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

Heart failure (HF) is a common disorder that is associated with significant mortality and morbidity. However, the diagnosis of HF may at times be difficult when using conventional tools. The cardiac natriuretic peptides, particularly brain (B-type) natriuretic peptide (BNP), have evolved to be useful biomarkers of cardiac function and prognosis in HF and other cardiovascular disorders. Multiple observational studies have established the close association between plasma BNP as well as the N-terminal fragment of the BNP prohormone (NT-proBNP) with the diagnosis of HF and an independent prediction of mortality and HF events. Although there are confounding variables to consider, when used in the correct clinical settings, BNP or NT-proBNP testing can be extremely useful. Furthermore, preliminary data from randomized controlled trials suggest that knowledge of BNP and/or NT-proBNP level may optimize the management of patients with HF. Large-scale randomized controlled trials that evaluate BNP/NT-proBNP-guided therapy are ongoing.
Heart Fail Monit 2005
PMID:BNP in the diagnosis and risk stratification of heart failure. 1623 98

Recent studies have demonstrated the inefficacy of nutritional supplements containing various combinations of vitamins and minerals for otherwise healthy elderly people and patients with ischemic heart disease. However, patients with chronic heart failure (CHF) have, up until recently, been excluded from such studies. CHF has a high mortality and morbidity and patients are often elderly with poor general nutrition and high levels of micronutrient deficiency. It is in this population that nutritional supplementation has the most potential benefit. Evidence is accumulating that a strategy of long-term highdose multiple micronutrient supplementation might improve symptoms and cardiac function in elderly patients with CHF. In this article, we review the effects of individual micronutrients and how they might impact on CHF, and present recent data that dietary supplementation might offer an addition to standard therapy for CHF.
Heart Fail Monit 2005
PMID:Chronic heart failure and multiple micronutrient supplementation: realistic hope or idealistic conjecture? 1623 99

A classic hallmark of chronic heart failure (CHF) is exercise intolerance; however, the extent of exercise limitation is not correlated with the degree of left ventricular dysfunction. Over the past 2 decades it has become more and more evident that peripheral factors, such as skeletal muscle dysfunction, ventilatory abnormalities, and endothelial dysfunction, contribute the greater part to the limitation of exercise capacity. The molecular and pathophysiological changes observed in these organ systems are not always specific to the underlying CHF but rather represent a common pathway that is activated in several chronic disease processes, including severe chronic obstructive pulmonary disease, cancer, and in the normal aging process. A major contributing factor for skeletal muscle catabolism (i.e. elevated cytokine expression in the skeletal muscle) can be found in both normal healthy aging and in heart failure patients. It is reasonable to assume that the overlap of aging and CHF-associated changes in the skeletal muscle partially explains the disabling consequences of the CHF syndrome among elderly patients (nearly 80% of all patients hospitalized for CHF are >65 years old). Peripheral alterations in CHF are often not adequately treated in routine clinical care since standard pharmacological therapy is still focused on the cardiac function and neurohormonal alteration. Exercise training is a guideline-oriented adjuvant therapy with well-documented beneficial effects on exercise tolerance, skeletal muscle function, endothelial function, and respiration. In this review, the effects of exercise in aging and in CHF are compared and the parallel mechanisms are explored.
Heart Fail Monit 2005
PMID:Aging and heart failure--similar syndromes of exercise intolerance? Implications for exercise-based interventions. 1623

Diabetes mellitus and heart failure frequently coexist and often lead to poor prognosis. However, data regarding glycemic control and treatment patterns in heart failure are sparse, partly because clinical studies specifically targeting diabetic heart failure patients are lacking. In registry data, although patients with heart failure often have poor glycemic control, almost all hypoglycemic drug classes have safety concerns regarding use in the setting of heart failure. Furthermore, there is a poor understanding of the relative contributions of glucose and fatty acids to the metabolism of the failing heart and a poor understanding of the pathogenesis of heart failure in patients with diabetes mellitus.
Heart Fail Monit 2006
PMID:Glycemic control and treatment patterns in patients with heart failure. 1654 30

The number of patients with newly diagnosed heart failure continues to grow worldwide, to some extent reflecting the increase in survival after acute coronary syndromes and the aging of the population. The search for new and effective therapies for this condition remains a priority in the 21st century. The use of beta-blockers is now well established in the clinical context of mild and moderate systolic heart failure. The effects of beta-blockade on mortality are additive to those with angiotensin-converting enzyme inhibitor therapy. Recently completed, large, randomized trials provided strong evidence for the use of beta-blockers in severe (NYHA functional class IV) heart failure and in asymptomatic patients with left ventricular systolic dysfunction and recent myocardial infarction. Obviously, patient selection still remains the key to the safe use of beta-blockers in patients with heart failure. Further data from clinical trials have emerged to support similar benefits in terms of mortality and morbidity, a good safety record, and tolerability in patients at extremes of age (children and adults >70 years of age) and in specific clinical circumstances (including diabetes, chronic obstructive airways disease, renal failure, and atrial fibrillation). Recent use of beta-blockers with vasodilatory properties in patients with heart failure and preserved systolic function (so-called diastolic heart failure) appears promising but will require large-scale, long-term trials prior to widespread clinical use.
Heart Fail Monit 2006
PMID:A continued role for beta-blocker therapy in heart failure. 1654 31

