Influence of UDCG-115 on hemodynamics and myocardial energetics in patients with idiopathic dilated cardiomyopathy

Hasenfuß, Gerd; Holubarsch, Christian; Heiß, H. W.; Just, Hanjörg

doi:10.1016/0002-8703(89)90266-4

Cited by 24 publications

(5 citation statements)

References 33 publications

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“…Haemodynamics and tissue perfusion were recorded at the time intervals described above. The doses of levosimendan, pimobendan, and milrinone used in the present investigation were chosen to produce similar dose-related increases in cardiac output and also represent clinically meaningful doses in man (Monrad et al, 1984;Hasenfuss et al, 1989;Pouleur et al, 1989;Lilleberg et al, 1994;. At the end of each experiment, the heart was electrically fibrillated, the positions of the fluid-filled catheters and the micromanometer-tipped catheter were confirmed, and tissue specimens obtained for analysis of blood flow.…”

Section: Experimental Protocolmentioning

confidence: 99%

“…These drugs also partially inhibit phosphodiesterase (PDE) isoforms in cardiac and vascular smooth muscle (Fujino et al, 1988;Bohm et al, 1991) producing systemic and pulmonary vasodilatation and further augmentation of contractility (Hajjar & Gwathmey, 1991). Myofilament Ca2+ sensitizers have been shown to improve cardiac performance in patients with congestive heart failure (Thormann et al, 1983;Baumann et al, 1989;Hasenfuss et al, 1989;Remme et al, 1989;Katz et al, 1992) and represent another important therapeutic approach in the pharmacological management of the failing heart (Hajjar & Gwathmey, 1991).…”

Section: Introductionmentioning

confidence: 99%

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Influence of levosimendan, pimobendan, and milrinone on the regional distribution of cardiac output in anaesthetized dogs

Pagel

Hettrick

Warltier

1996

British J Pharmacology

108

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1 The distribution of cardiac output during administration of levosimendan, a new myofilament calcium sensitizer, is unknown. We examined and compared the effects of levosimendan, pimobendan, and milrinone on regional tissue perfusion by use of the radioactive microsphere technique in barbiturate-anaesthetized dogs. 2 Haemodynamics and regional blood flow were determined before and during infusions of levosimendan (0.75, 1.5, and 3.0 Mg kg-' min-'), pimobendan (10, 20, and 40 ig kg-' min-'), or milrinone (1.0, 2.0, and 4.0 ,ug kg-' min-'). 3 All three drugs caused similar increases in heart rate, cardiac output, and left ventricular + dP/dt and decreases in end-diastolic pressure and systemic vascular resistance. No changes in subendocardial, midmyocardial, and subepicardial blood flow occurred during administration of levosimendan. However, a redistribution of blood flow from subendocardium to subepicardium was observed. Pimobendan increased midmyocardial and subepicardial blood flow and reduced the endo/epi ratio to a greater degree than levosimendan. Milrinone did not affect myocardial perfusion. 4 Levosimendan increased blood flow to the renal medulla and decreased renal medullary and cortical vascular resistance. Levosimendan increased blood flow to the small intestine and liver and reduced vascular resistance in these organs. Pimobendan increased hepatic blood flow to a greater degree than levosimendan but did not alter small intestinal perfusion. All three drugs decreased splenic blood flow to similar degrees. Levosimendan and pimobendan reduced cerebral vascular resistance. Levosimendan and milrinone reduced skeletal muscle vascular resistance. 5The results indicate that levosimendan, pimobendan, and milrinone cause subtlety different alterations in regional tissue perfusion while producing similar haemodynamic effects.

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Section: Experimental Protocolmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Influence of levosimendan, pimobendan, and milrinone on the regional distribution of cardiac output in anaesthetized dogs

Pagel

Hettrick

Warltier

1996

British J Pharmacology

108

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“…13,14) Pimobendan significantly improves the myocardial contractility and reduces myocardial oxygen consumption. 15) In a doubleblind multicenter trial, Kubo, et al reported that pimobendan improved the quality of life (QOL) and reduced the hospitalization rate in patients with moderate to severe HF.…”

