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Query: UMLS:C0011860 (type 2 diabetes)
 57,723 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Whole body insulin resistance characterizes patients with NIDDM, but it is not known whether insulin also has impaired ability to stimulate myocardial glucose uptake (MGU) in these patients. This study was designed to evaluate MGU as measured by 2-[18F]fluoro-2-deoxy-D-glucose ([18F]FDG) and positron emission tomography (PET) in patients with NIDDM and stable coronary artery disease (CAD) under standardized metabolic conditions. Eight patients with NIDDM, 11 nondiabetic patients with CAD, and 9 healthy control subjects were enrolled in the study. MGU was quantitated in the normal myocardial regions with [18F]FDG and PET and the whole body glucose disposal by glucose-insulin clamp technique (serum insulin, -430 pmol/l). Plasma glucose and serum insulin concentrations were comparable in all groups during PET studies. The whole body glucose uptake was 45% lower in NIDDM patients (22 +/- 9 micromol x min(-1) X kg(-1) body wt [mean +/- SD]), compared with healthy control subjects (40 +/- 17 micromol x min(-1) x kg(-1) body wt, P < 0.05). In CAD patients, whole body glucose uptake was 30 +/- 9 micromol x min(-1) x kg(-1) body wt (NS between the other groups). MGU was similar in the normal segments in all three groups (69 +/- 28 micromol x min(-1) x 100 g(-1) in NIDDM patients, 72 +/- 17 micromol x min(-1) x 100 g(-1) in CAD patients, and 76 +/- 10 micromol x min(-1) x 100 g(-1) in healthy control subjects, NS). No correlation was found between whole body glucose uptake and MGU. As studied by [18F]FDG PET under stable normoglycemic hyperinsulinemic conditions, MGU is not reduced in patients with NIDDM and CAD in spite of peripheral insulin resistance. These findings suggest that there is no significant defect in MGU in patients with NIDDM.
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PMID:Myocardial glucose uptake in patients with NIDDM and stable coronary artery disease. 928 51

Recent studies at our institution using positron emission tomography (PET) provide evidence that both myocardial blood flow (MBF) and glucose metabolism may be affected in patients with diabetes mellitus. A retrospective study revealed inadequate myocardial glucose uptake as assessed by 2-[18F]fluoro-2-deoxyglucose (18FDG) in 64% of type I (insulin-dependent diabetes mellitus, IDDM) and 36% of type II (non-insulin-dependent diabetes mellitus, NIDDM) patients. However, a study in 7 patients with IDDM and 9 controls showed that metabolic standardization using hyperinsulinemic-euglycemic clamp is associated with similar myocardial glucose uptake in both groups (0.43 +/- 0.16 vs 0.44 +/- 0.12 micromol/g per min; p = nonsignificant). Furthermore, we studied MBF as assessed by [13N]ammonia in 15 IDDM patients without coronary artery disease. We found an impairment in flow reserve in diabetic patients as compared with a control group of 13 healthy volunteers (2.6 +/- 1.3 vs 4.0 +/- 0.6; p <0.01), which was primarily due to a significantly higher resting MBF (95.3 +/- 27.7 vs 69.1 +/- 8.1 mL/100 g per min; p <0.01). Hyperemic flow during adenosine infusion tended to be lower in diabetics, but was not significantly different (236.3 +/- 105.7 vs 273.0 +/- 26.0 mL/100 g per min; p = nonsignificant). Morphologic and functional abnormalities of the coronary microcirculation have been reported in diabetic animals and humans. Furthermore, there is an ongoing controversy regarding the existence of a specific diabetic cardiomyopathy that is not related to epicardial coronary disease. However, few studies have explored the effect of diabetes, hyperinsulinemia, or hyperglycemia on MBF and glucose metabolism in humans. With PET it is possible to perform comprehensive noninvasive studies of various aspects of cardiac function in patients with diabetes mellitus.
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PMID:Myocardial blood flow and glucose metabolism in diabetes mellitus. 929 61

