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Pimobendan for Congestive Heart Failure

I think it is possible that we might save the lives of 100,000 who are going to die sooner than they have to from Congestive Heart Failure {CHF].

From the net I get, roughly, that about 6 million adults have congestive heart failure and half of them won’t make five years after being diagnosed, half that after being hospitalized.

An easy 360,000 deaths a year; a thousand a day or so.

I think we can get back 100,000 a year by getting the FDA to approve a drug, Pimobendan, they already approved for your dog with CHF, and which is used in Japan for humans.

 

The problem, in my jaundiced view, is that it is so cheap. But all the “trials” anyone could want have been going on for years with American pets and Japanese humans. Far more than was done for some vaccines. 

I want you to know heart failure is not fun. It is not heart attack where pop, and you are gone. You can’t breathe!!!  Not fun. Stairs were murder for me. Even getting off a plane and going up the ramp had me huffing and pumping. Now I train hard five hours a week. 

I have to get mine from vets outside the country. I heard of another fellow whose friend is a vet, and so he has a prescription and gets his off the net. 

*FULL DISCLOSURE!! One person’s experience can’t be extrapolated to a large population. There may have been other factors. 

So I am going to turn you loose to do your own research so you can decide for yourself. Below are excerpts from research on this drug Pimobendan. 

What I want you to do is: 

  • Give this research to your cardiologist. It won’t do any good, but who knows!? 
  • Pass this on to anyone with congestive heart failure [CHF]. 
  • Send a copy to your congressman requesting his attention. You might be saving his life.

   SIDE EFFECTS:

 

Look for yourself at the research below and you get the feeling that they are little to none. Each of us is more different than the other than snow flakes differ. SO EACH IS RESPONSIBLE FOR NOTING HIS OWN SIDE EFFECTS. You might say, as I do, that not breathing is a nasty side effect of not taking the pills. There is also the possible interaction with whatever else you might be taking. It is my impression that any of the side effects would be far less than many current vaccines.

 

RESEARCH  

 

Effects of pimobendan on adverse cardiac events and physical activities in patients with mild to moderate chronic heart failure: the effects of pimobendan on chronic heart failure study (EPOCH study).

  • Published 2002
  • Medicine
  • Circulation journal : official journal of the Japanese Circulation Society

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

Background: This multicenter trial was conducted to determine the efficacy and safety of pimobendan, an inotropic agent with calcium-sensitizing properties and activity as a phosphodiesterase inhibitor, in patients with heart failure.

Methods and results: One hundred ninety-eight ambulatory patients with symptoms of moderate to severe heart failure despite therapy with digitalis and diuretics with or without a single vasodilator were randomly assigned to receive either placebo (n = 49) or pimobendan (n = 149) in a double-blind fashion for 12 weeks. A dose range of pimobendan was used including 2.5 (n = 49), 5 (n = 51), or 10 mg/day (n = 49). 

One hundred fifty-eight (80%) patients were taking a converting enzyme inhibitor (CEI) and 28 (14%) patients were taking a non-CEI vasodilator.

 At end point, the 5-mg dose of pimobendan significantly increase exercise duration compared with placebo (121.6 +/- 19.1 seconds, p less than 0.001), whereas the 10-mg dose produced an increase of borderline significance (81.1 +/- 19.5 seconds, p = 0.05).

 Peak VO2 was significantly increased by 2.23 +/- 0.58 ml/kg/min in the 5-mg group (p less than 0.01 versus placebo). Furthermore, quality of life measured with the Minnesota Living With Heart Failure Questionnaire improved by 8.5 +/- 2.3 units in the 5-mg group compared with 1.3 +/- 2.2 units in the placebo group (p less than 0.01).

There were a total of 23 all-cause hospitalizations in the placebo group, which was significantly greater compared with 33 in the three groups treated with pimobendan (p less than 0.01). There were no significant differences between the placebo and pimobendan groups with respect to changes in ejection fraction and plasma norepinephrine measured at baseline and at the completion of the 12-week study, proarrhythmic effect, or the number of patients with a significant adjustment in background therapy.

Eleven patients died, including three (6%) on placebo and eight (5%) on pimobendan (p = NS). Among all adverse events, headache tended to be more common in the pimobendan groups compared with placebo, with the incidence increasing with dose (p less than 0.05).

