Left ventricular diastolic dysfunction secondary to hyperglycemia in patients with type II diabetes.

Diabetes mellitus type II, a cause of preclinical left ventricular dysfunction that can progress to cardiac insufficiency ventricular dysfunction in diabetic patients, is attributed to systemic arterial hypertension, or ischemic cardiopathy. Diastolic ventricular dysfunction takes place during the course of diabetes mellitus. The purpose of the present article is to report on the influence of hyperglycemia on the left ventricular diastolic dysfunction independently of dyslipidemia, obesity, and systemic arterial hypertension, usually present in diabetic patients. Left ventricular diastolic function was studied by Doppler echocardiography in asymptomatic type II diabetic patients without ischemic or valvular cardiopathies, cardiomegaly, or systemic arterial hypertension. Two groups of patients were integrated: patients with and without left ventricular diastolic dysfunction, i.e., groups A and B, respectively. Glycemia, cholesterol, triglycerides, and body mass index (BMI) were determined in each subject. Bivariate statistical tests (Student t, chi-square, or Mann-Whitney U tests) were applied to study the influence of the previously mentioned variables on the ventricular diastolic function. To evaluate the influence of hyperglycemia on ventricular diastolic function separately from dyslipidemia, systemic arterial hypertension, and the influence of obesity, logistic regression, and multivariate statistical analysis were applied. Independently of dyslipidemia and obesity, a relationship was found between hyperglycemia and diastolic dysfunction of the left ventricle in patients belonging to group A (p <0.05, odds ratio [OR] 12.1). No statistical significance was found between glycemia and the diastolic function of the left ventricle in group B patients. Even in type II diabetic patients without cardiopathy, uncontrolled hyperglycemia provokes diastolic left ventricular dysfunction.

Hyperinsulinemia in patients with coronary heart disease in absence of overt risk factors.

The objective of the study was to determine if male subjects with coronary atherosclerotic heart disease (CHD) without major CHD risk factors have hyperinsulinemia and related metabolic changes. Previous studies suggested that hyperinsulinemia is a CHD risk factor, but they did not entirely exclude concurrent metabolic abnormalities. A prospective, comparative, cross-sectional study in a tertiary care teaching hospital in Mexico City was conducted in 15 men who had suffered myocardial infarction 6 to 24 months before and had significant coronary occlusion on angiography. Control group was formed by 15 age-matched healthy men. None had hypertension, obesity, diabetes, gout, glucose intolerance or hyperlipidemia. Body mass index (BMI), waist/hip ratio (WHR), blood pressure (BP); oral glucose tolerance test (OGTT) with measurement of serum glucose, insulin and C-peptide every 30 min for 2 h, fasting serum cholesterol, triglycerides and uric acid, areas under curve (AUC) of glucose and insulin, insulin/glucose ratio and insulin sensitivity index were calculated. BMI, WHR and BP were similar in both groups. Fasting and post-load serum glucose and insulin concentrations were significantly higher in CHD than in control group (p < 0.01); fasting glucose 5.9 +/- 0.6 vs. 4.8 +/- 0.7 nmol/1, 2-h glucose 8.3 +/- 0.6 vs. 7.3 +/- 0.9 mmol/l, fasting insulin 17.5 +/- 1.2 vs. 15.3 +/- 1.7 pmol/l, 2 h insulin 448 +/- 108 vs. 282 +/- 87 pmol/l in CHD and control group, respectively. AUC of glucose, AUC of insulin, insulin/glucose ratio, post load C-peptide, serum cholesterol, triglycerides and uric acid levels were also significantly higher in CHD than in healthy controls. Insulin sensitivity index was significantly lower in patients with CHD (27.7 +/- 8.3) than in healthy control subjects (73.9 +/- 18) (p < 0.001). Patients with CHD have hyperinsulinemia and subtle metabolic abnormalities related with insulin resistance even in absence of overt risk factors.

Acute effect of cigarette smoking on glucose tolerance and other cardiovascular risk factors.

