INDIAN JOURNAL OF - · PDF filesuch as an infectious agent (virus, bacteria, fungus), ... a 36...

EDITORS | Dr. Yash Lokhandwala � Dr. Rabin Chakraborty

INDIAN JOURNAL OF

2012 : Vol. 2

GUEST EDITOR | Dr. Sanjay Bindra

ISECON 20135, 6 & 7 April, 2013 • Gurgaon

Dr. Balbir SinghPresident, ISE & Organizing Secretary, ISECON 2013

Senior Consultant, Interventional Cardiologist & Cardiac ElectrophysiologistMedanta – The Medicity Hospital

Sector 38, Gurgaon 122001Mobile : 09818898479

C o n t e n t s

Editorial ....................................................................................................... 2

Message from President Elect ................................................................... 3

REVIEW ARTICLESECG Manifestations of Myocarditis ......................................................... 5

Recycling Pacemakers, Challenges and Solutions ................................... 7

Calming The Storm By Sympatholysis ................................................... 10

Autonomic Denervation for the Treatment of Atrial Fibrillation......... 12

CASE REPORTSThe Classic Confounder of ST-Elevation Myocardial Infarction ......... 16

Aborted Sudden Death in a 38 Year Old Male ....................................... 17

ECG Quiz ................................................................................................... 19

ISE Membership Form ............................................................................ 31

executive Committee ofIndIan soCIety

ofeleCtroCardIology

PRESIDENTBalbir singh, New Delhi

IMM. PaST PRESIDENTPrakash Kamath, Cochin

PRESIDENT ELECT sB gupta, Mumbai

VICE PRESIDENTSPraveen Jain, Jhansigeetha subramaniam, Chennaisatish V Vaidya, Mumbai

HON. GENERaL-SECRETaRYamit Vora, Mumbai

TREaSURERUday M Jadhav, Navi Mumbai

JOINT SECRETaRIESramesh dargad, MumbaiKetan K Mehta, Mumbai

MEMBERSajay naik, Ahmedabadashish nabar, MumbaiUlhas Pandurangi, ChennaiVinod Vijan, Nashiksadanand shetty, MumbaiVijay garg, UjjainJitendra Makkar, Jaipurgs Parale, Solapur

JOURNaL EDITORSyash lokhandwala, Mumbairabin Chakraborty, Kolkata

CO-OPTED MEMBERSajit BhagwatOrganising Secretaryaurangabad arrhythmia Course

ORGaNISING SECRETaRYBalbir singhIseCon 2013 (new delhi)

SECRETaRIaTS. B. GUPTAPRESIDENT ELECT

Indian Society of ElectrocardiologyHead, Department of Medicine and Cardiology, C. Rly, Head Quarters Hospital, Byculla, Mumbai - 400 027. Phone : 2371 7246 (Ext. 425), 2372 4032 (ICCU), 2373 2911 (Chamber) • Resi: 2262 4556 Fax : 2265 1044 • Mobile : 0 98213 64565 / 0 99876 45403 E-mail : [email protected] • Website : www.iseindia.org

Dear Friends,

We are very excited to bring you the current issue of IJe. It includes interesting eCg related original manuscripts as well as clinical relevant review articles.

as always, the eCg Quiz is one of the highlights of the IJe.

two motivated college students, Vivek reddy and Vidhatha reddy from the Bay area (silicon valley) in California are researching the issue of pacemaker reuse. they have written a succinct review on the issues and opportunities that lie ahead. this should provoke interest from interested institutions and hopefully lead to the creation of standardized processes and increase the scale of these operations, thereby benefiting more individuals.

Dr Soni and Dr Nathani have described the ECG findings in myocarditis. Often ECG findings in this condition are often nonspecific with a myriad of clinical presentation. the predeliction of the aV conduction system in diphtheria in the Indian subcontinent, lyme’s disease in north america and Chagas in south america was succinctly described. fulminant cases of giant cell myocarditis, needs to be kept in the differential for subjects with no coronary disease or stress cardiomyopathy. the association of new left BBB, wide Qrs, abnormal Qrs axis with poor clinical prognosis is a clinical pearl.

drs Contractor and ayub describe an interesting case of transient Brugada type 1 eCg, in a patient with febrile illness. this signature pattern needs to be remembered to avoid thrombolytic therapy or an unnecessary trip to the cardiac catheterization lab.

dr Balakrishanan has described a case of aborted sudden death from a left posterior accessory pathway. The degeneration of preexcited AFib into Vfib is shown on the eCg tracings.

two articles from IPeJ highlight the role of autonomics in cardiac arrhythmias and their manipulation in management are important for the clinician to be aware of. atrial fibrillation and the role of ganglionic autonomic denervation. And an editorial by the group from UCla, on the role of sympatholysis and thoracic epidural analgesia in patients with ventricular storm. these have been re-printed with permission from the web-based Indian Pacing and electrophysiology journal.

Happy reading and we hope to have more contributions from you for future issues.

Sanjay Bindra California, USA, Guest Editor

Editorial

From President Elect’s DeskDear Members,

It is our great pleasure in bringing out the 2nd issue of Indian Journal of electrocardiology of the year 2012 on the eve of Mid term Conference of Indian society of electrocardiology at aurangabad.

IseCon 2012 – the annual Conference of Indian society of electrocardiology was organized by dr Jitendra Makkar and the team at Jaipur from 17th to 19th February 2012. It was a great scientific feast! Our heartiest congratulations to dr Jitendra Makkar and his team.

Indian society of electrocardiology also organized many programs during the year :

a. “eCg learning Courses” for postgraduate students were organized at Bangalore on 7th and 8th april 2012, at sri lanka on 21st and 22nd april 2012, 9th and 10th June 2012 at Chennai, 16th and 17th June 2012 at Pune and 18th and 19th august 2012 at rohtak. about 60-100 delegates participated in each course and successful candidates were awarded the Certificate of Competence for eCg reading

b. Ise satellite symposium at Mumbai on 6th July 2012 and 19th august 2012.

My sincere thanks to dr yash lokhandwala, dr sanjay Bindra and the editorial team for bringing out the Ise Journal – 2012, 2nd Volume.

long live Indian society of electrocardiology

Dr. S.B. GuptaPresident Elect Indian Society of Electrocardiology

5

Introduction

Myocarditis is an under-diagnosed cardiac disease resulting from a broad range of infectious, immune and toxic causes. Myocarditis usually results from external inflammatory trigger, such as an infectious agent (virus, bacteria, fungus), or a drug inducing an immune response. the severity ranges from minimal transient lV dysfunction with no eCg changes to fulminant myocarditis with a host of eCg changes ranging from aV blocks to life-threatening arrhythmias. affected patients may recover, develop dilated cardiomyopathy or die. although remarkable advances in diagnosis, understanding of pathophysiology and treatment of myocarditis have been achieved during the last years, standard treatment strategies remain limited to evidence-based Hf therapy in the most cases. Its precise characterization and natural history have been limited by the extraordinary variability of its clinical presentations, laboratory findings, and the diversity of etiology.

the clinical manifestation of myocarditis varies with a broad spectrum of symptoms ranging from asymptomatic course to presentations with signs of myocardial infarction to devastating illness with cardiogenic shock. Hence, the diagnosis of myocarditis based on the clinical presentation alone is usually not possible. Biomarkers (such as troponins or creatine kinase) and electrocardiographic changes lack specificity, but may help to confirm the diagnosis of myocarditis.

