Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aim of this study was to determine the significance of new electrocardiographic (ECG) ST elevation during coronary artery bypass surgery. Multilead ECGs were recorded intraoperatively approximately every 3 min on 105 patients. Cases of new ST elevation were divided into ischemic and those considered to be due to nonischemic causes such as cooling during cardiopulmonary bypass (CPB), defibrillation, new cardiac conduction abnormalities, and pericarditis. The myocardial fraction of creatine kinase (CK-MB) > or = 25 IU/L was considered to be indicative of myocardial injury. Both patients who had ischemic ST elevation prior to CPB and all seven patients who had ST elevation in temporal association with the administration of protamine had peak CK-MB > or = 25 IU/L. One patient with peak CK-MB > or = 25 IU/L did not have ST elevation and was considered to have injury during CPB. Two of these ten patients had Q wave myocardial infarctions (MIs). For the detection of patients with peak CK-MB > or = 25 IU/L, the sensitivity of ischemic ST elevation was 90% and the specificity was 100%. A history of MI prior to surgery and a history of Type I diabetes were associated with peak CK-MB > or = 25 IU/L (P < 0.05).
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PMID:Significance of electrocardiographic ST elevation during coronary artery bypass surgery. 813 80

Age-adjusted 28-day case-fatality rates were higher among Mexican Americans than among non-Hispanic whites and higher among women than among men hospitalized for definite or possible myocardial infarction in Corpus Christi, Nueces County, Texas, from May 1, 1988, through April 30, 1990. The authors therefore examined whether these higher case-fatality rates were associated with greater prevalence of previously diagnosed coronary heart disease or diabetes; with greater age, frequency of definite myocardial infarction, or congestive heart failure; with higher values of indicators of severity of infarction, including peak creatine phosphokinase levels and scales prognostic of early mortality after myocardial infarction; and with differences in receipt of in-hospital therapy. The overall 28-day case-fatality rate among 1,228 patients hospitalized for myocardial infarction during a 24-month period was 7.3%. After adjustment for age; diabetes; myocardial infarction class (definite vs. possible); congestive heart failure; the Norris and Peel severity indices; peak total creatine phosphokinase; and receipt of thrombolytic therapy, aspirin, calcium channel blockers, beta-blockers, anticoagulants, angioplasty, and bypass surgery, the risk of 28-day case-fatality for Mexican Americans in relation to non-Hispanic whites was 1.49 (95% confidence interval 0.92-2.40). The corresponding risk for women in relation to men was 1.80 (95% confidence interval 1.12-2.89). These findings should alert clinicians to the high-risk status of these groups of patients.
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PMID:Greater case-fatality after myocardial infarction among Mexican Americans and women than among non-Hispanic whites and men. The Corpus Christi Heart Project. 779 39

A 61-year-old woman with hyperlipidemia was treated with gemfibrozil. She also had insulin-treated diabetes mellitus and chronic renal failure and was admitted because of severe chest pain. The ST segment was depressed and creatine kinase levels were elevated. The original diagnosis was acute myocardial infarction. In the presence of increasing chest pain, the onset of limb muscle tenderness, and increasing levels of creatine kinase, the diagnosis of myopathy secondary to gemfibrozil therapy was made and the drug was discontinued. All symptoms then subsided and creatine kinase levels returned to normal. Myopathy is a well-known complication of blood lipid-lowering drugs, especially in patients with renal failure.
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PMID:[Gemfibrozil-induced myopathy]. 825 19

