The morphology of unipolar potentials predicts the depth of activation foci

Background: The depth of an arrhythmic focus is a major determinant of ablation procedural outcome. This study examined the relationship between the morphology of unipolar potentials and the depth and horizontal distance to activation foci. Methods: Unipolar left ventricular epicardial mapping was performed in 7 open-chest dogs, using silicon sheets with 12 unipolar electrodes 1 mm apart, during bipolar pacing from an octopolar plunge electrode with 1-mm interelectrode spacing. The morphology of the unipolar electrograms was classified as QS, rS, qrS, qRS, rsr’S, or rsR’S. Results: A QS complex was recorded immediately above a subepicardial or mid-myocardial pacing site. An rS complex was recorded away from a subepicardial pacing site. A positive wave originating from a down sloping deflection (R-in-QR) such as r wave in qrS, R wave in qRS, r′ wave in rsr’S or R′ wave in rsR’S complexes was observed when the recording was above a deep myocardial pacing site or away from a mid-myocardial pacing site. The amplitude of negative wave immediately before R-in-QR (Q-in-QR) was inversely correlated with the horizontal (R=−0.40; P<0.0001) and linear (R=−0.22; P=0.0006) distance to the pacing site, and the amplitude of R-in-QR was positively correlated with the horizontal (R=0.25; P=0.0001) and linear (R=0.29; P<0.0001) distance to the pacing site. The amplitude of the initial r wave was not correlated with the depth or horizontal and linear distance to the pacing site. Conclusion: The morphology of unipolar electrograms predicted the horizontal distance and the depth of nearby foci of activation

The origin of lumbar subcutaneous edema: two case reports

Since magnetic resonance imaging (MRI) is widely used to evaluate complaints of low back pain, there have been many reports of lumbar subcutaneous edema (LSE). However, the mechanism underlying its development is unknown. We herein report 2 cases that showed the reduction of LSE. These cases suggest details concerning the mechanism underlying the development of LSE. The first case was an obese 70-year-old woman with a history of chronic back pain due to lumbar canal stenosis. MRI revealed LSE extending from the level of the L2 vertebral body to the sacrum. However, LSE was reduced following weight loss due to a stomach ulcer. This case clearly indicated obesity as the cause of LSE. The second case was a nonobese 31-year-old woman with acute excruciating low back pain due to thoracolumbar fascia strain. LSE was observed at the level of the L3-L4 vertebral body. Two weeks later, her low back pain and LSE were reduced. This case suggests that the origin of LSE was impairment of the thoracolumbar fascia due to strain. We hypothesize that the mechanism underlying the development of LSE may be lymphatic or interstitial fluid pooling due to disturbance of the lumbar fascia

Left intraventricular dyssynchrony caused by a false tendon

Left ventricular (LV) false tendons are usually benign, intraventricular myocardial structures, which may cause functional malfunction or deformation of the LV cavity due to mechanical stretching and dilatation of the LV wall. We present a case of non-ischemic cardiomyopathy complicated with intraventricular dyssynchrony that was caused by complete left bundle branch block and the mechanical pressure exerted by the stiff false tendon on the weakened mid-septum during systole

Measurement of the ventriculoatrial interval from the coronary sinus during para-Hisian pacing may fail to distinguish ventriculoatrial nodal conduction from conduction over a septal accessory pathway

Background: Para-Hisian pacing (PHP) helps differentiate retrograde conduction over an accessory pathway (AP) from retrograde conduction over the atrioventricular (AV) node. This study examined a potential limitation of this technique, focusing on the measurement of the ventriculoatrial (V–A) interval from the coronary sinus (CS) during PHP. Methods: Our subjects were 9 patients undergoing electrophysiological studies before successful catheter ablation of a posteroseptal AP. During PHP, retrograde conduction occurred over an AP when the pacing stimulus to atrium (S–A) interval recorded near the AP remained unchanged whether the His bundle (HB) was captured or not (pattern 1), or when a loss of HB capture was associated with an increase in the S–A interval and no change in the V–A interval near the AP (pattern 2). Results: Patterns 1 and 2 were observed in 5 (56%) and 2 (22%) patients, respectively. However, in the remaining 2 patients (22%), loss of HB capture during PHP was associated with an increase in the S–A interval (as in pattern 2), whereas the V–A interval near the AP could not be measured because no ventricular electrogram was visible on the CS recording (pattern 3); therefore, the presence of AP could not be confirmed by PHP. In patterns 2 and 3, the atrial activation sequence remained unchanged whether the HB was captured or not. Conclusions: PHP may not be able to discriminate between a retrograde septal AP and AV nodal conduction in patients whose proximal CS recording shows no visible ventricular electrogram