Conclusions: These data demonstrate that pimobendan significantly increases exercise duration, peak VO2, and quality of life in patients with heart failure. Pimobendan appears to be useful adjunctive therapy when added to digitalis, diuretics, and vasodilators.

 

 

 

Effect of pimobendan in addition to standard therapy for heart failure on prevention of readmission in elderly patients with severe chronic heart failure

Hiroaki Kawano 1, Shuji Arakawa, Osami Satoh, Yuji Matsumoto, Motonobu Hayano, 

 

Aim: We evaluated the effect of pimobendan, a positive inotropic agent, in elderly patients with frequent readmission as a result of heart failure despite conventional therapy.

Methods: Pimobendan was given to five male patients with severe chronic heart failure (New York Heart Association class III-IV) (age range 69-89 years; mean 78 ± 8 years; ischemic cardiomyopathy in three cases, dilated cardiomyopathy in two cases) who required repeated admission for heart failure despite conventional therapy with angiotensin inhibitors, beta-blockers, diuretics and anti-arrhythmic agents. After the addition of pimobendan at a dose of 1.25-3.75 mg/day, we evaluated serum levels of brain natriuretic peptide (BNP), left ventricular ejection fraction (LVEF), septal e’ and left ventricular end-diastolic diameter (LVDD) by echocardiography, as well as readmission rates for more than 2 years.

 

Results: The serum level of BNP significantly decreased after treatment with pimobendan, although its level returned to pretreatment levels after 2 years.

LVEF significantly improved after the treatment, with the improvement continuing beyond the 2 years, although LVDD did not change after treatment. Septal e’ significantly improved after the treatment, although its level returned to pretreatment levels at 2 years after the treatment.

Readmission rates significantly decreased for 2 years after the treatment, although one patient required cardiac resynchronization therapy for severe heart failure, and another patient required cardiac pacemaker implantation for sick sinus syndrome 2 years after adding pimobendan.

Conclusions: Pimobendan in conjunction with conventional therapy for heart failure decreases the readmission rate in elderly patients with severe heart failure for at least 2 years

Beneficial effects of pimobendan on exercise tolerance and quality of life in patients with heart failure. Results of a multicenter trial. The Pimobendan Multicenter Research Group

S H Kubo 1, S Gollub, R Bourge, P Rahko, F Cobb, M Jessup, S Brozena, M Brodsky, P Kirlin, J Shanes, et al.

Full text linksCite

Abstract

Background: This multicenter trial was conducted to determine the efficacy and safety of pimobendan, an inotropic agent with calcium-sensitizing properties and activity as a phosphodiesterase inhibitor, in patients with heart failure.

Methods and results: One hundred ninety-eight ambulatory patients with symptoms of moderate to severe heart failure despite therapy with digitalis and diuretics with or without a single vasodilator were randomly assigned to receive either placebo (n = 49) or pimobendan (n = 149) in a double-blind fashion for 12 weeks. A dose range of pimobendan was used including 2.5 (n = 49), 5 (n = 51), or 10 mg/day (n = 49). One hundred fifty-eight (80%) patients were taking a converting enzyme inhibitor (CEI) and 28 (14%) patients were taking a non-CEI vasodilator. At end point, the 5-mg dose of pimobendan significantly increase exercise duration compared with placebo (121.6 +/- 19.1 seconds, p less than 0.001), whereas the 10-mg dose produced an increase of borderline significance (81.1 +/- 19.5 seconds, p = 0.05). Peak VO2 was significantly increased by 2.23 +/- 0.58 ml/kg/min in the 5-mg group (p less than 0.01 versus placebo). Furthermore, quality of life measured with the Minnesota Living With Heart Failure Questionnaire improved by 8.5 +/- 2.3 units in the 5-mg group compared with 1.3 +/- 2.2 units in the placebo group (p less than 0.01). There were a total of 23 all-cause hospitalizations in the placebo group, which was significantly greater compared with 33 in the three groups treated with pimobendan (p less than 0.01). There were no significant differences between the placebo and pimobendan groups with respect to changes in ejection fraction and plasma norepinephrine measured at baseline and at the completion of the 12-week study, proarrhythmic effect, or the number of patients with a significant adjustment in background therapy. Eleven patients died, including three (6%) on placebo and eight (5%) on pimobendan (p = NS). Among all adverse events, headache tended to be more common in the pimobendan groups compared with placebo, with the incidence increasing with dose (p less than 0.05).