Ninety-four consecutive patients (60 men and 34 women; mean age 68.5 +/- 11.5 years) with acute myocardial infarction (MI) were investigated retrospectively, in order to evaluate the prevalence, clinical features, and short-term course of the atypical forms (symptoms other than chest pain). An atypical MI was found in 30 patients, with a prevalence of 32% (95% confidence limits 27-36%). It was most prevalent in women above sixty-five years old (P < 0.05). Abdominal pain, paroxysmal dyspnea, and pulmonary edema were the most frequent symptoms (33%, 17%, 13%, respectively). No differences were observed between typical and atypical MI in regard to risk factors (hypercholesterolemia, arterial hypertension, diabetes mellitus, cigarette smoking) and history of MI, cerebrovascular disease, peripheral vascular disease, or chronic lung disease. Significantly fewer patients with atypical MI had a history of angina pectoris (P < 0.05). No differences were observed in regard to previous medication, except for antiarrhythmic drugs, more often used by atypical patients (P < 0.05). Location and severity of MI (as judged by ECG and peak levels of creatine kinase in the serum) were similar in both subgroups, as were the complications (34% typical and 50% atypical) and death rate (12.5% and 16.7%, respectively). In conclusion, atypical MI is not less severe than typical. This emphasizes the need for a high suspicion index in many different clinical settings, but particularly (although not exclusively) in elderly females, in the presence of abdominal pain or otherwise unexplained paroxysmal dyspnea.
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PMID:Prevalence, clinical features, and acute course of atypical myocardial infarction. 828 84

Skeletal muscle energetics can be studied noninvasively at rest, during exercise, and in recovery using phosphorus nuclear magnetic resonance (31P-NMR). In resting muscle, inorganic phosphate (P(i)) and total cellular phosphate concentration are regulated by Na(+)-dependent P(i) transport. Insulin was shown to stimulate P(i) uptake in G-8 muscle cells, in isolated rat soleus muscle, and in human muscle in vivo under conditions of hyperinsulinemic-euglycemic clamp. The relationship between plasma P(i) and intracellular muscle P(i) was examined in a group of patients with elevated plasma P(i) resulting from renal failure. The total creatine content of muscle cells is controlled by an active creatine uptake in which beta 2-receptor stimulation and the activity of the Na(+)-K(+)-ATPase play a significant role. Recovery after exercise is entirely oxidative; the rate of ATP synthesis is largely controlled by ADP, the concentration of which is determined by the creatine kinase equilibrium that includes the concentration of H+. At the onset of aerobic dynamic exercise, ATP is maintained largely by glycolysis, producing lactic acid, and by phosphocreatine breakdown. After vasodilation, ATP synthesis becomes predominantly oxidative. The above processes can be quantitatively evaluated by 31P-NMR.
Diabetes 1996 Jan
PMID:Control of energy metabolism during muscle contraction. 852 7

Physiologically, a postprandial glucose rise induces metabolic signal sequences that use several steps in common in both the pancreas and peripheral tissues but result in different events due to specialized tissue functions. Glucose transport performed by tissue-specific glucose transporters is, in general, not rate limiting. The next step is phosphorylation of glucose by cell-specific hexokinases. In the beta-cell, glucokinase (or hexokinase IV) is activated upon binding to a pore protein in the outer mitochondrial membrane at contact sites between outer and inner membranes. The same mechanism applies for hexokinase II in skeletal muscle and adipose tissue. The activation of hexokinases depends on a contact site-specific structure of the pore, which is voltage-dependent and influenced by the electric potential of the inner mitochondrial membrane. Mitochondria lacking a membrane potential because of defects in the respiratory chain would thus not be able to increase the glucose-phosphorylating enzyme activity over basal state. Binding and activation of hexokinases to mitochondrial contact sites lead to an acceleration of the formation of both ADP and glucose-6-phosphate (G-6-P). ADP directly enters the mitochondrion and stimulates mitochondrial oxidative phosphorylation. G-6-P is an important intermediate of energy metabolism at the switch position between glycolysis, glycogen synthesis, and the pentose-phosphate shunt. Initiated by blood glucose elevation, mitochondrial oxidative phosphorylation is accelerated in a concerted action coupling glycolysis to mitochondrial metabolism at three different points: first, through NADH transfer to the respiratory chain complex I via the malate/aspartate shuttle; second, by providing FADH2 to complex II through the glycerol-phosphate/dihydroxy-acetone-phosphate cycle; and third, by the action of hexo(gluco)kinases providing ADP for complex V, the ATP synthetase. As cytosolic and mitochondrial isozymes of creatine kinase (CK) are observed in insulinoma cells, the phosphocreatine (CrP) shuttle, working in brain and muscle, may also be involved in signaling glucose-induced insulin secretion in beta-cells. An interplay between the plasma membrane-bound CK and the mitochondrial CK could provide a mechanism to increase ATP locally at the KATP channels, coordinated to the activity of mitochondrial CrP production. Closure of the KATP channels by ATP would lead to an increase of cytosolic and, even more, mitochondrial calcium and finally to insulin secretion. Thus in beta-cells, glucose, via bound glucokinase, stimulates mitochondrial CrP synthesis. The same signaling sequence is used in the opposite direction in muscle during exercise when high ATP turnover increases the creatine level that stimulates mitochondrial ATP synthesis and glucose phosphorylation via hexokinase. Furthermore, this cytosolic/mitochondrial cross-talk is also involved in activation of muscle glycogen synthesis by glucose. The activity of mitochondrially bound hexokinase provides G-6-P and stimulates UTP production through mitochondrial nucleoside diphosphate kinase. Pathophysiologically, there are at least two genetically different forms of diabetes linked to energy metabolism: the first example is one form of maturity-onset diabetes of the young (MODY2), an autosomal dominant disorder caused by point mutations of the glucokinase gene; the second example is several forms of mitochondrial diabetes caused by point and length mutations of the mitochondrial DNA (mtDNA) that encodes several subunits of the respiratory chain complexes. Because the mtDNA is vulnerable and accumulates point and length mutations during aging, it is likely to contribute to the manifestation of some forms of NIDDM.(ABSTRACT TRUNCATED)
Diabetes 1996 Feb
PMID:Mitochondria and diabetes. Genetic, biochemical, and clinical implications of the cellular energy circuit. 854 53

