Acute Hemodynamic Effects of Tolvaptan, a Vasopressin V2 Receptor Blocker, in Patients With Symptomatic Heart Failure and Systolic Dysfunction

Udelson, James E.; Orlandi, Cesare; Ouyang, John; Krasa, Holly B.; Zimmer, Christopher; Frivold, Geir; Haught, W. Herbert; Meymandi, Sheiba; Macarie, Cezar; Raef, Dimitar; Wedge, Patricia; Konstam, Marvin A.; Gheorghiade, Mihai

doi:10.1016/j.jacc.2008.08.013

Cited by 160 publications

(41 citation statements)

References 17 publications

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“…Previous clinical studies, such as EVEREST and the Effect of Tolvaptan on Hemodynamic Parameters in Subjects with Heart Failure (ECLIPSE) trial, 10,11,13,17 have shown that tolvaptan increases urine output in a dose-dependent manner. However, no significant differences were reported for the secondary end points of BP, HR, systemic vascular resistance, or cardiac index.…”

Section: Discussionmentioning

confidence: 99%

Tolvaptan Improves Left Ventricular Dysfunction after Myocardial Infarction in Rats

Yamazaki

Izumi

Nakamura

et al. 2012

Circ: Heart Failure

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Arginine vasopressin (AVP) is a 9-amino acid peptide secreted from the posterior pituitary, in response to high plasma osmolality and hypotension. AVP is known to play an important role in water metabolism by inducing water reabsorption at the renal collecting duct via the V 2 receptor (V 2 R). AVP is also involved in the maintenance of blood pressure © 2012 American Heart Association, Inc. Background-Arginine vasopressin, which promotes the reabsorption of renal water is increased in chronic heart failure.Here, we compared the effects of tolvaptan, a newly developed nonpeptide V 2 receptor antagonist, with those of furosemide, a loop diuretic, and a combination of these 2 agents in rats with left ventricular dysfunction after myocardial infarction (MI). Methods and Results-After 10 weeks of MI induction, the rats were separated them into the following 6 groups adjusted to the infarct size: a vehicle group, a group treated with 15 mg·kg tolvaptan. Each treatment agent was administered for 4 weeks, and all groups had similar blood pressure levels and infarct size. The tolvaptan-treated groups were found to have lower levels of left ventricular end-diastolic and systolic cardiac volumes than the vehicle group did. Furthermore, the improvement in the ejection fraction in the tolvaptan-treated groups was significantly greater than those in the vehicle group. ED-1 immunostaining and Sirius red staining revealed that tolvaptan significantly repressed MI-induced macrophage infiltration and interstitial fibrosis in the left ventricle, respectively. Tolvaptan attenuated the MI-induced mRNA expressions of atrial and brain natriuretic peptides, monocyte chemotactic protein-1, transforming growth factor-β1, arginine vasopressin V 1a receptor, and endothelin-1 in the marginal infarct region. Conclusions-Tolvaptan may improve cardiac dysfunction after MI, which is partially mediated by the suppression of V 1a receptor, neurohumoral activation and inflammation. (Circ Heart Fail. 2012;5:794-802.)

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Section: Discussionmentioning

confidence: 99%

Tolvaptan Improves Left Ventricular Dysfunction after Myocardial Infarction in Rats

Yamazaki

Izumi

Nakamura

et al. 2012

Circ: Heart Failure

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“…Some studies have shown a beneficial effect of tolvaptan on renal function in heart failure [10], and tolvaptan has also been reported to decrease the pulmonary capillary wedge pressure and dose-dependently increase urine output in patients with heart failure [11]. …”

Section: Introductionmentioning

confidence: 99%

Safety and Efficacy of Tolvaptan for the Prevention of Contrast-Induced Acute Kidney Injury in Patients with Heart Failure and Chronic Kidney Disease

et al. 2018

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Background: Tolvaptan is a promising drug for the prevention of contrast-induced acute kidney injury (CI-AKI) because it induces aquaresis without adversely affecting renal hemodynamics. CI-AKI is a major cause of acute renal failure associated with increased morbidity and mortality. Objective: To investigate the effectiveness of different doses of tolvaptan for the prevention of CI-AKI. Method: Ninety-one consecutive patients with congestive heart failure (CHF) and chronic kidney disease (CKD) were prospectively enrolled as the tolvaptan group in this study (T-group; 7.5-mg: n = 42, 15-mg: n = 49). In addition, 91 consecutive patients with CHF and CKD were collected retrospectively as a control group (C-group, n = 91). All patients received continuous intravenous infusion of isotonic saline, and tolvaptan was administered to the T-group. Results: One patient developed CI-AKI in the T-group versus 3 in the C-group (1.1 vs. 3.3%, p = 0.61). On the other hand, the change of serum creatinine in the T-group was lower than that in the C-group. Additionally, in the 7.5-mg group, serum creatinine was unchanged up to 72 h after contrast administration, showing a significant difference from the 15-mg group (–0.00 ± 0.09 vs. 0.05 ± 0.12 mg/dL, p = 0.009). Similarly, the change of eGFR was significantly smaller in the 7.5-mg group than that in the 15-mg group (0.7 ± 5.4 vs. –2.8 ± 5.1 mL/min/1.73 m², p = 0.002). No patient required hemodialysis and there was no prolongation of hospitalization due to exacerbation of heart failure. Conclusions: Compared to hydration alone, tolvaptan combined with hydration could be a safer method for preventing CI-AKI while avoiding exacerbation of heart failure, and a dosage of 7.5-mg might be safer than 15-mg.

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“…The results suggest that tolvaptan reduces pulmonary capillary wedge pressure and decreases filling pressure without adversely affecting blood pressure or renal function [59]. …”

Section: Acute Crs (Type 1)mentioning

confidence: 99%

Pharmacologic Therapies for Chronic and Acute Decompensated Heart Failure: Specific Insights on Cardiorenal Syndromes

et al. 2014

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In the setting of cardiorenal syndrome(s) (CRS), the main pathophysiological triggers of renal disease progression include increases in renal venous pressure, maladaptive activation of the renin-angiotensin-aldosterone (RAAS) and the sympathetic nervous systems, and a chronic inflammatory state. In acute decompensated heart failure (HF)/type 1 CRS, diuretics remain the mainstay of first-line therapy in order to prevent congestion and renal venous hypertension. In chronic HF/type 2 CRS, RAAS multiple inhibition has been recommended in addition to diuretics. However, cotreatment with angiotensin-converting enzyme inhibitors/angiotensin receptor blockers and mineralocorticoid receptor antagonists is likely to lead to more frequent occurrences of hyperkalemia and worsening renal function. In this review, the main pharmacological therapies of acute and chronic CRS are discussed regarding their indication as well as intended and side effects. Future therapies are suggested, underlining that a multidisciplinary approach to a deeper understanding of the pathophysiology of CRS is still required to improve specific treatment and clinical outcome.

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Acute Hemodynamic Effects of Tolvaptan, a Vasopressin V2 Receptor Blocker, in Patients With Symptomatic Heart Failure and Systolic Dysfunction

Cited by 160 publications

References 17 publications

Tolvaptan Improves Left Ventricular Dysfunction after Myocardial Infarction in Rats

Tolvaptan Improves Left Ventricular Dysfunction after Myocardial Infarction in Rats

Safety and Efficacy of Tolvaptan for the Prevention of Contrast-Induced Acute Kidney Injury in Patients with Heart Failure and Chronic Kidney Disease

Pharmacologic Therapies for Chronic and Acute Decompensated Heart Failure: Specific Insights on Cardiorenal Syndromes

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