ECG Manifestations of MyocarditisMahipat Soni, PJ Nathanidept of Cardioology, lokmanya tilak Municipal Medical College and general Hospital, sion, Mumbai

Figure 1 : a 36 year old man cam with recent heart failure and global lV hypokinesia which improved over a few weeks. the coronary angiogram was normal.

Figure 2 : a 42 yr old lady with granulomatous myocarditis (tB proved in thoracic lymph node biopsy)

Review Article

ECG changes in myocarditis

although widely use as screening tool, sensitivity of eCg for myocarditis is only 47% but its specificity remain unknown. It may be hypothesized that these eCg parameters are associated with myocardial inflammation. The electrocardiogram (ECG) is widely used as a screening tool despite low sensitivity. the ECG findings in patients with myocarditis vary from nonspecific t-wave and st-segment changes to st-segment elevation mimicking an acute myocardial infarction.1 also, atrial or ventricular conduction delays as well as supraventricular and ventricular arrhythmias can occur in patients with inflammatory heart disease.

Myocarditis masquerading as an acute coronary syndrome (figure 1) has also been well described eCg changes suggestive of acute myocardial ischemia typically may include ST-segment elevation in ≥2 contiguous leads (54%), T-wave inversions (27%), widespread st-segment depressions (18%), and pathological Q waves (18% to 27%) 2. segmental or global echocardiographic wall motion abnormalities are frequently evident despite angiographically normal coronary anatomy. In series of 34 patients with known normal coronary anatomy presenting with symptoms and eCg changes consistent with an acute coronary syndrome, 11 (32%) of the patients were found to have myocarditis on biopy.3 Clinicians should consider acute myocarditis in younger patients who present with acute coronary syndromes when i) coronary risk factors are absent, ii) eCg abnormalities extend beyond a single coronary artery territory, or iii) global rather than segmental left ventricular dysfunction is evident on echocardiography.

6 Indian Journal of Electrocardiology

predictor for cardiac death or heart transplantation in patients with suspected myocarditis.5 the presence of Q waves or a new left bundle branch block are associated with higher rates of cardiac death or heart transplantation.6 Morgera et al. described in a small study of biopsy-proved myocarditis that an abnormal Qrs complex was associated with a lower lV function and poorer survival.7 A prolonged QRS duration of ≥120 ms was found to be an independent predictor for cardiac death or heart transplantation. Hence, the eCg represents an easily available tool for risk stratification in patients with suspected myocarditis.

High-grade aV block and tachyarrhythmias may be treated with placement of temporary or permanent pacemaker or antiarrhythmic medication as needed. arrhythmias usually resolve after several weeks. Patients with symptomatic or sustained ventricular tachycardia may require antiarrhythmic therapy and possibly implantable cardioverter defibrillator or cardiac transplantation if arrhythmias persist after the acute inflammatory phase.

Conclusion

Myocarditis has wide range of eCg manifestations. despite having low sensitivity, eCg is good prognostic tool in patients with myocarditis. QRS duration of ≥120 ms, QTc prolongation >440 ms, an abnormal Qrs axis, ventricular ectopic beats and new left bundle branch block is associated with poor clinical outcome.

References

1. Cooper lt. Jr; Myocarditis. N Engl J Med 360 2009 1526-1538.

2. angelini a, Calzolari V, Calabrese f, Boffa gM, Maddalena f, Chioin r, thiene g. Myocarditis mimicking acute myocardial infarction: role of endomyocardial biopsy in the differential diagnosis. Heart 2000;84:245–250.

3. dec gW, Waldman H, southern J, fallon Jt, Hutter aM, Palacios I. Viral myocarditis mimicking acute myocardial infarction. J Am Coll Cardiol 1992;20:85–89.

4. Cooper lt, Berry gJ, shabetai r, for the Multicenter giant Cell Myocarditis study group Investigators. Idiopathic giant-cell myocarditis: natural history and treatment. N Engl J Med 1997;336:1860–1866.

5. Ukena C., Mahfoud F., Kindermann I., Kandolf R., Kindermann M., Bohm M.; Prognostic electrocardiographic parameters in patients with suspected myocarditis. Eur J Heart Fail 2011;13:398-405.

6. nakashima H., Katayama t., Ishizaki M., takeno M., Honda y., yano K.; Q wave and non-Q wave myocarditis with special reference to clinical significance. Jpn Heart J 1998;39:763-774.

7. Morgera t., di lenarda a., dreas l.; et al. electrocardiography of myocarditis revisited: clinical and prognostic significance of electrocardiographic changes. Am Heart J 1992;124:455-467.

Table 1 : eCg changes in various myocarditis

Viral Myocarditis(adeno, Coxsackie,Parvo, Hepatitis C, epstein Barr, Mixed)

sinus tachycardia,atrial ar-rythmias,st-t segment changes,t-wave inversions,Bundle branch blocks (intra-ventricular conduction defects)diffuse st segment depres-sion, st segment elevation.

Pertussis sinus node and aV nodal blocks

rubella abnormal st-t segment changes and axis deviation.

lyme disease aV blocks.Chagas disease rBBB, laHB, aV nodal

block.diphtheria Pr prolongation, IVCd, aV

nodal blocks, t wave changes.rheumatic fever Prolonged Pr,

aV blocks (rare).HIV infection sinus tachycardia, non –spe-

cific ST-T wave changes, Bundle branch blocks, low voltage complexes, Poor r progression, prolonged Qtc.

Myocarditis can produce variable effects on the cardiac conduction system. Ventricular tachycardia is an uncommon initial manifestation of myocarditis but often develops during long-term follow-up. the giant Cell Myocarditis study group reported an initial incidence of ventricular tachycardia of <5% in a multicenter cohort. Ventricular tachycardia due to either lymphocytic or granulomatous myocarditis (figure 2) may infrequently result in sudden cardiac death. Myocarditis should be considered in patients who lack evidence of coronary atherosclerosis or other pathophysiological etiologies such as stress-induced cardiomyopathy (takotsubo syndrome).

diphtheria in particular has a predilection to cause conduction blocks and may require pacing. associated lV dysfunction also predicts the outcome. early institution of antitoxin may be life saving. other infections which may directly damage conduction system and lead to blocks include lyme disease, tuberculosis (rarely involves myocardium), Whipples disease and Chagas disease (not seen in our country). a wide range of eCg changes may present in myocarditis of infective origin (table 1).