Coronary flow reserve is used as an indicator to assess coronary microvascular function in the absence of obstructive coronary atherosclerosis. Diabetic patients, even with angiographically normal coronary arteries, show significantly reduced coronary flow reserve. This study evaluated coronary microcirculation in coronary artery disease complicated by glucose intolerance. Thirty-three patients with coronary artery disease were divided into three groups: Fourteen patients without glucose intolerance (control group), 8 with impaired glucose tolerance (IGT group), and 11 with noninsulin dependent diabetes mellitus (DM group). A Doppler guide wire was used to measure phasic coronary blood flow velocity in the left anterior descending artery without significant stenosis (> or = 40% diameter narrowing). Coronary flow reserve was determined by intracoronary 10 mg papaverine hydrochloride administration which induced maximal hyperemia. Coronary flow reserve was decreased in the DM group compared with the control group (2.1 +/- 0.6 vs. 3.1 +/- 0.9, p = 0.004), and that in the IGT group (2.5 +/- 0.9) did not show a significant difference compared with the other two groups. Vessel characteristics, such as infarct- or noninfarct-related artery and previous coronary angioplasty, did not have an influence on the results. Other coronary risk factors, left ventricular function, and hemodynamic findings were comparable in the three groups. This study demonstrates that diabetes mellitus may cause functional microvascular abnormalities in coronary artery disease.
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PMID:[Coronary microvascular dysfunction in coronary artery disease associated with glucose intolerance]. 930 Feb 85

The presence or absence of coronary artery disease (CAD) in diabetic patients has been related to the level of circulating plasma lipoproteins. This study examines whether there is a relationship between the actual severity of CAD and the plasma concentration of major classes of plasma lipoproteins (HDL, LDL, triglyceride-rich lipoproteins (TRL), and their Sf 12 to 60 and Sf 60 to 400 subfractions), particularly the numbers of lipoprotein particles, in men and women with type 2 diabetes. 174 diabetic patients (136 men, 38 women) who underwent angiography were studied. Nine specific coronary segments were scored. The population was divided into tertiles according to the angiographic severity of their coronary disease: mild CAD: coronary score 1 to 10; moderate CAD: coronary score 11 to 13; or severe CAD: coronary score 14 to 22. The main findings were that the numbers of particles (as reflected by the apoB levels) of the TRL were greater in those with moderate and severe disease than in those with mild disease (P = .001). There was a significant correlation between the coronary score and the apoB in TRL (P = .006). There were parallel but nonsignificant changes in triglyceride levels. ApoA-I was lower in patients with moderate and severe disease (P = .01). These differences were more striking in women than they were in men. There were no differences in plasma, LDL, or HDL cholesterol or in LDL apoB or Lp(a). Multiple linear regression analysis, when adjusted for sex, age, and BMI, showed that three lipid variables (TRL apoB, LDL cholesterol, and plasma apoA-I) significantly and independently predicted the coronary score. This study demonstrates that in type 2 diabetes, the severity of angiographically evaluated CAD is positively related to the numbers of TRL particles in the plasma. This relationship is stronger in women than in men, and it is independent of HDL and LDL.
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PMID:The severity of coronary atherosclerosis in type 2 diabetes mellitus is related to the number of circulating triglyceride-rich lipoprotein particles. 943 15

In this article the authors present a case of successful treatment of a 54-year old male patient with non-insulin dependent diabetes mellitus (NIDDM) and triple-vessel coronary artery disease who underwent surgical myocardial revascularization and was reoperated on the same day because of excessive bleeding. The patient was given cca 5000 mL of whole blood and cca 3000 mL of blood derivatives. The first postoperative chest X-ray showed radiological signs of ARDS. The therapy was based upon authors' experience and was consisted of controlled mechanical ventilation (respiratory volume 12-15 mL/kg, 10-14 cycles/min, I/E ratio 1:2, FIO2 0.6, PEEP 2-5 cm H2O), daily bronchoscopies with bronchoaspiration, aggressive diuresis, negative fluid balance, specific antibiotic therapy, and last but not least, of prostaglandin E1 (PGE1) 0.5-20 micrograms/kg/min combined with dopamine inotropic support (2-5 micrograms/kg/h). Simple but careful clinical observation still remains a milestone for all therapeutic measures taken in ARDS patients.
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PMID:Adult respiratory distress syndrome. 947 4

