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 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Previous studies have reported conflicting results on gender differences in the management of acute myocardial infarction (AMI) and have not evaluated hospital length of stay or costs. To determine gender-based differences in presentation, management, length of stay, costs, and prognosis after AMI, we studied 561 patients with AMI. Women were older, had systemic hypertension, diabetes mellitus, and a non-Q-wave AMI more frequently, whereas more men smoked cigarettes. Predictors of coronary angiography were: male gender (RR 1.9; 95% CI 1.2 to 3.1), chest pain at presentation (RR 1.8; 95% CI 1.0 to 3.3), recurrent angina (RR 4.1; 95% CI 2.5 to 6.8), admission via the emergency room (RR 0.2; 95% CI 0.1 to 0.3), and younger age. Gender did not predict mortality. Among presenting features, the predictors of length of stay were diabetes, prior coronary bypass and prior coronary angioplasty in men, and age alone in women. Pulmonary edema and need for coronary bypass during the hospital course were predictors of length of stay in men only. Among presenting features, predictors of cost were diabetes in men and congestive heart failure in women. Predictors of cost during hospitalization for men were pulmonary edema, coronary angiography, intraaortic balloon pump use, and coronary bypass; for women, they were peak levels of creatine kinase and coronary bypass. Thus, predictors of length of stay and hospitalization costs differ based on gender. Efforts at cost containment may need to be gender-specific.
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PMID:Do gender-based differences in presentation and management influence predictors of hospitalization costs and length of stay after an acute myocardial infarction? 748 95

One feature of the diabetic cardiomyopathy is the appearance of contractile dysfunction as the workload increases. We hypothesized that this resulted from an impaired creatine kinase/phosphocreatine system and therefore examined the creatine kinase kinetics at both low and high workloads. Creatine kinase flux (by 31P nuclear magnetic resonance saturation transfer method), cardiac performance, and oxygen consumption were measured in control and streptozotocin-induced diabetic rat hearts. Creatine kinase flux was inhibited by iodoacetamide in control hearts to confirm the role of the creatine kinase/phosphocreatine system in cardiac performance. In diabetic hearts, 1) the contractile dysfunction became apparent only at high workloads, 2) the ATP synthesis rate was not significantly different from control hearts, 3) the creatine kinase flux was reduced by 30.8% (257.5 +/- 7.7 mumol.g wet wt-1.min-1 in control vs. 178.3 +/- 9.4 in diabetes, P < 0.001), and 4) the creatine kinase flux did not increase as the workload increased. In control hearts, 5) iodoacetamide inhibited the creatine kinase flux to the same degree as that in diabetic hearts, and 6) the contractile dysfunction was not as severe as that observed in diabetic hearts. These results suggest that the impaired creatine kinase/phosphocreatine system is, at least in part, responsible for the contractile dysfunction in the diabetic cardiomyopathy.
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PMID:Creatine kinase kinetics in diabetic cardiomyopathy. 761 80

Rhabdomyolysis (RM) is a clinical and laboratory syndrome resulting from leakage of muscle cell contents into plasma. The increased plasma concentration of the substances released such as creatine kinase (CK) permits the clinician to diagnose this syndrome. Non-traumatic RM has occasionally been reported in patients with diabetic decompensation. We encountered about 44 cases of RM in 265 diabetic emergencies (including DKA or hyperosmolar, or both) during the period from 1984-1 to 1990-6, diagnosed based on (1) serum creatine kinase (CK) > 1000 IU/l and (2) the absence of acute myocardial infarction, stroke and end-stage renal disease. On admission, those who presented with RM had significantly higher concentration of blood urine nitrogen (BUN) (83.3 +/- 5.9 vs. 58.8 +/- 2.4 mg/dl, P < 0.05), creatine (4.45 +/- 0.4 vs. 2.97 +/- 0.1 mg/dl, P < 0.05) and serum osmolarity (386.5 +/- 5.2 vs. 351.6 +/- 2.4 mOsm/kg, P < 0.05). The mortality within 1 week of diabetic emergencies (38.5% for DKA, 35.5% for HHNK) was higher in patients with RM than those without RM (9.7% for DKA, 26.7% for HHNK). There was a correlation (r = 0.49, P < 0.05) between the levels of serum creatinine and CK in patients with RM.(ABSTRACT TRUNCATED AT 250 WORDS)
Diabetes Res Clin Pract 1994 Dec 31
PMID:Rhabdomyolysis in diabetic emergencies. 773 1

The clinical and echocardiographic variables related to postinfarction angina were evaluated in 54 patients with acute myocardial infarction. All patients underwent 2D echocardiography at 2-3 weeks after infarction. Wall motion analysis was quantified with a wall motion score index (WMSI) based on 16 left ventricular wall segments. Among the 54 patients with acute myocardial infarction 23 (42.6%) had early postinfarction angina. Multiple regression analysis demonstrated no significant difference between the patients with and without postinfarction angina in age, sex, location of infarction, Killip classification, previous angina, hypertension, hyperlipidemia, diabetes mellitus, creatine kinase level and left ventricular ejection fraction. In comparison with patients without postinfarction angina, patients with postinfarction angina had higher WMSI. It indicates that postinfarction angina appears to be related more to myocardial ischemia rather than to the infarct of myocardium.
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PMID:[Analysis of risk factors in postinfarction angina]. 788 38

In this preliminary report of a 20-week trial, 66 patients with non-insulin-dependent diabetes mellitus (NIDDM) and hyperlipidaemia who remained eligible after an 8-week dietary stabilization phase were randomly allocated to receive 20 mg of fluvastatin or placebo once daily for 6 weeks. Fluvastatin was subsequently increased to 20 mg twice daily and administered according to the same schedule, versus placebo, for a further 6 weeks. Both dosages of fluvastatin substantially improved serum lipid profiles compared with baseline and placebo. Both dosages of fluvastatin significantly reduced low-density- and very-low-density-lipoprotein (LDL, VLDL), cholesterol and triglyceride (TG) compared with placebo, and both dosages significantly elevated high-density-lipoprotein (HDL) cholesterol. The ratio of LDL to HDL was also significantly decreased. Amongst the 58 patients who completed the study, there was no evidence either of myopathy or of hepatotoxicity; mean creatine kinase values remained stable in the fluvastatin arm. Fasting glucose, glycosylated haemoglobin, and fructosamine levels were not markedly affected by active treatment. No serious adverse events attributable to the drug were reported. In conclusion, both dosages of fluvastatin appear to be effective and safe in the management of hyperlipidaemia in this outpatient, maturity-onset, diabetic population.
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PMID:Efficacy and safety of fluvastatin in hyperlipidaemic patients with non-insulin-dependent diabetes mellitus. 798 2

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

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


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