Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Peritoneal dialysis (PD) is the first option for patients in end stage renal disease (ESRD). Several complications such as peritonitis, exit-site or tunnels infections are encountered during PD. Other complications such as pain, proteic malnutrition, hyperglycemia, hypertension, cardiac failure are described in patients on continuous ambulatory peritoneal dialysis (CAPD) or APD (automated peritoneal dialysis). Rare complications are incapsulated sclerosing peritonitis, hemoperitoneum or pneumoperitoneum. We present the case of a female patient, 66 years old, on cyclic continuous peritoneal dialysis (APD-CCPD) admitted for pneumoperitoneum developed during a dialysis change from a CCPD schedule, due to an error in the Tenckhoff catheter and peritoneal dialysis manipulation. The treatment consisted in extracting the air during manual peritoneal dialysis changes, with the patient in Trendelenburg position and pressing on the abdominal wall, without any other complications.
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PMID:Pneumoperitoneum--rare complication in end stage renal disease patient on automated peritoneal dialysis. 1948 Mar 2

Advanced glycation end products (AGEs) contribute significantly to diabetic complications, both macro- and microvascular. TRC4186 is an AGE-breaker that has been evaluated in vitro and in vivo and shown to reduce AGE burden. The aim of this study was to determine the effect of TRC4186 on diabetic cardiomyopathy and nephropathy in obese Zucker spontaneously hypertensive fatty rats (Ob-ZSF1), an animal model of diabetes with progressive cardiac and renal dysfunction. Ob-ZSF1 rats loaded with 0.5% salt were treated with TRC4186, 9 or 27 mg/kg twice daily intraperitoneally or vehicle control and monitored telemetrically throughout the study. Cardiac function was assessed terminally by Millar catheter. Markers of cardiac and renal dysfunction were measured and changes evaluated histopathologically. TRC4186 at 27 mg/kg prevented rise in blood pressure (BP) and also improved cardiac output (CO) secondary to better diastolic relaxation as well as systolic emptying in association with the reduction in afterload. At 9 mg/kg, CO was improved by compensatory increase in pre-load however afterload reduction was not adequate to allow efficient systolic emptying. Brain natriuretic peptide (BNP) and interleukin-6 (IL-6) expression was reduced with treatment. Deterioration in renal function was retarded as evident from albumin to creatinine ratio and renal histopathology. TRC4186, an AGE-breaker, clearly preserved cardiac function and reduced the severity of renal dysfunction in Ob-ZSF1, an animal model with persistent severe hyperglycemia leading to diabetic heart failure and renal failure.
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PMID:TRC4186, a novel AGE-breaker, improves diabetic cardiomyopathy and nephropathy in Ob-ZSF1 model of type 2 diabetes. 1954 15

Patients with chronic heart failure (CHF) represent a group with high risk of repetitive hospitalizations. In order to assess frequency of repetitive hospitalizations and elucidate their risk factors we included in this study 962 patients with stage IIA-III and functional class II-IV CHF hospitalized in a multiprofile hospital once or repeatedly during 1 year. Rate of rehospitalizations during 1 year was 59%. The following factors of risk of rehospitalizations were revealed: admission because of progression of CHF, history of myocardial infarction, atrial fibrillation, systolic left ventricular dysfunction, hyperuricemia, and hyperglycemia.
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PMID:[Repetitive hospitalizations of patients with chronic heart failure according to data of one year follow-up study]. 1965 92

Metabolic syndrome (MetS) includes some parameters which are associated with cardiovascular events and risk of developing heart failure (HF). The aim of the present study was to explore the prevalence of metabolic syndrome and individual MetS parameters among heart failure patients. Stable HF patients who had an ejection fraction (EF) < or = 35% were included. They were evaluated for MetS and parameters according to the Adult Treatment Panel III (ATP III) of the National Cholesterol Education Program (NCEP). One hundred and nine patients (72 males, 37 females; mean age, 67 +/- 12 years) were included. The most prevalent parameters were low HDL-C (69%) and hypertension (69%) in all participants. No significant change was observed in the prevalence of these parameters due to gender (P > 0.05). Hypertension, increased waist circumference, and hypertriglyceridemia were all significantly more common in women (P < 0.05). The prevalences of hypo-HDL-emia, hyperglycemia, and hypertension did not differ significantly with an advanced age (P > 0.05), whereas hypertriglyceridemia and high waist circumference were significantly decreased in the elderly (P < 0 05). The overall MetS prevalence was 51% and it was significantly higher in women (76% versus 37%, P : 0.003). The prevalence of MetS clearly decreased with age, although the difference was not statistically significant (61% versus 46%, P : 0.57). The mean number of positive MetS parameters also changed significantly with age (3 +/- 1.4 versus 2.5 +/- 1.3, P : 0.046). EF did not change with mean number of MetS parameters (P > 0.05). Hypo-HDL-emia and similarly hypertension were the 2 most common MetS parameters in HF patients. Hypo-HDL-emia and hypertension were the most common parameters observed in all participants and no significant difference was seen due to gender or age. Even though the prevalence of MetS and the mean number of parameters were significantly more common in females and young patients, EF did not change with changes in these parameters. Based on the results obtained, we conclude that the early diagnosis and treatment of MetS as well as the measurement of individual parameters, especially the most frequent ones, may prevent heart failure or improve its status.
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PMID:Low HDL levels as the most common metabolic syndrome risk factor in heart failure. 1980 6

