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Background: Appropriate left ventricle (LV) lead placement is integral to successful cardiac resynchronization therapy (CRT). Lead dislodgement and phrenic nerve stimulation (PNS) are major obstacles. A recent trial of an active fixation LV lead (Attain Stability 20066, Medtronic Inc., Tilburg, the Netherlands) has shown promising results. We share our initial experience with this novel active fixation LV lead., Methods: A Medtronic active fixation lead 20066 was used in eight consecutive patients for CRT. An optimal site was chosen and recommended maneuvers were applied for lead fixation. Push and pull maneuvers were used to test stability., Results: There were two initial dislodgements after which we used a transvalvular insertion (TVI) tool that was used in the hemostatic valve during rotation of the lead so that the torque was easily transmitted to the tip. It also allowed better tactile feedback during push-pull tests. There were no further dislodgements in the subsequent six patients. However, in one patient the lead could not be unscrewed due to the tip getting wedged at a distal smaller vein. Repositioning of the LV lead was done in three patients due to PNS or pacing issues. The median time for LV lead placement was 16.5 minutes (interquartile range 9-25 minutes)., Conclusion: The Medtronic Attain Stability 20066 active fixation LV lead can potentially be implanted at any pacing site avoiding PNS and providing better stability. The learning curve is short and additional tricks can be learnt to improve success. Use of TVI while the lead is rotated is beneficial., (© 2014 Wiley Periodicals, Inc.)

We report a case of recurrent postcardiac injury syndrome (PCIS) after pacemaker lead insertion. Each episode was attended by hemorrhagic pleuro-pericardial effusion with drop in hemoglobin levels leading us to consider cardiac perforation and subject the patient to surgical pericardiotomy. However, no perforation or active bleeding was detected on exploration. This unusual case illustrates the occurrence of PCIS following pacemaker lead insertion, mimicking cardiac perforation. This entity should be considered in patients who, after pacemaker lead insertion, develop pericardial and pleural effusion associated with markers of inflammation.

Idiopathic left ventricular tachycardia (ILVT) is a distinct entity that arises in the left ventricle, may have reentrant mechanism and is verapamil-sensitive. Pleomorphism as defined by multiple ventricular tachycardia morphologies is usually associated with either coronary artery disease or cardiomyopathy but very rare in cases of ILVT. In this case report, we describe an unusual case of ILVT with two ECG morphologies of the opposite axis that were successfully eliminated with radiofrequency ablation. The successful ablation sites were closely located to each other in the left lower ventricular septum.

We encountered a 40-year-old man with recurrent symptomatic palpitations manifested as monomorphic ventricular tachycardia (VT) of a right bundle branch block (RBBB) pattern with an inferior frontal axis. Physical examination, chest roentgenogram, and echocardiogram were unremarkable. The VT could be provoked by treadmill exercise testing. Electrophysiologic study revealed that the VT could be reproducibly initiated with either atrial or ventricular pacing at cycle lengths between 500 and 400 ms. With overdrive ventricular pacing, the VT could be terminated. Of note was the observation that intravenous adenosine was not effective, but intravenous verapamil could interrupt the VT. The VT was pace mapped to be arising from a site at the left ventricular outlet tract (LVOT). Notably, during pace mapping, the pacing spike was immediately followed by the beginning of the paced QRS complex, and during VT, there was no time delay between the earliest local activation and the onset of QRS complex. Furthermore, there was no mid-diastolic activity or Purkinje potential that could be recorded during sinus rhythm and VT. Subsequently, the VT was successfully ablated with radiofrequency energy as guided by pace mapping. In summary, an idiopathic VT arising from the LVOT was found to be cycle lengths- and catecholamine-dependent, adenosine-insensitive but verapamil responsive. These unusual features suggest that either microreentry or triggered activity could be the underlying mechanism.

Electrophysiological characteristics of an accessory pathway (AP) with a long ventriculoatrial (VA) interval (arbitrarily defined as > or = 50 ms and absence of continuous electrical activity) and no retrograde decremental property are described in this study. Fifteen patients (group 1) were compared with 171 patients with normal VA conduction (group 2). Mean VA conduction time was 77 +/- 24 versus 34 +/- 12 ms in group 1 versus group 2, respectively. Group 1 patients were older (55 +/- 14 vs 40 +/- 14 years), the male to female ratio was higher (2.8 vs 1.6), and APs were more prevalent on the right (60%) but manifest APs were lower (20% vs 54%) compared to group 2 patients (P < 0.05 in all cases). QRS morphology during induced atrioventricular reciprocating tachycardia was identical in both groups but the tachycardia cycle length was longer in group 1 (373 +/- 29 vs 344 +/- 50 ms, P < 0.05). Retrograde AP block cycle length and effective refractory period were greater in group 1 (362 +/- 59 vs 293 +/- 57 ms; 330 +/- 58 vs 273 +/- 55 ms, both P < 0.05). Adenosine (up to 18 mg) and verapamil (5-10 mg) failed to block the VA conduction via AP during ventricular pacing. In group 1 the number of radiofrequency lesions for a successful ablation were significantly less (3 +/- 2 vs 6 +/- 5, P < 0.05). In conclusion, APs with a long VA interval and no decremental retrograde conduction have electrophysiological characteristics that are different from those with a short VA interval. Role of aging deserves further exploration., (Effect of Pacing Site and Lead Tip to Ring Distance)

This article describes the additional use of incremental atrial burst pacing (A1A1) and double atrial extrastimulation with a predefined fast pathway conducted A2 (A1A2A3), rather than single atrial extrastimulation (A1A2) only, to characterize typical atrioventricular nodal reentrant tachycardia (AVNRT). The authors noted an additional 32% of patients had multiple anterograde AV nodal physiology demonstrated when A1A1 or A1A2A3 protocols were deployed compared to more conventional A1A2 protocols. The A2H2max (449 +/- 147 vs 339 +/- 94 ms) and A3H3max (481 +/- 120 vs 389 +/- 85 ms) were higher in 31 patients where multiple jumps in the AV nodal conduction curve were obtained (group 1) compared to 192 patients where only single jump was obtained (group 2) (both P < 0.01). Postablation, the degree of reduction of A2H2max (49%) and A3H3max (50%) in group 1 was greater than in group 2 (38% and 42%, respectively, P < 0.05). In seven of group 1 patients in whom A1A2A3 stimulation was required to reveal multiple jumps, the A2H2max remained unchanged after ablation (237 +/- 89 vs 214 +/- 59, P > 0.05). A3H3max was the only parameter that shortened significantly after ablation. Generally, successful ablation resulted in loss of multiple discontinuities in A1A1/A1H1 or A2A3/A3H3 curves. In conclusion, a combination of A1A2, A1A1, and A1A2A3 are required to fully elucidate AVNRT. Significant shortening of AHmax or loss of multiple jumps after ablation indicates successful elimination of AVNRT in these patients.

We described a 55-year-old woman with recurrent syncope, complete atrioventricular (AV) block, sparsely scattered idioventricular beats lasting for 56 seconds, and long sinus arrest recorded during the syncopal episode. Paroxysmal atrial flutter-fibrillation was also presented during Holter electrocardiograph (ECG) monitoring without clinical symptom. During tilt test, atrial flutter with variable AV block was induced and the patient suddenly passed out. The vasovagal syncope was successfully treated with a DDD permanent pacemaker with a rate drop response algorithm. Vasovagal syncope with concomitant ventricular asystole and sinus arrest is rare. Aggressive management with permanent pacemaker is strongly advocated in malignant vasovagal syncope.