Asymptomatic hyperglycaemia is associated with increased intimal plus medial thickness of the carotid artery

Summary Atherosclerotic changes have not been demonstrated directly in asymptomatic hyperglycaemic non-diabetic subjects, although high mortality due to coronary heart disease has been reported. We measured arterial wall thickness non-invasively, in order to directly demonstrate atherosclerosis of the carotid arteries of hyperglycaemic non-diabetic subjects and to evaluate its risk factors.The thicknesses of the intimal plus medial complex (IMT) of the carotid arteries of 112 asymptomatic hyperglycaemic non-diabetic subjects (aged 22–81, 95 males and 17 females) were compared with those of 55 healthy male subjects and 211 non-insulin-dependent NIDDM male diabetic patients. The subjects were subgrouped into impaired glucose-tolerant (IGT) subjects who had a 2-h glycaemic level of more than 7.8 mmol/l, and non-IGT subjects whose 2-h glycaemic levels were within 6.7–7.7 mmol/l.Non-IGT and IGT subjects showed significantly greater IMTs than age-matched healthy males and showed no significant differences compared to age-matched NIDDM patients. Multivariate analysis demonstrated that the risk factors for IMT of non-IGT and IGT subjects were age and systolic blood pressure. According to data on the accumulation of atherogenic risks (hypertension, dyslipidaemia, and smoking), IMT increased linearly in non-IGT and IGT subjects. However, non-IGT and IGT subjects without hyperlipidaemia, hypertension, or smoking risk still had significantly greater IMT than age-matched normal males (1.019±0.063 vs 0.770±0.111 mm, p<0.05). Prevalence of ECG-indicated coronary heart disease was significantly higher in hyperglycaemic non-diabetic subjects and NIDDM with increased carotid arterial wall thickness (IMT 1.1 mm) than in those without increased thickness (IMT<1.1 mm). Asymptomatic hyperglycaemic non-diabetic subjects have increased thickness of their carotid arteries compared to age-matched male NIDDM patients. As one of several independent risk factors, mild hyperglycaemia advances atherosclerosis, which leads to coronary heart disease.Abbreviations IMT Intimal plus medial complex - NIDDM non-insulin-dependent diabetes mellitus - IGT impaired glucose tolerance - CHD coronary heart disease - T-Chol serum total cholesterol - HDL-C high-density lipoprotein cholesterol - TG serum triglycerides     

糖代谢异常对冠状动脉病变的影响

目的:探讨冠心病并发糖代谢异常患者的冠状动脉病变特点。方法:回顾分析2000~2004年冠状动脉造影阳性患者468例,分为糖尿病组(101例)、糖耐量减低组(70例)和非糖代谢异常组(297例),所有患者均测定空腹血糖、餐后2h血糖、血胆固醇、三酰甘油、低密度脂蛋白、高密度脂蛋白,观察其年龄、冠心病危险因素(包括高血压、高胆固醇血症和吸烟)和冠状动脉受累情况。结果:3组在年龄、性别、危险因素等方面均差异无统计学意义。糖尿病组冠状动脉双支和3支病变发生率(59.4%,36.6%)均明显高于非糖代谢异常组(29.6%,10.1%),双支病变发生率(59.4%)明显高于糖耐量减低组(11.4%),而单支病变发生率(3.9%)均显著低于糖耐量减低组(51.4%)和非糖尿病组(60.3%)(P<0·05),多节段病变发生率(43.5%)则显著高于非糖代谢异常组(11.1%)(P<0·05)。结论:糖代谢异常的冠心病患者冠状动脉病变严重,对预后和经皮冠状动脉腔内成形术的效果均有影响。     