ECG as prognostic marker

recently, the prognostic role of eCg parameters was investigated in patients with suspected myocarditis. Ukena et al described that prolonged Qrs duration is an independent

7

Review Article

Background

as an integral part of cardiac electrophysiology, pacemaker use is unfortunately not without considerable cost. Heart Beat International estimates that more than 1million people die annually due to inability to afford this lifesaving technology. In the past, philanthropic actions of some motivated physicians have provided a small pool of donated devices to be reused to the needy underprivileged. Currently, there is an urgent need to a creative solution to this humanitarian mission.

Sources of Donated Devices

Upgrades or Infections

some patients with pacing indications may require device upgrades to an ICd and/or cardiac resynchronization therapy device, potentially making the old pulse generators available for reuse.

devices explanted secondary to infection can be reimplanted after adequate sterilization.

death

the largest source of pacemakers is obtained postmortem. since over 30% of pacemaker implants occur in patients over 80 years of age, these devices, often with adequate battery life of greater than 3 years, can be recovered prior to burial or cremation.

reuse of explanted pacemakers by funeral homes is an obvious source of devices,1 most of which are currently discarded as waste.

Pacemaker Reuse

low and middle income countries (lMIC) understandably have restricted access to cardiac pacemakers, despite the fact that many of these devices have been discarded by funeral homes and mortuaries in the developed world as medical waste or stored with no intended purpose.3

recent evidence has underscored the feasibility of developing a process for wide-scale redistribution for pacemaker reuse.4

Societal Views

furthermore, there is also strong support among private citizens and patients for donating pacemakers for reuse. according to one study conducted at the University of Michigan and University of Pennsylvania, 84% of the 210 patients surveyed

Recycling Pacemakers, Challenges and SolutionsVivek Reddy1a, Vidhatha Reddy1b, Sanjay Bindrac

1aUrsinus College, Collegeville, Pa; 1bUniversity of California Berkeley, Ca; cWashington Hospital Health Care, fremont Ca

were willing to donate their device for reuse.5

to better utilize the availability of used pacemakers from mortuaries, funeral homes and from patients willing to donate their devices, initiatives such as the University of Michigan’s Project My Heart - your Heart have begun to raise awareness and distribute reusable pacemakers to low and middle income countries.

Challenges

Before regulated pacemaker redistribution can occur, there are several regulatory, ethical and legal issues regarding the, safety and efficacy of pacemaker reuse that must be addressed. Issues related to distribution of devices and monitoring of quality control needs to be standardized.

1. legal and ethical Barriers

there are major legal and ethical barriers to reusing refur-bished implantable pacemakers.

legal issues include who should have jurisdiction over pacemakers as well as laws that restrict or prohibit the reuse of the devices. furthermore, the governments of various countries have contrasting opinions regarding jurisdiction and the legality of pacemaker reuse. In sweden for exam-ple, the implanting center has jurisdiction while the patient has jurisdiction in Canada, netherlands, the U.s. and India. In the U.s., the food and drug administration (fda) pro-hibits the introduction into interstate commerce of any de-vice that is adulterated or misbranded in the United states.5 the United Kingdom prohibits the reuse of pacemakers as well. on the other hand, Canada, sweden, switzerland, In-dia, Israel, and france allow pacemakers to be reused.

the ethical issues relate to procurement of devices, their distribution and allocation to deserving individuals.

2. Safety and Efficacy

Current research has shown that the safety of pacemaker reuse can be assured through protocolized resterilization and redistribution procedures. In these cases, there are comparable rates of infections and technical malfunctions for both reusable pacemakers and new ones. one study by Baman et al7. involved a sample of 2270 patients in 18 stud-ies with reusable devices, with an infection rate of 1.97% and device malfunction rate of 0.68%. the infection rates


of reused pacemakers have been comparable to those of new pacemakers.

3. Challenges during distribution and Cost of leads

It is also possible that allocation can lead to a black market, diverting devices away from those who need them most to the select few in developing and underdeveloped countries that can afford to monopolize these devices. furthermore, reused devices would not be available completely free to patients because the patient would still be responsible for obtaining new leads ($200), a cost that is still considerably high for the patients that pacemaker reuse would be geared towards. a possible alternative, however, would be dual chamber pacemakers that can be implanted as single Vdd lead devices resulting in significant cost savings compared to the purchase of two new leads.8

4. Quality at Implant Center

Non-profit organizations can assess the quality and safety records of implanting centers and lMIC device implanta-tion centers 5.

Process Standardization and Sterilization

Providence Hospital and Medical Center at Wayne state University has coordinated with an implanting institution in Nicaragua, carrying out specific protocols for explantation, sterilization, and implantation8.

a. donors consented to removal and donation of pacemak-ers, and all devices were interrogated to assess function, remove prior data and ensure adequate battery life (70% life or greater than 3 years). all previous patients’ data.

b. the sterilization protocol involved the removal and clean-ing of devices, aerating and transport of devices, and ac-countance of quality assurance.9 devices were cleaned with sterile water and isopropyl alcohol in the electrophysiology laboratory, and the devices were then aerated and transport-ed to the Center for sterilization Processing department (CsPd), within 24 hours of explanation. at the CsPd, the devices were placed in a peel pouch with an ethylene oxide chemical indicator and sterilized with a biological test pack (B1 spore).9

c. Quality assurance: then, these devices were incubated for 15 hours, and if the B1 incubator was negative, steriliza-tion was complete. for quality assurance, devices under-went surveillance in vitro cultures-aerobic, anaerobic, and fungal-every 3 months until the time of device implantation abroad.9

d. transportation: then, these devices were re-sterilized and repackaged, and all were delivered and implanted within 6 months of initial sterilization. these devices were trans-ported to the Centro de Cardiology nacional and Hospital

Militar de Managua in nicaragua.

e. distribution and Implant

a senior investigator would review each case with respect to indication of implant, and third party payers donated de-vice leads.

f. followup

all patients with donated devices, underwent device evalu-ation before discharge, and complications were recorded.

g. results

Ultimately, there were no infections, early battery deple-tion, or device malfunctions while this initiative was con-ducted.

through the use of strict guidelines such as those outlined in this case, life span, time last implanted, recovery, ster-ilization methods, testing, and final preparation can all be verified and ensured.

While great strides have been made in recent years to facili-tate the distribution of used pacemakers to lMIC, there is still significant work to be done.

