Factors Associated with Blunt Cerebrovascular Injury in Patients with Cervical Spine Injury

Blunt cerebrovascular injury (BCVI) is known to be a potentially fatal complication of cervical spine injury (CSI). Methods for screening the appropriate population remain to be elucidated, especially in Japan. This retrospective study was conducted to predict the risk factors relevant to BCVIs. Among 92 patients with CSI transferred to our institution from April 2007 to March 2012, 40 patients (35 men, 5 women) with neurological deficits and/or significant cervical spine fracture including fracture of transversarium, facet, body, lamina, and spinous process, underwent multi-detector computed tomography angiography (MDCTA) and magnetic resonance angiography (MRA), which identified 10 patients with BCVI [2 carotid artery injuries (BCAIs) and 9 vertebral artery injuries (BVAIs); 1 patient suffered both]. Univariate analyses exploring associations between individual risk factors and BCVI and BVAI were performed using Fisher''s exact test and Chi-square test for dichotomous variables and the unpaired t-test for continuous variables. Multiple logistic regression analyses for BCVI and BVAI were carried out using stepwise methods. On univariate and multivariate analysis, hyperextension injury was significantly associated with BVAI (p = 0.01 and p = 0.02), and subluxation (dislocation of vertebral body > 5 mm) was a significant predictor of BCVI (p = 0.04 and p = 0.03) and BVAI (p = 0.01 and p = 0.01). Prompt evaluation for BCVIs is recommended in CSI patients with hyperextension injury and dislocation of the vertebral body.     

Mid-Diastolic Potential is Related to the Reentrant Circuit in a Patient with Verapamil-Sensitive Idiopathic Left Ventricular Tachycardia

Mid-Diastolic Potential in Idiopathic VT. We report a case of verapamil-sensitive idiopathic ventricular tachycardia in which a mid-diastolic potential (MDP) 45 msec preceding the Purkinje potential ( P potential) was recorded. Pacing during the tachycardia caused concealed entrainment, and the stimulus–QRS interval was equal to the P potential–QRS interval. The interval between the last pacing stimulus and the next P potential (postpacing interval) was longer than the ventricular tachycardia cycle length, but the MDP was orthodromically activated. These findings suggest that the MDP was on the reentrant circuit and the P potential was not on the reentrant circuit, but a bystander.     

Radiofrequency Catheter Ablation of Concealed Atrioventricular Accessory Pathways Using a "Simultaneous Pacing Method"

The retrograde atrial potential at a successful ablation site is usually obscured by the wide and large ventricular potential during atrioventricular reentrant tachycardia or ventricular pacing, which makes it difficult to determine the appropriate ablation site for concealed accessory pathway. A pacing maneuver named the “simultaneous pacing method” is proposed herein to differentiate the retrograde atrial potential from the ventricular potential for a successful ablation of the concealed accessory pathway. Catheter ablation was performed in 12 patients with a single left free-wall concealed accessory pathway. The atrial insertion site was determined by the simultaneous pacing method in six patients (group I) and by ventricular pacing in six patients (group II), In the simultaneous pacing method, electrograms recorded during ventricular pacing in the earliest retrograde atrial activation site are a fusion of the ventricular potential and the following retrograde atrial potential. When atrial and ventricular pacings are performed simultaneously (simultaneous pacing), the end portion of the electrograms recorded at the same site is solely the ventricular component, because atrial is activated earlier. The atrial potential can be confirmed during ventricular pacing in comparison with the electrograms during the “simultaneous pacing.” Radiofrequency catheter ablation was successful in eliminating conduction through the accessory pathway in all 12 patients. The radiofrequency applications in group I were significantly fewer than those in group II (1.7 ± 1.0 in group I, 5.3 ± 3.2 in group II, P < 0.05). The total procedure time in group I was significantly shorter than in group II (57.8± 15.7 vs 106.7 ± 41.6 mins in group II. respectively, P < 0.05). The fluoroscopy time in group I was significantly shorter than in group II (54.0 ± 7.9 vs 81.3± 26.3 mins, respectively, P < O.05). We were able to determine the atrial insertion site of accessory pathways by the simultaneous pacing method. The simultaneous pacing method was useful in eliminating concealed left free-wall accessory pathways.     

Significance of Ventricular Pacing Site in Manifest Entrainment During Orthodromic Atrioventricular Reentrant Tachycardia with Left-Sided Accessory Pathway

We examined entrainment by ventricular pacing in six patients during orthodromic atrioventricular reentrant tachycardia (AVRT) utilizing a left-sided lateral accessory pathway. Constant fusion and progressive fusion were demonstrated in all patients by left ventricular pacing during tachycardia, but in none of the patients by right ventricular pacing. When left ventricular pacing was performed during AVRT, the antidromic wave front from the pacing impulse (n) collided with the orthodromic wave front of the previous pacing beat (n - 1) within the ventricle, therefore, constant fusion and progressive fusion were demonstrated in the surface electrocardiographic QRS complexes. On the other hand, when right ventricular pacing was performed during orthodromic AVRT, the antidromic wave front from the pacing impulse (n) collided with the orthodromic wave front of the previous paced beat (n - 1) within the normal atrioventricular pathway, and constant fusion and progressive fusion were therefore not demonstrated. These phenomena were explained by the relationship of the ventricular pacing site and the reentrant circuit. This study demonstrates the importance of the pacing site in manifest entrainment of orthodromic AVRT during ventricular pacing.     

