Simultaneous dual AV node antegrade conduction (2 for 1) and lower common pathway (2-1) block illustrate AVNRT physiology.

We report a rare case of spontaneous initiation of Atrioventricular nodal reentry tachycardia (AVNRT) via 2 for 1 phenomenon, into a 2:1 AV block due to lower common pathway block and finally transition to 1:1 tachycardia. The premature atrial p wave traverses down both the fast and slow pathway simultaneously during 2 for 1 initiation and is met with subsequent typical AVNRT with 2:1 block. Infranodal location of the block is confirmed on electrophysiologic testing and is also cured by intervention. This rare electrographic presentation is not only pathognomonic for AVNRT with lower common pathway block but also illustrates its dual conduction physiology.

KCNE regulation of KvLQT1 channels: structure-function correlates.

K(+) channels play a central role in determining resting membrane potential and cellular excitability. There is growing recognition that the channels exist not as independent units but as macromolecular complexes able to integrate a plethora of cellular signals to fine-tune channel activities. Interaction of K(+) channels with accessory proteins and subunits is increasingly reported as providing mechanisms for channels to respond to a variety of stimuli beyond just changes in membrane potential. One such association is that between some voltage-gated K(+) channels and the proteins encoded by the KCNE family of genes. The significance of these interactions is manifest in reports of genetic disorders such as the Long QT Syndrome linked to KCNE mutations and proarrhythmic drug susceptibilities from KCNE polymorphisms. The mechanism by which KCNE-encoded proteins control channel behavior is an emerging story. This article reviews some of the recent work addressing the prototypical KCNE-channel interaction between minK and KvLQT1.

Heart rate variability and diastolic heart failure.

Diastolic heart failure accounts for up to 40% of patients with congestive heart failure (CHF), and is associated with a better prognosis as compared to patients with systolic dysfunction. Nevertheless, patients with diastolic dysfunction have a significantly higher mortality as compared to the normal population. Reduced heart rate variability (HRV), a marker of autonomic dysfunction, is associated with increased mortality in patients with systolic heart failure. We therefore sought to determine to what extent HRV is altered in a population of patients with diastolic heart failure. Twenty-four hour ambulatory (Holter) recordings were performed in 19 consecutive patients with diastolic heart failure, in 9 patients with systolic heart failure, as well as in 9 healthy volunteers (normal controls). Time and frequency domain HRV variables were obtained for all three groups of patients. Both Time and Frequency domain variables were found to be reduced in both heart failure groups compared to normal controls. When compared with each other, patients with diastolic function had relatively higher values of HRV variables, compared to those with systolic dysfunction (SDNN, Total power, ULF power, all P