Solutions

Logistical barriers: A “pacemaker living will” filled out by patients at the time of implantation could we used to authorize pacemaker recovery for reuse after upgrade or death.

education and involvement of mortuary directors and personnel may assist in retrieval of suitable devices.

ensuring a meticulous chain of custody from explant to reimplant. Careful patient selection based on indication and financial hardship. Detailed preimplantation and followup documentation with clear policies for fair distribution and a mechanism to audit the process.

the creation of an internationally recognized system for pacemaker redistribution, resolution of conflicting legal issues and circumventing ethical challenges will assist the process to be safe, efficient and ethical in the near future.

Conclusion

With further research and greater awareness in both the medical community and the general public, a systematic and regulated retrieval and distribution of used pacemakers in low and middle income countries is certainly possible.

References

1. Kantharia et al. reuse of explanted permanent pacemakers donated by funeral homes. Am J Cardiol 2012;109:238-40.

2. gakenhemier et al. societal views of pacemaker reutilization for those

9

with untreated symptomatic bradycardia in underserved nations. J Interv Card Electrophysiol 2011;30:261-6.

3. Romero et al. Pacemaker Reuse in a 65 Year-Old Woman in the Philippines with severe Medical need. PACE 2010;33:8-9.

4. Baman et al. Pacemaker reuse: an Initiative to alleviate the Burden of symptomatic Bradyarrhythmia in Impoverished nations around the World. Circulation 2010;122:1649-1656.

5. Kolettis, Theofilos. Reuse of Electrode Catheters and Pacemakers. Hospital Chronicles 2007;2:160-163.

6. Jackson. Issues affecting refurbishment and re-use of pacemakers. Australian Health Review 1996;19:68-80.

7. Baman s, timir and eagle a, Kim. Cardiac device reutilization: Is it time to “go green” in Underserved Countries? PACE 2011;34:651-52.

8. Hasan et al. Safety, Efficacy, and Performance of Implanted Recycled Cardiac rhythm Management (CrM) devices in Underprivileged Patients. Pacing Clin Electrophysiol 2011;34:653-8.

9. linde et al. re-used pacemakers – as safe as new? a retrospective case-control study. European Heart Journal 1998;19:154-157.


Keywords: electrical storm, sympathetic chain blockade, thoracic epidrual anaesthesia, stellate ganglionectomy

This Article has been Reprinted from IPEJ with Permission from the Editor

Calming The Storm By SympatholysisJohnson Francis, MBBS, MD, DM, FaCC, FRCP1; Tara Bourke, MD2; Kalyanam Shivkumar, MD, PhD2

1KMCt Heart Insitute & research Centre, KMCt Medical College, Calicut, Kerala, India; 2UCla Cardiac arrhythmia Center, Ronald Reagan UCLA Medical Center, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095, USA

an electrical storm is a fearful and life threatening experience for the patient while it is a therapeutic challenge of the extreme degree for the physician. In this issue of the Journal, Proietti and sagone have presented an in depth discussion on the various aspects of the electrical storm including the current day management.1 as rightly mentioned by them, the present definition of an electrical storm would be the occurrence of three or more episodes of ventricular tachycardia or ventricular fibrillation in 24 hours, requiring either anti-tachycardia pacing or a shock. this editorial note will focus on the management of a refractory electrical storm with sympatholytic measures, other than the conventional pharmacologic beta adrenergic blockade.

the concept of sympathetic blockade for the management of an electrical storm is not new as intravenous beta-blocker therapy is a well known therapeutic option in this setting.2 similarly left cardiac sympathetic denervation (lCsd) has been in use for prevention of the sympathetically driven life threatening arrhythmias in congenital long Qt syndrome and catecholaminergic polymorphic ventricular tachycardia.3,4 lCsd has also been shown to contribute to a reduction in the incidence of sudden cardiac death among subgroups of post myocardial infarction patients at high risk.5 Mahajan et al initially reported the use of thoracic epidural anaesthesia (tea) for the control of an electrical storm.6 Bourke et al from the same institution have further studied the efficacy of both LCSD and tea in the management of electrical storms.7 these measures were considered only when the storm or malignant ventricular arrhythmia were refractory to all conventional measures including intra venous beta-blocker therapy, antiarrhythmic drugs, device reprogramming to minimize shocks, treatment of reversible causes such as myocardial ischemia and electrolyte disturbances, deep sedation and intubation with induction of general anaesthesia where necessary and catheter ablation when feasible. tea was planned if the surgeon performing lCsd was not available or the patient was awaiting cardiac transplant or catheter ablation. otherwise an lCsd was preformed, which is a more definitive therapeutic option.7

thoracic epidural anaesthesia involves application of local anaesthetic directly onto the sympathetic chain which results in almost immediate sympatholysis. tea was given via an epidural catheter placed at the t1-2 or t2-3 interspace via a paramedian approach. Intrathecal or intravascular placement was excluded by the lack of aspiration of cerebrospinal fluid or

blood. Bupivacaine was the agent used to obtain the anaesthesia and subsequent antiarrhythmic response, a 1ml bolus of 0.25% Bupivicane followed by an infusion at a rate of 2ml/hour was administered.7 the effects of tea on hemodynamic parameters including heart rate, mean arterial pressure, cardiac index and central venous pressure are minimal.8 tea was well tolerated by all the patients in their series in which 6/8 patients had a greater than 80% reduction in arrhythmia burden following tea. no adverse effects were reported.7

lCsd was done by a video-assisted thorascopic approach (Vats). the pleural cavity was entered through three small incisions in the left subaxillary area; a double lumen endotracheal tube allowed ventilation of the contralateral lung while the ipsilateral lung was deflated and non ventilated to facilitate access to the sympathetic chain. resection of the lower half of the stellate ganglion, along with t2–4 ganglia of the sympathetic chain was performed.7 Patients in this series had diverse aetiologies of cardiomyopathy including ischaemic and nonischaemic, sarcoid, arVd and hypertrophic. five out of nine patients with refractory ventricular arrhythmias had a complete or partial reduction in arrhythmia burden following lCsd with 7/9 patients surviving to hospital discharge. Complications in this series included one partial Horner’s syndrome which resolved after 6 months, an apical pneumothorax (which was managed conservatively) and transient facial paresthesia occurred in one patient. no procedural deaths occurred. the safety and feasibility of Vats lCsd has been reported in several small series previously.9-12 atallah J et al12 used Vats left cardiac sympathetic denervation for treating children with intractable ventricular arrhythmias. four each of their patients had long Qt syndrome and catecholaminergic polymorphic ventricular tachycardia while one had idiopathic ventricular tachycardia.

another older approach to the problem of electrical storm is a left stellate ganglionic blockade (lsgB). lsgB can be given percutaneously by an anterior approach between the trachea and the carotid artery, within several millimeters anterior to the lateral process of the spine. the blockade was done using 1% xylocaine which was injected until a Horner’s syndrome or partial Horner’s syndrome developed2 however repeated dosing and inability to use concurrent anticoagulation are limitations in the clinical setting.