 

Conclusions: These data demonstrate that pimobendan significantly increases exercise duration, peak VO2, and quality of life in patients with heart failure. Pimobendan appears to be useful adjunctive therapy when added to digitalis, diuretics, and vasodilators.

Cardiovascular profile of UDCG 115 BS-pimobendane and reversibility of catecholamine subsensitivity in severe congestive heart failure secondary to idiopathic dilated cardiomyopathy

G Baumann 1, K Ningel, B Permanetter

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      • PMID: 2472521

Cite

Abstract

The pyridazoline derivative UDCG 115 BS (pimobendane) is a new, noncatecholamine, nonglycoside inotropic compound with potent vasodilative properties which exerts its stimulatory myocardial effect by increasing the Ca2+ affinity of cardiac contractile proteins and thus improving Ca2+ utilization.

The aim of this study was to characterize and quantify the hemodynamic profile of oral UDCG 115 BS in 25 patients suffering from idiopathic congestive cardiomyopathy (NYHA III) and compare these effects with the action of the beta 1-receptor agonist dobutamine.

 UDCG 115 BS 5 mg p.o. increased cardiac output, cardiac index, and stroke volume index by approximately 60%. With only minor changes in heart rate, ventricular filling pressures decreased by 40%. A decline in pulmonary and systemic vascular resistance (-50%), as well as in systolic, diastolic, and mean pulmonary artery pressures (-35%) were also observed.

The effects of 5 mg UDCG 115 BS were comparable to those that occurred with the optimal dose of dobutamine, whereas 10 mg UDCG 115 BS induced significantly more pronounced hemodynamic changes. The effects of UDCG lasted for at least 12 h. No major side effects were observed. Continuous treatment with 10 mg UDCG 115 BS/day for greater than 5 days resulted in a significantly improved response in beta-adrenoceptor stimulation as well as a drop in endogenous plasma catecholamines to nearly normal values.

We therefore conclude that UDCG 115 BS, with its unique receptor-independent mechanism of action, may represent a new therapeutic approach in the management of patients with congestive heart failure (CHF).

 

Efficacy and limitations of oral inotropic agents for the treatment of chronic heart failure.

The 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.

Pimobendan, a new oral cardiotonic and vasodilator agent, increases myocardial contractile force through specific inhibition of phosphodiesterase type III and increased calcium sensitivity of the myocardial contractile elements. The effects of pimobendan on left ventricular performance and maximal exercise capacity were studied in a multicenter, randomized, double-blind, placebo-controlled trial involving 52 patients with severe congestive heart failure despite diuretics, digoxin, and angiotensin-converting enzyme inhibitors. The acute hemodynamic evaluation included three single doses of 2.5, 5.0, and 10.0 mg of oral pimobendan, which was subsequently administered at a daily dose of 5 or 10 mg for 4 weeks. Acute administration of pimobendan significantly increased the resting cardiac index and lowered pulmonary capillary wedge pressure in a dose-dependent manner, whereas heart rate and systemic arterial pressure were not substantially altered. 

Patients receiving pimobendan, 5 and 10 mg daily, had a significantly greater increase in maximal exercise duration than those receiving placebo, that is, 144 +/- 30 and 124 +/- 33 seconds versus 58 +/- 25 seconds (p = 0.05). Peak oxygen uptake increased by 1.7 +/- 0.8 and 2.2 +/- 1.3 ml/kg/min in patients receiving pimobendan at a daily dose of 5 and 10 mg, respectively, whereas it decreased by 0.1 +/- 0.6 ml/kg/min in patients receiving placebo (p = 0.06). 

Thus pimobendan acutely improves resting left ventricular performance and chronically increases exercise duration and peak oxygen uptake in patients with severe congestive heart failure concomitantly treated with digoxin, diuretics, and angiotensin-converting enzyme inhibitors.

 

 

 

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The effects of pimobendan (UD-CG 115) on hemodynamics and exercise capacity after acute (single dose) and chronic (6 month) oral treatment, as well as acute treatment after 6 months were investigated in 67 patients with chronic heart failure of NYHA classes II or III, which had persisted in spite of treatment with diuretics and digitalis. They were treated with pimobendan (2.5 mg bid or 5 mg) or placebo in a randomized, double-blind multicenter trial.

