New strategies for the management of acute decompensated heart failure

Koerner, Michael M.; Loebe, Matthias; Lisman, Kevin A.; Stetson, Sonny J.; Lafuente, Javier; Noon, George P.; Torre‐Amione, Guillermo

doi:10.1097/00001573-200105000-00002

Cited by 6 publications

(7 citation statements)

References 65 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The favorable electrochemical driving force for Na ϩ influx is maintained by the ouabain-sensitive basolateral Na ϩ /K ϩ -ATPase that also transports Na ϩ into the interstitial space (22). Hydrostatic pulmonary edema is a common complication of congestive heart failure, resulting in substantial morbidity and mortality (23,24). Moreover, acute pulmonary edema or pulmonary reimplantation response frequently occurs after lung transplantation (25), and is caused by ischemic vascular injury of the allograft, resulting in increased permeability of the lung after reperfusion and in turn leading to interstitial and alveolar edema.…”

Section: Discussionmentioning

confidence: 99%

Functional Identification of the Alveolar Edema Reabsorption Activity of Murine Tumor Necrosis Factor-α

Elia¹,

Tapponnier²,

Matthay³

et al. 2003

Am J Respir Crit Care Med

View full text Add to dashboard Cite

Tumor necrosis factor-alpha (TNF-alpha) activates sodium channels in Type II alveolar epithelial cells, an important mechanism for the reported fluid resorption capacity of the cytokine. Both TNF-alpha receptor-dependent and -independent effects were proposed for this activity in vitro, the latter mechanism mediated by the lectin-like domain of the molecule. In this study, the relative contribution of the receptor-dependent versus receptor-independent activities was investigated in an in situ mouse lung model and an ex vivo rat lung model. Fluid resorption due to murine TNF-alpha (mTNF-alpha) was functional in mice that were genetically deficient in both types of mTNF-alpha receptor, establishing the importance of mTNF-alpha receptor-independent effects in this species. In addition, we assessed the capacity of an mTNF-alpha-derived peptide (mLtip), which activates sodium transport by a receptor-independent mechanism, to reduce lung water content in an isolated, ventilated, autologous blood-perfused rat lung model. The results show that in this model, mLtip, in contrast to mTNF-alpha, produced a progressive recovery of dynamic lung compliance and airway resistance after alveolar flooding. There was also a significant reduction in lung water. These results indicate that the receptor-independent lectin-like domain of mTNF-alpha has a potential physiological role in the resolution of alveolar edema in rats and mice.

show abstract

Section: Discussionmentioning

confidence: 99%

Functional Identification of the Alveolar Edema Reabsorption Activity of Murine Tumor Necrosis Factor-α

Elia¹,

Tapponnier²,

Matthay³

et al. 2003

Am J Respir Crit Care Med

View full text Add to dashboard Cite

show abstract

“…Acutely decompensated heart failure may develop in a previously asymptomatic patient for example due to massive acute myocardial infarction leading to severe pump failure, aortic dissecation leading to massive aortic valve insufficiency, endocarditis or acute myocarditis [62]. More often, however, acute decompensation occurs in a patient with previously existing heart failure.…”

Section: Drug Therapy In Acute Heart Failurementioning

confidence: 99%

“…For example, acute massive myocardial infarction warrants revascularisation therapy -thrombolytic treatment, PTCA or cardiac bypass; acute valvular catastrophe may warrant emergency surgical treatment etc. [62]. In case of worsening chronic heart failure, the pre-existing maintenance therapy is continued, although hypotension may require temporary discontinuation or dose reduction of betablocking agents and of ACE inhibitor [46].…”

Section: Drug Therapy In Acute Heart Failurementioning

confidence: 99%

Levosimendan: A New Inodilatory Drug for the Treatment of Decompensated Heart Failure