11

sympathetic hyperactivity is an important modulator of ventricular arrhythmias, including electrical storm13 therefore neuraxial modulation is an attractive option for arrhythmia management. these treatment modalities can be considered when standard treatments fail, they may be used as a bridge to cardiac surgery or catheter ablation procedures or may be used as definitive therapy when revascularization, transplantation or catheter ablation procedures are not feasible. large prospective randomized studies are needed to further define the clinical role of these therapeutic strategies in the future.

References

1. Proietti r, sagone a. electrical storm: Incidence, Prognosis and therapy. Indian Pacing electrophysiol. J. 2011;11:34.

2. nademanee K, taylor r, Bailey We, et al. treating electrical storm: sympathetic blockade versus advanced cardiac life support-guided therapy. Circulation 2000;102:742–747.

3. schwartz PJ, locati eH, Moss aJ, Crampton rs, trazzi r, ruberti U. left cardiac sympathetic denervation in the therapy of congenital long Qt syndrome: a worldwide report. Circulation. 1991;84:503–511.

4. Collura Ca, Johnson Jn, Moir C, ackerman MJ. left cardiac sympathetic denervation for the treatment of long Qt syndrome and catecholaminergic polymorphic ventricular tachycardia using video-assisted thoracic surgery. Heart Rhythm. 2009;6:752–759.

5. Schwartz PJ, Motolese M, Pollavini G, Lotto A, Ruberti U, Trazzi R, Bartorelli C, Zanchetti a. the Italian sudden death Prevention group. Prevention of sudden cardiac death after a first myocardial infarction by pharmacologic or surgical interventions. J Cardiovasc electrophysiol 1992; 3:2-16.

6. Mahajan a, Moore J, Cesario da, shivkumar K. Use of thoracic epidural anesthesia for management of electrical storm: a case report. Heart Rhythm. 2005;2:1359 –1362.

7. Bourke t, Vaseghi M, Michowitz y, sankhla V, shah M, swapna n, Boyle ng, Mahajan a, narasimhan C, lokhandwala y, shivkumar K. neuraxial modulation for refractory ventricular arrhythmias: value of thoracic epidural anesthesia and surgical left cardiac sympathetic denervation. Circulation. 2010;121:2255-62.

8. Hasenbos M, Liem TH, Kerkkamp H, Gielen M. The influence of high thoracic epidural analgesia on the cardiovascular system. acta Anaesthesiol Belg 1988; 39:49-54.

9. li J, liu y, yang f, Jiang g, li C, Hu d, Wang J. Video-assisted thoracoscopic left cardiac sympathetic denervation: a reliable minimally invasive approach for congenital long-Qt syndrome. ann thorac surg 2008; 86:1955-1958.

10. Collura Ca, Johnson Jn, Moir C, ackerman MJ. left cardiac sympathetic denervation for the treatment of long Qt syndrome and catecholaminergic polymorphic ventricular tachycardia using video-assisted thoracic surgery. Heart Rhythm 2009; 6:752-759.

11. li J, Wang l, Wang J. Video-assisted thoracoscopic sympathectomy for congenital long Qt syndromes. Pacing Clin electrophysiol 2003; 26:870-873.

12. atallah J, fynn-thompson f, Cecchin f, diBardino dJ, Walsh eP, Berul CI. Videoassisted thoracoscopic cardiac denervation: a potential novel therapeutic option for children with intractable ventricular arrhythmias. Ann Thorac Surg 2008; 86:1620-1625.

13. Credner, s.C., Klingenheben t, Mauss o, sticherling C, Hohnloser sH. electrical storm in patients with transvenous implantable cardioverter-defibrillators: incidence, management and prognostic implications. J Am Coll Cardiol, 1998; 32:1909-15.


Abstract

The influence of the autonomic nervous system (ANS) on triggering and perpetuation of atrial fibrillation (AF) is well established. ganglionated plexi (gP) ablation achieves autonomic denervation by affecting both the parasympathetic and sympathetic components of the ans. an anatomic approach for gP ablation at relevant atrial sites appears to be safe, and improves the results of PV isolation in patients with paroxysmal and persistent af. gP ablation can be accomplished endocardially or epicardially, ie, during the maze procedure or thoracoscopic approaches. further experience is needed to assess the clinical value of this promising technique.

Keywords: atrial fibrillation, ablation, ganglionated plexi, autonomic nervous system

This Article has been Reprinted from IPEJ with Permission from the Editor

Autonomic Denervation for the Treatment of Atrial FibrillationDemosthenes G. Katritsis, MD, PhD, FRCPdepartment of Cardiology, athens euroclinic, athens, greece

Introduction

The influence of the autonomic nervous system (ANS) on the triggering and perpetuation of atrial fibrillation (AF) is well established. Variations of the autonomic tone have been associated with paroxysms of af and both sympathetic and parasympathetic activation may be proarrhythmic by shortening of atrial refractoriness.1-3 Vagal reflexes from clusters of autonomic ganglia, so-called ganglionated plexi (gP), at sites around the circumference of the left atrial-pulmonary vein (PV) junction (figure 1), may induce and perpetuate af through spatial heterogeneity of refractoriness.1,4 In clinical practice, inadverted parasympathetic denervation has been proposed as a potential mechanism of circumferential or antral PV ablation for the treatment of atrial fibrillation.5,6 Initial studies on partial vagal denervation via epicardial fat pad ablation indicated that such a dedicated approach may prevent af,7,8 although results have not been consistent.9-11 ablation of areas with prominent sympathetic innervation has also prevented sympathetic af. the ligament of Marshall is a left atrial epicardial neuromuscular bundle, rich in sympathetic innervation, that has been associated with the genesis of atrial tachyarrhymias and af.12-15 epicardial ablation of the ligament of Marshall in the canine can terminate spontaneous atrial activity and prevent af,13 whereas in the human epicardial (through the coronary sinus)16 or endocardial14,15 ablation at the insertion site of the Marshall bundle may terminate af. We know now that selective parasympathetic or sympathetic denervation may not be feasible. Both sympathetic and parasympathetic elements reside in all four major left atrial ganglionated plexi,16,17 and ablation lesions may unavoidably affect both components of the autonomic nervous system. the area around the ligament of Marshall that has been previously thought to represent an area of predominantly sympathetic innervation has been shown to contain parasympathertic fibers as well.18 thus, although initial studies on GP ablation were characterized as attempts at specific parasympathetic denervation, this may not be true. actually,

ablation of atrial areas containing gP unavoidably results in autonomic denervation.