To test whether insulin is a regulatory factor of myocardial MB creatine kinase content, we investigated the correlation between the ability of insulin secretion and the MB fraction of cumulative CK released in patients with acute myocardial infarction. We analyzed 18 patients who underwent successful direct angioplasty within 10 hours of the onset of their first myocardial infarction. Exclusion criteria were age more than 75 years, heart failure, severe obesity, multivessel disease, and history of diabetes mellitus. Cumulative activity of serum MB CK divided by that of total CK was defined as MB%, which was considered to represent myocardial MB CK content. Two weeks or more after the onset of myocardial infarction, 75 gm oral glucose tolerance test with serial determination of plasma glucose and serum insulin (0, 0.5, 1, 2, 3 hours) was done. Urinary and plasma catecholamines and echocardiographic left ventricular (LV) mass were measured. MB% significantly correlated with insulinogenic index (r = 0.564, p = 0.019), insulin area (r = 0.594, p = 0.012), insulin area/glucose area (r = 0.630, p = 0.007), and urinary adrenaline (r = -0.542, p = 0.025) and tended to correlate with plasma adrenaline (r = -0.431, p = 0.084). Age, body mass index, infarct size, glucose metabolism, and LV mass were not significant univariate predictors of MB%. Multivariate analysis showed that the ability of insulin secretion contributed to MB% more than catecholamines did and that insulin area/glucose area was the strongest independent predictor of MB% (t = 3.01, p = 0.015). Thus MB fraction of cumulative CK released, indicative of Myocardial MB CK distribution, strongly related to the ability of insulin secretion in subjects without overt insulin resistance. Regulation by insulin of myocardial MB CK is suggested.
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PMID:MB fraction of cumulative creatine kinase correlates with insulin secretion in patients with acute myocardial infarction: insulin as a possible determinant of myocardial MB creatine kinase. 855 15

