Current pacemaker therapy requires the use of an electronic pacemaker and implantable leads (What is a Pacemaker? ).  There have been reports of leadless pacemakers that use an implantable yet leadless means to pace the heart (Nanostim Leadless Pacemaker).  A group has recently reported results of their study examining the implantation of pacemaker-related genes.  (Biological Pacemaker using Genes)  A biological pacemaker has the advantages of no indwelling hardware and may eliminate risk of infection from traditional pacemakers.

Cingolani et al utilized a right femoral vein transvenous approach to deliver pacemaker-related genes to the atrioventricular (AV) junction.  Genes expressing dominant-negative inward rectifier potassium channel (Kir2.1AAA) and hyperpolarization-activated cation channel (HCN2) genes were used;  these are responsible for the pacemaker current (If, HCN2) and suppression of the inward rectifier current (Kir2.1).  This overexpression results in junctional pacemaker activity for up to 2weeks.  They found a septal activation pattern similar to those seen during sinus rhythm;  thus, this biological pacemaker may not cause dyssynchrony seen in right ventricular (RV) apical pacing.

Aside from gene overexpression, pluripotent stem cells and specific factors (T box transcription factors) may offer biological pacemaker activity as well.  Obviously, these are all preclinical techniques that may offer an exciting alternative to current electronic, implantable pacemakers.

Nokia has introduced a smart phone that can charge itself wirelessly. (  It is safe to assume that Nokia uses induction based technology to charge the phone. The phone (equipped with a special receiver) is placed on a mat that generates an electromagnetic field. The phone’s special receiver uses this electromagnetic field to charge the phone’s battery. This technology can only power one device at a time and may generate heat during the charging process.

Recently, IDT and Intel partnered to announce the development of an integrated transmitter and receiver chipset for Intel’s wireless charging technology based on resonance technology. (IDT and Intel Partnership)  Magnetic resonance uses electrical components (a coil and a capacitor) to create magnetic resonance. This resonance can then transmit electricity to the receiver (device to be charged) from the transmitter (charging base). Magnetic resonance can power multiple devices at a time and may not generate excessive heat. A nice summary of this technology is available at Fujitsu Summary of Wireless Charging.

These technologies can be disruptive forces in the medical device industry that rely on battery depletion and replacement for subsequent sales (e.g., pacemakers, defibrillator, and noncardiac pulse generators). The device company that incorporates wireless charging into their devices may minimize replacement procedures for patients (and limiting procedural risk) while at the same time stabilizing their market position. Future device upgrades may be software upgrades and licensing that can be performed wirelessly without need for invasive procedure.

Approximately 180000 patients undergo pacemaker implantation in the U.S each year [1]. In addition, the extreme elderly are the most rapidly growing segment of the U.S. [2,3] and pacemakers are commonly implanted in this population. There are reports of pacemaker implant complications (generally clinical trials reporting outcomes and incident complication rates) and fewer reports of complication rates in the extreme elderly (with a persistent exclusion of elderly patients from ongoing clinical trials [4]). A comprehensive review of pacemaker implant complications can help improve informed consent in preoperative patients. Major and minor complications are defined based upon prior reports of device-related complications. [5,6,7,8] Major complications have been defined as death, cardiac arrest, cardiac perforation, cardiac valve injury, coronary venous dissection, hemothorax, pneumothorax, transient ischemic attack, stroke, myocardial infarction, pericardial tamponade, and arterial-venous fistula. Minor complications have been defined as drug reaction, conduction block, hematoma or lead dislodgement requiring reoperation, peripheral embolus, phlebitis, peripheral nerve injury, and device-related infection. This chapter will include discussion of common and uncommon complications of pacemaker implantation including associated incidence as well as the associated radiographs and common clinical signs of these complications.
Complications of Pacemaker Implantation

The heart’s natural pacemaker (the SA node) is located in the top right chamber of the heart, the right atrium. The SA node sends a signal to the upper right (right atrium) and left chambers (left atrium) and lower chambers (the right and left ventricles) via the atrioventricular (AV) node. Often, the patient has a slow heart rate because the electrical connection between the top (the signal from the SA node) and bottom (the ventricles) of the heart (right ventricle) is diseased and a pacemaker lead can be placed in this chamber.

The most common type of pacemaker involves placing a lead in the right atrium and right ventricle.  The image above (taken from displays a pacing lead in the right atrium and right ventricle.  It also shows a typical implant scenario where the device is positioned under the left clavicle below the skin but above the chest muscle.  The leads are then placed through the subclavian vein where they are threaded to position into the heart.  The following video (taken from shows the sequence of events during lead implantation.

You can see the site of the incision is under the left collarbone and insertion of the needle, guide wire, and introducer (hollow tube used to carry lead into the vein).  The pacing lead is then advanced into the right ventricle where the screw-in mechanism is activated – views of both the helix extending out and the implant tool operation are shown.

