Milrinone: Basic and Clinical Pharmacology and Acute and Chronic Management

Shipley, Joshua B.; Tolman, David; Hastillo, A; Heß, Michael

doi:10.1016/s0002-9629(15)41723-9

Cited by 66 publications

(30 citation statements)

References 23 publications

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“…The plasma concentrations of milrinone increase dose-dependently and its elimination half-life is approximately 2 hours [102]. Due to the relatively long elimination half-life, a loading dose is recommended in order to get immediate hemodynamic response [103]. Elimination is prolonged in renal impairment and thus caution should be exercised when milrinone is used in patients with renal insufficiency [104,105].…”

Section: Milrinonementioning

confidence: 99%

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

Kivikko¹,

Lehtonen²

2005

CPD

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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...

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Section: Milrinonementioning

confidence: 99%

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

Kivikko¹,

Lehtonen²

2005

CPD

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“…Milrinone increases cardiac output and reduces systemic vascular resistance and pulmonary capillary wedge pressure; it rarely causes thrombocytopenia [22]. The Outcomes of a Prospective Trial of Intravenous Milrinone for Exacerbations of Chronic HF (OPTIME-CHF) [23] was designed to evaluate the use of milrinone in acute decompensated HF.…”

Section: Milrinonementioning

confidence: 99%

Inotropic Drugs and Neurohormonal Antagonists in the Treatment of HF in the Elderly

O’Connor

Arumugham

2007

Clinics in Geriatric Medicine

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“…Cardiac output is increased due to its direct inotropic effects as well as secondary to the decrease in afterload [41,42]. Mean blood pressure and heart rate tend to be unchanged but at higher doses (0.5 mg/kg), hypotension and tachycardia may develop [43].…”

Section: Pde Inhibitorsmentioning

confidence: 99%

“…Mean blood pressure and heart rate tend to be unchanged but at higher doses (0.5 mg/kg), hypotension and tachycardia may develop [43]. Milrinone can be administered as a loading dose followed by a continuous infusion [42]. There is a dose response relationship for loading dose increments of 37.5-50 μg/kg.…”

Section: Pde Inhibitorsmentioning

confidence: 99%