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
Author: Heart Rhythm Center
Dr. Williams obtained his undergraduate degree with a double major in Biomedical and Electrical Engineering at Vanderbilt University. He was then awarded a Keck Fellowship for graduate school at the University of Pittsburgh where he obtained his Master’s degree in Bioengineering.
Dr. Williams went on to obtain his medical degree at Drexel University in Philadelphia and completed 5 years of Fellowship training in both Cardiovascular Diseases and Clinical Cardiac Electrophysiology at the University of Pittsburgh Medical Center.
His unique background and extensive knowledge of both engineering and cardiology have earned Dr. Williams many accolades in both clinical and academic settings. He’s published over 20 manuscripts and abstracts in the field of cardiology/electrophysiology and has received awards from both the American College of Cardiology Foundation and the National Institutes of Health.
Dr. Williams started in the Invasive Electrophysiology Laboratory at The Good Samaritan Hospital in 2008 and the Heart Rhythm Center published outcomes on pacemaker and defibrillator implantations as well as the safety and efficacy of high frequency jet ventilation during EP studies with ablation under his direction. He is Chair of the Quality Committee at the Florida Chapter of the American College of Cardiology.
Radiofrequency Ablation for Minimally-Invasive Repair of Mitral Valve Prolapse
The effects of intracardiac ablation have been well characterized (See Effects of RFA) and prior work has suggested that it can be used to repair mitral valve prolapse causing severe mitral regurgitation (MR). Minimally invasive repair of mitral valve prolapse (MVP) causing severe mitral regurgitation (MR) should increase the rigidity of the valve leaflet, decrease the leaflet surface area, and decrease redundant chordal length. Ex-vivo studies suggest that direct application of radiofrequency ablation (RFA) to mitral leaflets and chordae can effect these repair goals to decrease MR. We used a naturally occurring model of MVP (similar macroscopically and microscopically to primary MVP in humans) causing severe MR. RFA was applied to the prolapsed leaflets of the mitral valve and any associated elongated chordae. Mitral regurgitant volume was calculated using the proximal isovelocity surface area method on pre- and post-ablation echocardiograms. Subjects found to have anterior leaflet, posterior leaflet, and bileaflet MVP prolapse causing severe MR with a mean ejection fraction of 66±3%(±SD) underwent direct RFA. Echocardiograms performed before and after RFA demonstrated a 66.9±20.6% reduction in mitral regurgitant volume. The first video below shows the severe MR prior to RFA application to leaflets and chordae. The second video shows the degree of MR 6weeks after RFA applied. One can note the qualitative decrease in MR that was quantified by doppler.
These data suggest that myxomatous mitral valve repair using radiofrequency energy delivered via catheter may be feasible. Further investigation is necessary to evaluate whether such a technique could be adapted to a percutaneous, closed chest, beating heart environment.
More information about this study can be found at: http://www.lebanoncardiology.com/downloads/JLW%20JOIC%202008.pdf.
Pathophysiology of Intracardiac Ablation: How Does Ablation Work?
Radiofrequency catheter ablation (RFA) of cardiac tissue has been well-characterized in animal models. Both unipolar (HUA88) and bipolar (TAN91) radiofrequency ablation cause similar acute and chronic effects, the extent of which is determined by the amount of energy applied to the tissue. It has been shown that the application of microwave (LIE98,WOR02), cryogenic (DUB98,WOR02), laser, (WOR02), and ultrasonic (WOR02) energy result in similar cellular damage as radiofrequency energy.
Radiofrequency energy produces cell damage by heating the tissue and causing coagulative necrosis (cell death). These areas of cell death will eventually be replaced with fibrosis (scar tissue). (WOL94,REM98,LIE00) As one increases the energy applied to tissue, one will see an increase in the coagulation area and an increase in thermal damage. (REM98) Interestingly, this technique has been used to stiffen the palate (roof of the mouth) to prevent snoring. (MAI00) It has been speculated that RFA may cause direct valve tissue injury in patients undergoing ablation of accessory pathways.(MIN92) In fact, Wolfsohn et al (WOL94) found that when they accidentally applied energy to one of the valves of the heart they caused a fibrous scar. Another group (TAN91) found pathologic changes in the tricuspid valve when AV node or His bundle ablation was attempted in dogs. These changes included edema, swelling of the spongiosa, degenerative change of collagen fibers, endocardial thickening, and slight fibrosis and destruction of the valvular tissue. Additionally, collagen is the substance in the body that forms the support structure of tissue. Collagen in heart tissue denatures (breaks down) and contracts when heated to >65° CelciusVIC02. In fact, the chordae tendinae also contract when heated to >65° Celcius (VIC02). This contraction of heart tissue has also been noted by another group.LIE00 Though this technique has not been studied on heart valves one can infer that similar cellular changes may occur when this energy is applied to cardiac valves. RFA has been used to stiffen the palate (roof of the mouth) to prevent snoring. (MAI00) In fact, Wolfsohn et al (WOL94) found that when they accidentally applied energy to one of the valves of the heart they caused a similar fibrous scar.
