Therapy With Verapamil or Carvedilol in Chronic Heart Failure

The recruitment status of this study is unknown because the information has not been verified recently.
Verified September 2006 by Medical University of Silesia.
Recruitment status was  Recruiting
Sponsor:
Information provided by:
Medical University of Silesia
ClinicalTrials.gov Identifier:
NCT00374465
First received: September 8, 2006
Last updated: NA
Last verified: September 2006
History: No changes posted

September 8, 2006
September 8, 2006
January 2006
Not Provided
  • Sserum level of NT-proBNP,LVEF, LV diameters, exercise capacity (NYHA, V02,6 min walking test, changes in quality of life (MLHFQ).
  • In addition to secondary endpoints efficacy, patients will be classified as improved if they meet an increase of > 10 percentage points in the absolute EF and decrease in NT-proBNP levels at least 50% as compared with baseline study.
Same as current
No Changes Posted
Combined: mortality, heart transplantation, and readmission to hospital due to heart failure progression
Same as current
Not Provided
Not Provided
 
Therapy With Verapamil or Carvedilol in Chronic Heart Failure
Prospective, Randomized Comparison of Therapy With Verapamil or Carvedilol on Long-Term Outcomes of Patients With Chronic Heart Failure Secondary to Non-Ischemic Cardiomyopathy

The aim of this study is to compare the effect of treatment with verapamil or carvedilol on long-term outcomes in stable, chronic heart failure secondary to non-ischemic cardiomyopathy.

Heart failure, irrespective of its etiology may be viewed as a progressive disorder initiated by a different events and sustained by a multifaceted pathophysiological mechanisms. Regardless of the nature of the initiating events and optimized therapy used, loss of functioning cardiac myocytes developed and the disease progressed. One potential explanation for such progression is that not all pathological mechanisms underlying the disease are antagonized enough by currently used therapeutic strategy. Accordingly, impaired myocardial perfusion secondary to microvascular dysfunction has been postulated to play a major role in the progression of heart failure despite standard therapy for heart failure. It has been hypothesized that diffuse subendocardial ischemia due to altered coronary physiology may contribute to the global cardiac dysfunction seen in heart failure patients. Accordingly, coronary endothelial dysfunction at the microvascular and epicardial level in patients with acute-onset idiopathic dilated cardiomyopathy and chronic congestive heart failure has been reported. Thus, taking all mentioned above into account, the improvement in endothelial function and diminishing of subendocardial ischemia with calcium antagonists may be promising in terms of using these drugs for therapy of patients with stable chronic heart failure. The previous randomized study (5) and our long-term pilot study support this point of view.

Interventional
Phase 4
Allocation: Randomized
Endpoint Classification: Efficacy Study
Intervention Model: Parallel Assignment
Masking: Single Blind
Primary Purpose: Treatment
Dilated Cardiomyopathy
  • Drug: Verapamil
  • Drug: Carvedilol
Not Provided
Not Provided

*   Includes publications given by the data provider as well as publications identified by ClinicalTrials.gov Identifier (NCT Number) in Medline.
 
Recruiting
100
May 2008
Not Provided

Inclusion Criteria:

  • Chronic heart failure (NYHA II and III; LV ejection fraction, ≤ 35%) secondary to non-ischemic cardiomyopathy
  • Stable condition at least 6 months before enrollment on conventional therapy (beta-blockers, ACE inhibitors and diuretics).

Exclusion Criteria:

  • Improvement in clinical status on conventional therapy in out-patients period preceded hospitalization,
  • Any changes narrowing epicardial coronary arteries in coronary angiography,
  • Insulin dependent diabetes,
  • Valvular heart disease (except the relative mitral regurgitation),
  • Endocrine disease
  • Significant renal and liver disease
  • Alcohol abuse
  • Lack of written informed consent
Both
18 Years to 65 Years
No
Contact: Jan Wodniecki, MD, PhD +48 32 2716471 ext 228 wojnicz@dom.zabrze.pl
Contact: Ewa Nowalany Kozielska, MD, PhD +48 32 2525767 ewakozielska@wp.pl
Poland
 
NCT00374465
CavsBe.06
Not Provided
Not Provided
Medical University of Silesia
Not Provided
Study Chair: Jan Wodniecki, Prof. Medical University of Silesia
Medical University of Silesia
September 2006

ICMJE     Data element required by the International Committee of Medical Journal Editors and the World Health Organization ICTRP