Introduction: Catheter-based radiofrequency (RF) ablation is generally regarded as the standard approach for patients with ventricular tachycardia (VT) refractory to antiarrhythmic drug therapy and may be considered as a first-line approach when there is a preference to avoid these agents. Patients with a history of cardiac surgery may have VT substrate inaccessible to catheter ablation due to intervening prosthetic materials or scar.
Methods And Results: This article describes a 55-year-old patient with a history of surgically repaired subvalvular aortic stenosis and subsequent valve-sparing root replacement who presented with sustained VT.
Background: Many genetic nonischemic dilated cardiomyopathies (NICMs) cause ventricular tachycardias (VTs) originating from scar substrate identified as areas of low electrogram voltage. Substrate locations vary, and the causes of scar are not well defined.
Objective: This study evaluated VT substrate locations in genetic NICM patients undergoing VT ablation to evaluate spatial relationships between specific variants and substrate locations.
Objective: Inhibition of adenosine kinase (ADK), via augmenting endogenous adenosine levels exerts cardiovascular protection. We tested the hypothesis that ADK inhibition improves microvascular dilator and left ventricle (LV) contractile function under metabolic or hemodynamic stress.
Methods And Results: In Obese diabetic Zucker fatty/spontaneously hypertensive heart failure F1 hybrid rats, treatment with the selective ADK inhibitor, ABT-702 (1.