OBJECTIVE: To investigate the acute effect of cigarette smoking on glucose tolerance, insulin sensitivity, serum lipids, blood pressure, and heart rate. RESEARCH DESIGN AND METHODS: This nonrandomized experimental control trial in a tertiary care center included 20 healthy chronic smokers and 20 age-, sex-, and BMI-matched healthy volunteers. Two oral glucose tolerance tests (OGTTs) were performed on each subject. Three cigarettes were smoked during the first 30 min in one of the tests. Serum glucose, insulin, and C-peptide levels were measured every 30 min; the area under the curve (AUC) and the insulin sensitivity index (ISI) were calculated; serum total cholesterol, LDL cholesterol, HDL cholesterol, and triglyceride levels were measured at 0 and 180 min; and blood pressure and heart rate were recorded every 5 min throughout 180 min. RESULTS: Smoking acutely impaired glucose tolerance: the AUC for glucose in smokers was 25.5 +/- 1.03 mmol/l (mean +/- SE) (95% CI 22.9-28) during the smoking OGTT and 21.8 +/- 0.85 mmol/l (CI 19.2-24.3) in the control OGTT (P < 0.01); in nonsmokers, it was 19.7 +/- 0.3 mmol/l (CI 18.8-20.5) in the smoking OGTT and 18.7 +/- 0.35 mmol/l (CI 17.8-19.5) in the control OGTT (P < 0.05). Smoking acutely increased serum insulin and C-peptide levels and decreased ISI only in smokers: ISI in smokers was 55 +/- 2.8 (CI 47.4-62.6) in the control OGTT and 43 +/- 2.7 (CI 35.4-50.6) in the smoking OGTT (P < 0.05). Smoking acutely caused a rise of serum total cholesterol levels in both groups and increased LDL cholesterol and triglyceride serum levels significantly only in smokers (P < 0.05). A significant rise of blood pressure and heart rate while smoking was present in all the subjects. CONCLUSIONS: Smoking acutely impaired glucose tolerance and insulin sensitivity, enhanced serum cholesterol and triglyceride levels, and raised blood pressure and heart rate. These findings support the pathogenetic role of cigarette smoking on cardiovascular risk factors.

The effect of two sequential doses of Opuntia streptacantha upon glycemia.

To find out if a second dose of O. streptacantha may enhance its hypoglycemic effect, three tests were performed in fasting condition to 8 type II diabetic subjects and 6 healthy individuals. The tests were as follows: A. 500 g of broiled stems of O. streptacantha were given orally initially and two hours later. B. Only the initial dose. C. Control test with water. Serum glucose and C peptide were measured every two hours from 0 to 6 hours. In diabetic patients a significant (P < 0.01 vs control) decrease of serum glucose reaching from 41 to 46% less than initial value, was noticed in tests A and B, without differences between them. C peptide did not change. In healthy subjects serum glucose and C peptide did not significantly differ between tests. A second dose of O. streptacantha, two hours after the first one, did not improve its hypoglycemic activity.

Influence of nopal intake upon fasting glycemia in type II diabetics and healthy subjects.

To assess if the acute hypoglycemic effect of nopal which occurs in diabetic patients also appears in healthy individuals, 500 g of nopal stems (O. streptacantha Lem.) were given orally to 14 healthy volunteers and to 14 patients with NIDDM. Serum glucose and insulin levels were measured at 0, 60, 120 and 180 minutes after nopal ingestion. A control test was performed with the intake of 400 ml of water. The intake of nopal by the NIDDM group was followed by a significant reduction of serum glucose and insulin concentration reaching 40.8 + 4.6 mg/dl (n = 14) (mean+SEM) and 7.8 + 1.5 uU/ml (n = 7) less than basal value, respectively, at 180 minutes. (P less than 0.001 vs control test). No significant changes were noticed in the healthy group as compared with the control test (P greater than 0.05). Acute hypoglycemic effect of nopal was observed in patients with NIDDM but not in healthy subjects, thus the mechanisms of this effect differs from current hypoglycemic agents.

[The effect of acute hyperinsulinemia on arterial pressure in healthy individuals]. / Effecto de la hiperinsulinemia aguda en la tensión arterial de individuos sanos.