Increased plasma fibrinogen levels have been identified as a risk indicator for myocardial infarction, stroke, and thrombosis. Both environmental and genetic factors make an important contribution to plasma fibrinogen levels in humans. In the present study we evaluated, in patients with serum cholesterol levels between 4 and 8 mmol/L, the relation of plasma levels and polymorphisms of fibrinogen with coronary artery disease (CAD), cross-sectionally at baseline and after a 2-year follow-up period in which they received either a placebo or pravastatin. Higher plasma fibrinogen levels (3.9 g/L) were observed at baseline in patients with the -455AA genotype than in patients with the -455GA (3.2 g/L) and -455GG (3.1 g/L) genotypes of the -455G/A fibrinogen beta gene polymorphism (P<.05). Plasma levels of fibrinogen were not related to the baseline angiographic variables (mean segment diameter [MSD] and minimum obstruction diameter [MOD]), nor to the quantitative changes in these angiographic variables. However, in the placebo group, patients with the -455AA genotype had more progression of CAD, expressed by a significantly greater decrease of the MSD and MOD, after the 2-year follow-up period than patients with the other genotypes. The -455G/A polymorphism was related to the progression of CAD, and pravastatin therapy seemed to offset this deleterious effect. We hypothesized that the -455A allele may promote a stronger acute-phase response in fibrinogen and that the resulting higher fibrinogen levels may form the pathogenetic basis for the stronger progression of coronary atherosclerosis. Experiments to verify this hypothesis are being proposed and advocated, in view of the possibility of identifying a genetic marker that can recognize a subgroup of patients with an increased risk who may benefit from early treatment with lipid-lowering or anticoagulant drugs.
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PMID:-455G/A polymorphism of the beta-fibrinogen gene is associated with the progression of coronary atherosclerosis in symptomatic men: proposed role for an acute-phase reaction pattern of fibrinogen. REGRESS group. 948 92

Most people with diabetes die from thrombotic complications superimposed to degenerative arterial vascular lesions, mostly myocardial infarction. Diabetes is a risk factor per se for such complications, but often clusters with dyslipoproteinemia, hypertension and obesity. In NIDDM (Type-II) patients this is referred to as "metabolic syndrome" and often operates on a genetically programmed susceptibility which accelerates the pathogenesis of coronary artery disease in front of a much wider diabetes specific cardiopathy. From a pathophysiological point of view none of these associated risk factors explains the pathogenetic series of events leading to the precipitation of an occlusive thrombus at sites of complicated coronary plaques. In patients with diabetes the coagulation system is switched towards a prethrombotic state, involving increased plasmatic coagulation, diminished fibrinolysis, decreased endothelial thromboresistance and predominantly platelet hyperreactivity ("diabetic thrombocytopathy"). Some of these factors are associated with an increased coronary risk (e.g. fibrinogen, PAI-1, platelets), but are also directly linked to the pathogenesis of "atherothrombosis". Altered cardiac remodelling together with adhesion and coagulation mechanisms appears suitable to explain decreased functional performance of infarcted organs, decreased success of acute (reduced fibrinolytic response, reperfusion injury) and longterm intervention strategies (PTCA, CABG) in diabetes. Glucose adjustment alone will not adequately neutralize these complex mechanisms. Particularly in diabetes a multidimensional interventional repertoire is required including antihypertensive, antidyslipoproteinemic and antithrombotic drugs, customized according to the individual patients needs as assessed by early diagnostic measures ("early secondary prevention").
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PMID:Heart disease in diabetes mellitus: a challenge for early diagnosis and intervention. 951 54

The prevention of coronary artery disease is based on the control of several factors associated with a disease or clinical condition and suspected to play a pathogenetic role, defined as 'risk factors'. Smoking is a powerful risk factor for coronary artery disease, with risk of events increasing in relation to the number of cigarettes smoked daily. Smoking cessation is associated within 3-4 years, with a significant reduction in cardiovascular risk. Hyperlipidaemia is a powerful predictor of coronary disease with a strong, independent, continuous and graded positive association between cholesterol levels and risk of coronary events. Several large studies have shown the benefit of cholesterol reduction, and there is clear evidence of the efficacy of statins in the reduction of events in primary and secondary prevention. Hypertension is a significant, strong and independent risk factor for coronary artery disease morbidity and mortality and the reduction of events and mortality by antihypertensive treatment is well documented. Obesity is associated with an increase in all-cause mortality and cardiovascular mortality, with a particularly high risk for subjects with central obesity. Central obesity is also part of the so-called 'metabolic X syndrome' including insulin resistance, which appears to be associated with a particularly high risk of coronary artery disease. Type 1 and type 2 diabetes mellitus are associated with an increased risk of cardiovascular disease, especially in women. Several studies have shown that good metabolic control and multifactorial risk factor reduction significantly lower the coronary risk in these patients. Recent evidence is accumulating that some clotting factors (fibrinogen, factor VII, von Willebrand factor) and fibrinolytic factors (t-PA and PAI-1) are associated with an increased risk of coronary artery disease. The European Concerted Action on Thrombosis (ECAT) showed that the levels of fibrinogen, von Willebrand factor antigen, and t-PA antigen are independent predictors of subsequent coronary syndromes in patients with angina pectoris, and that low fibrinogen is associated with a low risk of events despite high cholesterol levels. Post-menopausal status is associated with increased risk of coronary artery disease, particularly when menopause is premature (before the age of 45) or abrupt (surgical). There is strong, thought not yet completely definite evidence that post-menopausal hormone replacement therapy may significantly reduce the risk of events and improve survival. Hyperhomocysteinaemia is an emerging risk factor independently associated with an increased risk of coronary artery disease, cerebral vascular disease, and peripheral vascular disease. The administration of vitamin B6, B12 or folate seems to be useful and is currently under further evaluation. Recently, attention has been focused on the correlation between coronary artery disease and genetic factors, such as ACE gene polymorphism or the gene polymorphism for the IIIa-moiety of the platelet fibrinogen receptor IIb-IIIa. In primary prevention, control of the major risk factors mainly in patients with clustered factors will substantially reduce the risk of ischaemic events. Secondary prevention of CHD is based on: aggressive behavioural advice, blood pressure reduction in hypertensives, good metabolic control of diabetes, and cholesterol reduction. Aspirin, beta-blockers, ACE inhibitors, and oral anticoagulants, may be useful in selected patients.
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PMID:Classical risk factors and emerging elements in the risk profile for coronary artery disease. 951 44