葡萄糖耐量低减与动脉粥样硬化

目的　观察葡萄糖耐量低减 (IGT)与动脉粥样硬化 (AS)的关系。方法　在曾经有血糖异常升高 (但未达糖尿病标准 )、患有心血管疾病 (如冠心病、中风或高血压 )或其危险因素 (如血脂异常 )的人群进行 75g口服葡萄糖耐量试验 (OGTT)筛查IGT病人 ,并同时记录病史、体检。空腹血脂指标由自动生化分析完成。同时用B型超声检查双侧颈总动脉 ,观察内膜连续性、内膜 中层厚度 (IMT)、斑块等指标。结果　IGT组 (n =5 1)的内膜连续性比正常糖耐量 (NGT)组 (n =97)明显差 (P <0 .0 5 ) ,IGT组双侧平均IMT和动脉粥样硬化 (AS)积分均显著高于NGT组 (均P <0 .0 5 ) ,IGT的平均IMT异常增高的发病率显著高于NGT。但以上指标IGT与糖尿病组 (n =73 )差异无显著性。多元分析发现 ,IGT的AS指标增加效应经同时校正甘油三酯、胆固醇、冠心病史、中风史、吸烟、性别、体重指数仍具有显著意义 ;但是分别校正年龄、腰臀围比值、高密度脂蛋白胆固醇和高血压病史 ,三种AS指标有不同程度的减弱。结论　与NGT人群相比 ,IGT人群已经存在明显的AS表现 ,其程度与糖尿病类似。IGT的动脉粥样硬化现象独立于部分心血管危险因子和已经存在的心血管疾病。     

Post-challenge hyperglycaemia relates more strongly than fasting hyperglycaemia with carotid intima-media thickness: the RIAD Study. Risk Factors in Impaired Glucose Tolerance for Atherosclerosis and Diabetes.

AIMS: Only scarce information exists on the distribution and atherosclerosis risk in different types of hyperglycaemia at diabetes detection. This study aimed to analyse the occurrence of isolated fasting (IFH), isolated post-challenge (IPH) and combined hyperglycaemia (FH/PH) among subjects detected to have diabetes and the association of these types of hyperglycaemia with cardiovascular risk factors and carotid intima-media thickness (IMT). METHODS: A total of 785 middle-aged subjects of the Risk Factors in Impaired Glucose Tolerance (IGT) for Atherosclerosis and Diabetes (RIAD) study underwent a 75-g oral glucose tolerance test and examination of various atherosclerosis risk factors. IMT was measured by B-mode ultrasound. RESULTS: One hundred and nineteen (15.2%) asymptomatic diabetic subjects were detected: of these, 35.3% with IFH, 26% with IPH and 38.7% with FH/PH. The level of risk factors was higher in diabetic vs. non-diabetic subjects. HbA1c and cardiovascular risk factors were in the same range for IFH and IPH except for active plasminogen activator inhibitor (PAI)-1 which was significantly higher in IFH. A higher risk burden was found in the FH/PH group vs. both IFH and IPH. IMT was as follows: non-diabetic subjects 0.85 +/- 0.18 mm, IFH 0.91 +/- 0.20 mm, IPH 0.94 +/- 0.18 mm, FH/PH 0.98 +/- 0.17 mm (P < 0.05 vs. non-diabetes). 2 h post-challenge glucose (2hPG) correlated more closely (r = 0.23, P < 0.001) to IMT than fasting plasma glucose (FPG) (r = 0.14, P = 0.004). The importance of 2hPG was confirmed by the direct comparison of FPG and 2hPG in a three dimensional analysis. A significant increase of IMT was only observed in the subgroups with abnormal post-challenge hyperglycaemia for both combinations with normal FPG and IFG. FPG category did not significantly add to IMT in either group of post-challenge hyperglycaemia. Regression analysis in the whole sample revealed 2hPG but not FPG as a significant determinant of IMT. Further significant risk factors were age, male sex, total cholesterol, HDL-cholesterol and hypertension. CONCLUSIONS: The RIAD study population at high risk for Type 2 diabetes mellitus, post-challenge hyperglycaemia was found to relate more strongly than fasting hyperglycaemia with carotid IMT.     

Hypoglycaemia unawareness in type 1 diabetes: a lower plasma glucose is required to stimulate sympatho-adrenal activation.