To assess if induced hyperinsulinemia enhances blood pressure (BP), three tests were performed to nine healthy volunteers as follows: A. After an oral dextrose load (75 g), 250 ml of 0.9% NaCl plus 25 g dextrose were infused in three hours. B. The same procedure, plus 15 U of regular insulin in the intravenous solution. C. (control) The same procedure but without insulin and dextrose. Pulse and BP were measured every 15 minutes, serum glucose and insulin were determined hourly. Hyperinsulinemia from 2 to 7-fold the basal value was induced in the test A, and from 7 to 30-fold in the test B (P less than 0.01). BP did not rise with hyperinsulinemia, but a slight and nonsignificant decrease of mean BP and higher heart rate (P less than 0.05) were noticed at the third hour in the test B. Acute hyperinsulinemia do not cause high BP. A cause-effect relationship between hyperinsulinemia and hypertension is still unproved.

[Changes in ventricular function in diabetes mellitus. Relation to the duration of the diabetes and its complications]. / Alteraciones de la función ventricular en la diabetes mellitus. Relación con la duración de la diabetes y sus complicaciones.

To find out if ventricular dysfunction is related with diabetes duration or diabetic chronic complications, resting and exercise electrocardiograms, chest X-ray, echocardiograms and dynamic scintigraphy with left ventricular ejection fraction measurement (LVEF) were performed to three groups of diabetic subjects without known cardiopathy or hypertension: (I) twelve subjects with less than five-years diabetes, (II) eleven with five to ten years, (III) nineteen with diabetes lasting more than ten years. Results were compared with ten healthy volunteers. 90.4% of diabetics had at least one abnormality. LVEF was significantly lower in diabetics (P less than 0.001) than in control group. No important differences were found according to diabetes duration. Lower fractional shortening and lower cardiac output were found in group III than in control group (P less than 0.05). Impaired ventricular function in group III was related (P less than 0.05) with the evidence of diabetic late complications. Relationship between ventricular dysfunction and other microvascular abnormalities might suggest that microangiopathy participates in some extent to the pathogenesis of ventricular disorder.

Alteraciones de las hormonas tiroideas en hepatopatias agudas y cronicas. / Changes of thyroid hormones in acute and chronic liver diseases

Para investigar la relacion de las enfermedades hepaticas con la concentracion serica de hormonas tiroideas, se estudiaron 30 pacientes con cirrosis hepatica, 10 con hepatitis cronica activa y 40 con hepatitis viral aguda. Se determinaron T3, T4, TBG y TSH sericas, y pruebas de funcion hepatica. Se encontro una relacion directa significativa entre la albumina serica y la TBG con la T3 y la T4 en el conjunto de los casos, en los cirroticos y en los que tenian hepatitis aguda (excepto entre albumina y T4 en estos ultimos). De los 24 casos con disminucion de T3 11 tuvieron disminucion de albumina y dos TBG baja.Los 15 casos con hepatitis aguda e hipertiroxinemia tuvieron TBG elevada o en limites normales superiores. A una misma con centracionn de albumina, los casos con ci rrosis y hepatitis cronica tuvieron menor TBG, T3 y T4 que aquellos con hepatitis aguda. Los niveles sericos de T3 y T4 y TBG en las hepatopatias parecen depender parcialmente de la concentracion de proteinas sericas transportadoras y son similares a las observadas en enfermedades no hepaticas

Determinacion rapida y precisa de cifras altas de glucemia con el metodo de dilucion y un reflectometro. / Rapid determination and cipher of high glucose with dilution method and reflectante meter

Los metodos para determinar la glucemia rapidamente a la cabecera del enfermo (tiras reactivas y aparadas de reflexion) no pueden medir mas de 400 mg/dl (22.2 mmol/ 1) de glucosa o carecen de precision. El metodo de dilucion, que consiste en diluir una muestra de sangre capilar, leer la concentracion de glucosa con una tira reactiva y multiplicar el resultado segun la dilucion, logra medir glucemias muy altas, pero la lectura visual es imprecisa. En este trabajo se intenso mejorar la precision con lectura en un reflectometro

[Familial neoplasms and childhood dermatomyositis]. / Neoplasia familiar y dermatomiositis infantil.

Familial frequency of malignant neoplasms from 20 children with dermatomyositis was investigated and compared with 225 controls. Eight patients with dermatomyositis (40 per cent) had nine family members with a malignant tumour; this frequency is significantly higher than those found in the controls with juvenile rheumatoid arthritis (P less than 0.01), neoplasms (P less than 0.01), and a variety of diseases (P less than 0.05). This finding and the known association of neoplasm-dermatomyositis might suggest an hereditary predisposing factor, possibly a subtle inmune deficiency, common for tumours and dermatomyositis.