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This is a research study that is evaluating blood markers which may predict which patients who receive CRT will improve. Congestive heart failure (CHF) is associated with increased oxidative stress, a condition where abnormal oxygen forms are produced. These forms harm the cells of the heart and cause damage to the heart muscle. We would like to see if blood levels of these forms improve after CRT, and if they can be measured early after surgery to predict who will and who will not benefit from surgery.
Congestive heart failure (CHF) is a common diagnosis with significant clinical impact. Although medical therapy exists, many patients on optimal medical treatment are still highly symptomatic. About 1/3 of these patients have a condition known as "dyssynchrony", where the walls of the heart beat in an uncoordinated way, causing worsening of CHF symptoms. A newer therapy known as cardiac resynchronization therapy (CRT) has been successful in decreasing symptoms in these dyssynchronous patients. It involves surgical placement of a pacemaker containing 3 wires- one in the top part of the heart (atrium) to coordinate the top and bottom parts of the heart beat, and two on the bottom to coordinate the bottom parts of the heart beat (ventricles). This treatment, however, does not work for up to 1/3 of patients with dyssynchrony.
Recent studies have found that CHF is associated with increased oxidative stress. This is a condition where abnormal oxygen forms are produced. These forms harm the cells of the heart, causing them to beat abnormally and causing damage to the heart muscle. We would like to see if levels of these forms improve after CRT, and if they can be measured early after surgery to predict who will and who will not benefit from surgery.
In this study, we will compare blood markers of oxidative stress between patients with CHF and an already-collected set of control patients to confirm these levels are elevated at baseline. Then, we will perform CRT surgery and implant pacemakers in the CHF patients. At 1 week and 3 months postoperatively, we will measure blood markers again, and see if they have improved in patients whose symptoms have improved. Patients will undergo echocardiograms to document their abnormal hearts, do a 6 minute hall walk to measure their exercise tolerance, and take a standardized questionnaire to measure their symptoms of CHF. These test results will be compared pre and post CRT to assess response to therapy.
Intervention Model: Single Group Assignment, Masking: Open Label, Primary Purpose: Treatment
Congestive Heart Failure
Active, not recruiting
Published on BioPortfolio: 2014-08-27T03:12:37-0400
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A cardiotonic glycoside obtained mainly from Digitalis lanata; it consists of three sugars and the aglycone DIGOXIGENIN. Digoxin has positive inotropic and negative chronotropic activity. It is used to control ventricular rate in ATRIAL FIBRILLATION and in the management of congestive heart failure with atrial fibrillation. Its use in congestive heart failure and sinus rhythm is less certain. The margin between toxic and therapeutic doses is small. (From Martindale, The Extra Pharmacopoeia, 30th ed, p666)
Agents that have a strengthening effect on the heart or that can increase cardiac output. They may be CARDIAC GLYCOSIDES; SYMPATHOMIMETICS; or other drugs. They are used after MYOCARDIAL INFARCT; CARDIAC SURGICAL PROCEDURES; in SHOCK; or in congestive heart failure (HEART FAILURE).
A semisynthetic digitalis glycoside with the general properties of DIGOXIN but more rapid onset of action. Its cardiotonic action is prolonged by its demethylation to DIGOXIN in the liver. It has been used in the treatment of congestive heart failure (HEART FAILURE).
A heterogeneous condition in which the heart is unable to pump out sufficient blood to meet the metabolic need of the body. Heart failure can be caused by structural defects, functional abnormalities (VENTRICULAR DYSFUNCTION), or a sudden overload beyond its capacity. Chronic heart failure is more common than acute heart failure which results from sudden insult to cardiac function, such as MYOCARDIAL INFARCTION.
Disease of CARDIAC MUSCLE resulting from chronic excessive alcohol consumption. Myocardial damage can be caused by: (1) a toxic effect of alcohol; (2) malnutrition in alcoholics such as THIAMINE DEFICIENCY; or (3) toxic effect of additives in alcoholic beverages such as COBALT. This disease is usually manifested by DYSPNEA and palpitations with CARDIOMEGALY and congestive heart failure (HEART FAILURE).
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