Techniques of GP ablation

In the electrophysiology laboratory and the operating theater, identification of major GP has been mainly accomplished through high-frequency stimulation (Hfs) and induction of vagal responses in the atria.19,20 Hfs is delivered at 1,200 bpm (20 Hz) with a pulse width of 10 ms at 12-24 V.21 a predominant efferent vagal response is defined as induction of AV block (> 2 sec) and hypotension or prolongation of the R-R interval by >50% during AF, following a 5-second application of high-frequency stimulation. during these studies the anatomic locations of these plexi in the human have been well characterized. However, the method usually entails the discomfort of general anaesthesia, since conscious patients may not tolerate more than 15 V. Furthermore, we have recently shown that that anatomic ablation, ie targeting the areas known to host gP in the left atrium (Figure 1) without previous identification of GP, yields superior clinical results than HFS-identification and ablation of gP in patients with paroxysmal af.22

Clinical Experience

Ablation in the Electrophysiology Laboratory

Isolated gP ablation has been employed for both paroxysmal and persistent af with variable success. In paroxysmal af, arrhythmia-free survival within the first year after the procedure ranged between 26 to 77%.22-26 success rates of <40% have been reported for persistent af after a single procedure.27 gP ablation in combination with pulmonary vein (PV) isolation has yielded better results than PV isolation alone with reported success rates up to 80%.4,26,28-30 We have conducted the only randomized study that has compared the efficacy of PV isolation vs PV isolation+gP ablation in 67 patients with paroxysmal AF. Recurrence of arrhythmia was documented in 18 (54.5%) patients in the PV group 4.7 ± 1.0 months after ablation, and

13

Figure 1 : anatomic position of the major gP targeted for catheter ablation. Presumed gP clusters are ablated 1-2 cm outside the PV-la junctions at the following sites: left superolateral area (superior left gP-slgP), right superoanterior area (anterior right gP-argP), left inferoposterior area (inferior left gP-IlgP), and right inferoposterior area (inferior right gP-IrgP). another gP (crux gP) the inferoposterior area between the IlgP and IrgP is not indicated. reprinted from from Katritsis dg et al. rapid pulmonary vein isolation combined with autonomic ganglia modification: a randomized study. Heart Rhythm. 2011;8:672-8. Copyright (2011), with permission from elsevier.

repeat PV isolation was performed in 7 (21.2%) of these patients 5.1 ± 1.1 months after the first procedure. Recurrence of arrhythmia was documented in 9 (26.5%) patients in the GP+PV group 5.0 ± 1.3 months after ablation, and repeat ablation was performed in 6 (17.6%) of these patients 4.3 ± 0.5 months after the first procedure. At the end of follow-up, 20 (60.6%) patients in the PV group and 29 (85.3%) patients in the GP+PV group remained arrhythmia-free (log rank test, P = 0.019).29

Intraoperative Ablation

addition of gP ablation to the conventional Maze procedure has produced improved outcomes with success rates 83-93% over the following year.31-33 although this approach is interesting it is associated by the risks of open heart surgery and the Maze which nowadays is only considered in patients subjected to valve surgery.

Thoracoscopic Approaches

thoracoscopic approaches combine PV isolation with selective gP ablation, with or without ligament of Marshall ablation or left atrial appendage amputation.34-38 the reported success rates over one year follow-up range from 65 to 86%, and the procedure does not appear to have any associated mortality, with pleural effusion, pneumothorax, hemothorax, and phrenic nerve injury the reported complications so far.

Complications of GP ablation

ablation-induced atrial or ventricular proarrhythmia has been reported with both endocardial and epicardial (thoracoscopic) approaches.28,39-40 Anatomic GP modification appears to carry a higher risk of iatrogenic left atrial tachycardias than PV isolation. In our experience, anatomic or Hfs-mediated gP ablation is complicated by atrial macroreentry in 2-10% of patients treated, but does not always require a repeat procedure, since these


tachycardias may spontaneously resolve with time.22,25,27,29

The Future

GP ablation appears to be a safe and efficacious method to improve PV isolation in patients with af, and has been used in the electrophysiology laboratory, and during the maze procedure or thoracoscopic approaches.41 However experience is limited and mainly based in patients with paroxysmal af. furthermore, the long-term efficacy is not known, and this is particularly important since restoration of autonomic activity may occur as early as 4 weeks following ablation.41 Controlled, randomized studies and more clinical experience are needed to accurately assess the clinical usefulness of this promising technique.

References

1. liu l, nattel s. differing sympathetic and vagal effects on atrial fibrillation in dogs: role of refractoriness heterogeneity. Am J Physiol 1997;273:H805-16.

2. Chiou CW, eble Jn, Zipes dP. efferent vagal innervation of the canine atria and sinus and atrioventricular nodes. the third fat pad. Circulation 1997;95:2573–2584.

3. Bettoni M, Zimmermann M. autonomic tone variations before the onset of paroxysmal atrial fibrillation. Circulation 2002;105:2753–2759.

4. scherlag BJ, nakagawa H, Jackman WM, yamanashi Ws, Patterson e, Po s, lazzara r. electrical stimulation to identify neural elements on the heart: their role in atrial fibrillation. J Interv Card Electrophysiol 2005;13 suppl 1:37-42

5. Nakagawa H, Jackman WM, Scherlag BJ, Lazzara R. Pulmonary vein isolation during atrial fibrillation: insight into the mechanism of pulmonary vein firing. J Cardiovasc Electrophysiol 2003;14:261-272.

6. Pappone C, santinelli V, Manguso f, Vicedomini g, gugliotta f, augello g, Mazzone P, tortoriello V, landoni g, Zangrillo a, lang C, tomita T, Mesas C, Mastella E, Alfieri O.Pulmonary vein denervation enhances long-term benefit after circumferential ablation for paroxysmal atrial fibrillation. Circulation 2004;109:327-34.

7. scanavacca M, Pisani Cf, Hachul d, lara s, Hardy C, darrieux f, trombetta I, negrão Ce, sosa e. selective atrial vagal denervation guided by evoked vagal reflex to treat patients with paroxysmal atrial fibrillation. Circulation 2006;114:876-85.

8. schauerte P, scherlag BJ, Pitha J, scherlag Ma, reynolds d, lazzara r, Jackman WM. Catheter ablation of cardiac autonomic nerves for prevention of vagal atrial fibrillation. Circulation 2000;102:2774-80.

9. oh s, Zhang y, Bibevski s, Marrouche nf, natale a, Mazgalev tn. Vagal denervation and atrial fibrillation inducibility: epicardial fat pad ablation does not have long-term effects. Heart Rhythm 2006; 3:701-8.

10. Hirose M, leatmanoratn Z, laurita Kr, Carlson Md. Partial vagal denervation increases vulnerability to vagally induced atrial fibrillation. J Cardiovasc Electrophysiol 2002;13:1272-9.

11. Cummings Je, gill I, akhrass r, dery M, Biblo la, Quan KJ. Preservation of the anterior fat pad paradoxically decreases the incidence of postoperative atrial fibrillation in humans. J Am Coll Cardiol 2004;43:994–1000.

