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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The pathogenesis of hypertension in haemodialyzed uraemic patients is multifactorial. The following are involved: sodium and water retention as a result of the impaired excretory capacity of the kidneys, excessively increased activity of the RAAS and sympathetic nerve, increased levels of the vascular constrictor endothelin-1, cumulation of endogenous inhibitors of NO synthesis and reduced formation of vasodepressor factors. As to other factors in the development of hypertension raised intracellular calcium associated with hyperparathyroidism may participate, the stiffness of calcified arteries, erythropoietin treatment and preexisting essential hypertension. Treatment comprises salt restriction below 5 g/day, systematic control of the volume of extracellular fluid by ultrafiltration during every haemodialysis to the level of so-called dry weight and pharmacological treatment in patients where volume control dos not suffice. All drug groups are used. In their selection contraindications are taken into consideration as well as co-morbidity, the dialyzability of antihypertensive drugs and compelling evidence. In patients with a preserved residual diuresis furosemide is administered--125-750 mg/day. Beta-blockers are indicated in patients with IHD, in particular after IM. Calcium blockers are recommended in ventricular hypertrophy and diastolic dysfunction, when beta-blockers are contraindicated and in elderly patients. ACEI indicated in congestive heart failure and left ventricular hypertrophy with systolic dysfunction. Inhibitors of AT1 receptors are an alternative in case of undesirable effects od ACEI. Alpha-blockers and central alpha agonists are used mainly in combinations. In case of failure the haemodialyzation method can be altered or changing the patients to CAPD may be considered. The relationship between BP and the survival of haemodialyzed patients is bimodal. An adverse effect is exerted by a high as well as low BP and in particular by interdialyzation hypotension. The target BP for the haemodialyzed population has not been defined so far. There is, however, evidence that a high BP is independently associated with the de novo development of IHD and MAP above 106 mm Hg with de novo development of cardiac failure. MAP below 98 mm Hg minimalizes the development and progression of left ventricular hypertrophy and MAP below 106 mm Hg the development of heart failure. Long-term survival for 15 and more years is statistically significantly associated with MAP lower than 99 mm Hg.
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PMID:[Hypertension in hemodialyzed uremic patients]. 1095 54

Since the first publication of isosorbide mononitrate 30% immediate-release 70% sustained-release (IR-SR) formulation in 1985, a considerable body of literature concerning its clinical efficacy and safety has become available. Theoretically, the formulation has the advantage over conventional isosorbide mononitrate or dinitrate (ISMN/ISDN) that it has a simpler and more predictable pharmacokinetic profile. The objectives of this paper are to review published data so far and to see whether the theoretical advantages translate into better clinical effectiveness. 1. After oral administration, isosorbide mononitrate IR-SR has a rapid onset of action (30 minutes), and effects are evident for up to 17 hours. 2. The antianginal effects of once-daily isosorbide mononitrate IR-SR increased with increasing dosages, were generally larger than those of either placebo or equipotent doses of conventional ISMN/ISDN, and were somewhat larger than those of the beta blocker bupranolol. The effects were generally similar to those of sustained release nifedipine. 3. Patients showed significantly greater improvement in some quality-of-life indices with once-daily isosorbide mononitrate IR-SR than with twice or three times daily regimens of conventional ISMN/ISDN. This was particularly so with mobility, psychological distress, and life satisfaction indices. 4. Tolerance did not develop after 13 months of once daily isosorbide dinitrate IR-SR. No rebound increase in incidence of ischemic episodes was observed after discontinuation of treatment. 5. Long-term efficacy data both of isosorbide mononitrate IR-SR and of conventional ISMN/ISDN are limited so far. Large studies in patients with angina pectoris and patients with heart failure addressing long-term effects are ongoing, and some of the data will be completed within the next months. Isosorbide mononitrate IR-SR has a rapid onset of action and has been shown to be clinically efficient and, in addition, to be more so than conventional ISMN / ISDN. Nitrate tolerance with continued use of the formulation has not yet been reported. Long-term effects on morbidity and mortality are currently being assessed.
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PMID:Isosorbide mononitrate 30% immediate-release 70% sustained-release formulation: a review. DUMQOL (DUtch Mononitrate Quality of Life) Study Group. 1095 15

