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)

The present study was designed to determine if changes in function and metabolism of heart muscle induce alterations in characteristics of skeletal muscle. We investigated the histochemical and biochemical properties of soleus (SOL) and extensor digitorum longus (EDL) muscles in Wistar rats at the chronic phase after coronary artery occlusion/reperfusion. The size of myocardial infarct region was evaluated using a high resolution pinhole single photo emission computed tomography (SPECT) system. 4 wk after left coronary artery occlusion/reperfusion, the SOL and EDL of hindlimb were dissected out and immersed in isopentane cooled with liquid nitrogen for subsequent histochemical and biochemical analysis. From SPECT imaging, the blood circulation was recovered, but the recovery of fatty acid metabolism was not observed in infarct region of heart. Citrate synthase (CS) and 3-hydroxyacyl-CoA dehydrogenase (HAD) activities in infarct region of heart were lower in the myocardial infarction (MI, n = 6) group compared with that of age-matched sham-operated (Sham, n = 6) group. In addition, heart muscle hypertrophy caused by the dysfunction in MI group was observed. In skeletal muscle, the atrophy and transition of fiber type distribution in MI group, reported in previous studies of heart failure, were not observed. However, the succinate dehydrogenase (SDH) activity in the slow twitch oxidative (SO) from SOL of MI group decreased by 9.8% and in the fast twitch oxidative glycolytic fibers (FOG), 8.0% as compared with sham group. Capillary density of the SO fibers from SOL of MI group also reduced by 18.5% and in the FOG fibers, 18.2% as compared with Sham group. Decreased capillary density in this study related significantly to decreased SDH activity of single muscle fibers in chronic phase of perfusion after surgical infarction. Our results make it clear that there is a difference in the reaction of skeletal muscle to coronary artery occlusion/reperfusion compared with chronic heart failure. However, our data would support the notion that there is a linkage between the function of heart and physiological properties of skeletal muscle.
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PMID:[Adaptation in properties of skeletal muscle to coronary artery occlusion/reperfusion in rats]. 1250 Apr 16

In renal failure, blood urea nitrogen and serum creatinine usually rise in tandem; the normal BUN: Cr ratio is 10-15: 1. Disproportionate rises in BUN: Cr (> 20: 1) often imply pre-renal azotemia but may be caused by increased protein catabolism or an excessive protein load. In this study we looked at intensive care patients who acutely developed markedly increased BUN (> or = 100 mg/dL) with only modest elevation of Cr (< or = 5 mg/dL) for possible causes of the disproportionate azotemia. There were 19 such cases collected over 6 months, nine women and ten men, with mean age 69.2 +/- 4.4 years (13/19 > 75 years). Peak BUN was 156 +/- 11 mg/dL; peak Cr 4.3 +/- 0.5 mg/dL. Eleven patients expired. Mean serum albumin at the time of consultation was 2.7 +/- 0.2 g/dL; mean total lymphocyte count 1.0 +/- 0.1/mm3. Of possible factors causing the azotemia, nine patients had documented hypovolemia; eight had congestive heart failure; six were in septic or hypovolemic shock, and two received high-dose steroids. As contributing factors, eight patients had Salb < 2.5 g/dL; eight were given a high protein intake > 100 g/d; two had HIV, and two others had gastrointestinal bleeding. Infection was present in 14 patients; seven had sepsis (bacteremia with hypotension). All patients had at least one of these factors present and 16/19 had two or more. Fractional Na excretion was < 1% (consistent with pre-renal azotemia) in only four of the 11 patients in whom it was measured. We conclude that severely disproportionate BUN : Cr is frequently multifactorial and is most common in the elderly, perhaps due to their lower muscle mass, and in ICU patients given a high protein intake. It is often not indicative of uncomplicated renal hypoperfusion, although low renal perfusion (hypovolemia, shock, or heart failure) is common. Mortality is high due to the severe illnesses, especially infection, worsened by decreased renal function and hypercatabolic state.
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PMID:Massive and disproportionate elevation of blood urea nitrogen in acute azotemia. 1254 57