The emergence of resynchronization therapy has led to an increase in attempts at left ventricular lead placement via the coronary sinus (CS).  The MIRACLE study program [LEO05] reported a 91.6% success rate for LV lead placement, while COMPANION [BRI04] revealed an 89%  success rate for LV lead placement.  Another report indicated a similar 92% success rate with LV lead placement. [DIV08]  Though we counsel our patients on a LV lead placement success rate at 88-92%, our center demonstrated a 97% success rate (64 of 66 patients) with LV lead placement within the range from 2:30 to 5:30 o’clock in the left anterior oblique (LAO) view. [WIL10]

There are many reasons for difficult CS access including Thebesian valves, cardiac vein ostial valves, and Chiari networks.  The image shown below is representative of the ostial valve of the coronary sinus (aka, Thebesian valve) that prevents engagement of the CS and ultimately precludes LV lead placement.  Routine attempts at engaging the coronary sinus with deflectable EP catheters as well as hydrophilic guide wires were met without success.  A 9MHz radial intracardiac echo (ICE) probe (UltraICE, Boston Scientific Corp) was introduced via a steerable sheath (Agilis, St. Jude Medical) to evaluate the CS anatomy.  This image demonstrates a Thebesian valve covering the entire CS osmium with no obvious accessible fenestration or defect.  LV lead placement was aborted and patient was referred for epicardial LV lead placement via cardiothoracic surgery.

Prior reviews of CS anatomy (PEJ08) revealed the presence of Thebesian valves in 80% of cases and Chiari networks were found in 10% of cases.  It covered one-fifth in 7%, one-third the os in 29%, one-half in 27%, two-thirds in 14%, and the entire os in 5%.  The average diameter of the CS os was 8mm with a range of 3-15mm.  Appreciation for the anatomic variations of the normal human CS as well as experience with ICE may help reduce complications and improve success of LV lead implantation.


LEO05     Leon AR, Abraham WT, Curtis AB, et al.; for the MIRACLE Study Program, “Safety of Transvenous Cardiac Resynchronization System Implantation in Patients with Chronic Heart Failure: Combined Results of Over 2000 Patients from a Multicenter Study Program,” J Am Coll Cardiol, 2005;46(12):2348–56.

BRI04     Bristow MR, Saxon LA, Boehmer J, et al., “Cardiac-Resynchronization Therapy with or without an Implantable Defibrillator in Advanced Chronic Heart Failure for the Comparison of Medical Therapy, Pacing, and Defibrillation in Heart Failure (COMPANION) Investigators,” N Engl J Med, 2004;350(21):2140–50.

DIV08     D’Ivernois C, Lesage J, Blanc P, “Where are left ventricular leads really implanted? A study of 90 consecutive patients,” Pacing Clin Electrophysiol, 2008;31(5):554–9.

WIL10     Williams JL, Lugg D, Gray R, Hollis D, Stoner M, Stevenson R, “Patient Demographics, Complications, and Hospital Utilization in 250 Consecutive Device Implants of a New Community Hospital Electrophysiology Program,” American Heart Hospital Journal, V. 8, No. 1 (Summer, 2010), pp. 33-39.

PEJ08     Pejkovic B, Krajnc I, Anderhuber F, Kosutic D, “Anatomical Variations of the Coronary Sinus Ostium Area of the Human Heart,” J Int Med Research, V. 36 (2008), pp. 314-321.

Right Atrial (A), Right Ventricular (B), and Left Ventricular (C) Leads Before (Pre) and After (Post) Dislodgements. Right atrial lead became dislodged after patient twiddled with device. Right ventricular lead dislodged by moving more basilar in position (arrow) one day after implant. Left ventricular lead dislodged and reseated itself in the body of coronary sinus 3 months after initial placement (arrow).

     There are scant data for pacemaker implant complications and readmission rates in the extreme elderly (age≥80 years) despite their common use in this population.   We performed a retrospective chart review of consecutive patients (n=149, age≥80 years) who underwent pacemaker implantation at our community hospital Electrophysiology program from July 2008 through June 2010.  Single-, dual-, and biventricular-chamber pacemakers and generator changes were included for analysis; cardioverter-defibrillator devices, temporary pacemakers, and loop recorders were excluded.  Standard procedures for implantation were used.   Major complications defined as death, cardiac arrest, cardiac perforation, cardiac valve injury, coronary venous dissection, hemothorax, pneumothorax, transient ischemic attack, stroke, myocardial infarction, pericardial tamponade, and arterial-venous fistula.  Minor complications defined as drug reaction, conduction block, hematoma or lead dislodgement requiring reoperation, peripheral embolus, phlebitis, peripheral nerve injury, and device-related infection.

     The overall mean age of implantation was 86 years.  There were no intraprocedural complications. There was one major in-hospital (0.7%) and one minor in-hospital complication (0.7%).  Within 30 days of implant, there was an overall 5.4% rate of complications; 4 minor (2.7%) and 4 major (2.7%).  There was a 30d cardiovascular-attributable mortality of 0.7% and an all-cause mortality of 2%.  There was a 5.4% rate of readmission within 30days of implantation.

Our report of pacemaker implantations in the extreme elderly reveals rates of implant complications comparable to data from younger patient populations while experiencing a higher 30day all-cause mortality (that may be attributable to elevated all-cause mortality rates in this age-group).