Section: Discussionmentioning

confidence: 99%

Efficacy and Limitations of Oral Inotropic Agents for the Treatment of Chronic Heart Failure

et al. 2013

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SummaryThe heart failure guideline in Japan has stated the necessity of investigating the role of oral inotropic agents in patients with chronic heart failure (CHF), which are clinically available only in Japan. A total of 1,846 consecutive patients with heart failure (mean: 69.5 years old, 1,279 males) treated at our institute from November 2009 to August 2010 were investigated retrospectively. Thirty-one patients (1.84%) who had taken oral inotropic agents (pimobendan 27, docarpamine 6, and denopamine 4) were extracted for this study, and the efficacy and limitations of the treatments were analyzed. Following the oral inotropic treatment, the NYHA functional class (P = 0.017), cardiothoracic ratio (P = 0.002) and B-type natriuretic peptide levels (P = 0.011) were significantly improved, and the number of emergency room (ER) visits (P < 0.001) and hospitalizations (P < 0.001) were significantly reduced. The nonsurviving patients (n = 7/31, 22.6%) were significantly older (P = 0.02) and tended to have a larger cardiothoracic ratio (P = 0.084) compared with the survivors. An absence of concomitant beta-blocker therapy was significantly associated with a worse prognosis (oneyear mortality 2/21 versus 5/10, log rank, P = 0.011). Oral inotropic agents brought about improvements in the clinical parameters of CHF and a reduction in ER visits and hospitalizations. However, concomitant beta-blocker therapy should be considered for patients receiving oral inotropic treatment. (Int Heart J 2013; 54: 75-81) Key words: Pimobendan, Denopamine, Docarpamine, Beta-blocker A lthough several oral inotropic agents have been developed for the treatment of advanced heart failure, such as oral catecholamines, phosphodiesterase III (PDE III) inhibitors, and Ca-sensitizers, [1][2][3][4][5] there have been no reports showing improvement in the patient survival for these treatments. On the other hand, beta-blocker therapy, [6][7][8] which is pharmacologically active in an opposite site to the inotropic agents, has brought about not only improvement in the longterm outcomes, but also improvement in cardiac function in patients with chronic heart failure (CHF). However, many patients with advanced heart failure have difficulty being weaned from intravenous inotropic therapy or recovering from their low output condition. There are few countries where oral inotropic agents are available for such instances. In Japan, a few oral inotropic agents, including pimobendan, denopamine, and docarpamine, are clinically available for inotropic treatment in patients with advanced heart failure 1,5) or as supportive treatment for beta-blocker therapy.9) The guidelines for the treatment of chronic heart failure from the Japanese Circulation Society have pointed out the necessity for clinical investigations concerning the efficacy and limitation of the oral inotropic treatments, which are available only in Japan, and are not approved in Western countries. Thus, the present study analyzed the real-world use, efficacy, and limitations of oral inotropic ag...

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“…6 In patients with idiopathic dilated cardiomyopathy and moderate CHF, the systemic hemodynamic actions induced by pimobendan were associated with advantageous effects on myocardial oxygen consumption. 36 Therefore, the increase in myocardial oxygen force by pimobendan is accomplished in a more economical way, making this agent better suited for long-term treatment of heart failure.…”

Section: Discussionmentioning

confidence: 99%

Effects of Pimobendan on Adverse Cardiac Events and Physical Activities in Patients With Mild to Moderate Chronic Heart Failure

Group

2002

Circ J

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The long-term beneficial effects of pimobendan in the treatment of chronic heart failure (CHF) have not been established, so the present trial compared pimobendan (1.25 or 2.5mg twice daily) vs placebo in 306 patients with stable New York Heart Association class IIm or III CHF, and a radionuclide or echocardiographic left ventricular ejection fraction (LVEF) < or =45% despite optimal treatment with conventional therapy, for up to 52 weeks in a double-blind protocol. At the end of the 52 weeks of treatment, combined adverse cardiac events had occurred in 19 patients in the pimobendan group (15.9%) vs 33 patients in the placebo group (26.3%). The cumulative incidence of combined adverse cardiac events was 45% lower (95% confidence interval of hazard ratio: 0.31-0.97, log-rank test: p=0.035) in the pimobendan group than in the placebo group. Death and hospitalization for cardiac causes occurred in 12 patients in the pimobendan group (10.1%), vs 19 patients in the placebo group (15.3%), but without significant difference. Treatment with pimobendan also increased the mean Specific Activity Scale score from 4.39+/-0.12 at baseline to 4.68+/-0.15 at 52 weeks (p<0.05). In conclusion, long-term treatment with pimobendan significantly lowered morbidity and improved the physical activity of patients with mild to moderate CHF.

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Influence of UDCG-115 on hemodynamics and myocardial energetics in patients with idiopathic dilated cardiomyopathy

Cited by 24 publications

References 33 publications

Influence of levosimendan, pimobendan, and milrinone on the regional distribution of cardiac output in anaesthetized dogs

Influence of levosimendan, pimobendan, and milrinone on the regional distribution of cardiac output in anaesthetized dogs

Efficacy and Limitations of Oral Inotropic Agents for the Treatment of Chronic Heart Failure

Effects of Pimobendan on Adverse Cardiac Events and Physical Activities in Patients With Mild to Moderate Chronic Heart Failure

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