 With a single administration before and after 6 months’ treatment there was-compared to placebo-a significant fall in pulmonary capillary pressure (PCP) at rest (R) and during exercise (E) of 7% to 24%. Right atrial pressure (R) and pulmonary arterial pressure (PAP) (R, E) decreased after pimobendan on day 1; cardiac index (E) increased significantly. All other parameters were not influenced. After chronic therapy, PCP (E), PAP (E), LV stroke work index (E), and pulmonary resistance (R and E) values were significantly lowered by pimobendan when compared to day

1. Exercise duration was prolonged after 6 months by 83 s and 47 s after 5 and 10 mg/day, resp., compared to the placebo group (group difference not significant).

Subjective wellbeing was improved in all three groups (no group difference). Clinical symptoms were not altered; six patients (two in each group) died suddenly. Another nine patients discontinued the trial prematurely because of poor efficacy or adverse events (no group difference). Overall, pimobendan was well-tolerated and had favorable effects on both acute and chronic hemodynamics and on exercise capacity. There was no evidence of any tolerance development.

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.

 

 

A comment on the images. They have utterly no relevance to the subject matter. I thought so much printed material boring so I stuck them in.

 

 

 

 

 

 

 

 

 

 

 

Pimobendan seems to be a potent inhibitor of platelet aggregation, analecta that may be mediated by inhibition of platelet thromboxane A production [36,37].

Veterinary pimobendan studies

Although there are still few published reports, there have been a number of studies in dogs examining the use of pimobendan in dilated cardiomyopathy and chronic mitral valve disease. 

Short-term studies

Early open-label trials included a dose-ranging study in 45 dogs with chronic mitral valve disease or dilated cardiomyopathy. Pimobendan was started at 0.2 mg/kg/d and was increased up to 0.4 or 0.6 mg/kg/d in two divided doses until improvement was observed [38]. This dose was maintained for a further 2 weeks until the final examination. The authorsconcluded that 0.4 to 0.6 mg/kg/d seemed to be an effective dose in dogswith heart failure. Another open-label study compared the effects of pimobendan versus digoxin over 4 weeks in 109 dogs with congestive heart failure [39]. The NYHA score was significantly better in the pimobendan group than in the digoxin group after 4 weeks. One of the most comprehensive randomized, blind, controlled studies todate of pimobendan in canine congestive heart failure was the PiTCH study[40,41]. Dogs were recruited with NYHA class III or IV heart failure caused by dilated cardiomyopathy (n = 81) or chronic mitral valve disease, with105 dogs enrolled in total. Dogs were randomized to receive pimobendanand placebo, pimobendan and benazepril, or placebo and benazepril for a28-day period. A greater proportion of dogs failed to finish the initial study period because of lack of efficacy or death in the benazepril group (34%)compared with the pimobendan group (11%) or the combined group (9%).The low numbers of mitral insufficiency cases in the PiTCH trialprompted initiation of further trials in this subset of patients. One suchtrial compared the use of pimobendan with the ACE inhibitor ramipril indogs with myxomatous mitral valve disease over a 6-month period [42,43].Dogs showing signs of modified NYHA class II to III heart failure were randomized to pimobendan or ramipril in a single-blind fashion (owners were aware of the drug identity). Of 44 dogs recruited, there were  significantly fewer adverse outcomes in the pimobendan group comparedwith ramipril group (odds ratio = 5.03, 95% CI: 1.12–22.6).

Long-term studies

The PiTCH study also had a long-term arm, with an option to continuewith the medication after the 28-day initial study period. The pimobendan and combination groups continued with pimobendan and benazepril,whereas the benazepril-only group continued with benazepril and placebo.Additional medications could be added at the clinician’s discretion. Median survival time in the placebo group was 42 days compared with 217 days in the pimobendan group [41].It should be recognized that the above studies represent preliminary and as yet unpublished data. A small, double-blind, randomized, placebo-controlled study of dilated cardiomyopathy in Doberman Pinschers and English Cocker Spaniels reported use of pimobendan as an add-on therapy to background treatment with furosemide, enalapril, and digoxin [44]. An improvement in NYHA heart failure classification was seen in 8 of 10 dog sreceiving pimobendan compared with 1 of 10 of the dogs in the placebo group (

P

 = 0.005). Median survival was improved in the Doberman Pinschers in this study, from 50 days in the placebo group to 329 days in the pimobendan-treated group (hazard ratio = 3.4, 95% CI: 1.4–39.8).Similar benefits for Doberman Pinschers with dilated cardiomyopathy were shown in another randomized placebo-controlled study [45]. Doberman Pinschers with congestive heart failure caused by dilated cardio myopathyand receiving ACE inhibitors and diuretics (n = 15) were randomized to placebo or pimobendan. Quality-of-life scores were significantly better in the  pimobendan group, and mean survival times were 128, 29 days in thepimobendan group compared with 63

 14 days in the placebo group.