The debate on whether resting myocardial blood flow (MBF) to hibernating myocardium is reduced or not has attracted a lot of interest and has contributed to stimulate new research on heart failure in patients with coronary artery disease (CAD). Positron emission tomography with oxygen-15 labeled water (H(2)(15)O) or nitrogen-13 labeled ammonia (13NH(3)) has been used for the absolute quantification of regional MBF in human hibernating myocardium. When hibernating myocardium is properly identified, i.e. a dysfunctional segment subtended by a stenotic coronary artery that improves function upon reperfusion, the following conclusions can be reached based on the available literature: (a) in the majority of these studies resting MBF in hibernating myocardium is not different from either flow in remote tissue in the same patient or MBF in normal healthy volunteers; (b) a reduction in MBF of approximately 20% compared to MBF in remote myocardium or age matched normal subjects has been demonstrated in a minority of truly hibernating segments; (c) hibernating myocardium is characterized by a severely impaired coronary flow reserve which improves after revascularization in parallel with contractile function. Thus, the pathophysiology of hibernation in humans is more complex than initially postulated. The recent evidence that repetitive ischemia in patients with coronary artery disease can be cumulative and lead to more severe and prolonged stunning, lends further support to the hypothesis that, at least initially, stunning and hibernation are two facets of the same coin.
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PMID:Myocardial blood flow in patients with hibernating myocardium. 1256 3

A case of fatal suicidal bentazon poisoning is presented along with a description of the different analytical methods involved. A 56-year-old farmer was examined by the family doctor 1 h after voluntarily ingesting 500 mL of FIGHTER (bentazon, 480 g/L water). He presented a Glasgow score of 15, polypnea, diarrhea, and vomiting. During transport by ambulance to the hospital, he tossed, sweated, and suddenly presented breathing difficulty followed by heart failure. Tracheal intubation was impossible (H1.5) despite use of different diameter cannulas because of extreme general muscle rigidity. All attempts at resuscitation failed, and the patient died within 2 h postingestion. Blood and urine samples were taken just before death. General basic and neutral drug screening by high-performance liquid chromatography-diode-array detection and gas chromatography-nitrogen-phosphorus detection showed no strychnine or other drugs or toxics except for citalopram (< 0.1 mg/L) and bentazon, but this weak acidic molecule (pKa3.3) was badly extracted in alkaline conditions. Plasma and urine levels, measured after acidic extraction, protein precipitation, or simple dilution, were 1500 and 1000 mg/L, respectively. Bentazon (M.W. 240) was confirmed by its basic mass spectrum (ESI-, m/z 239, 197, 175, 132) or by that of methylated derivative (El+, m/z 254, 212, 175). An hydroxylated metabolite (ESI-, m/z 255, 213, 191, 148; El+, m/z 284, 242, 163) and the N1-glucuronide conjugate of bentazon (ESI-, m/z 415, 239) were also detected in urine. (Quantitation ions are underlined.) This first case of bentazon poisoning with available analytical data revealed the high toxicity of this compound after large dose ingestion with early and heavy symptoms such as muscle rigidity probably related to muscular toxicity. Comparison with another nonfatal case and with toxicological data on animals is discussed.
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PMID:Fatal acute poisoning by bentazon. 1267 7

Nitric oxide (NO) plays an important role in the physiologic modulation of coronary artery tone and myocardial function. However, increased formation of NO within the myocardium can also have detrimental effects, contributing to the pathophysiology of myocardial dysfunction in ischaemic heart diseases. The role of reactive nitrogen species in the pathogenesis of myocardial dysfunction after ischaemia has been investigated in numerous studies. They reveal divergent and opposed effects of nitric oxide: from a cardioprotective action leading to ischaemic preconditioning after short ischaemic periods to a cardiodepressive action after severe ischaemia/reperfusion injury and heart failure. This review describes the determining role of reactive oxygen species on these opposite myocardial effects of NO. The final action of NO, whether cardioprotective or cardiodepressive, strongly depends on the level of oxidative stress in the myocardium. Nitric oxide disrupts free radical and oxidant-mediated reactions, due to a strong attraction and interaction with superoxide.The level of oxidative stress is positively related to the severity of the ischaemic injury, making the results in different myocardial syndromes more concordant. If the increased production of NO is well in balance with a moderate increase in oxygen radicals, then NO will exert beneficial effects. However, if the oxygen radicals are produced in excess of NO as in prolonged ischaemic injury, then deleterious effects will be induced. Consequently, the balance between NO and free oxygen radicals is crucial in modulating the outcome after an ischaemic insult.
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PMID:Role of nitric oxide and oxidative stress in ischaemic myocardial injury and preconditioning. 1271 3