To investigate the relationship between awareness of symptoms and the autonomic reaction of hypoglycaemia, acute hypoglycaemia was induced with intravenous insulin (2.5 mU kg-1 min-1) in diabetic and non-diabetic subjects, all of whom had normal cardiovascular autonomic function tests. Three groups were studied: (1) nine patients with Type 1 diabetes with loss of awareness of hypoglycaemia; (2) eight patients who had normal awareness of hypoglycemia, matched for duration of diabetes and blood glucose control; (3) eleven non-diabetic volunteers. The onset of the acute autonomic reaction was identified objectively by the sudden and rapid responses of heart rate and sweating. Cognitive function and hypoglycaemia symptom scores were estimated serially. Acute autonomic activation was observed to occur in all subjects in response to hypoglycaemia. In the 'unaware' diabetic patients, onset of the reaction occurred at a significantly lower plasma glucose (1.0 +/- 0.1 mmol l-1) than in the 'aware' diabetic patients (1.6 +/- 0.2 mmol l-1) (p less than 0.05) or in the non-diabetic control group (1.4 +/- 0.1 mmol l-1) (p less than 0.05). Obvious neuroglycopenia was observed only in the 'unaware' diabetic group and developed when plasma glucose had declined to approximately 1.4 +/- 0.1 mmol l-1, and thus preceded the reaction (p less than 0.02 vs the autonomic threshold). The maximal rise in plasma adrenaline was of similar magnitude in all three groups but a lower plasma glucose was required to stimulate this hormonal response in the 'unaware' patients, in whom the plasma adrenaline concentration was lower at the time of the reaction. Thus, the plasma glucose at which activation of the autonomic reaction was observed was lower in the diabetic patients with unawareness of hypoglycaemia.     

Impaired glucose tolerance in the third trimester of pregnancy

When the methods and interpretation of glucose tolerance as recommended by the World Health Organisation were applied to 247 patients in the third trimester of pregnancy selected on account of glycosuria, previous large-for-dates offspring, diabetic family history, maternal obesity or a fetus large for gestational age, impaired glucose tolerance (IGT) was found in 20 (8.1%). Patients with IGT were older than those with normal tests: 30.5 +/- 4.8 years (mean +/- S.D.) vs 27.8 +/- 4.8 years (p less than 0.02) and more having IGT had a first degree family history of diabetes (25% vs 10%, p less than 0.05). The majority (15) of the IGT patients then received dietary advice to restrict refined carbohydrate. Post-prandial blood glucose and HbA1 concentrations in these subjects remained within the normal range except for one patient who was treated with insulin. Pregnancy outcome was satisfactory in the patients with impaired tolerance and further studies will be required to assess the clinical significance of IGT in pregnancy.     

Marked impairment of the effect of hyperglycaemia on glucose uptake and glucose production in insulin-dependent diabetes

The effect of hyperglycaemia per se on glucose utilization and glucose production was evaluated in 12 patients with insulin-dependent diabetes and in 9 non-diabetic control subjects. In diabetic patients normoglycaemia was maintained during the night preceding the study by a variable intravenous insulin infusion. During the study endogenous insulin secretion was suppressed by somatostatin (300 micrograms h-1) and replaced by infusion of insulin (0.2 mU kg-1 min-1). Glucose utilization and hepatic glucose production rates were quantified at two plasma glucose concentrations (6.7 and 16.7 mmol l-1) using the two-step sequential hyperglycaemic clamp technique in combination with 3-3H-glucose tracer infusion. Duration of each step was 120 min. In diabetic patients glucose utilization, at a glucose concentration of 6.7 mmol l-1, was not different from normal (mean +/- SE: 2.9 +/- 0.2 vs 3.6 +/- 0.3 mg kg-1 min-1, 0.05 less than p less than 0.10), but the response to marked hyperglycaemia was significantly reduced (5.4 +/- 0.5 vs 9.4 +/- 1.0 mg kg-1 min-1, p less than 0.01). Hepatic glucose production was also normal at 6.7 mmol l-1 (1.4 +/- 0.1 vs 1.4 +/- 0.1 mg kg-1 min-1, NS), but whereas in control subjects glucose production was suppressed during hyperglycaemia of 16.7 mmol l-1 (0.3 +/- 0.4 mg kg-1 min-1, p less than 0.01), a slight increase was observed in diabetic patients (2.0 +/- 0.2 mg kg-1 min-1, p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)     

Hypoadiponectinemia is associated with impaired glucose tolerance and coronary artery disease in non-diabetic men.

