Renal Denervation in Patients With Heart Failure and Severe Left Ventricular Dysfunction.
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|ClinicalTrials.gov Identifier: NCT01870310|
Recruitment Status : Unknown
Verified June 2013 by doc. MUDr. Miloš Táborský, CSc., FESC, MBA, University Hospital Olomouc.
Recruitment status was: Recruiting
First Posted : June 6, 2013
Last Update Posted : June 6, 2013
|Condition or disease||Intervention/treatment||Phase|
|Heart Failure||Procedure: Catheterised renal denervation||Not Applicable|
Chronic heart failure in the European countries occurs in 2-3% of the population with a significant increase in the higher age groups (1). Improved treatment of acute conditions (especially myocardial infarction) has resulted in more patients entering into the category of chronic heart failure. Chronic heart failure has a poor prognosis. Diagnosis and treatment are challenging both medically and economically. Half of the patients with systolic heart failure die within 4 years and more than 50% of patients with severe heart failure (NYHA functional class of IV) die within one year (1). The current treatments for heart failure are not only aimed at influencing the symptoms, but also preventing the progression of heart failure to reduce mortality.
Heart failure leads to the activation of compensatory mechanisms designed to restore adequate cardiac output. These mechanisms are initially beneficial, but their long-term activation leads to further progression of the pathological process and deterioration of cardiac function. One of the basic pathophysiological processes in heart failure is excessive activation of the sympathetic nervous system. This causes increased levels of circulating catecholamines which is proportional to the severity of the disease that is patients with the highest levels of norepinephrine have the worst prognosis. Beta-blocker therapy which is designed to inhibit activity of sympathetic nervous system causes milder symptoms of heart failure in patients by modifying disturbed hemodynamics and ultimately the clinical status. In recent years, the therapeutic efficacy of beta-blockers in chronic heart failure has been verified in a number of controlled clinical trials (2-5). These studies have confirmed that long-term treatment with beta-blocker therapy alleviates the symptoms of heart failure, improves the clinical condition of the patients and reduces mortality like ACE inhibitors.
High activity of renal sympathetic nerves in patients with chronic heart failure is an early predictor of increased mortality (6). The main pathophysiological basis of this finding is probably excessive sodium retention due to direct activation of sympathetic fibers innervating renal tubules (7). Recent experimental work on animals have shown that surgical renal denervation inhibits an increase in renal vascular resistance, prevents a decrease in renal blood flow (8), and also prevents changes in expression of angiotensin receptors in the kidney (8).
Surgical sympathectomy began to be used for the treatment of severe and malignant hypertension more than 50 years ago. But this was a rather complicated procedure, which was accompanied by a number of adverse effects (orthostatic hypotension and tachycardia, shortness of breath, bowel and sexual disorders]. Moreover it required a long hospitalization of 2-4 weeks and then required a recovery period of 1-2 months. However this intervention led to a rapid decrease in pressure and a higher survival rate after surgery in a large observational study(9).
In recent years a method has been developed in which destruction of renal sympathetic nerves that are present in the adventitia of renal arterial walls is done by catheterization (10). This procedure uses a catheter with a radiofrequency ablator at its tip (Symplicity, Ardian / Medtronic, USA), which is introduced through the femoral artery and then progressively introduced into the renal arteries. A randomized study has demonstrated that this procedure has a high degree of safety for the patients and a high rate of efficacy as well. In patients with resistant hypertension treated with transcatheter renal denervation there was a significant drop in blood pressure of 33/11 mmHg (p < 0.0001) that occurred after 6 months compared to a control group receiving unmodified pharmacological treatment (11).
|Study Type :||Interventional (Clinical Trial)|
|Estimated Enrollment :||50 participants|
|Intervention Model:||Parallel Assignment|
|Masking:||None (Open Label)|
|Official Title:||Long Term Study on the Possible Beneficial Effects of Catheterised Renal Denervation in Patients With Heart Failure and Left Ventricular Systolic Dysfunction Who Are Already on Standard Medical Therapy.|
|Study Start Date :||June 2012|
|Estimated Primary Completion Date :||September 2013|
|Estimated Study Completion Date :||June 2016|
|No Intervention: Standard medical therapy|
Experimental: Renal denervation + standard medical therapy
Patients in this arm will undergo catheterised renal denervation in addition to having optimization of medical therapy for heart failure.
Procedure: Catheterised renal denervation
Other Name: Symplicity, Ardian / Medtronic, USA
- Change in serum NT-proBNP at 6 months and 1 year from baseline in both groups. [ Time Frame: 6 months and 1 year ]The level of NT-proBNP (N-terminal prohormone of Brain Natriuretic Peptide) is a reliable indicator of the severity of heart failure. Lowering levels will indicate improvement in the heart function.
- Reduction in the number of hospitalizations and/or deaths due to cardiovascular causes. [ Time Frame: 1 year to 4 years ]
- Significant Renal impairment and symptomatic hypotension. [ Time Frame: 6 months to 1 year ]Increase in serum creatinine of 2 times the baseline or decrease in estimated glomerular filtration according to MDRD (Modification of Diet in Renal Disease) by more than 50% from baseline will be used to assess renal function.
To learn more about this study, you or your doctor may contact the study research staff using the contact information provided by the sponsor.
Please refer to this study by its ClinicalTrials.gov identifier (NCT number): NCT01870310
|Contact: Dagmar Strnkova, Mgr.||+420 588 443 email@example.com|
|Contact: Albert Louis, MUDr.||+420 588 443 firstname.lastname@example.org|
|University Hospital, Olomouc||Recruiting|
|Olomouc, Czech Republic, 775 20|
|Contact: Miloš Táborský, doc., MUDr., CSc., FESC, MBA +420 588 443 201 email@example.com|
|Contact: Albert Louis, MUDr. +420 588 443 238 firstname.lastname@example.org|
|Principal Investigator: Miloš Táborský, doc., MUDr., CSc., FESC, MBA|
|Sub-Investigator: Albert Louis, MUDr.|
|Principal Investigator:||Miloš Táborský, doc., MUDr., CSc., FESC, MBA||Head of Department of First Clinic of Internal Medicine - Cardiology, University Hospital, Olomouc.|