Abstract
Coronary artery disease and heart failure carry concurrent risk for atrial fibrillation and life-threatening ventricular arrhythmias. We review evidence indicating that at therapeutic concentrations, ranolazine has potential for dual suppression of these arrhythmias. Mechanisms and clinical implications are discussed.
Publication types
-
Research Support, Non-U.S. Gov't
-
Review
MeSH terms
-
Acetanilides / therapeutic use*
-
Action Potentials
-
Animals
-
Anti-Arrhythmia Agents / therapeutic use*
-
Atrial Fibrillation / etiology
-
Atrial Fibrillation / metabolism
-
Atrial Fibrillation / physiopathology
-
Atrial Fibrillation / prevention & control*
-
Coronary Artery Disease / complications
-
Coronary Artery Disease / drug therapy
-
Coronary Artery Disease / physiopathology
-
Electrocardiography
-
Heart Conduction System / drug effects*
-
Heart Conduction System / metabolism
-
Heart Conduction System / physiopathology
-
Heart Failure / complications
-
Heart Failure / drug therapy*
-
Heart Failure / physiopathology
-
Humans
-
Myocardial Ischemia / complications
-
Myocardial Ischemia / drug therapy*
-
Myocardial Ischemia / physiopathology
-
Piperazines / therapeutic use*
-
Ranolazine
-
Sodium / metabolism
-
Sodium Channel Blockers / therapeutic use*
-
Treatment Outcome
-
Ventricular Fibrillation / etiology
-
Ventricular Fibrillation / metabolism
-
Ventricular Fibrillation / physiopathology
-
Ventricular Fibrillation / prevention & control*
Substances
-
Acetanilides
-
Anti-Arrhythmia Agents
-
Piperazines
-
Sodium Channel Blockers
-
Sodium
-
Ranolazine