 1.9) and CHD (prevalence ratio = 4.6 vs. 1.8) in women than in men. Prevalence rates of heart disease were lowest in the communities in Arizona; prevalence rates were similar in Oklahoma and South Dakota/North Dakota and were two- to threefold higher than those in Arizona. By logistic regression, prevalent CHD among American Indians was significantly and independently related to age, diabetes, hypertension, albuminuria, percentage of body fat, smoking, high concentrations of plasma insulin, and low concentrations of high density lipoprotein cholesterol. In contrast to reports from other non-Indian populations, diabetes was the strongest risk factor. The lower prevalence of CHD among Indians in Arizona is distinctive in view of their higher rates of diabetes, obesity, hypertension, and albuminuria, but it may be partly related to their low frequency of smoking and their low concentrations of total and low density lipoprotein cholesterol. These findings from the initial Strong Heart Study examination emphasize the importance of diabetes and its associated variables as risk factors for CHD in Native American populations.

HomeCirculationVol. 82, No. 1The compelling case for smoking cessation in diabetics. Free AccessAbstractPDF/EPUBAboutView PDFSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessAbstractPDF/EPUBThe compelling case for smoking cessation in diabetics. B V Howard and W J Howard B V HowardB V Howard Medlantic Research Foundation, Washington, D.C. 20010. and W J HowardW J Howard Medlantic Research Foundation, Washington, D.C. 20010. Originally published1 Jul 1990https://doi.org/10.1161/01.CIR.82.1.299Circulation. 1990;82:299–301 eLetters(0) eLetters should relate to an article recently published in the journal and are not a forum for providing unpublished data. Comments are reviewed for appropriate use of tone and language. Comments are not peer-reviewed. Acceptable comments are posted to the journal website only. Comments are not published in an issue and are not indexed in PubMed. Comments should be no longer than 500 words and will only be posted online. References are limited to 10. Authors of the article cited in the comment will be invited to reply, as appropriate. Comments and feedback on AHA/ASA Scientific Statements and Guidelines should be directed to the AHA/ASA Manuscript Oversight Committee via its Correspondence page. Sign In to Submit a Response to This Article Previous Back to top Next FiguresReferencesRelatedDetailsCited By Chiong Y and Evans-Molina C (2015) Vascular Complications of Diabetes Mellitus PanVascular Medicine, 10.1007/978-3-642-37078-6_49, (1541-1593), . Chiong Y and Evans-Molina C (2014) Vascular Complications of Diabetes Mellitus PanVascular Medicine, 10.1007/978-3-642-37393-0_49-1, (1-65), . Tonstad S (2009) Cigarette smoking, smoking cessation, and diabetes, Diabetes Research and Clinical Practice, 10.1016/j.diabres.2009.04.013, 85:1, (4-13), Online publication date: 1-Jul-2009. Peters R, Brooks M, Todd L, Liebson P and Wilhelmsen L (1995) Smoking cessation and arrhythmic death: The CAST experience, Journal of the American College of Cardiology, 10.1016/0735-1097(95)00328-2, 26:5, (1287-1292), Online publication date: 1-Nov-1995. July 1, 1990Vol 82, Issue 1 Advertisement Article Information Metrics Copyright © 1990 by American Heart Associationhttps://doi.org/10.1161/01.CIR.82.1.299 Originally publishedJuly 1, 1990 PDF download Advertisement

A method is described for the establishment of diploid fibroblast cell cultures from human foreskins. Foreskins are minced and digested for a relatively long period of time in standard tissue culture medium containing trypsin and antibiotics. Undigested tissue is removed by filtration, and the cells are isolated by centrifugation and dispensed in culture vessels. This procedure circumvents the explanation of large amounts of minced tissue fragments and yields larger numbers of cells in a short period of time.

Cultures of human diploid fibroblasts were shown to accumulate elevated levels of intracellular triglyceride when grown in medium supplemented with sera from patients with endogenous hypertriglyceridemia (Type IV hyperlipoproteinemia). Time course studies indicated cell triglyceride levels reached maximum in 6 to 12 hours. Isotopic studies indicated that the source of the accumulated cell triglyceride was serum triglyceride, and that most of the triglyceride was taken up without hydrolysis. Triglyceride was not significantly removed by trypsinization or extensive washing. The accumulated triglyceride was also demonstrated to be metabolized, as indicated by conversion to phospholipids and free fatty acids.

Serum thyroxine (T4) and triiodothyronine (T3) concentrations were measured at frequent intervals in 9 hyperthyroid patients treated with iodide alone. Serum T4 and T3 levels fell initially in all patients. In 6 patients, after a mean fall in serum T4 of 46% and in serum T3 of 47% after 4 to 11 days of therapy, thyroid hormone levels began to rise. In the 3 remaining patients a rise in thyroid hormone levels was not seen following the initial fall. However, in one of this group T4 and T3 levels did not reach the normal range despite 60 days of therapy. These data support the concept that iodide alone is not an ideal agent for the treatment of hyperthyroidism.

6 patients with active acromegaly were treated with 10 mg of medroxyprogesterone acetate (MPA) every 6 hours daily for 2 weeks to 6 months. Oral glucose tolerance tests, growth hormone (GH) levels, and insulin tolerance tests (ITT) were done before and during MPA treatment. Basal GH levels varied widely during control and therapy periods; no significant lowering of GH levels occurred during treatment. Carbohydrate tolerance was not significantly affected by MPA therapy, although 5 out of 6 patients had deterioration at least once during treatment. Blood glucose response to ITT was unchanged by MPA. MPA did not affect the clinical features of acromegaly. There was no consistent effect of MPA on insulin-induced or arginine-induced GH secretion. It is concluded that MPA is not an effective agent for treating acromegaly.

Lipoid proteinosis is an inherited disorder characterized histologically by the deposition of an amorphous eosinophilic material in skin and other tissue. Histochemical demonstration of lipid in the deposits led early investigators to suspect that the disorder was a lipoidosis. However, recent biochemical and electron microscopical studies have suggested that the material is principally a glycoprotein elaborated by fibrocytes. Fibroblast cultures were established with the use of tissue from a cutaneous lesion of a woman with this disorder to determine whether an error of lipid metabolism occurred in the disease. An assay of fibroblast lipids revealed normal quantities of all lipid fractions. This appears to confirm that the accumulation of lipids in the lesions of this disease is not due to a primary metabolic defect, but is a secondary phenomenon, probably due to the affinity between lipoproteins and glycoproteins.

Eight patients with active acromegaly were treated with 100–200 mg chlorpromazine (CPZ) daily for 3 to 6 months. Clinical improvement did not occur in any patient. Mean basal growth hormone (MBGH) levels decreased substantially in only one patient in whom the MBGH fell from 94.3 ng/ml to 56.3 ng/ml after one month of therapy; further reduction in the MBGH did not occur in spite of continued treatment and doubling of the initial dose of CPZ. The MBGH increased in three patients during therapy. Oral glucose tolerance tests were performed before and during treatment in all patients; insulin and arginine tolerance tests were performed before and during therapy in six patients. Patterns of growth hormone (GH) secretion following administration of glucose, insulin, and arginine were highly variable in individual patients before and throughout treatment. Our data are consistent with the hypothesis that GH secretion is not truly autonomous in most patients with aeromegaly.