The hypothesis proposed is that heart failure (HF) is associated with a reactive hyperadrenergic state that increases circulating plasma free fatty acids (FFAs), which leads to impaired glucose metabolism and insulin resistance. We propose that increased FFA-induced mitochondrial uncoupling and substantial oxygen wastage is closely associated with the generation of reactive oxygen species, inflammatory markers, and the development of insulin resistance. The therapeutic aims of metabolic therapy are as follows: 1) to decrease hyperadrenergic drive; 2) to inhibit lipotoxicity and glucotoxicity; and 3) to increase glucose uptake by muscle. These aims are achieved, respectively, by the following: 1) the use of beta-adrenergic blockade and all measures that relieve the mechanical load on the heart; 2) the use of drugs that inhibit fatty acid oxidation (trimetazidine, perhexiline), although without clinical evidence that the heart is their major site of action in HF; and 3) increase of the transport of glucose into the cells by exercise and metformin. Of these measures, only data concerning the reduction of mortality as the result of exercise are available. Of all the other measures, there are substantial positive data on the use of trimetazidine that demonstrate metabolic and clinical benefit with almost no side effects, but data from a large outcome trial are lacking. Our data suggest a major extracardiac site of trimetazidine action. Ranolazine, which inhibits the late sodium inward current, requires testing in human HF. Insulin to reduce hyperglycemia and FFAs is untested in HF, with incretins such as glucagon-like peptide-1 on the horizon. Other future therapies may include malonyl-coenzyme A regulators to inhibit fatty acid oxidation, fish oil omega-3, and activators of protein kinase C-epsilon.
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PMID:The adrenergic-fatty acid load in heart failure. 1985 Feb 4

Diabetes is a major metabolic disorder and leading cause of morbidity and mortality in the developed world. Indeed, vascular complications are the major cause of mortality in diabetics. Impaired glucose metabolism has been implicated as a cause for the observed cardiac dysfunction in diabetics. Dramatic increase in polyol pathway flux during hyperglycemia could cause damage to blood vessels that leads to heart failure. Recent investigations and patent applications suggest the interesting and important role of polyol pathway enzyme, aldose reductase (AR) in mediating oxidative stress-induced inflammatory signals. AR inhibitors have been shown to prevent or delay the onset of cardiovascular complications such as ischemic injury, restenosis and atherosclerosis. In this review, we have focused on describing the pivotal role of AR in the pathogenesis of cardiovascular complications and use of AR inhibitors as emerging therapeutic strategies in preventing cardiovascular complications.
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PMID:Aldose reductase inhibition: emerging drug target for the treatment of cardiovascular complications. 1988 61

Diabetic cardiomyopathy has been defined as "a distinct entity characterized by the presence of abnormal myocardial performance or structure in the absence of epicardial coronary artery disease, hypertension, and significant valvular disease". The diagnosis stems from the detection of myocardial abnormalities and the exclusion of other contributory causes of cardiomyopathy. It rests on non-invasive imaging techniques which can demonstrate myocardial dysfunction across the spectra of clinical presentation. The presence of diabetes is associated with an increased risk of developing heart failure, and the 75% of patients with unexplained idiopathic dilated cardiomyopathy were found to be diabetic. Diabetic patients with microvascular complications show the strongest association between diabetes and cardiomyopathy, an association that parallels the duration and severity of hyperglycemia. Metabolic abnormalities (that is hyperglycemia, hyperinsulinemia, and hyperlipemia) can lead to the cellular alterations characterizing diabetic cardiomyopathy (that is myocardial fibrosis and/or myocardial hypertrophy) directly or indirectly (that is by means of renin-angiotensin system activation, cardiac autonomic neuropathy, alterations in calcium homeostasis). Moreover, metabolic abnormalities represent, on a clinical ground, the main therapeutic target in the patients with diabetes since the diagnosis of diabetes is made. Since diabetic cardiomyopathy is highly prevalent in the asymptomatic type 2 diabetic patients, screening for its presence at the earliest stage of development can lead to prevent the progression to chronic heart failure. The most sensitive test is standard echocardiogram, while a less expensive pre-screening method is the detection of microalbuminuria.
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PMID:The diabetic cardiomyopathy. 2019 91

