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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An 87-year-old man had been treated under a diagnosis of idiopathic dilated cardiomyopathy and sick sinus syndrome since 1996. His heart failure was worsened by atrial fibrillation in August 2004. He received amiodarone from October 2004. He was admitted to our hospital with shortness of breath in February 2005. Chest radiography revealed a diffuse reticular shadow in the right lung field and pleural effusion. The diagnosis was interstitial pneumonitis induced by amiodarone. However, 10 days after the discontinuation of amiodarone, the serum sodium concentration fell to 114mEq/l. The blood and urine chemical data were consistent with syndrome of inappropriate antidiuretic hormone secretion (SIADH). The serum sodium concentration improved with fluid restriction. Clinicians should be aware that SIADH may occur during amiodarone therapy.
J Cardiol 2006 Oct
PMID:[Interstitial pneumonitis followed by syndrome of inappropriate antidiuretic hormone secretion induced by amiodarone therapy for dilated cardiomyopathy: a case report]. 1706 25

Vasopressin administration has been suggested during cardiopulmonary resuscitation, and a previous clinical trial has suggested that vasopressin is most effective when administered with epinephrine. Adult subjects (n = 325) who received > or =1 dose of intravenous epinephrine during cardiopulmonary resuscitation for nontraumatic, out-of-hospital cardiac arrest were randomly assigned to receive 40 IU of vasopressin (n = 167) or placebo (n = 158) as soon as possible after the first dose of epinephrine. The rate of return of pulses was similar between the vasopressin and placebo groups (31% vs 30%), as was the presence of pulses at the emergency department (19% vs 23%). No subgroup appeared to be differentially affected, and no effect of vasopressin was evident after adjustment for other clinical variables. Additional open-label vasopressin was administered by a physician after the study drug for 19 subjects in the placebo group and 27 subjects in the vasopressin group. Results were similar if these subjects were excluded or were assigned to an actual drug received. Survival duration for subjects admitted to the hospital did not differ between groups. In conclusion, vasopressin administered with epinephrine does not increase the rate of return of spontaneous circulation.
Am J Cardiol 2006 Nov 15
PMID:Usefulness of vasopressin administered with epinephrine during out-of-hospital cardiac arrest. 1713 21

While pharmaceutical innovation has been highly successful in reducing mortality in chronic heart failure, this has not been matched by similar success in decompensated heart failure syndromes. Despite outstanding issues over definitions and end points, we argue in this paper that an unprecedented wealth of pharmacologic innovation may soon transform the management of these challenging patients. Agents that target contractility, such as cardiac myosin activators and novel adenosine triphosphate-dependent transmembrane sodium-potassium pump inhibitors, provide inotropic support without arrhythmogenic increases in cytosolic calcium or side effects of more traditional agents. Adenosine receptor blockade may improve glomerular filtration and diuresis by exerting a direct beneficial effect on glomerular blood flow while vasopressin antagonists promote free water excretion without compromising renal function and may simultaneously inhibit myocardial remodeling. Urodilatin, the renally synthesized isoform of atrial natriuretic peptide, may improve pulmonary congestion via vasodilation and enhanced diuresis. Finally, metabolic modulators such as perhexiline may optimize myocardial energy utilization by shifting adenosine triphosphate production from free fatty acids to glucose, a unique and conceptually appealing approach to the management of heart failure. These advances allow optimism not only for the advancement of our understanding and management of decompensated heart failure syndromes but for the translational research effort in heart failure biology in general.
J Am Coll Cardiol 2006 Dec 19
PMID:Emerging therapies for the management of decompensated heart failure: from bench to bedside. 1717 76

Acute decompensated heart failure is the most common cause for hospitalization among patients over 65 years of age. It may result from new onset of ventricular dysfunction or, more typically, exacerbation of chronic heart failure symptoms. In-hospital mortality remains high for both systolic and diastolic forms of the disease. Therapy is largely empirical as few randomized, controlled trials have focused on this population and consensus practice guidelines are just beginning to be formulated. Treatment should be focused upon correction of volume overload, identifying potential precipitating causes, and optimizing vasodilator and beta-adrenergic blocker therapy. The majority of patients (>90%) will improve without the use of positive inotropic agents, which should be reserved for patients with refractory hypotension, cardiogenic shock, end-organ dysfunction, or failure to respond to conventional oral and/or intravenous diuretics and vasodilators. The role of aldosterone antagonists, biventricular pacing, and novel pharmacological agents including vasopressin antagonists, endothelin blockers, and calcium-sensitizing agents is also reviewed.
Curr Probl Cardiol 2007 Jun
PMID:Management of acute decompensated heart failure. 1753 3

In a national heart failure registry, hyponatremia (serum sodium < 130 mEq/L) was initially reported in 5% of patients and considered a risk factor for increased morbidity and mortality. In a chronic heart failure study, serum sodium level on admission predicted an increased length of stay for cardiovascular causes and increased mortality within 60 days of discharge. Hyponatremia in patients with congestive heart failure (CHF) is associated with a higher mortality rate. Also, by monitoring and increasing serum sodium levels during hospitalization for CHF, patient outcomes may improve. This review describes the pathophysiology of hyponatremia in relation to CHF, including the mechanism of action of vasopressin receptors in the kidney, and assesses the preclinical and clinical trials of vasopressin receptor antagonists--agents recently developed to treat hyponatremia. In hospitalized patients with CHF, hyponatremia plays a major role in poor outcomes. Vasopressin receptor antagonists have been shown to be safe and effective in clinical trials in patients with hyponatremia.
Clin Cardiol 2007 Nov
PMID:Hyponatremia and vasopressin antagonism in congestive heart failure. 1784 41