BACKGROUND: Impaired glucose tolerance (IGT) is a significant risk factor for cardiovascular disease, but is not always recognized in the clinical setting. An anti-atherogenic adipocytokine, adiponectin, is decreased in type 2 diabetes mellitus, but its role in non-diabetic subjects has not been clarified. The hypothesis investigated in the present study was that plasma adiponectin levels correlate with IGT and coronary artery disease (CAD) in non-diabetic men. METHODS AND RESULTS: Glucose intolerance was evaluated by an oral glucose tolerance test and plasma adiponectin levels were measured in 232 non-diabetic men who underwent coronary angiography. Patients with IGT (n=102) had significantly lower adiponectin levels than those with normal glucose tolerance (n=130) (4.47 [3.23-6.39] vs 5.85 [3.99-8.65] mug/ml, p=0.003). Plasma adiponectin levels were associated with IGT in multiple logistic regression analysis (odds ratio (OR) 0.623, 95% confidence interval (CI) 0.397-0.980; p=0.041). Non-diabetic patients with CAD (n=122) had lower adiponectin levels than those without CAD (n=110) (4.60 [3.32-6.38] vs 6.08 [4.10-9.88] microg/ml, p<0.001). Multiple logistic regression analysis demonstrated adiponectin independently correlated with the presence of CAD (OR 0.432, 95% CI 0.256-0.728; p=0.002). CONCLUSIONS: Hypoadiponectinemia is associated with IGT and CAD in non-diabetic men, suggesting that the adiponectin level can provide valuable information regarding the risk of CAD even in non-diabetic subjects.     

Clinical characteristics in diabetic stroke patients

The impact of diabetes was prospectively studied during a 5-year period in 428 unselected and consecutive patients with acute cerebrovascular disease of whom 18% were diabetic. Cerebral infarction was more frequent in diabetics (81 vs 70%, p less than 0.02) whereas transient cerebral ischaemia was less frequent (4 vs 14%, p less than 0.01). Case fatality rate during hospitalization was higher in the diabetic than in the non-diabetic patients (28 vs 15%, p less than 0.02). Patients who died during hospitalization, diabetic as well as non-diabetic, had significantly higher blood glucose concentrations on admission compared with patients who survived. Hematocrit values were higher in the diabetic than in the non-diabetic patients (p less than 0.02). Diabetics had higher systolic blood pressure levels than the non-diabetics in the acute phase (p less than 0.005). The diabetic stroke patients more often had a history of hypertension, atrial fibrillation, heart failure and angina pectoris than non-diabetics stroke patients and diabetic control patients without stroke. Stroke patients, not known to be diabetic, had larger mean oral glucose tolerance test curve areas when compared with healthy controls but not when compared with hospitalized controls. We propose that diabetes increases the risk for stroke through other concurrent risk factors, cardiac disorders in particular.     

Coronary arterial calcification is associated with albuminuria in type 2 diabetic patient