12. Hwang C, Karagueuzian Hs, Chen Ps. Idiopathic paroxysmal atrial fibrillation induced by a focal discharge mechanism in the left superior pulmonary vein. Possible role of the ligament of Marshall. J Cardiovasc Electrophysiol 1999;10:636-648.

13. doshi rn, Wu tJ, yashima M, Kim yH, ong JJC, Cao JM, Hwang C, yashar P, fishbein MC, Karagueuzian Hs, Chen P-s. relation between ligament of Marshall and adrenergic atrial tachyarrhythmia. Circulation 1999;100:876-883.

14. Hwang C, Wu tJ, doshi rn, Peter Ct, Chen Ps. Vein of Marshall cannulation for the analysis of electrical activity in patients with focal af. Circulation 2000;101:1503-1505.

15. Katritsis D, Ioannidis JP, Anagnostopoulos CE, Sarris GE, Giazitzoglou E, Korovesis S, Camm AJ. Identification and catheter ablation of extracardiac and intracardiac components of ligament of Marshall tissue for treatment of paroxysmal atrial fibrillation. J Cardiovasc Electrophysiol 2001;12:750-8.

16. armour Ja, Murphy da, yuan BX, Macdonald s, Hopkins da. gross and microscopic anatomy of the human intrinsic cardiac nervous system. Anat Rec 1997;247:289-98.

17. Kawashima t. the autonomic nervous system of the human heart with special reference to its origin, course, and peripheral distribution. Anat Embryol (Berl) 2005;209:425-38.

18. Ulphani Js, arora r, Cain JH, Villuendas r, shen s, gordon d, Inderyas f, Harvey la, Morris a, goldberger JJ, Kadish aH. the ligament of Marshall as a parasympathetic conduit. Am J Physiol Heart Circ Physiol 2007;293:H1629-35.

19. lemery r, Birnie d, tang as, green M, gollob M. feasibility study of endocardial mapping of ganglionated plexuses during catheter ablation of atrial fibrillation. Heart Rhythm 2006;3:387-96.

20. Mehall Jr, Kohut rM Jr, schneeberger eW, taketani t, Merrill WH, Wolf rK. Intraoperative epicardial electrophysiologic mapping and isolation of autonomic ganglionic plexi. Ann Thorac Surg 2007;83:538-41.

21. lemery r. How to perform ablation of parasympathetic ganglia of the left atrium. Heart Rhythm 2006;3:1237-1239.

22. Pokushalov e, romanov a, shugayev P, artyomenko s, shirokova n, turov a, Katritsis dg. selective ganglionated plexi ablation for paroxysmal atrial fibrillation. Heart Rhythm 2009;6:1257-64.

23. danik s, neuzil P, d’avila a, Malchano ZJ, Kralovec s, ruskin Jn, reddy Vy. evaluation of catheter ablation of periatrial ganglionic plexi in patients with atrial fibrillation. Am J Cardiol 2008;102:578-83.

24. Katritsis d, giazitzoglou e, sougiannis d, goumas n, Paxinos g, Camm aJ. anatomic approach for ganglionic plexi ablation in patients with paroxysmal atrial fibrillation. Am J Cardiol 2008;102:330-4.

15

25. Pokushalov E, Romanov A, Artyomenko S, Turov A, Shirokova N, Katritsis dg. left atrial ablation at the anatomic areas of ganglionated Plexi for Paroxysmal atrial fibrillation. Pacing Clin Electrophysiol 2010;33:1231-8.

26. Mikhaylov e, Kanidieva a, sviridova n, abramov M, gureev s, szili-torok t, lebedev d. outcome of anatomic ganglionated plexi ablation to treat paroxysmal atrial fibrillation: a 3-year follow-up study. Europace 2011;13:362-70.

27. Pokushalov e, romanov a, artyomenko s, et al. ganglionated plexi ablation for longstanding persistent atrial fibrillation. Europace 2010;12:342-6.

28. Po ss, nakagawa H, Jackman WM. localization of left atrial ganglionated Plexi in Patients with atrial fibrillation. J Cardiovasc Electrophysiol 2009;20:1186-9.

29. Katritsis dg, giazitzoglou e, Zografos t, Pokushalov e, Po ss, Camm aJ. rapid pulmonary vein isolation combined with autonomic ganglia modification: a randomized study. Heart Rhythm 2011;8:672-8.

30. Zhou Q, Hou Y, Yang S. A Meta-Analysis of the Comparative Efficacy of ablation for atrial fibrillation with and without ablation of the ganglionated Plexi. Pacing Clin Electrophysiol 2011 sep 28. [epub ahead of print]

31. doll n, Pritzwald-stegmann P, Czesla M, et al. ablation of ganglionic plexi during combined surgery for atrial fibrillation. Ann Thorac Surg 2008;86:1659-63.

32. Ware al, suri rM, stulak JM, sundt tM 3rd, schaff HV. left atrial ganglion ablation as an adjunct to atrial fibrillation surgery in valvular heart disease. Ann Thorac Surg 2011;91:97-102.

33. onorati f, Curcio a, santarpino g, torella d, Mastroroberto P, tucci L, Indolfi C, Renzulli A. Routine ganglionic plexi ablation during Maze procedure improves hospital and early followup results of mitral surgery. J Thorac Cardiovasc Surg 2008;136:408-18.

34. McClelland JH, duke d, reddy r. Preliminary results of a limited thoracotomy: new approach to treat atrial fibrillation. J Cardiovasc Electrophysiol 2007;18:1289-95.

35. Han FT, Kasirajan V, Kowalski M, Kiser R, Wolfe L, Kalahasty G, shepard rK, Wood Ma, ellenbogen Ka. results of a minimally invasive surgical pulmonary vein isolation and ganglionic plexi ablation for atrial fibrillation: single-center experience with 12-month follow-up. Circ Arrhythm Electrophysiol 2009;2:370-7.

36. yilmaz a, geuzebroek gs, Van Putte BP, et al. Completely thoracoscopic pulmonary vein isolation with ganglionic plexus ablation and left atrial appendage amputation for treatment of atrial fibrillation. Eur J Cardiothorac Surg 2010;38:356-60.

37. edgerton Jr, Brinkman Wt, Weaver t, et al. Pulmonary vein isolation and autonomic denervation for the management of paroxysmal atrial fibrillation by a minimally invasive surgical approach. J Thorac Cardiovasc Surg 2010;140:823-8.

38. Krul sP, driessen aH, van Boven WJ, linnenbank aC, geuzebroek gs, Jackman WM, Wilde aa, de Bakker JM, de groot Jr. thoracoscopic video-assisted pulmonary vein antrum isolation, ganglionated plexus ablation, and periprocedural confirmation of ablation lesions: first results of a hybrid surgical-electrophysiological approach for atrial fibrillation. Circ Arrhythm Electrophysiol 2011;4:262-70.