Clinical observations suggest that flecainide might pass the placenta more easily than digoxin, and that its transfer is less disturbed in case of hydrops fetalis than that of digoxin. The purpose of the study was to compare the materno-fetal transplacental transfer of digoxin, flecainide, and amiodarone, another antiarrhythmic agent used in the treatment of fetal tachyarrhythmia, and to assess the effect of an elevated umbilical venous pressure (UVP) on the transfer rate. Isolated lobules of 16 human placentas were dually perfused after spontaneous delivery or caesarean section. The transplacental transfer (area under the curve in the maternal compartment [maternal AUC], area under the curve in the fetal compartment [fetal AUC], kinetic parameters) of digoxin, flecainide, and amiodarone was calculated after these drugs were added to the maternal circuit. In five experiments, the effect of increased UVP on the transplacental transfer rate was assessed by elevating the UVP by 10 cm H2O. Flecainide efflux out of the maternal compartment was significantly greater than that of digoxin (maternal AUC 57.4% +/- 5.1 %/min vs 73.9% +/- 1.5%/min), whereas the flecainide influx into the fetal circulation was smaller (fetal AUC 9.3% +/- 4.1%/min vs 11.5% +/- 2.0%/min). Only in 50% of the experiments were the smallest amounts of amiodarone detectable in the fetal compartment. An elevation of the UVP reduced the influx of digoxin and flecainide into the fetal compartment (fetal AUC) from 11.5% +/- 2.0%/min to 7.4% +/- 1.9%/min and from 9.3% +/- 4.1% to 4.7% +/- 1.4%/min, respectively. Materno-fetal transplacental transfer of digoxin, flecainide, and amiodarone decreases in this sequence. Fetal cardiac insufficiency accompanied by an elevation of the UVP might reduce the transplacental transfer of these drugs, although no significant difference could be found between the reduction of transfer of digoxin and flecainide.
Ther Drug Monit 2000 Oct
PMID:Digoxin, flecainide, and amiodarone transfer across the placenta and the effects of an elevated umbilical venous pressure on the transfer rate. 1103 64

The objective of this study was to determine the accuracy of administrative data (by use of hospital discharge codes) for measuring comorbidity in patients with heart disease. One thousand seven hundred and sixty-five medical records of subjects admitted to hospital for AMI, unstable angina, angina pectoris, chronic IHD or heart failure were reviewed. The number and types of comorbidities were determined from the medical records (regarded as the "gold standard"). These were compared with the 10 discharge codes obtained from the hospital administrative records (referred to as the "administrative data"). The rate of false-negative and false-positive comorbidity diagnoses were determined. Twenty of the 21 comorbidities studied were underreported in the administrative data. For these 20 comorbidities, the median false-negative rate was 49.5% and ranged from 11% for diabetes to 100% for dementia. False-positive rates were low, less than 1.5%, except for chronic arrythmia (4.8%) and hypertension (4.2%). Mean percent agreement was high, ranging from 88% for hypertension to 100% for AIDS/HIV. Administrative data based on hospital discharge codes consistently underestimate the presence of comorbid conditions in our population. This has implications for administrators when estimating mortality, length of stay and disability. Researchers also need to be aware when using administrative data based on hospital discharge codes to assess subject's comorbidities that they may be widely underreported.
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PMID:Accuracy of administrative data to assess comorbidity in patients with heart disease. an Australian perspective. 1143 9

Patients with advanced congestive heart failure have a very high 5-year mortality despite medical treatment. In such patients, heart transplantation is the treatment of choice. The number of patients awaiting transplantation is several-fold higher than the number of procedures performed. Heart transplantation therapy has numerous limitations and is associated with serious complications. The left ventricular assist device is a step towards this goal. It can be attached to the weakened left ventricle to temporarily increase blood flow to the body. The use of left ventricular assist devices helps the failing heart to recover and extends the duration over which a patient's heart can wait for a replacement donor heart. This therapy is in use for only up to a few months. The total artificial heart, Jarvik-7, first implanted in 1982, did not succeed due to a poor quality of a patient's life and numerous complications leading to death. Recently, a successful implantation of the AbioCor (Abiomed), the first fully implantable replacement heart, was accomplished. The AbioCor's internal battery system eliminates the need for the patient to be permanently immobilized through tubes or wires connected to an external power source. Innovative transcutaneous energy transmission permits the recharging of internal batteries. The total artificial heart will require adapting it to different human body sizes as well as further improving its technical features. The total artificial heart is a remedy of the future coming to fruition right now, giving a chance to numerous heart failure patients by extending and improving their lives.
Med Sci Monit 2002 Mar
PMID:The artificial heart-- past, present, and future. 1188 44

The aim of this review is to outline the characteristics of pulmonary circulation in health and disease and to define the value of exhaled NO (eNO) as a means to assess the involvement of pulmonary circulation in pathology. The discovery of the endocrine role of the endothelium has generated great interest in its potential role in regulating the vascular tone of the pulmonary vascular bed. Nitric oxide (NO)-mediated, endothelium-dependent relaxation has been demonstrated in the pulmonary arteries of animals and humans. Changes in the NO pathway in pulmonary hypertension are not completely understood. It is clear that NO has an important role in modulating the response to acute hypoxia, increased flow, and shear stress. The amount of exhaled NO (eNO) in different species may be easily measured, reflecting the overall NO metabolism from the lung (thus including epithelial, endothelial and other cell activity). The development of pulmonary hypertension secondary to systemic (systemic sclerosis, chronic heart failure) or pulmonary (COPD) diseases appears to be associated with a decrease in eNO production both at rest and during exercise. Chronic inhalation of NO appears to protect against pulmonary hypertension in animal models. Exhaled NO is attracting interest for its in vivo ability to represent the features of pulmonary circulation in pathology.
Med Sci Monit 2002 Aug
PMID:Nitric oxide and pulmonary circulation. 1216 55