The functional relevance of autoantibodies (Abs) against cardiac myosin (CM) in clinical idiopathic dilated cardiomyopathy (DCM) remains controversial. The study sought to determine effects of human Abs affinity-purified (AF) by immunoaffinity column chromotography on excitation-contraction coupling in isolated myocytes. Effects of CM-Abs from heart failure patients with DCM (n=19) and ischemic heart disease (IHD, n=19) on contractility, L-type Ca2+ current, and Ca2+ transients in continuously perfused rat ventricular myocytes were studied. Immunofluorescence studies using confocal microscopy were carried out to determine whether Abs were internalized. AF-Abs from either group did not differ in IgG titer but differed in their elution profiles. The IgG3 subclass response was higher in AF fractions from DCM (21%) than IHD (5%) patients. The Abs reduced the capacity of field-stimulated myocytes to contract in a dose-dependent manner. Inhibition of contraction, as a percentage of untreated cells, was greater with DCM than IHD-Abs (P=0.004), and the effect was independent of Ab titer. An increase in frequency of the beating myocytes (0.2 to 3.0 Hz) raised peak systolic and diastolic levels of [Ca2+]i of cells treated with DCM but not IHD-Abs (P<0.005). The AF-Abs were not internalized by myocytes and had no effect on L-type Ca2+ currents. The altered sensitivity of the myofilaments to [Ca2+]i by CM-Abs may represent a potential mechanism of autoantibody-mediated impairment in clinical DCM.
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PMID:Human cardiac myosin autoantibodies impair myocyte contractility: a cause-and-effect relationship. 1658 73

Recent studies suggest that adipose tissue hormones ("adipokines") are involved in the pathogenesis of various complications of obesity, including hyperlipidemia, diabetes mellitus, arterial hypertension, atherosclerosis, and heart failure. Apelin and visfatin are two recently described adipokines, although they are also synthesized outside adipose tissue. Apelin exists in at least three forms, consisting of 13, 17, or 36 amino acids, all originating from a common 77-amino-acid precursor. In the cardiovascular system, apelin elicits endothelium-dependent, nitric oxide-mediated vasorelaxation and reduces arterial blood pressure. In addition, apelin demonstrates potent and long-lasting positive inotropic activity which is preserved even in injured myocardium and is not accompanied by myocardial hypertrophy. Apelin synthesis in adipocytes is stimulated by insulin, and plasma apelin level markedly increases in obesity associated with insulin resistance and hyperinsulinemia. In addition to regulating cardiovascular function, apelin inhibits water intake and vasopressin production. Visfatin, previously recognized as a pre-B cell colony-enhancing factor (PBEF), is abundantly expressed in visceral adipose tissue and is upregulated in some, but not all, animal models of obesity. Preliminary studies suggest that plasma visfatin concentration is also increased in humans with abdominal obesity and/or type 2 diabetes mellitus. Visfatin binds to the insulin receptor at a site distinct from insulin and exerts hypoglycemic effect by reducing glucose release from hepatocytes and stimulating glucose utilization in peripheral tissues. Thus, apelin and visfatin are unique among adipose tissue hormones in that they are upregulated in the obese state and both exert primarily beneficial effects.
Med Sci Monit 2006 Jun
PMID:Apelin and visfatin: unique "beneficial" adipokines upregulated in obesity? 1694 Sep 39

The authors present a case of an elderly female patient with heart failure and renal dysfunction treated with digoxin, where 2 commercial immunoassay methods (DRI, Microgenics, and DGNA, Dade Behring) showed a clinically very significant discrepancy on the same plasma sample, viz. 0.5 and 2.3 nmol/L, respectively. The sample was also referred to a third external laboratory that returned a result of 0.9 nmol/L using mFPIA (AxSYM, Abbott). Subsequent ultrafiltration (30,000 Dalton) on the sample essentially eliminated the difference, suggesting an interference from a large molecular weight compound(s), potentially the well-described digoxin-like immunoreactive substance(s) (DLIS). Although further study is required to verify that the DLIS implicated was indeed the interfering species, it does again highlight the importance of careful method selection in the clinical therapeutic drug monitoring laboratory to ensure that such well-established potential problems do not result in inappropriate dosage reduction with consequent lack of adequate drug exposure and serious clinical sequelae.
Ther Drug Monit 2006 Jun
PMID:Suspected DLIS interference in the dimension DGNA digoxin assay method and the clinical application of the revised digoxin target range. 1677 33

Hypertension is a major risk factor for the development of cardiac failure. Patients with severe heart failure and left ventricular ejection fraction <40% are excluded from the majority of hypertension trials. The European Guidelines recommend treatment of hypertension in patients with heart failure and the introduction of blood pressure-lowering drugs that deal with the underlying disease. Several of the drugs may be needed in combination to achieve target blood pressure.
Heart Fail Monit 2006
PMID:Treatment of hypertension in patients with congestive cardiac failure. 1681 75

Heart failure is a multifactorial and complex debilitating disease facing limitations in available pharmacological therapeutics. To cure such a disease, cardiac regeneration has been envisioned using stem cells. A few clinical trials using bone marrow-derived stem cells have been carried out without conclusive results. Stem cells of other origins should therefore be considered for future trials. In this article, the advantages and disadvantages of the most promising stem cells to be used in cell therapy are reviewed. The remaining challenges of cell therapy of heart failure are also presented.
Heart Fail Monit 2006
PMID:Stem cell therapy in heart failure: where do we stand and where are we heading? 1681 76


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