The acute (1-7 days) effects of RFA (50-300J) include a lesion that is round-oval in shape, centrally-pale with varying amounts of a hemorrhagic rim.(HUA88) Occasionally, there is a mural thrombus over the lesion (~20% occurrence). There is central coagulation necrosis, peripheral contraction band necrosis, and interstitial edema and fibrinous material on the endocardium. (TAN91) During days 3-7, one observes a rim of granulation tissue composed of proliferating capillaries and fibroblasts admixed with acute and mononuclear inflammatory cells. (HUA88) Finally, the chronic effects are usually evident at 4-6 weeks after RFA. Chronic lesions are round-oval to irregular in shape, well-circumscribed, and fibrotic.(HUA88) The acute edema has almost disappeared and there are almost mature collagen fibers and a mild increase in elastic fibers.(TAN91) Much of these pathological observations were made in dog models however, Huang et al (HUA88) found that dog tissue damage was very similar to the tissue damage found in postmortem humans. RFA lesion size is, in part, determined by the amount of energy applied (typically, 50-700Joules). However, energy levels of 100-300J have been shown to cause similar lesion sizes (LxWxDepth, ~4.8×4.6×4.3mm) (HUA91). Earlier work by Huang et al (HUA87), demonstrated the application of unipolar RFA with an energy level of 50J caused an average subacute (7-10d) lesion size of 4x4x2mm.
References:
WOL94 Wolfsohn AL, Green MS, and Walley VM, “Pathology of Radiofrequency Catheter Ablation of the Atrioventricular Node,” Modern Pathology, Vol. 7, No. 4 (1994), pp. 494-496.
REM98 Remorgida V, “Tissue thermal damage caused by bipolar forceps can be reduced with a combination of plastic and metal,” Surgical Endoscopy, Vol. 12 (1998), pp. 936-939.
LIE00 Liem LB, Pomeranz M, et al, “Electrophysiological Correlates of Transmural Linear Ablation,” PACE, Vol. 23 (January 2000), pp. 40-46. MAI00 Mair EA and Day RH, “Cautery-assisted palatal stiffening operation,” Otolaryngol Head Neck Surg, Vol. 122 (April 2000), pp. 547-555.
MIN92 Minich LL, Snider AR, Dick M II, “Doppler Detection of Valvular Regurgitation After Radiofrequency Ablation of Accessory Connections,” Am J Cardiol, V. 70 (July 1, 1992), pp. 116-117.
VIC02 Victal OA, Teerlink JR, et al, “Left Ventricular Volume Reduction by Radiofrequency Heating of Chronic Myocardial Infarction in Patients with Congestive Heart Failure,” Circulation, Vol. 105 (March 19, 2002), pp. 1317-1322.
LIE98 Liem LB and Mead RH, “Microwave Linear Ablation of the Isthmus Between the Inferior Vena Cava and Tricuspid Annulus,” PACE, Vol. 21 (November 1998, Part I), pp. 2079-2086.
WOR02 Liem LB, “Catheter Ablation Using Alternative Energy Sources,” EP Lab Digest, (September/October 2002), pp. 10-12. DUB98 Dubuc M, Talajic M, et al, “Feasibility of Cardiac Cryoablation Using a Transvenous Steerable Electrode Catheter,” J Interventional Cardiac Electrophysiology, Vol. 2 (1998), pp. 285-292.
TAM95 Tamura K, Fukuda Y, Ishizaki M, Masuda Y, Yamanaka N, Ferrans V. “Abnormalities in elastic fibers and other connective-tissue components of floppy mitral valve,” Am Heart J, V. 129, No. 6 (June 1995), pp. 1149-1158.
NAS04 Nasuti JF, Zhang PJ, Feldman MD, Pasha T, Khurana JS, Gorman JH III, Gorman RC, Narula J, and Narula N, “Fibrillin and Other Matrix Proteins in Mitral Valve Prolapse Syndrome,” Ann Thorac Surg, V. 77 (2004), pp. 532-536.
DAV78 Davies MJ, Moore BP, Braimbridge MV, “The floppy mitral valve – Study of incidence, pathology, and complications in surgical, necropsy, and forensic material,” Br Heart J, V. 40 (1978), pp. 468-481.