AIM: Although microalbuminuria has been suggested as an independent risk factor for ischemic heart disease, the relationship between diabetic nephropathy and macroangiopathy remains unclear. Previously, we reported that coronary artery calcification detected by electron beam computed tomography (EBCT) could indicate the degree of coronary atherosclerosis in type 2 diabetic patients. In this study, we examine the association between coronary arterial calcification and microalbuminuria and aortic calcification and microalbuminuria. METHODS: Two hundred and fifty-six patients, including 177 type 2 diabetic patients (106 patients with normoalbuminuria, 71 with microalbuminuria) and 79 non-diabetic patients were evaluated by assessing the urinary albumin excretion rate and using EBCT to determine a coronary calcification score (CCS) and an aortic calcification score (ACS). RESULTS: No differences were observed regarding age, smoking index or BMI. Diabetic patients exhibited a greater CCS than non-diabetic subjects (non-diabetes 33 +/- 75 vs. diabetes 203 +/- 467, p < 0.05). Diabetic patients with microalbuminuria exhibited the most advanced CCS (253 +/- 491, p < 0.05). In contrast, no difference was observed in ACS among three groups. Multiple regression analysis showed that CCS is significantly associated with urinary albumin excretion rate as well as age, duration of diabetes and serum creatinine (R(2) = 0.31), while ACS is strongly associated with age, smoking, serum creatinine, systolic blood pressure and low-density lipoprotein cholesterol level (R(2) = 0.29). CONCLUSION: Increased urinary albumin excretion is associated with coronary arterial calcification in diabetic patients.     

Statistical analysis of clinical risk factors for coronary artery spasm: identification of the most important determinant.

Coronary artery spasm plays an important role in acute ischemic events, and it has a close relationship with coronary atherosclerosis. Thus we attempted to determine the most significant risk factor for coronary artery spasm. Among 3000 consecutive patients who underwent coronary cineangiography with ergonovine maleate testing, 330 with typical angina pectoris (group 1) and 294 with old myocardial infarction (group 2) were studied. We divided each group into three or four subgroups according to the presence of fixed organic stenosis (FOS+) or a positive reaction to ergonovine maleate (coronary artery spasm [CAS]+). We examined the relationship between coronary artery spasm and eight coronary risk factors: age, sex, hypertension, diabetes mellitus, smoking, and serum cholesterol, uric acid, and high-density lipoprotein cholesterol levels. The proportion of smokers in the subgroups with CAS(+) was significantly higher than in the subgroups with CAS(-)(p less than 0.01). There was no correlation between smoking and fixed organic stenosis. According to the results of multiple regression analysis, there was a positive correlation between smoking and CAS(+) and between serum high-density lipoprotein cholesterol levels and CAS(+)(p less than 0.01). Thus we concluded that smoking is the most significant risk factor in discriminating between patients with and without coronary artery spasm.     

Glucagon-stimulated insulin secretion in patients with type 2 diabetes mellitus: support for the concept of glucose toxicity.

Parameters of blood glucose control and insulin secretion were evaluated in 114 patients with type 2 diabetes mellitus, who were no longer controlled satisfactorily by maximal doses of oral hypoglycaemic agents, and compared with those obtained in 11 healthy control subjects, 32 patients with recently-diagnosed type 2 diabetes, and 16 tablet-treated and 36 insulin-treated patients. Newly-diagnosed patients were slightly younger (60 +/- 13 yr) and had a slightly higher body mass index (29.4 +/- 6.5 kg/m2). Known duration of diabetes was 9 yr (range 1-37) in secondary failure, and 11 yr (range 1-31) in insulin-treated patients. Fasting blood glucose was the highest (13.8 +/- 2.8 mmol/l) in secondary failure and newly-diagnosed patients (12.6 +/- 3.8 mmol/l) compared to tablet-treated (8.7 +/- 3.3 mmol/l) and insulin-treated patients (9.6 +/- 3.2 mmol/l, p less than 0.05). HbA1c levels were comparably elevated. In insulin-treated patients, fasting plasma C-peptide levels were lower relative to the mutually comparable levels in the other 3 diabetic groups. Fasting plasma insulin levels did not differ between the 4 diabetic groups. C-peptide release after glucagon (C-peptide AUC) was comparable in all 4 diabetic groups, although in tablet-treated patients the ratio C-peptide AUC/fasting blood glucose was higher (p less than 0.05). We conclude that the clinical usefulness of determining residual insulin secretion in type 2 diabetic patients is limited, and that the similar reduction of insulin secretion in severely hyperglycaemic newly-diagnosed and secondary failure type 2 diabetic patients supports the concept of "glucose toxicity".     