We examined whether beraprost sodium (beraprost), a stable prostacyclin analogue, prevented cardiomyopathy in diabetic rats in vivo. Diabetes was induced by a bolus injection of streptozotocin in rat-tail vein. Four weeks after the induction of diabetes, the animals were treated with beraprost (30 micrograms/kg/day, p.o.) for 4 weeks until they were used for the measurement of hemodynamics, electrocardiogram (ECG), and plasma creatine phosphokinase (CK) activity. Nontreated diabetic rats have lower mean blood pressure, heart rate, left ventricular systolic pressure, and peak positive dP/dt at basal levels compared to age-matched normal rats. All of these changes were not improved in beraprost-treated rats. The left ventricular end-diastolic pressure and ST/R ratio in the ECG were significantly increased in diabetic rats. These parameters were significantly improved by beraprost compared with nontreated diabetic rats. Additionally, beraprost significantly suppressed the elevation of plasma CK activity as compared with that in non-treated diabetic rats. Changes in peak positive dP/dt in response to isoproterenol were attenuated in nontreated diabetic rats as compared with age-matched normal rats and beraprost-treated diabetic rats. These results suggest that beraprost is capable of preventing diabetic cardiomyopathy without affecting hyperglycemic condition.
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PMID:Beneficial effects of beraprost sodium, a stable prostacyclin analogue, in diabetic cardiomyopathy. 856 22

This study examined the profile and management of acute myocardial infarction in patients hospitalized in the coronary care unit of Henry Ford Hospital to determine risk factors or treatments that best explained a decline in in-hospital mortality rates. During the 1980s and early 1990s, many therapeutic advances occurred in management of acute infarction. Overall and in-hospital mortality were observed also to decline, but little is known about the relation of newer treatments to clinical outcome. The study population consisted of 1798 patients with a confirmed diagnosis of myocardial infarction. Of these, 982 consecutive patients were hospitalized in the coronary care unit of Henry Ford Hospital from January 1981 through December 1984 and compared with the 816 consecutive patients hospitalized from January 1990 through October 1992. Data on baseline demographics, initial clinical features, in-hospital management, and in-hospital outcome were compared for the two groups. Logistic regression was used to define independent predictors of the improved outcome of the two groups. Demographic features of the earlier group were similar to those of the later cohort, with the exception of a greater incidence of diabetes and hypertension and a lesser incidence of angina and prior heart failure. The occurrence of non-Q wave infarction increased from 27% in the earlier to 39% in the later group, whereas the magnitude of peak creatine kinase elevation in serum was higher in the later group. Medical management differed significantly, with increased use of aspirin, thrombolytics, heparin, warfarin, nitrates, and beta-blockers and decreased use of antiarrhythmic agents, digoxin, and vasopressors in the later group. Coronary revascularization was performed during hospitalization in 6.4% of the earlier group of patients and 31.6% of the later group. In-hospital mortality was 14.7% in the earlier group and 7.4% in the later group. Multivariate logistic regression analysis showed that the difference in mortality between the two groups was best accounted for by increased use of beta-blockers, angioplasty, and thrombolytics, decreased incidence of cardiogenic shock and asystole, and decreased use of lidocaine. In conclusion, the presentation and in-hospital management of patients with acute myocardial infarction has changed from the early 1980s to the early 1990s. The improved hospital mortality rate may be associated with both the expanded use of effective therapies and a more favorable in-hospital course, although these are not mutually exclusive.
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PMID:Decline in the rate of hospital mortality from acute myocardial infarction: impact of changing management strategies. 857 16

This study included 25 patients receiving hemodialysis (HD) but in whom diabetes mellitus was not the primary disease (HD-non DM group), 25 patients receiving hemodialysis with diabetes mellitus as the primary disease (HD-DM group), and 50 patients with diabetes mellitus who had not yet been treated with hemodialysis (DM group). The following markers of myocardial injury were measured in these patients: troponin T (TnT), creatine kinase (CK), myoglobin (Mb), and myosin light chain-1 (MLC-1). No significant correlation was found between myocardial TnT and Cr in any study group. The Mb and MLC-1 values in patients receiving HD were markedly higher than normal regardless of the primary disease involvement, while myocardial TnT was found to be only slightly abnormal. These results suggest that myocardial TnT may be a more useful marker of myocardial injury in HD patients than the markers in current use. In the present investigation, myocardial TnT was the only marker that was higher in the HD-DM group than in the HD-non DM group. This suggests the possibility that the HD-DM group included more patients with arteriosclerotic lesions, such as myocardial injury.
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PMID:A comparative study of myocardial troponin T levels in patients undergoing hemodialysis. 858


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