WHI87 Whittaker P, Boughner DR, Perkins DG, Canham PB, “Quantitative structural analysis of collagen in chordae tendinae and its relation to floppy mitral valves and proteoglycan infiltration,” Br Heart J, V. 57 (1987), pp. 264-269.
BAK88 Baker PB, Bansal G, Boudoulas H, Kolibash AJ, Kilman J, Wooley CF, “Floppy Mitral Valve Chordae Tendinae: Histopathologic Alterations,” Hum Pathol, V. 19 (1988), pp. 507-512.
GRA03 Grande-Allen KJ, Griffin BP, Ratliff NB, Cosgrove DM, Vesely I, “Glycosaminoglycan Profiles of Myxomatous Mitral Leaflets and Chordae Parallel the Severity of Mechanical Alterations,” JACC, V. 42, No. 2 (July 16, 2003), pp. 271-277.
HUA88 Huang SKS, Graham AR, Bharati S, Lee MA, Gorman G, and Lev M, “Short- and Long-Term Effects of Transcatheter Ablation of the Coronary Sinus By Radiofrequency Energy,” Circulation, V. 78, No. 2 (August 1988), pp. 416-427.
TAN91 Tanaka M, Satake S, Kawahara Y, Sugiura M, Hirao K, Tanaka K, Kawara T, Masuda A, Nishikawa T, and Kasajima T, “Pathological Aspects of Radiofrequency Ablation of the Canine Atrioventricular Node and Bundle of His: With Special Reference to Chronic Incomplete Atrioventricular Block,” Acta Pathol Jpn, V. 41, No. 7 (1991), pp. 487-498.
HUA91 Huang SKS, Graham AR, Lee MA, Ring ME, Gorman GD, and Schiffman R, “Comparison of Catheter Ablation Using Radiofrequency Versus Direct Current Energy: Biophysical, Electrophysiologic and Pathologic Observations,” JACC, V. 18, No. 4 (October 1991), pp. 1091-1097.
HUA87 Huang SK, Bharati S, Graham AR, Lev M, Marcus FI, and Odell RC, “Closed Chest Catheter Dessication of the Atrioventricular Junction Using Radiofrequency Energy- A New Method of Catheter Ablation,” JACC, V. 9, No. 2 (February 1987), pp. 349-358.
DAV78 Davies MJ, Moore BP, and Braimbridge MV, “The floppy mitral valve: Study of incidence, pathology, and complications in surgical, necropsy, and forensic material,” British Heart Journal, V. 40 (1978), pp. 468-481.
KIN82 King BD, Clark MA, Baba N, Kilman JW, Wooley CF, “Myxomatous Mitral Valves: Collagen Dissolution as the Primary Defect,” Circulation, V. 66, No. 2 (August 1982), pp. 288-296.
COS89 Cosgrove DM and Stewart WJ, “Mitral Valvuloplasty,” Curr Probl Cardiol, V. 14, No. 7 (July 1989), pp. 353-416.
ZOO83 Zook BC, Blackbourne BD, Katz RJ, and Bradley EW, “Mitral Valve Prolapse,” Comparative Pathology Bulletin, Vo. 15 (August 1983), pp.3-4.
Intracardiac Echo (ICE) for Heart Rhythm Procedures
Most intracardiac EP procedures are analogous to painting the inside of a room; I have found that in many procedures, without ICE you are painting in the dark. Charles Darwin said, “It is not the strongest of the species that survives, nor the most intelligent, but rather the one most responsive to change.” Within the last decade, the field of Electrophysiology has progressed in term of technology and breadth of procedural variety. Part of this development has been the use of adjunctive imaging during EP procedures. The following video depicts an ex-vivo heart preparation undergoing a radio frequency ablation.
One can imagine the trauma that a steam pop could cause during an EP study in which the ablation catheter is confined within a small trabeculation in the right or left atrium. Direct visualization of the ablation electrode-endocardial interface is possible with intracardiac echo (ICE). ICE permits us to watch for increasing echogenicity of endocardium and possible overheating. In addition, the development of catheter or sheath thrombus can be detected by direct visualization with ICE.
There are two main types of ICE: Phased-Array and Radial.
1. Phased Array: 8-10 French, 5.5–10 Mega Hertz catheter with 90° sectorial sector image and Doppler capability (AcuNav®, Acuson, a Siemens Corporation, Mountain View, California). Phased-array generally offers better image resolution/definition and doppler capability. The doppler capability permits assessment of valve disorders such as stenosis (blockage) or regurgitation (leaking). The cost is higher.