High plasma insulin and triglyceride concentrations and blood pressure in offspring of people with impaired glucose tolerance

The plasma glucose and insulin response to an oral glucose challenge, fasting plasma lipid concentration, and blood pressure were compared in 13 offspring of parents previously diagnosed as having impaired glucose tolerance (IGT) and 13 offspring of parents previously shown to have normal glucose tolerance. The parents with IGT had higher plasma glucose, insulin and triglyceride concentration, and blood pressure than parents with normal glucose tolerance. The two groups of offspring were young and non-obese, and similar in terms of age, gender distribution, and body mass index. However, the total integrated plasma insulin response during a 75 g oral glucose tolerance test was significantly higher (p less than 0.05, Student's t-test) in offspring of parents with IGT (718 +/- 71 pmol l-1 h) than in the subjects whose parents had normal glucose tolerance (524 +/- 47 pmol l-1 h). In addition, serum triglyceride concentration was somewhat higher in offspring of parents with IGT (1.17 +/- 0.11 vs 0.92 +/- 0.08 mmol l-1, 0.10 greater than p greater than 0.05), as were both systolic (132 +/- 5 vs 118 +/- 3 mmHg, p less than 0.05) and diastolic (79 +/- 3 vs 70 +/- 2 mmHg, p less than 0.05) blood pressure. Demonstration of similar abnormalities in plasma insulin response to glucose and blood pressure regulation in patients with IGT and in their offspring is consistent with the view that these changes have a genetic component.     

Coronary vasomotor response to acetylcholine relates to risk factors for coronary artery disease

In animals, acetylcholine dilates normal arteries and produces vasoconstriction in the presence of hypercholesterolemia, hypertension, or atherosclerosis, reflecting endothelial cell dysfunction. In patients with angiographically smooth coronary arteries, acetylcholine has been reported to produce both vasodilation and constriction. To test the hypothesis that the acetylcholine response relates to risk factors for coronary artery disease, acetylcholine 10(-8) to 10(-6) M was infused into the left anterior descending or circumflex coronary artery, and diameter changes were assessed with quantitative angiography in 34 patients with angiographically smooth coronary arteries. The acetylcholine response ranged from +37% (dilation) to -53% (constriction) at the peak acetylcholine dose. All coronary arteries dilated in response to nitroglycerin (26 +/- 17%), suggesting an abnormality of endothelial function in the patients with a constrictor response to acetylcholine. By multiple stepwise regression analysis, serum cholesterol (p less than 0.01), male gender (p less than 0.001), family history (p less than 0.05), age (p less than 0.05), cholesterol level (p less than 0.01), and total number of risk factors (p less than 0.0001) were independently associated with the acetylcholine response. Thus, coronary risk factors are associated with loss of endothelium-dependent vasodilation. The development of vasoconstriction is likely to be an abnormality of endothelial function that precedes atherosclerosis or an early marker of atherosclerosis not detectable by angiography.     

Non-insulin-dependent diabetes mellitus and hyperlipoproteinemia in patients with ischemic cardiopathy

Cardiovascular disease (CVD) constitutes the main cause of death in diabetes mellitus (DM): Previous studies at the "Instituto Nacional de Cardiología de México" have investigated the metabolic alterations of survivors of a myocardial infarction (MI), but none of them had focused on the metabolic profile of the diabetic patient. We compared two groups of patients with ischemic heart disease (IHD), one with (DMG) and one without (NDMG) Diabetes Mellitus, to investigate differences in the prevalence and nature of hyperlipoproteinemias (HLP) and other risk factors of atherosclerosis. DMG consisted of 117 patients (75 male, 42 female) and NDMG consisted of 119 patients (91 male y 28 female). (Female NDMG vs female DMG p less than 0.05). The presence of risks factors of atherosclerosis was investigated in all patients, and total cholesterol (chol) triglycerides (TG) and glucose were measured in post-absorptive phase. There were no differences regarding mean age (DMG: 60 +/- 8 years, NDM: 60 +/- 11 years), Quetelet Index (Kg./mt2: DMG: 26.5 +/- 3, NDMG: 26.7 +/- 3), TG: (DMG: 246.2 +/- 125, NDMG: 223.5 +/- 129) or Chol (DMG: 216 +/- 42 mg/dl, NDMG: 225 +/- 45 mg/dl). Hypertriglyceridemia was significantly higher in patients with DM, as a whole and when both sexes were studied separately (p less than 0.05). Hypercholesterolemia was significantly higher in NDMG (p less than 0.05) and without significance, in diabetic women. (p less than 0.05). Type IV phenotype was higher in DMG (p less than 0.05) whereas phenotypes IIa and IIa + IIb were more prevalent among non-diabetics (p less than 0.001, p less than 0.0001, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)     

