Minimalistic strategy for coronary sinus lead implant: A single tool capable of electrophysiological mapping, pressure measurement, and angiography

2020 ◽  
Vol 43 (10) ◽  
pp. 1072-1077
Author(s):  
Rahul Samanta ◽  
Ben Ng ◽  
Andrew Ha ◽  
Abhishek Bhaskaran ◽  
Mahmoud Bokhari ◽  
...  
Keyword(s):  
Coronary Sinus ◽  
Pressure Measurement ◽  
Coronary Sinus Lead

scholarly journals Ratchet mechanism selectively causing idiopathic macrodislodgement of an active-fixation coronary sinus lead: a case report

2020 ◽  
Author(s):  
Pier Giorgio Golzio ◽  
Arianna Bissolino ◽  
Raffaele Ceci ◽  
Simone Frea
Keyword(s):  
Coronary Sinus ◽  
Pulse Generator ◽  
Thoracic Inlet ◽  
Ratchet Mechanism ◽  
Active Fixation ◽  
First Case ◽  
Time In Literature ◽  
Pacemaker Leads ◽  
Coronary Sinus Lead ◽  
Arm Motion

Abstract Background ‘Idiopathic’ lead macrodislodgement may be due to Twiddler’s syndrome depending on active twisting of pulse generator within subcutaneous pocket. All leads are involved, at any time from implantation, and frequently damaged. In the past few years, a reel syndrome was also observed: retraction of pacemaker leads into pocket without patient manipulation, owing to lead circling the generator. In other cases, a ‘ratchet’ mechanism has been postulated. Reel and ratchet mechanisms require loose anchoring, occur generally briefly after implantation, with non-damaged leads. We report the first case of an active-fixation coronary sinus lead selective macrodislodgement involving such ratchet mechanism. Case summary A 65-year-old man underwent biventricular defibrillator device implantation, with active-fixation coronary sinus lead. Eight months later, he complained of muscle contractions over device pocket. At fluoroscopy, coronary sinus lead was found near to pocket, outside of thoracic inlet. Atrial and ventricular leads were in normal position. After opening pocket, a short tract of coronary sinus lead appeared anteriorly dislocated to generator, while greater length of lead body twisted a reel behind. The distal part of lead was found outside venous entry at careful dissection. Atrial and ventricular leads were firmly anchored. Discussion Our case is a selective ‘Idiopathic’ lead macrodislodgement, possibly due to a ratchet mechanism between the lead and the suture sleeve, induced by normal arm motion; such mechanism incredibly, and for first time in literature involves a coronary sinus active-fixation lead. Conclusion Careful attention should always be paid to secure anchoring even of active-fixation coronary sinus leads.

Optimization of coronary sinus lead placement targeted to right-to-left delay in patients undergoing cardiac resynchronization therapy

EP Europace ◽  
2018 ◽  
Vol 21 (3) ◽  
pp. 502-510 ◽  
Author(s):  
Daniele Oddone ◽  
Diana Solari ◽  
Giuseppe Arena ◽  
Roberto Mureddu ◽  
Renè Nangah ◽  
...  
Keyword(s):  
Cardiac Resynchronization Therapy ◽  
Coronary Sinus ◽  
Cardiac Resynchronization ◽  
Resynchronization Therapy ◽  
Lead Placement ◽  
Coronary Sinus Lead

scholarly journals Requirement for coronary sinus lead interventions and effectiveness of endovascular replacement during long-term follow-up after implantation of a resynchronization device

EP Europace ◽  
2009 ◽  
Vol 11 (5) ◽  
pp. 607-611 ◽  
Author(s):  
C. J. W. Borleffs ◽  
R. J. van Bommel ◽  
S. G. Molhoek ◽  
J. G. de Leeuw ◽  
M. J. Schalij ◽  
...  
Keyword(s):  
Coronary Sinus ◽  
Long Term Follow Up ◽  
Coronary Sinus Lead

Retrograde Buddy Wire Technique for Coronary Sinus Lead Placement-An Approach to Overcome Coronary Vein Angulation

2011 ◽  
Vol 36 (2) ◽  
pp. e41-e44
Author(s):  
DAVID P. DOBESH ◽  
CONSTANTINOS A. COSTEAS ◽  
MANDHAVI PAMIDI ◽  
MARC ROELKE ◽  
DONALD G. RUBENSTEIN
Keyword(s):  
Coronary Sinus ◽  
Coronary Vein ◽  
Lead Placement ◽  
Coronary Sinus Lead ◽  
Buddy Wire

Extraction of a coronary sinus lead

2017 ◽  
Vol 18 (10) ◽  
pp. 807-810 ◽  
Author(s):  
Luca Bontempi ◽  
Francesca Vassanelli ◽  
Alessandro Lipari ◽  
Elisa Locantore ◽  
Marco Belotti Cassa ◽  
...  
Keyword(s):  
Coronary Sinus ◽  
Coronary Sinus Lead

Abstract 3071: Reversible Transmural Electrical Dyssynchrony in Pacing-Induced Congestive Heart Failure

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Nilesh Mathuria ◽  
Jianwen Wang ◽  
April L Gilbert ◽  
Daryl G Schulz ◽  
Mihir Naware ◽  
...  
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Wall Thickness ◽  
Coronary Sinus ◽  
Electrical Conduction ◽  
Recovery Of Function ◽  
Conduction Delay ◽  
Conduction Time ◽  
Ventricular Dyssynchrony ◽  
Coronary Sinus Lead

Introduction: Inter and Intra-ventricular dyssynchrony can develop during congestive heart failure (CHF). We investigated transmural electrical conduction properties within the LV wall during CHF and subsequent recovery. Methods: Biventricular pacemakers were implanted in 8 normal mongrel dogs (mean weight: 38 kg), and continuous RV pacing (230 –250 bpm) was initiated to induce CHF. Echocardiography, catheterization, and LV myocardial biopsy were performed biweekly while pacing was temporarily stopped. At each catheterization, an intracardiac electrode-catheter was placed at the LV endocardium against the pacemaker coronary sinus lead tip located at the LV epicardium. Intrinsic transmural electrical conduction delay was measured by recording endocardial electrograms via the electrode-catheter and epicardial electrograms via the pacemaker coronary sinus lead, both in posterolateral LV. The conduction delay was also assessed during LV pacing via the endocardial catheter and measuring the time to the coronary sinus lead tip. Pacing was stopped in 4 dogs with CHF to allow for recovery of function. All times were corrected for heart rate. Results: All dogs developed CHF within 2– 4 wks of pacing from baseline (EF: 27±8 vs. 49±4%; LVEDP: 20±9 vs. 6±3 mmHg; QRS: 98±8 vs. 70±14 msec with no LBBB). There was no change in LV wall thickness during CHF compared to baseline (0.9 cm), while LV myocyte size increased (21.7±6.6 vs. 16.2±1.5 μm). Transmural endocardial-to-epicardial intrinsic electrical conduction time lengthened during CHF compared to baseline (35±13 vs. 10±5msec, P<0.001). In dogs recovering from CHF 2– 4 wks after cessation of pacing, intrinsic transmural endocardial-to-epicardial conduction time shortened compared to CHF (10±9 vs. 39±1ms, n=4), which was consistent with LV endocardial pacing (recovery: 47.5±6 ms; CHF: 70.7±9 ms, n=3). Conclusions: Electrical transmural dyssynchrony develops as a consequence of pacing-induced CHF, and is reversible upon recovery of cardiac function. These changes are not associated with LV wall thickness. This novel finding suggests another aspect of ventricular dyssynchrony that may not be reflected by routine noninvasive modalities and warrants further investigation.

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