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)

Metformin is associated with decreased mortality and morbidity in stable heart failure patients with diabetes mellitus type II. Diabetic heart failure patients with elevated systolic blood pressure are at increased risk for developing acute decompensated heart failure, which is often associated with decreased kidney function. Metformin-associated lactic acidosis is a rare but fatal side effect that may occur when kidney function is decreased. During acute decompensated heart failure, timely treatment may prevent the decrease in kidney function to the threshold associated with an increased risk of metformin-associated lactic acidosis. Metformin should not be withheld in diabetic patients with stable heart failure who do not have other risk factors for acute decompensated heart failure or lactic acidosis.
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PMID:Metformin use in decompensated heart failure. 1870 28

There is increasing evidence to suggest that chronic heart failure (CHF) is an insulin resistant (IR) state and that the degree of IR correlates with the severity and mortality of CHF. The pathophysiology of IR in CHF has yet to be fully defined. Additionally, it remains to be determined if IR is merely a marker reflecting the severity of CHF or whether it contributes to the disease in CHF. If IR is truly a culprit that worsens CHF, it will potentially be a new target for therapy as strategies that can reverse IR in CHF may potentially result in an improvement in symptoms and even mortality in these patients. However, there are concerns regarding the use of certain insulin sensitizers, most notably, the thiazolidinediones (TZDs) which have been associated with increased risk of hospitalizations for CHF. Despite previous concerns of lactic acidosis (LA), there is now evidence that metformin may not only be safe but could potentially be useful in the setting of CHF. There are now ongoing prospective studies, including the TAYSIDE study, to determine if reversing IR with metformin will have beneficial effects in patients with CHF.
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PMID:Insulin resistance: a potential new target for therapy in patients with heart failure. 1878 90

Diabetes mellitus and heart failure (HF) commonly coexist, and together these conditions are associated with increased morbidity and mortality compared with either condition alone. Although the optimal treatment strategy to achieve glucose control in HF patients with type 2 diabetes has not been well studied, given the common coexistence of these conditions and the need to adequately treat hyperglycemia to prevent microvascular complications, it is important for clinicians to understand the potential implications of diabetic therapy in patients with established HF. Until recently, metformin was contraindicated in patients with HF because of the potential risk of lactic acidosis; however, recent retrospective studies of metformin use in HF patients have shown that this medication may be used safely and indeed may be beneficial in patients with stable HF. The association between thiazolidinediones (TZDs) and HF remains controversial, but recent prospective randomized trials of TZD use in HF patients suggest that worsening volume retention associated with these agents may lead to worsening of HF symptoms. The recently developed incretin-based therapies, such as exenatide and sitagliptin, also have not been extensively studied in HF populations; however, small pilot studies of glucagon-like peptide-1 have shown potential promise in the treatment of diabetic patients with HF. Although they may be difficult to perform, future randomized controlled trials are needed to establish optimal treatment goals and strategies in this population.
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PMID:Management of type 2 diabetes in patients with heart failure. 1902 77

A 49-year-old woman was admitted to hospital because of heart failure. She was diagnosed as having mitochondrial cardiomyopathy and diabetes mellitus. Echocardiography revealed a hypertrophic and poorly contracting left ventricle. A diagnosis of mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes was established by muscle biopsy. She underwent technetium-99m-sestamibi ((99m)Tc-MIBI) and beta-methyl-p-(123)I-iodophenyl-pentadecanoic acid ((123)I-BMIPP) scintigraphic examinations. (99m)Tc-MIBI single-photon emission computed tomography revealed reduced tracer uptake in the hypertrophic left ventricular inferior wall. In contrast, there was an increase in (123)I-BMIPP uptake in the in the region of reduced (99m)Tc-MIBI uptake ((99m)Tc-MIBI/(123)I-BMIPP mismatch). There was rapid washout of (99m)Tc-MIBI from the myocardium (washout rate increased by 30%). Decreased (99m)Tc-MIBI and increased (123)I-BMIPP uptake ((99m)Tc-MIBI/(123)I-BMIPP mismatch) were the characteristics of cardiac involvement in mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes.
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PMID:Cardiac scintigraphic findings of mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes: A case report. 1934 24