2. Radial (mechanical rotation of the transducer): 8.5 French, 9 MHz catheter with 360° radial image (Ultra ICE, Boston Scientific, Natick, Massachusetts). This catheter has no Doppler capability and image definition is not as good. 360° scan has a larger field of view and allows for a more comprehensive depiction of both atrial chambers and atrioventricular valves with their relationships and it also can be used as IVUS for great vessels.
Floating Potential and Far-Field Left Atrial Appendage Signals During Atrial Fibrillation Ablation
Atrial fibrillation ablations are often like exploring a new forest; there are interesting findings unique to every patient and it is “what keeps you coming back.” This is an electrogram recorded during an ablation after completing a left atrial pulmonary venous antrum isolation and assessing the left superior pulmonary vein for entrance/exit block. On first exam, it looks as if some work needs to be done but on closer inspection there is evidence of a “floating potential” and far-field sensing of atrial appendage activity. The longer cycle length electrogram (~3100msec) is a pulmonary vein potential that is firing regularly but not conducting out to the left atrium (exit block). In addition, the shorter cycle length (~1000msec) is a slightly lower frequency left atrial appendage signal that is often recorded from the proximate left superior pulmonary vein. I get the “floating potentials” less than 10-20% of cases but it is a welcome finding.
How are Pacemaker Leads Implanted?
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 MedtronicConnect.com) 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 MedtronicConnect.com) 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.
Difficult Access of Coronary Sinus During Attempted Percutaneous LV Lead Insertion
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.
References:
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.
Development and Characterization of an Implantable Biosensor for Telemetric Monitoring of Ethanol in the Brain of Freely Moving Rats
These researchers describe an amperometric sensor for the detection of ethanol in the extracellular fluid of animal brains.
http://pubs.acs.org/doi/abs/10.1021/ac301253h
Ethanol is one of the most widespread psychotropic agents in western society. While its psychoactive effects are mainly associated to GABAergic and glutamatergic systems, the positive reinforcing properties of ethanol are related to activation of mesolimbic dopaminergic pathways resulting in a release of dopamine in the nucleus accumbens. Given these neurobiological implications, the detection of ethanol in brain extracellular fluid (ECF) is of great importance. In this study we describe the development and characterization of an implantable biosensor for the amperometric detection of brain ethanol in real time. Ten different designs were characterized in vitro in terms of Michaelis–Menten kinetics (VMAX and KM), sensitivity (linear region slope, LOD and LOQ), and electroactive interference blocking. The same parameters were monitored in selected designs up to 28 days after fabrication in order to quantify their stability. Finally, the best performing biosensor design was selected for implantation in the nucleus accumbens and coupled with a previously-developed telemetric device for the real-time monitoring of ethanol in freely moving, untethered rats. Ethanol was then administered systemically to animals, either alone or in combination with ranitidine (an alcohol dehydrogenase inhibitor) while the biosensor signal was continuously recorded. The implanted biosensor, integrated in a low-cost telemetry system, was demonstrated to be a reliable device for the short-time monitoring of exogenous ethanol in brain ECF, and represents a new generation of analytical tools for studying ethanol toxicokinetics and the effect of drugs on brain ethanol levels.
Biosensor Market Increases to $13 Billion Annually
Biosensors are now generating $13 billion in annual sales up from $5 million 30 years ago. The combination of real-time biofeedback and the ability to deliver therapy has the promise to get us one step closer to a truly “personalized” approach to medicine. Examples such as home glucose monitors and in-ear thermometers demonstrate that point of care biosensors can decentralize health care delivery. Ultimately, the decentralization of health care will place patients once again at the forefront of their own care.
ECG Sensing Driver’s Seat
Biomonitoring will become more and more common as we move forward. The feasibility of us interacting with our electronic environment via biosensors will allow more personalized interactions. We already see personalized interactions with:
1. Websites that track our preferences and suggest information that is related to these preferences.
2. Pacemakers and defibrillators that can adjust pacing rates based upon activity and breathing.
3. Glucose monitors that automatically adjust insulin dosing based upon blood glucose levels.
Ford is investigating the use of leadless ECG monitoring system in the driver’s seat. Though it is investigational, one can see the possibility of tracking a driver’s heart for use in several ways such as monitoring for stress response prior to accident, ischemia, bradycardia (or heart block), and arrhythmias (such as atrial fibrillation). Interesting to think about the implications of this data and privacy issues.
See link below for more information:
http://medgadget.com/2011/05/ford-unveils-contactless-ecg-sensing-driver-seat.html
Heart Rhythm Center 