Recommendations for use of pimobendan

In Europe, pimobendan is available as 1.25-, 2.5-, and 5- g capsules. The recommended dose rate in dogs is 0.1 to 0.3 mg/kg administered every 12hours and given at least an hour before food. Dosing is usually started at the low end of the dose range. Pimobendan can be combined with diuretics ,ACE inhibitors, or digoxin. The positive inotropic effects may be reduced when given in conjunction with calcium channel antagonists or-adrenergicantagonists.

Future directions

Pimobendan is a highly interesting compound that is showing much promise in the treatment of canine congestive heart failure. Its calcium-sensitizing effect distinguishes it from other commercially available positive inotropes and may be responsible for its comparative lack of adverse effects compared with inotropic agents that rely on increasing cytosolic calcium levels. An alternative viewpoint is that PDE III inhibition is not uniformly harmful in all patient populations and that despite the findings of the PROMISE trial [27], it may be beneficial in dogs with nonischemic

1151

V. Luis Fuentes / Vet Clin Small Anim 34 (2004) 1145–1155

 

congestive heart failure. In fact, pimobendan has continued to be licensed for human use in Japan since 1994, and US investigators have re-examinedpimobendan in recent times as a means of facilitating tolerance of-adrenergic antagonists in human patients with severe heart failure [46].The combination of carvedilol and pimobendan was safe and seemed to result in favorable neurohormonal effects [46]. An additional possible use for pimobendan is in treating pulmonary hypertension [47].Trials are currently underway to elucidate the role of pimobendan in the treatment of chronic mitral valve disease. Early use of pimobendan tended to be focused on cases with systolic dysfunction, because it was thought that these patients would obtain the most benefit from a positive inotrope. New evidence is suggesting that pimobendan may relieve clinical signs even when systolic function is not impaired, and it is likely that the the rapeutic mechanisms are more complex than originally thought. The role of pimo-bendan’s effects on neurohormones and cytokines also requires further study. No work has been done on the effects of pimobendan in dogs with naturally occurring acute heart failure, and there are only anecdotal reports of its use in cats. Pimobendan’s antithrombotic effects may be particularly helpful in the latter species.

Summary

Pimobendan is a new inodilator compound available in many countries for use in canine heart failure. It combines calcium-sensitizing effects with PDE III inhibition, resulting in positive inotropic effects and veno- andarteriodilation. Because there is downregulation of the myocardial adren-ergic signal transduction pathway in the failing heart, the calcium-sensitizing effects may assume greater importance in patients with heart failure. Clinical studies in human patients have shown sustained improvement in hemodynamics and exercise tolerance, with favorable neurohormonal effects. One study showed a nonsignificant trend toward increased mortality [20], but proarrhythmic effects have not been observed. Studies in naturally occurring canine heart failure suggest that pimobendan’s effects are at least comparable to those of ACE inhibitors, if not superior. Pimobendan is likely toplay an increasing role in the future in the treatment of canine heart disease

67 german [Acute and long-term effects of pimobendan (UD-CG 115) in NYHA II and III heart failure. Results of a randomized multicenter double-blind study]

[Article in German]

I Assmann 1, P Kassel, H G Duck, H Fiehring, P Morgan, P K Schmidt, T HöfsG Nehmiz

      • PMID: 1792811

Abstract

The effects of pimobendan (UD-CG 115) on hemodynamics and exercise capacity after acute (single dose) and chronic (6 month) oral treatment, as well as acute treatment after 6 months were investigated in 67 patients with chronic heart failure of NYHA classes II or III, which had persisted in spite of treatment with diuretics and digitalis. 