Clinicians are faced with an expansive array of treatment choices when caring for patients with type 2 diabetes. Because patient compliance may be affected when media sensationalism about controversial findings is misunderstood, we sought to clarify the recent controversy surrounding the cardiovascular and bone-health risks of thiazolidinediones, the risk of lactic acidosis with metformin, and the risk of hypoglycemia with oral therapies. The side effect profile of thiazolidinediones includes fluid retention, heart failure; and an increased risk of fracture. A recent controversial meta-analysis suggested that rosiglitazone increases the risk of myocardial infarction, which is possibly related to thiazolidinedione-induced lipid changes, weight gain, congestive heart failure, and anemia. Metformin is restricted to patients with normal renal function because of concerns that metformin may cause lactic acidosis. However, few cases of metformin-associated lactic acidosis have been reported, and most have occurred in patients with other reasons for developing lactic acidosis, such as sepsis or renal failure. Although the use of metformin continues to increase, observational studies have not been able to demonstrate an increased incidence of lactic acidosis in metformin-treated patients, even when it is used in populations with relative contraindications. Some oral hypoglycemic medications can cause hypoglycemia. Hypoglycemia is especially common in older patients, alcoholics, and patients with liver or renal disease. Patients on sulfonylureas and meglitinides have the highest incidence of hypoglycemia because of their pharmacological action of increasing insulin secretion. Of the sulfonylureas, glyburide presents the highest risk of hypoglycemia. Combination therapies, especially those regimens containing a sulfonylurea, increase the risk of hypoglycemia.
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PMID:Balancing risk and benefit with oral hypoglycemic drugs. 1942 67

Metformin is a biguanide, insulin sensitiser that reduces blood sugar levels. There are concerns about the risk of lactic acidosis in patients receiving metformin who have procedures requiring iodinated contrast, and in those with renal impairment or heart failure. The data on which these concerns are based are reviewed, with the conclusion that metformin treatment is rarely to blame for lactic acidosis. A generic policy of stopping metformin 48 h before and 48 h after the procedure in all patients is counterintuitive, lacks any evidence base and does not conform to the principles of best practice. In patients with heart failure, although the underlying condition can predispose to lactic acidosis, existing evidence suggests that metformin use is associated with improved outcome rather than increased risk.
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PMID:Metformin: safety in cardiac patients. 1956 48

Classical non-insulin antihyperglycemic drugs currently approved for the treatment of type 2 diabetes mellitus (T2DM) comprise five groups: biguanides, sulfonylureas, meglitinides, glitazones and alpha-glucosidase inhibitors. Novel compounds are represented by the incretin mimetic drugs like glucagon like peptide-1 (GLP-1), the dipeptidyl peptidase 4 (DPP-4) inhibitors, dual peroxisome proliferator-activated receptors (PPAR) agonists (glitazars) and amylin mimetic drugs. We review the cardiovascular effects of these drugs in an attempt to improve knowledge regarding their potential risks when treating T2DM in cardiac patients. Metformin may lead to lethal lactic acidosis, especially in patients with clinical conditions that predispose to this complication, such as recent myocardial infarction, heart or renal failure. Sulfonylureas exert their effect by closing the ATP-dependent potassium channels. This prevents the opening of these channels during myocardial ischemia, impeding the necessary hyperpolarization that protects the cell. The combined sulfonylurea/metformin therapy reveals additive effects on mortality in patients with coronary artery disease (CAD). Meglitinides effects are similar to those of sulfonylureas, due to their almost analogous mechanism of action. Glitazones lower leptin levels, leading to weight gain and are unsafe in NYHA class III or IV. The long-term effects of alpha-glucosidase inhibitors on morbidity and mortality rates is yet unknown. The incretin GLP-1 is associated with reductions in body weight and appears to present positive inotropic effects. DPP-4 inhibitors influences on the cardiovascular system seem to be neutral and patients do not gain weight. The future of glitazars is presently uncertain following concerns about their safety. The amylin mimetic drug paramlintide, while a satisfactory adjuvant medication in insulin-dependent diabetes, is unlikely to play a major role in the management of T2DM. Summarizing the present information it can be stated that 1. Four out the five classical oral antidiabetic drug groups present proven or potential cardiac hazards; 2. These hazards are not mere 'side effects', but biochemical phenomena which are deeply rooted in the drugs' mechanism of action; 3. Current data indicate that the combined glibenclamide/metformin therapy seems to present special risk and should be avoided in the long-term management of T2DM with proven CAD; 4. Glitazones should be avoided in patients with overt heart failure; 5, The novel incretin mimetic drugs and DPP-4 inhibitors--while usually inadequate as monotherapy--appear to be satisfactory adjuvant drugs due to the lack of known undesirable cardiovascular effects; 6. Customized antihyperglycemic pharmacological approaches should be implemented for the achievement of optimal treatment of T2DM patients with heart disease. In this context, it should be carefully taken into consideration whether the leading clinical status is CAD or heart failure.
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PMID:A cardiologic approach to non-insulin antidiabetic pharmacotherapy in patients with heart disease. 1961 27