Kivikko¹,

Lehtonen²

2005

CPD

View full text Add to dashboard Cite

Levosimendan is a new calcium sensitizer developed for the treatment of congestive heart failure. Experimental studies indicate that levosimendan increases myocardial contractility and dilates both the peripheral and coronary vessels. Its positive inotropic effect is based on calcium-dependent binding of the drug to cardiac troponin C. It also acts as an opener of ATP-dependent potassium channels in vascular smooth muscle, thus inducing vasodilation. Although levosimendan acts preferentially as a calcium sensitizer it has also demonstrated selective phosphodiesterase III inhibitory effects in vitro. However, this selective inhibition does not seem to contribute to the positive action at pharmacologically relevant concentrations. Levosimendan has an active metabolite, OR-1896. Similarly to levosimendan, the metabolite exerts its positive inotropic and vasodilatory effects on myocardium and vasculature. The elimination half-life of levosimendan is about 1 hour. Thus, with intravenous administration, the parent drug rapidly disappears from the circulation after the infusion is stopped. The active metabolite, however, has a half-life of approximately 80 hours, and can be detected in circulation up to 2 weeks after stopping a 24-hour infusion of levosimendan. The intravenous formulation of levosimendan has been studied in several randomized comparative studies in patients with decompensated heart failure. Both patients with ischemic and non-ischemic etiology have participated in the studies. Levosimendan produces significant, dose-dependent increases in cardiac output, stroke volume and heart rate, and decreases in PCWP, mean blood pressure, mean pulmonary artery pressure, mean right atrial pressure and total peripheral resistance. With a loading dose, the effects on PCWP and cardiac ouput are seen within few minutes. There is no sign of development of tolerance even with a prolonged infusion up to 48 hours. Cardiac performance is improved with no significant increases in oxygen consumption or potentially malignant rhythm disorders. Due to the formation of an active metabolite, the hemodynamic effects are maintained up to several days after stopping levosimendan infusion. Compared to dobutamine, levosimendan produces similar increase in cardiac output but profoundly greater decrease in pulmonary capillary wedge pressure. On the contrary to dobutamine, the hemodynamic effects are not attenuated with concomitant beta-blocker use. Levosimendan has been shown to have favourable effects on symptoms of heart failure superior to placebo and at least comparable to dobutamine. Mortality and morbidity in levosimendan treated patients has been shown to be significantly lower when compared to dobutamine or placebo treated patients. The most common adverse events associated with levosimendan treatment are headache and hypotension, as a likely consequence of the vasodilating properties of the compound. In conclusion, levosimendan offers a new effective option for the treatment of acutely decompensated heart failure. Unlike traditio...

show abstract

“…These acute symptoms are caused by acute or chronic overloading of the heart due to arterial hypertension, coronary heart disease, and/or a reduction in ventricular mass after myocardial infarction. [10] The timely recognition and treatment of cardiogenic shock are crucial in reducing the incidence of death. [10,11] Patients with cardiogenic shock should be treated aggressively with a combination of pharmacologic agents and, when needed, mechanical support devices to stabilize them as early as possible.…”

Section: Discussionmentioning

confidence: 99%

Combination of Continuous Renal Replacement Therapies (CRRT) and Extracorporeal Membrane Oxygenation (ECMO) for Advanced Cardiac Patients

et al. 2003

View full text Add to dashboard Cite

We conclude that mortality rate for acute renal failure in cardiac patients under ECMO continues to be high. Our data suggest that acute renal failure is generally a part of multiorgan failure. This unique form of acute renal failure, causes generalized edema and fluid overload despite still low serum creatinine and azotemia, and deteriorates rapidly to death. From this study shows, advanced cardiac failure may need more aggressive and early initiation of ECMO support before acute renal failure develops. Acute renal failure in advanced heart failure under ECMO support means a grave sign, need aggressive heart transplantation therapy as soon as possible. Combination of CRRT and ECMO might serve an alternative therapy bridging the temporary replacement treatment and heart transplantation in advanced cardiac patients.

show abstract

New strategies for the management of acute decompensated heart failure

Cited by 6 publications

References 65 publications

Functional Identification of the Alveolar Edema Reabsorption Activity of Murine Tumor Necrosis Factor-α

Functional Identification of the Alveolar Edema Reabsorption Activity of Murine Tumor Necrosis Factor-α

Levosimendan: A New Inodilatory Drug for the Treatment of Decompensated Heart Failure

Combination of Continuous Renal Replacement Therapies (CRRT) and Extracorporeal Membrane Oxygenation (ECMO) for Advanced Cardiac Patients

Contact Info

Product

Resources

About