The impressive correlation between cardiovascular disease and alterations in glucose metabolism has raised the likelihood that atherosclerosis, heart failure, and type 2 diabetes may share common antecedents. Postprandial hyperglycemia has been shown to play an important role on the onset and development of heart failure and cerebral infarction in several large-scale clinical trials. Recently, chronic hyperglycemia has been reported to enhance the vasoconstrictor response by Rho-kinase. We have previously reported that phenylephrine enhanced the vasoconstrictor response in a spontaneous diabetes mellitus OLETF (Otsuka-Long-Evane-Tokushima fatty) rat model. However, the mechanism of hyperglycemia in these reactions, particularly the influence of hyperglycemia on the signal transduction pathway, is still not well understood. We, therefore, examined the effect of hyperglycemia on the cell growth and gene expression of rat aortic smooth-muscle cells (RASMCs). Hyperglycemia accelerated the growth of RASMCs in a concentration-dependent manner. Furthermore, the c-fos gene expression was also increased by hyperglycemia. Phenylephrine activated the c-fos gene expression. Hyperglycemia augmented the phenylephrine-induced c-fos gene expression synergistically in a dose dependent manner. The deletion analysis revealed that the c-fos serum response element (SRE) accounts for the c-fos gene expression. RhoA, and Rho-kinase were involved in hyperglycemia-induced c-fos gene expression. An HMG-CoA reductase inhibitor, Pitavastatin, inhibited these hyperglycemia-augmented reactions by inhibiting RhoA. Hyperglycemia itself increased the cell growth and gene expression. Furthermore, it modifies and augments the cell growth and gene expression by alpha1-AR-mediated stimulation. Statin might therefore be effective for the treatment of hyperglycemia-induced cardiovascular dysfunction.
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PMID:Hyperglycemia induced cell growth and gene expression via the serum response element through RhoA and Rho-kinase in vascular smooth muscle cells. 2021 75

An increasing body of evidence suggests that oxidant stress is involved in the pathogenesis of many cardiovascular diseases, including hypercholesterolemia, atherosclerosis, hypertension, heart failure and diabetes. Recent studies have also provided important new insights into potential mechanisms underlying the pathogenesis of vascular disease induced by diabetes. Glycosylation of proteins and lipids, which can interfere with their normal function, activation of protein kinase C with subsequent alteration in growth factor expression, promotion of inflammation through the induction of cytokine secretion and hyperglycemia-induced oxidative stress are some of these mechanisms. It is widely accepted that hyperglycemia-induced reactive oxygen species contribute to cell and tissue dysfunction in diabetes. A variety of enzymatic and non-enzymatic sources of reactive oxygen species exist in the blood vessels. These include NADPH oxidase, mitochondrial electron transport chain, xanthine oxidase and nitric oxide synthase. The present article reviews the effects of reactive oxygen species on endothelial function in diabetes and addresses possible therapeutic interventions.
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PMID:Reactive oxygen species and endothelial function in diabetes. 2037 Dec 38

Male gender is a major risk factor for premature cardiovascular death, a relationship not yet explained. Low testosterone in men is a risk factor for the metabolic syndrome and type 2 diabetes and is associated independently with individual components of the metabolic syndrome--visceral obesity, insulin resistance, hyperglycemia, hypertension and dyslipidemia. Epidemiological studies report increased mortality in men with low testosterone. Testosterone replacement in the short-term reduces waist circumference, cholesterol and circulating pro-inflammatory cytokines and improves insulin sensitivity and glycemic control in diabetics. Testosterone also has beneficial effects on cardiac ischemia, angina and chronic heart failure. This manuscript reviews the current evidence supporting a link between low testosterone and cardiovascular disease, highlighting the need for larger, longer-term studies.
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PMID:Testosterone deficiency: a risk factor for cardiovascular disease? 2038 74


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