Measuring Electrical Resistance of Different Tissues on the Outer Surface of the Heart
|Cardiomyopathies Ventricular Dysfunction Myocardial Infarction Arrhythmia|
|Study Design:||Observational Model: Cohort
Time Perspective: Prospective
|Official Title:||Impedance Measurement of Epicardial Substrate for Ventricular Arrhythmias: Case Control Series of Patients With and Without Myocardial Scarring|
|Study Start Date:||April 2006|
|Study Completion Date:||January 2008|
|Primary Completion Date:||July 2006 (Final data collection date for primary outcome measure)|
The treatment of cardiac arrhythmias with endocardial catheter ablation has evolved rapidly over the past few decades. At the time of this writing, the ablation of almost all atrial and ventricular arrhythmias has been described in the literature. Multiple energy modalities (e.g. radiofrequency, cryotherapy) and approaches (e.g. retrograde aortic, transseptal puncture) have been described, yet ablation of some rhythms is not as successful as others.
The realization that ventricular tachycardia (VT) in the setting of Chagas Disease can originate in the epicardium has lead to the development of a percutaneous, transthoracic epicardial approach to mapping and ablation of this arrhythmia. This approach has now been applied to patients with VT in the setting of ischemic and nonischemic heart disease at many centers throughout the world. Traditional mapping technologies are utilized on the epicardium to define scarred heart tissue and locate the VT circuit.
It is well known that human hearts display a variable amount of fat overlying the epicardium. Not only is the coronary vasculature embedded in a layer of adipose tissue, but the rest of the heart may have areas of epicardial fat. As fat is an insulator and does not generate or easily conduct electrical activity, current mapping techniques may classify epicardial fat incorrectly as myocardial scar. This may have important effects on the ability to diagnose and treat arrhythmias with epicardial ablation.
Please refer to this study by its ClinicalTrials.gov identifier: NCT00291174
|United States, Pennsylvania|
|Hospital of the University of Pennsylvania|
|Philadelphia, Pennsylvania, United States, 19104|
|Principal Investigator:||David J. Callans, MD||University of Pennsylvania, Dept of Medicine, Cardiology Division|