The extent of coronary artery disease in diabetic patients with myocardial infarction: an ECG study

In 91 non-diabetics (age 63 +/- 12, mean +/- SD, years range 31-94 years) and 85 patients with known diabetes or clearly abnormal levels of HbA1c (age 66 +/- 10 years, range 36-87 years) electrocardiograms were analysed sequentially after acute myocardial infarction (AMI). There was no significant difference in infarct site between the two groups. Generalized ischaemic change without ST elevation was seen in 33% of diabetics and 22% of non-diabetics (p greater than 0.1). In patients with transmural AMI, cardiogenic shock (CGS) was significantly commoner in diabetics (relative risk 3.1, CL 1.2-8.1) but there was no difference in the frequency of reciprocal change between the two groups. In both diabetic and non-diabetic patients the development of cardiogenic shock was more frequently associated with the presence of reciprocal change, the difference reaching significance in the diabetic group (chi 2 = 4.4, p less than 0.05). Thus cardiogenic shock in both diabetic and non-diabetic patients with AMI may be associated with the presence of extensive coronary artery disease, but differences in the prevalence of extensive disease do not explain the predisposition of diabetic patients to CGS.     

The relationship of hyperinsulinaemia to the development of hypertension in type 2 diabetic patients and in non-diabetic subjects

We have carried out a 5 year follow-up study of a group of 41 originally normotensive (BP less than 160/95 mmHg) newly diagnosed Type 2 (non-insulin-dependent) diabetic patients (26 men, 15 women) and 86 non-diabetic subjects (39 men, 47 women) to assess the predictive value of serum insulin levels with regard to the development of hypertension. Hypertension (BP greater than 160/95 mmHg and/or drug treatment) developed in 14% of diabetic patients and 10% of non-diabetic subjects (NS). The baseline postglucose insulin levels tended to be higher in those diabetic and non-diabetic subjects who developed hypertension during the 5 year follow-up than in those who remained normotensive, and in non-diabetic subjects the differences were statistically significant after adjustment for age, sex and body mass index for the baseline 1 hour serum insulin (104 +/- 18 vs. 68 +/- 5 mU/l; P less than 0.05) and area under the insulin curve (138 +/- 34 vs. 85 +/- 8 mU/l.h, P less than 0.05). Both diabetic and non-diabetic subjects who developed hypertension showed elevated total- and VLDL-triglycerides at baseline compared with those subjects who remained normotensive during the follow-up. In conclusion, the results support the hypothesis that hyperinsulinaemia or insulin resistance may play a role in the pathogenesis of hypertension.     

Insulin resistance, but normal basal rates of glucose production in patients with newly diagnosed mild diabetes mellitus