Differential Response of QTU Interval to Exercise, Isoproterenol, and Atrial Pacing in Patients with Congenital Long QT Syndrome

Sympathetic stimulation is well known to contribute to the genesis of QTU prolongation and ventricular lachyarrhythmias in patients with congenital long QT syndrome. In this study, we performed exercise treadmill testing, isoproterenol infusion (1–2 μg/min), and right atrial pacing (cycle length 500 msec) in 11 patients with congenital long QT (LQT) syndrome (LQT group) and in 12 age- and sex-matched controls (control group). The responses of the corrected QT (QT_c; Bazett's method) interval and the TU wave complex tvere evaluated. The QT_c interval was prolonged from 482 ± 63 msec^1/2 to 548 ± 28 msec^1/2 by exercise in the LQT group (n = 11; P < 0.005), and this was associated with fusion of the T waves with enlarged U waves, whereas the QT_c interval did not increase with exercise in the control group (n = 12; 402 ± 19 msec^1/2 vs 409 ± 22 msec^1/2). The QT_c interval was also prolonged from 466 ± 50 msec^1/2 to 556 ± 33 msec^1/2 by isoproterenol in the LQT group (n = 7; P < 0.005) in association with morphological changes of the TU wave complex like those seen with exercise, whereas it was only slightly increased from 399 ± 10 msec^1/2 to 436 ± 13 msec^1/2 by isoproterenol in the control group (n = 77; P < 0.001). However, the QT_c interval did not increase with atrial pacing in the LQT group (n = 8; 476 ± 57 msec^1/2 vs 486 ± 59 msec^1/2), whereas it was slightly increased from 400 ± 21 msec^1/2 to 426 ± 18 msec^1/2 by atrial paring in (he control group (n = 8; P < 0.005). These results suggest that sympathetic stimulation plays an important role in the QTU prolongation and marked TU wave complex abnormalities in patients with congenital long QT syndrome.     

Epinephrine-Induced Ventricular Premature Complexes Due to Early Afterdepolarizations and Effects of Verapamil and Propranolol in a Patient with Congenital Long QT Syndrome

Epinephrine-Induced VPCs and EADs in Congenital LQTS. We report a patient with congenital long QT syndrome in whom early afterdcpolarizations (RAl)s) were demonstrated on monophasic action potential (MAP) recordings in the left ventricular mid-base inferior wall. Epinephrine infusion at 5 fig/mm increased the amplitude of the EADs and the late component of the T(U) wave. Epinephrine also induced ventricular premature complexes (VPCs) with right hundle branch block morphology and left-axis deviation that occurred from the peak of the EADs. Verapamil injection (5 nig) during continuous epinephrine infusion abolished all VPCs with a slight reduction in the amplitude of the EADs. Propranolol injection (5 mg) in addition to verapamil further reduced the amplitude of the EADs and the late component of the T(U) wave. These findings suggest that the epinephrinc-induced VPCs were closely related to triggered rhythm arising from the EADs, and that both verapumil and propranoloi were effective for the suppression of VPCs and EADs.     

Increased Dispersion of Repolarization Time Determined by Monophasic Action Potentials in Two Patients with Familial Idiopathic Ventricular Fibrillation

Increased Dispersion of RT in Familial Idiopathic VF. Introduction: The role of increased dispersion of repolarization in the genesis of torsades de pointes in patients with long QT syndrome has been clarified, but its role in the genesis of idiopathic ventricular fibrillation (VF) is not yet known. To investigate the pathogenesis of VF, we recorded monophasic action potentials (MAPs) from two siblings (48- and 36-year-old males) with familial idiopathic VF. Methods and Results: The elder brother (patient I) showed a late r’ wave in lead V¹ and ST segment elevation in leads V¹ through V³. The younger brother (patient 2) had late r’ waves and ST segment elevation in leads II, III, and aVF, and the configurations were very similar to those of patient I. MAPs were recorded from several sites in the right ventricular (RV) and left ventricular (LV) endocardium during constant right atrial pacing. The repolarization time (RT) was defined as the sum of the activation time (AT) and action potential duration (APD) at 90% repolarization. In patient 1, marked prolongation of the AT (140 msec) and the RT (380 msec) was recorded in the RV septum of the outflow tract, and the RT dispersion was markedly increased (125 msec). In contrast, patient 2 showed prolongation of the AT (80 msec) and RT (310 msec), and fractionated electrograms in the RV floor of the inflow tract. The RT dispersion was also increased (80 msec). VF and nonsustained polymorphic ventricular tachycardia were induced by double premature stimulation in patients 1 and 2, respectively. Chronic amiodarone therapy decreased the RT dispersion and suppressed the induction of ventricular tachyarrhythmias in patient 2, although late r’ waves and slight ST segment elevation were unmasked in leads V₁, and V₂. Conclusion: Our data suggest that the increased dispersion of the RT, which was due mainly to a localized conduction delay in the RV, created an arrhythmogenic substrate in the two patients with familial idiopathic VF.