The aim of the present study was to determine the contributions of particle size versus number to differences in plasma triglyceride-rich lipoprotein concentrations in patients with type 2 diabetes. Fasting plasma was obtained from 174 consecutive eligible men and women with type 2 diabetes (with or without insulin treatment, mean age 57.0 + 6.3 years) who were undergoing coronary angiography. The triglyceride-rich (Sf 12-400) lipoproteins (TRL) were subfractionated into the Sf 12-60 and Sf 60-400 subfractions. Particle numbers, estimated by measuring apolipoprotein B by electroimmunoassay, in each of these lipoprotein fractions were related to enzymatically determined triglyceride levels in the triglyceride-rich lipoproteins. Approximately 87% of the triglyceride-rich lipoprotein particles were in the Sf 12-60 fraction and 13% in the Sf 60-400 fraction. Multiple linear regression indicated that 69% (i.e. r2=0.69) of the variance in the triglyceride levels could by explained by differences in TRL particle number and 17% (i. e. r2=0.17) by the differences in particle triglyceride content. These observations are similar in each gender and in those with or without insulin treatment. In conclusion, in type 2 diabetes, the vast majority of triglyceride-rich lipoproteins are smaller particles which are in the Sf 12-60 fraction. Differences in particle number, rather than triglyceride content, account for approximately 70% of the differences in triglyceride levels observed between individuals. Previous demonstrations, in those without diabetes, of an association between small triglyceride-rich lipoproteins with coronary artery disease suggest the importance of these findings to the increased atherosclerosis in diabetes.
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PMID:Important contribution of lipoprotein particle number to plasma triglyceride concentration in type 2 diabetes. 956 54

We set out to determine the genotype distributions of the PI(A) polymorphism of platelet glycoprotein IIIa, the HPA-3 polymorphism of platelet glycoprotein IIb, and the variable number tandem repeat (VNTR) polymorphism of platelet glycoprotein Ib in subjects with Type 2 diabetes mellitus (Type 2 DM) with (n = 125) and without (n = 90) a clinical history of macrovascular disease. In 215 white European subjects with Type 2 DM, presence of coronary artery disease was determined as a clinical history of angina, myocardial infarction (MI), coronary angioplasty or coronary artery by-pass grafting. Presence of peripheral vascular disease was defined as a clinical history of intermittent claudication with confirmatory vascular ultrasound or angiography, intermittent claudication with undetectable foot pulses and no history of arthralgia or surgery for leg ischaemia, confirmed by reference to medical case notes. Polymorphisms were detected by polymerase chain reaction amplification of DNA. There was no difference in the genotype distributions of subjects with and without macrovascular disease. In subjects with a first MI before the age of 60 years (n = 26), there was a 38% incidence of PI(A2) compared to 29% in subjects free from clinically evident macrovascular disease, but this difference did not reach statistical significance. This study does not support the hypothesis that polymorphisms of platelet glycoproteins, in particular the PI(A) polymorphism of platelet glycoprotein IIIa, play an important role in the pathogenesis of macrovascular disease in subjects with Type 2 DM.
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PMID:Polymorphisms of platelet glycoproteins in relation to macrovascular disease in type 2 diabetes mellitus. 958 97


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