Fasting hyperglycemia in Type II (non-insulin-dependent) diabetes has been suggested to be due to hepatic overproduction of glucose and reduced glucose clearance. We studied 22 patients (10 lean and 12 obese) with newly diagnosed mild diabetes mellitus (fasting plasma glucose less than 15 mmol/l, urine ketone bodies less than 1 mmol/l), and two age- and weight-matched groups of non-diabetic control subjects. Glucose turnover rates and sensitivity to insulin were determined using adjusted primed-continuous [3-3H]glucose infusion and the hyperinsulinemic euglycemic clamp technique. Insulin-stimulated glucose utilization was reduced in both diabetic groups (lean patients: 313 +/- 35 vs 531 +/- 22 mg.m-2.min-1, p less than 0.01; obese patients: 311 +/- 28 vs 453 +/- 26 mg.m-2.min-1, p less than 0.01). Basal plasma glucose concentrations decreased 0.43 +/- 0.05 mmol/l per h (p less than 0.01). Glucose production rates were smaller than glucose utilization rates (lean patients: 87 +/- 3 vs 94 +/- 3 mg.m-2.min-1, p less than 0.01; obese patients: 79 +/- 5 vs 88 +/- 5 mg.m-2.min-1, p less than 0.01), were not correlated to basal glucose or insulin concentrations, and were not different from normal (lean controls: 87 +/- 4 mg.m-2.min-1; obese controls: 80 +/- 5 mg.m-2.min-1). These results suggest that the basal state in the diabetic patients is a compensated condition where glucose turnover rates are maintained near normal despite defects in insulin sensitivity.     

Behaviour modification in obese subjects with type 2 diabetes mellitus.

We have followed prospectively, 46 obese, type 2 diabetic patients for a 55-week period, in order to evaluate the efficiency of an educational programme based on behaviour modification to enhance weight loss and changes of other cardiovascular risk factors. No patient received pharmacological treatment during the study. At the end of the follow-up the patients obtained an average weight loss of 9.250 kg (range: 0.500-17.500 kg); the BMI was reduced from 34.2 +/- 0.8 kg/m2 to 30.6 +/- 1.1 kg/m2 (P less than 0.01); fasting serum glucose descended from 7.9 +/- 0.4 to 6.1 +/- 0.5 mM (P less than 0.05); SBP (systolic blood pressure) decreased from 145.7 +/- 3 to 126.4 +/- 5.1 mmHg (P less than 0.01); DBP (diastolic blood pressure) decreased from 83.5 +/- 2.5 to 65 +/- 2.6 mmHg (P less than 0.01); triglyceride levels were lowered from 164.5 +/- 12 to 109.7 +/- 10 mg/dl (P less than 0.01); HDL-cholesterol levels increased from 1.27 +/- 0.05 to 1.53 +/- 0.12 mM (P less than 0.01). Serum glucose 2 h after a 75 g glucose oral load decreased from 14.9 +/- 0.6 to 12.7 +/- 0.9 mM (P less than 0.05) on week 35 of follow-up. Twelve patients no longer presented a diabetic curve (8 normal oral glucose tolerance test (OGTT) curves, and 4 impaired glucose tolerance (IGT) curves). No significant changes in the parameters studied were obtained in the group of patients on conventional treatment.(ABSTRACT TRUNCATED AT 250 WORDS)     

老年冠心病合并糖耐量减低患者不同血糖水平与冠状动脉病变的研究

目的探讨老年冠心病合并糖耐量减低患者不同血糖水平与冠状动脉病变的相关性。方法回顾分析经冠状动脉造影确诊冠心病的老年患者212例临床资料,根据口服葡萄糖耐量试验结果分为糖耐量正常(NGT)组64例,糖耐量减低(IGT)患者148例,又根据餐后2h血糖水平分为IGT1组50例,IGT2组58例和IGT3组40例,比较各组的冠状动脉病变支数、弥漫性病变状况以及冠状动脉病变Gensini总积分。结果与NGT组比较,IGT1组、IGT2组、IGT3组LDL-C水平、弥漫性病变比例、Gensini积分明显升高(P<0.05);IGT1组、IGT3组双支病变比例明显升高,IGT2组双支病变比例明显下降(P<0.05)。冠状动脉Gensini积分与餐后2h血糖呈正相关(r=0.512,P<0.05)。结论 IGT加重了冠状动脉病变程度。餐后2h血糖升高的患者是动脉粥样硬化的高危人群,对于此类人群应及时早期干预、治疗。