A 54-year-old man with diabetes mellitus, peripheral vascular disease, and hypertension was admitted to the hospital for an acute exacerbation of chronic heart failure. Therapy with intravenous furosemide and oral losartan 100 mg twice/day was begun. Ten days later, the patient's blood urea nitrogen and serum creatinine levels rose and peaked at 110 and 6.0 mg/dl, respectively. His serum potassium level increased to 5.7 mg/dl, urine output dropped to 400 ml over 24 hours, and mental status changes occurred. Magnetic resonance angiography revealed bilateral renal artery stenosis. After losartan was discontinued and hemodialysis was performed for 3 consecutive days, the patient's renal function returned to his baseline level. Reports in the medical literature reinforce the importance of recognizing that angiotensin-converting enzyme inhibitors should be used with caution in patients with bilateral renal artery stenosis. However, the literature is not as definitive about using of angiotensin II receptor blockers (ARBs) in these patients. Our patient's experience suggests that ARBs should be used with caution in patients with bilateral renal artery stenosis. Clinicians should be aware that renal failure might occur when using ARBs in these patients.
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PMID:Acute renal failure secondary to angiotensin II receptor blockade in a patient with bilateral renal artery stenosis. 1516 10

Increasing evidence suggests that oxidative and nitrosative stress play an important role in regulation of cardiac myocyte growth and survival. The cardiovascular system is continuously exposed to both reactive oxygen species (ROS) and nitrogen species (RNS), collectively termed reactive inflammatory species (RIS), and imbalances between the enzymes that regulate their bioavailability are associated with cardiac hypertrophy and the pathogenesis of cardiomyopathies, myocardial infarction and heart failure. It is now clear that RIS act as critical regulators of cardiac myocyte hypertrophy and apoptosis through control of redox-sensitive signaling cascades, such as tyrosine kinases and phosphatases, protein kinase C, and mitogen-activated protein kinases. This review will focus on the mechanisms by which ROS/RNS modulate cardiac myocyte growth and apoptosis induced by neurohormones and cytokines, and will discuss evidence for a role in the pathophysiology of heart failure.
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PMID:Regulation of hypertrophic and apoptotic signaling pathways by reactive oxygen species in cardiac myocytes. 1458 46

We investigated the nutritional adequacy and energy availability in 57 normal-weight patients with chronic heart failure (HF) and 49 matched healthy sedentary subjects. We found that the chronic HF patients had a higher total energy expenditure (1,700 +/- 53 vs 1,950 +/- 43 kcal/day; p <0.01), a negative calorie balance (104 +/- 35 vs -186 +/- 40 kcal/day; p <0.01), a negative nitrogen balance (2.2 +/- 0.5 vs -1.7 +/- 0.4 g/day; p <0.01), and a hypercatabolic hormonal status (cortisol/insulin ratio 32 +/- 1.7 vs 65 +/- 5.1; p <0.01). We conclude that patients with chronic HF had an inadequate calorie intake to support energetic needs for daily activities, with consequent important protein breakdown that causes muscular wasting.
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PMID:Inadequate nutritional intake for daily life activity of clinically stable patients with chronic heart failure. 1509 5

Heart failure is a common, progressive, complex clinical syndrome with high morbidity and mortality. Coronary artery disease is its most common cause. The evaluation of symptomatic patients with suspected heart failure is directed at confirming the diagnosis, determining the cause, identifying concomitant illnesses, establishing the severity of heart failure, and guiding therapy. The initial evaluation should include a focused history and physical examination, a chest radiograph, and an electrocardiogram. The presence of heart failure can be confirmed by an echocardiogram. Heart failure is highly unlikely in the absence of dyspnea and an abnormal chest radiograph or electrocardiogram. Radionuclide angiography or contrast cineangiography may be necessary when clinical suspicion for heart failure is high and the echocardiogram is equivocal. Patients with confirmed heart failure should undergo additional testing, including a more detailed history and physical examination; a complete blood count; blood glucose measurement; liver function tests; serum electrolyte, blood urea nitrogen, and creatinine measurements; lipid panel; urinalysis; and thyroid-stimulating hormone level. A serum ferritin level, human immunodeficiency virus test, antinuclear antibody assays, rheumatoid factor test, or metanephrine measurements may be required in selected patients. Patients with coronary artery disease, hypertension, diabetes mellitus, exposure to cardiotoxic drugs, alcohol abuse, or a family history of cardiomyopathy are at high risk for heart failure and may benefit from routine screening.
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PMID:Diagnosis of heart failure in adults. 1560 63

The recent determination that Angeli's salt may have clinical application as a nitrogen oxide donor for treatment of cardiovascular diseases such as heart failure has led to renewed interest in the mechanism and products of thermal decomposition of Angeli's salt under physiological conditions. In this report, several mechanisms are evaluated experimentally and by quantum mechanical calculations to determine whether HNO is in fact released from Angeli's salt in neutral, aerobic solution. The mechanism of product autoxidation is also considered.
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PMID:Mechanism of aerobic decomposition of Angeli's salt (sodium trioxodinitrate) at physiological pH. 1564 98


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