Therapy With Verapamil or Carvedilol in Chronic Heart Failure
Recruitment status was Recruiting
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.
|Study Design:||Allocation: Randomized
Endpoint Classification: Efficacy Study
Intervention Model: Parallel Assignment
Masking: Single Blind
Primary Purpose: Treatment
|Official Title:||Prospective, Randomized Comparison of Therapy With Verapamil or Carvedilol on Long-Term Outcomes of Patients With Chronic Heart Failure Secondary to Non-Ischemic Cardiomyopathy|
- 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.
- Combined: mortality, heart transplantation, and readmission to hospital due to heart failure progression
|Study Start Date:||January 2006|
|Estimated Study Completion Date:||May 2008|
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.
|Contact: Jan Wodniecki, MD, PhD||+48 32 2716471 ext email@example.com|
|Contact: Ewa Nowalany Kozielska, MD, PhD||+48 32 firstname.lastname@example.org|
|Silesian Centre for Heart Disease, 3rd Department of Cardiology||Recruiting|
|Zabrze, Szpitalna 2 st., Poland, 41800|
|Principal Investigator: Romuald Wojnicz, MD, PhD|
|Sub-Investigator: Ewa N Kozielska, MD, PhD|
|Sub-Investigator: Jolanta Nowak, MD|
|Sub-Investigator: Krzysztof Wilczek, MD|
|Sub-Investigator: Celina Wojciechowska, MD|
|Sub-Investigator: Bozena Szygula, MD|
|Study Chair:||Jan Wodniecki, Prof.||Medical University of Silesia|