A 74-year-old man with cardiac failure and renal impairment was admitted to the cardiothoracic intensive care unit with metformin-induced lactic acidosis and shock. He was successfully treated with high-dose (80 ml/kg/hour) continuous venovenous haemodiafiltration. Lactic acidosis is a known complication of metformin and is associated with a high mortality. The use of high-dose continuous venovenous haemodiafiltration for this condition has not previously been reported.
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PMID:Continuous venovenous haemodiafiltration for metformin-induced lactic acidosis. 1977 50

Mitochondrial trifunctional protein (MTP) is a heterocomplex composed of 4 alpha-subunits containing LCEH (long-chain 2,3-enoyl-CoA hydratase) and LCHAD (long-chain 3-hydroxyacyl CoA dehydrogenase) activity, and 4 beta-subunits that harbor LCKT (long-chain 3-ketoacyl-CoA thiolase) activity. MTP deficiency is an autosomal recessive disorder that causes a clinical spectrum of diseases ranging from severe infantile cardiomyopathy to mild chronic progressive polyneuropathy. Here, we report the case of a Korean male newborn who presented with severe lactic acidosis, seizures, and heart failure. A newborn screening test and plasma acylcarnitine profile analysis by tandem mass spectrometry showed an increase of 3-hydroxy species: 3-OH-palmitoylcarnitine, 0.44 nmol/ml (reference range, RR <0.07); 3-OH-linoleylcarnitine, 0.31 nmol/ml (RR <0.06); and 3-OH-oleylcarnitine, 0.51 nmol/ml (RR <0.04). These findings suggested either long-chain 3-hydroxyacyl-coA dehydrogenase deficiency or complete MTP deficiency. By molecular analysis of the HADHB gene, the patient was found to be a compound heterozygote for c.358dupT (p.A120CfsX8) and c.1364T>G (p.V455G) mutations. These 2 mutations of the HADHB gene were novel and inherited. Although the patient was treated by reduction of glucose administration and supplementation of a medium-chain triglyceride-based diet with L-carnitine, he died 2 mo after birth due to advanced cardiac failure.
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PMID:Two novel HADHB gene mutations in a Korean patient with mitochondrial trifunctional protein deficiency. 1988 Jul 69

Metformin is a biguanide, insulin sensitiser that reduces blood sugar levels. There are concerns about the risk of lactic acidosis in patients receiving metformin who have procedures requiring iodinated contrast, and in those with renal impairment or heart failure. The data on which these concerns are based are reviewed, with the conclusion that metformin treatment is rarely to blame for lactic acidosis. A generic policy of stopping metformin 48 h before and 48 h after the procedure in all patients is counterintuitive, lacks any evidence base and does not conform to the principles of best practice. In patients with heart failure, although the underlying condition can predispose to lactic acidosis, existing evidence suggests that metformin use is associated with improved outcome rather than increased risk.
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PMID:Metformin: safety in cardiac patients. 2054 5


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