They were treated with pimobendan (2.5 mg bid or 5 mg) or placebo in a randomized, double-blind multicenter trial. With a single administration before and after 6 months’ treatment there was-compared to placebo-a significant fall in pulmonary capillary pressure (PCP) at rest (R) and during exercise (E) of 7% to 24%. Right atrial pressure (R) and pulmonary arterial pressure (PAP) (R, E) decreased after pimobendan on day 1; cardiac index (E) increased significantly. All other parameters were not influenced. After chronic therapy, PCP (E), PAP (E), LV stroke work index (E), and pulmonary resistance (R and E) values were significantly lowered by pimobendan when compared to day 1. 

Exercise duration was prolonged after 6 months by 83 s and 47 s after 5 and 10 mg/day, resp., compared to the placebo group (group difference not significant). Subjective wellbeing was improved in all three groups (no group difference). 

Clinical symptoms were not altered; six patients (two in each group) died suddenly. Another nine patients discontinued the trial prematurely because of poor efficacy or adverse events (no group difference). Overall, pimobendan was well-tolerated and had favorable effects on both acute and chronic hemodynamics and on exercise capacity. There was no evidence of any tolerance development.

OBJECTIVE:

To assess the effects of a calcium sensitizer, pimobendan, in patients with mild to moderate chronic heart failure.

PATIENTS AND METHODS:

Pimobendan was administered at a dose of 2.5 mg/day for 12 months to 34 patients with chronic heart failure (New York Heart Association functional class IIm to III) after treatment with diuretics and angiotensin-converting enzyme inhibitors. The etiologies of heart failure were dilated cardiomyopathy (DCM), old myocardial infarction (OMI) and other heart disease (Others). The effects of pimobendan were assessed by echocardiography, blood pool scintigraphy, Holter monitoring, 123I-meta-iodobenzylguanidine (MIBG) imaging and 123I-β-methyl-p-iodophenyl-pentadecanoic acid (BMIPP) imaging. 

RESULTS:

Pimobendan produced improvement of symptoms in the majority of patients. Improvement was more common in the DCM group than in the OMI group. Left ventricular internal diameter measured by echocardiography was significantly decreased. Left ventricular ejection fraction was significantly increased in the DCM and Others groups. The heart to mediastinum ratio on MIBG imaging was significantly increased in the DCM and Others groups, and the heart to mediastinum ratio on BMIPP imaging was significantly increased in the DCM group. 

CONCLUSIONS:

Pimobendan is effective in patients with chronic heart failure but is less effective in patients with OMI than in patients with DCM or other heart diseases.

      • OI:10.1007/BF01745236  Corpus ID: 19329412 21 Clinical effects of long-term administration of pimobendan in patients with moderate congestive heart failure

Summary: The long-term efficacy of the positive inotropic and vasodilator drug, pimobendan, was assessed in 21 patients suffering from symptomatic heart failure. 

 Patients were randomized to 16 weeks of double-blind therapy with either 2.5 or 5.0mg/day of pimobendan (n = 10), or a matching placebo (n = 11). Patients were blinded on the study drug if their clinical status had not substantially worsened during the study. Of the placebo-treated patients, 5 patients were withdrawn from the study because of a deterioration of their heart failure, while none of the active treated group was withdrawn because of increased symptoms. Quality of life, assessed by the specific activity scale derived from the metabolic costs of individual physical activity, was 3.45 ± 0.90 (SD) mets in the baseline state and increased significantly after week 16, averaging 5.07 ± 1.40 and 4.67 ± 1.47 mets at weeks 16 and 24, respectively. In the placebo-treated group, the specific activity scale was 3.27 ± 1.21 mets at the baseline and remained unchanged throughout the study period. 

 Patients treated with pimobendan were able to significantly increase their exercise duration. The accompanying increase in peak oxygen uptake was statistically insignificant, due to the limited number of patients enrolled in the study. These results suggest that in contrast to the recent pessimistic view of the long-term efficacy of cardiotonic drugs, pimobendan is beneficial in treating patients with congestive heart failure and may favorably modify their prognosis. Further largescale evaluation of this agent is warranted

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.There you have enough to set you off on your own research.

At the beginning I suggested that we might save 100,000 lives in the next year, or grately improve them.

I have mentioned pimobendan to all my doctors and so far none have heard of it, or reacted to the information.

If you are one of the 100,000, or someone close to you is, you might be tempted to react. If you have a cardioliogist, give him a little of what you have just read, or give him the web site address.

Again I say that if your congressman would forward this to the FDA along with some concern, there is the finite chance he might save or improve his own life.

 

If you have friends in another country send this too them! It is probably easier for them to get it than you. 

100,000 easy!