Letter to the Editor in response to “Role of Subcutaneous Leadless Implantable Cardioverter Defibrillator in Young Patients
NaumanKhalid, M.D.; PoojaSareen, MD; Sarah Aftab Ahmad, M.D.; Sarah ;,Houston Methodist Hospital, Houston, Texas
December 8, 2018
To the Editor:
We enjoyed reading the article by Gwozdz et al. in the recent issue of the Methodist DeBakey Cardiovascular Journal.1 The authors have described therapeutic endovascular modalities of the upper and lower extremity central venous thrombosis in contemporary practice in the published special edition on venous interventions.
In the present article, the authors state that a 34-year-old woman received a permanent pacemaker for Brugada syndrome (BrS).1 The pacemaker should be correctly identified as a single-chamber implantable converter defibrillator (ICD) as it is the correct form of intervention for patients with BrS to prevent sudden cardiac death. BrS is a genetic channelopathy most commonly involving the SCN5A gene, which encodes the cardiac sodium channel function, and leads to increased incidence of ventricular arrhythmias. The illustrated venogram also appears to demonstrate a single lead, which appears to represent an ICD lead. Also relevant to the case, the rate of venous thrombosis and stenosis is usually directly proportional to the increasing diameter and the increasing number of leads. An ICD lead usually has a larger diameter than a pacemaker lead, thus being more prone to stenosis.
The current practice guidelines recommend the placement of an ICD for primary or secondary prevention of sudden cardiac death in symptomatic BrS patients.2,3 Leadless or subcutaneous ICDs have recently begun gaining favor, especially in younger patients (such as those with channelopathy), to prevent the associated complications of the transvenous cardiac device leads.4,5 The extrathoracic placement and elimination of transvenous endocardial leads makes these miniaturized devices particularly attractive options in the younger population since these patients often require multiple device exchanges in their lifetime, which increases the risks of other complications such as device infection.4,5
Nauman Khalid, M.D.a; Pooja Sareen, M.D.b; Sarah Aftab Ahmad, M.D.c; Lovely Chhabra, M.D.d
aMedStar Washington Hospital Center, Washington, DC
bHarrisburg Medical Center, Harrisburg, Illinois
cSaint Francis Medical Center, Monroe, Louisiana
dHeartland Regional Medical Center, Marion, Illinois
- Gwozdz AM, Silickas J, Smith A, Saha P, Black SA. Endovascular Therapy for Central Venous Thrombosis. Methodist Debakey Cardiovasc J. 2018 Jul-Sep;14(3):214-8.
- Khalid N, Chhabra L, Kluger J. PYREXIA-INDUCED BRUGADA PHENOCOPY. J Ayub Med Coll Abbottabad. 2015;27:228-31.
- Chhabra L, Spodick DH. Brugada pattern masquerading as ST-segment elevation myocardial infarction in flecainide toxicity. Indian Heart J. 2012 Jul;64(4):404-7.
- Abu-El-Haija B, Bhave PD, Campbell DN, et al. Venous Stenosis After Transvenous Lead Placement: A Study of Outcomes and Risk Factors in 212 Consecutive Patients. J Am Heart Assoc. 2015 Aug;4(8):e001878.
- Müller MJ, Dieks JK, Backhoff D, et al. Efficacy and safety of non-transvenous cardioverter defibrillators in infants and young children. J Interv Card Electrophysiol. 2018 Sep 25. doi: 10.1007/s10840-018-0451-y. [Epub ahead of print]
Response from the author:
We are grateful to the authors for identifying the error in our original manuscript and for elaborating on the role and function of pacemakers in Brugada Syndrome.
Stephen A. Black, M.D.
Guy’s and St Thomas’ NHS Trust