The authors summarize results of trials with acetysalicyl acid (ASA) in patients with ischaemic heart disease and in particular with chronic cardiac failure. They draw attention to the relatively frequent use this drug in common practice, although so far not a single trial was completed which would prove the effect of acetylsalicyl acid on long-term mortality. The authors discuss also possible interactions of acetylsalicyl acid and ACE inhibitors which in retrospective analyses indicate possible veakening of the ACE-I when administered concurrently with ASA in cardiac failure. The authors mention also other antiaggregation drugs, which similarly as ASA, significantly reduce the mortality in acute coronary syndrome. Their long-term administration is however not associated with further improvement of the diagnosis. Trials are mentioned which compare antiaggregation and anticolagulation treatment in patients with ischaemic heart disease. They analyze also the effect of dosage (benefit vs. risk). After ASA > 300 mg there are more frequent complications, and without a proved effect on total mortality, while doses < or = 100 mg seem to be safer but there is evidence that they are effective in reducing the total mortality of patients with IHD and/or cardiac failure.
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PMID:[Acetylsalicylic acid (ASA)--is everything clear?]. 1242 98

A novel algorithm for real-time detection and prediction of the dicrotic notch from aortic pressure waves was evaluated in arrhythmic aortic pressure signals from heart failure patients. A simplified model of the arterial tree was used to calculate real-time aortic flow from aortic pressure. The dicrotic notch was detected at the first negative dip from the calculated flow, prediction of the notch was performed using a percentage of the decreasing flow. The performance of the real-time dicrotic notch detection algorithm (RTDND) was evaluated during severe arrhythmia from aortic pressure signals of 12 patients. The RTDND was able to detect the dicrotic notch in 98.1%. No false positive dicrotic notch identifications were observed. Prediction of the dicrotic notch was tested at 40%, 20%, and 0% of the decreasing calculated aortic flow. The mean time-delays to the notch were 68 +/- 14 ms, 55 +/- 12 ms, and 43 +/- 8 ms, respectively. Given these small variability, intra-beat prediction of the dicrotic notch may be used for real-time intra-aortic balloon counterpulsation inflation timing.
J Clin Monit Comput
PMID:Performance of a real-time dicrotic notch detection and prediction algorithm in arrhythmic human aortic pressure signals. 1245 34

Clinical suspicion of congestive heart failure (CHF) always requires a careful diagnostic workup. This comprises the verification of the presence of CHF (in contrast to other conditions that cause nonspecific phenomena such as shortness of breath and edema), evaluation of the underlying cause of heart failure, and assessment of left ventricular (LV) systolic function. In addition to clinical examination, echocardiography is warranted in most cases. On the basis of this information, patients can be selected for further studies, such as exercise testing, cardiac catheterization and coronary angiography. In view of the serious prognosis of heart failure, especially systolic CHF, the threshold for specialist consultation should be low. Although the classification of CHF into systolic and diastolic forms is complex, clinically meaningful data can be derived simply by determining whether LV systolic function is impaired (predominantly systolic CHF) or not (probable diastolic CHF). In the latter case, treatment is mainly symptomatic in addition to the management of the underlying condition (e.g. hypertension). In systolic CHF, considerable therapeutic advances have recently been made and it is important that patients receive appropriate care to improve their prognosis. These measures include angiotensin-converting enzyme inhibitors, beta-blockers and spironolactone.
Heart Fail Monit 2001
PMID:Systolic and diastolic heart failure--diagnostic and therapeutic dilemmas. 1263 72

Congestive chronic heart failure (CHF) is a progressive disorder in which a complex interaction of haemodynamic, neurohormonal and metabolic disturbances leads to subsequent immune activation. The greatest attention has been given to the concept that the progression of heart failure is due to neurohormonal abnormalities and this has led to substantial therapeutic benefits for CHF. The aim of this review is to describe a number of the interactions between neurohormonal pathways and metabolic problems relevant in CHF. Besides the renin-angiotensin-aldosterone-system, steroid and thyroid hormones, growth factors, insulin and inflammatory cytokines (e.g. tumour necrosis factor-alpha [TNF-alpha]) are considered. TNF-alpha is potentially a key molecule with enormous interactive opportunities within a regulatory network of energy metabolism, immune function and neuroendocrine and hormonal function. The most dramatic metabolic problem in heart failure patients is the development of cardiac cachexia. Currently, no specific therapy exists and the prognosis is poor. There are promising approaches (counteracting TNF-alpha or applying anabolic growth factors) but these are not without risk and are expensive, and their application may, therefore, be limited to certain subgroups of patients. In the future, it will not be enough to monitor cardiac function and symptomatic status in heart failure patients. Rather, the patients' metabolic status may need to be taken, as well as an assessment of peak oxygen consumption, body composition and hormonal status.
Heart Fail Monit 2000
PMID:Chronic heart failure as a metabolic disorder. 1263 73


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