Regular atrial tachycardias classically are classified into flutter or tachycardia, depending on the rate and presence of a stable baseline on the ECG. However, current understanding of electrophysiology atrial tachycardias makes this classification obsolete, because it does not correlate with mechanisms. The proposed classification is based on electrophysiologic mechanisms, defined by mapping and entrainment. Radiofrequency ablation of a critical focus or isthmus can afford proof. Focal tachycardias are characterized by radial spread of activation and endocardial activation not covering the whole cycle. Ablation of the focus of origin interrupts the tachycardia. The mechanism of focal firing is difficult to ascertain by clinical methods. Macroreentrant tachycardias are characterized by circular patterns of activation that cover the whole cycle. Fusion can be shown during entrainment on the ECG or by multiple endocardial recordings. Ablation of a critical isthmus interrupts the tachycardia. Macroreentry can occur around normal structures (terminal crest, eustachian ridge) or around atrial lesions. The anatomic bases of these tachycardias must be defined, to guide appropriate treatment. Atrial flutter is a mere description of continuous undulation on the ECG, and only some strictly defined typical flutter patterns correlate with right atrial macroreentry bounded by the tricuspid valve, terminal crest, and caval vein orifices. This classification should be considered open, as some classically described tachycardias, such as reentrant sinus tachycardia, inappropriate sinus tachycardia, and type II atrial flutter, cannot be classified accurately. Furthermore, the possibility of fibrillatory conduction makes the limits with atrial fibrillation still ill defined.
In addition to the known effects of PKA and cAMP, HERG channels are also modulated by PKC. The molecular mechanisms of this PKC-dependent process are not completely understood but do not depend on direct PKC-dependent phosphorylation of the channel.
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