Acute heart failure syndrome (AHFS) is prevalent and costly, and clinical development of pharmacologic therapy remains challenging. Relieving congestion is still the central goal in the decompensated states, although the predominant approach remains the use of intravenous loop diuretics. Newer agents such as vasopressin receptor antagonists have yet to show incremental benefits. A resurgence of interest in vasodilator therapy has been supported by a better understanding of the pathophysiology of AHFS and the availability of nesiritide and other natriuretic peptides, but long-term clinical outcomes data are lacking and highly debated. Several promising drugs are currently undergoing clinical development for the treatment of AHFS, although many of the clinical challenges remain unresolved.
Cardiol Clin 2007 Nov
PMID:Pharmacologic therapy for acute heart failure. 1806 58

This article discusses the most important developments in heart failure reported during the last year. It contains a review of new findings on chronic heart failure, acute heart failure, cardiac resynchronization therapy, heart transplantation, with particular emphasis on the situation in Spain, and surgery in heart failure. In addition, the article describes progress in the treatment of anemia, vasopressin receptor antagonists, non-invasive ventilation, inotropic therapy, and resynchronization therapy in patients with heart failure and atrial fibrillation, and examines the current role of echocardiography in detecting asynchrony and in selecting patients.
Rev Esp Cardiol 2008 Feb
PMID:[Heart failure]. 1834 35

One of the most important comorbidities in heart failure is renal dysfunction. Diminished estimated glomerular filtration rate is a potent predictor of cardiovascular mortality and complications. On the other hand, worsening heart failure or acute decompensated heart failure can accelerate worsening of renal function--the so-called cardiorenal syndrome. Risk factors include hypertension, diabetes, elderly age, and prior history of heart or renal failure. The pathophysiology of the cardiorenal syndrome involves intrarenal hemodynamics, transrenal perfusion pressure and systemic neurohormonal factors. Clinical management of the patient with cardiorenal syndrome includes the challenge of diuretic resistance, which may involve correcting the underlying cause, combination diuretics or diuretic infusions. The key to improved outcome is the optimization of proven heart failure therapies. The use of vasodilator therapy is the current mainstay of treatment. Nesiritide, or recombinant B-type natriuretic peptide, has courted controversy regarding its role in cardiorenal syndrome. However, data are emerging that low doses appear to be renal-protective. Other more recent strategies include ultrafiltration, vasopressin antagonists and adenosine antagonists. All of these newer modalities promise more rapid volume removal, but their ultimate impact on survival or preservation of renal function is unknown at the present time. Because of the complex nature of these patients, and the compromised outcome, it is important that cardiologists, nephrologists and internists all work together toward the common goal of protecting the patient with cardiorenal syndrome, and use the best available evidence for management.
Can J Cardiol 2008 Jul
PMID:Cardiorenal syndrome in heart failure: a cardiologist's perspective. 1862 86

Antidiuretic hormone, also known as arginine vasopressin, is a hormone with a multitude of physiologic activities including the control of urinary free water excretion. Antidiuretic hormone also plays a role in vasoconstriction and has 3 receptors that have been identified. Vasopressin analogs and antagonists have been extensively studied in animal models as well as in humans. Because heart failure is associated with a state of water retention, several vasopressin antagonists have been evaluated for their potential aquaretic effect. Diuretics remain the mainstay of treatment in acute and chronic volume overload but are not shown to improve survival. In fact, they are associated with numerous side effects including hypotension, electrolyte abnormalities, worsening renal function, and activation of renin-angiotensin-aldosternone system. Tolvaptan, conivaptan, and lixivaptan are some of the vasopressin antagonists that have been studied in heart failure. The results were initially encouraging with alleviation of symptoms and effective aquaresis without worsening of hyponatremia or renal function, but yet failed to show any effect on mortality in heart failure. With an increasing number of more selective orally active vasopressin antagonists, further studies are underway to establish the role of "Vaptans" in the treatment of heart failure and other disease states with volume overload and hyponatremia.
Cardiol Rev
PMID:Vasopressin and vasopressin receptor antagonists in heart failure. 1909 65

Heart failure (HF) is still one of the most important causes of morbidity and mortality worldwide. Neurohormonal changes appear to play an important role in the development and continuation of HF. Among the mediators responsible for these changes, antidiuretic hormone (ADH) is probably the least known. However, elevated concentrations of ADH are frequently found in this syndrome and have prognostic value in addition to known biomarkers. Recent experimental studies and clinical trials have aroused interest in the possible benefits of ADH receptor antagonists. This article reviews the pathophysiological mechanisms of ADH in HF and the latest advances in ADH antagonism in the therapeutic management of HF.
Rev Port Cardiol 2009 Sep
PMID:The role of antidiuretic hormone in the pathophysiology and treatment of heart failure. 1999 8


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