39. Kron J, Kasirajan V, Wood Ma, Kowalski M, Han ft, ellenbogen Ka. Management of recurrent atrial arrhythmias after minimally invasive surgical pulmonary vein isolation and ganglionic plexi ablation for atrial fibrillation. Heart Rhythm 2010;7:445-51.

40. osman f, Kundu s, tuan J, Jeilan M, stafford PJ, andre ng g. ganglionic plexus ablation during pulmonary vein isolation - predisposing to ventricular arrhythmias? Indian Pacing Electrophysiol J 2010;10:104-7.

41. sakamoto s, schuessler rB, lee aM, aziz a, lall sC, damiano rJ Jr. Vagal denervation and reinnervation after ablation of ganglionated plexi. J Thorac Cardiovasc Surg 2010;139:444-52.


Case Report

A 59-year-old male with no prior cardiac history presented with altered mental status. He was unable to give any history. His vital signs revealed a temperature a 104.9 and a heart rate of 103. an initial electrocardiogram showed evidence of st-elevation in V1 and V2 (figure 1) prompting a concern for myocardial infarction in the emergency department. Comparison with the prior eKg (figure 2) showed the patient had a type 2 (saddle-back type) Brugada pattern, which progressed to type 1 Brugada pattern with hyperthermia giving the appearance of anteroseptal st-elevation MI (coved type). a bedside echocardiogram revealed normal left ventricular wall motion confirming the above. serial cardiac enzymes remained negative.

described twenty years ago (1), Brugada syndrome is an important channelopathy that causes sudden cardiac death in structurally normal hearts. Mutations in the SCN5A gene have been linked to this autosomal dominant condition (2). fever is an important trigger for eKg changes as well as ventricular arrhythmias in patients with Brugada syndrome (3). this

condition is an important differential of st-elevation in the anteroseptal leads, and a bedside echocardiography can rule out myocardial infarction if the history is unobtainable.

References

1. Brugada P, Brugada J. right bundle branch block, persistent st segment elevation and sudden cardiac death: a distinct clinical and electrocardiographic syndrome. a multicenter report. J Am Coll Cardiol 1992;20:1391-6.

2. Chen Q, Kirsch ge, Zhang d, Brugada r, Brugada J, Brugada P, Potenza d, Moya a, Borggrefe M, Breithardt g, ortiz-lopez r, Wang Z, antzelevitch C, o’Brien re, schulze-Bahr e, Keating Mt, towbin Ja, Wang Q.genetic basis and molecular mechanism for idiopathic ventricular fibrillation. Nature 1998;392:293-6.

3. amin as, Meregalli Pg, Bardai a, Wilde aa, tan Hl.fever increases the risk for cardiac arrest in the Brugada syndrome. Ann Intern Med 2008;149:216-8.

The Classic Confounder of ST-Elevation Myocardial InfarctionTahmeed Contractor, Bilal Ayub division of Cardiology, lehigh Valley Health network, allentown, Pa

Figure 1 : Brugada pattern during fever

Figure 2 : Basal eCg showing Brugada pattern

17

Case Report

Introduction

We present the case of a young male who suffered a cardiac arrest due to ventricular fibrillation (VFib) and was found to have preexcitation that was successfully ablated during his hospital stay.

Case Report

a 38-year-old male with a history of methamphetamine and alcohol abuse was brought to the emergency room by paramedics after finding him in wide complex tachycardia (Figure 1). His immediate preceding symptoms which occurred at rest included significant palpitations, shortness of breath, chest pressure and lightheadedness. emergency medical personnel arrived at the scene and noted wide-complex irregular tachycardia. He was diagnosed presumptively with ventricular tachycardia and was shocked to sinus rhythm prior to arrival to the er. after arrival, he went into wide complex irregular tachycardia which degenerated into ventricular fibrillation for which he received 5 shocks (figure 2). He was then started on an amiodarone drip and relatively stabilized. on further questioning, he states he recently went on a methamphetamine binge. He also had been having symptoms of palpitations and lightheadedness which he had ignored without seeking medical attention.

an electrophysiology consultation was then requested. a review of his eKg’s showed negative delta waves in the

Aborted Sudden Death in a 38 Year Old MaleSangeetha R Balakrishnan* *Cardiac electrophysiologist, Washington Hospital, fremont Ca

inferior leads and a positive delta wave in lead V1 with short Pr intervals (figure 3). the patient was taken to the eP lab and he underwent a left postero-septal pathway ablation using a trans-septal approach (figure 4). He did well post procedure and he was discharged to follow up as an outpatient.

Discussion

Atrial fibrillation occurs in roughly 20% of patients with Wolff-Parkinson-White (WPW) syndrome. Prolonged intra-atrial conduction times during rapid atrial rates tend to predispose these patients to atrial fibrillation.1 the incidence of sudden cardiac death has been reported between 0.5% to 4% in several case series and case reports.2 Patients at increased risk for degeneration to ventricular fibrillation have an accessory pathway with a very short antegrade refractory period (<250 msec), or have multiple pathways or left sided pathways, and have symptomatic tachycardia or epstein’s anomaly.3 In those

Figure 1 : Pre-hospital eMs 12 lead showing irregular wide complex tachycardia with preexcitation

Figure 2 : In the ER. Degeneration to Vfib requiring multiple shocks.

Figure 3 : resting eCg showing preexcitation suggestive of a posteroseptal pathway.

Figure 4 : Post-ablation eCg of the left posteroseptal pathway


individuals with symptoms, it might be prudent to perform electrophysiology testing to risk stratify the most appropriate therapy. our patient ignored his symptoms for the three months prior to presentation. He also likely put himself at increased risk with antecedent drug abuse with methampetamines.

References

1. riccardi r, gaita f, giustetto C, gardiol s. atrial electrophysiological features in patients with Wolff-Parkinson-White and atrial fibrillation: absence of rate adaptation of intraatrial conduction time parameters. Pacing Clin Electrophysiol 1997;20(5 Pt 1):1318.

2. teo Ws, Klein gJ, yee r. sudden Cardiac death In the Wolff-Parkinson-White syndrome. Singapore MED J 1992;33:247-251.

3. Klein gJ, Bashore tM, sellers td, Pritchett el, smith WM, gallagher JJ. Ventricular fibrillation in the Wolff-Parkinson-White syndrome. N Engl J Med 1979;301:1080.

4. Munger tM, Packer dl, Hammill sC, feldman BJ, Bailey Kr, Ballard dJ, Holmes dr Jr, gersh BJ. a population study of the natural history of Wolff–Parkinson–White syndrome in Olmsted County, Minnesota, 1953–1989. Circulation 1993;87:866–73.

19

eCg QuizYash Lokhandwala*, Gopi Krishna Panicker**

*arrhythmia associates; **Quintiles Cardiac safety services, Mumbai


The answers and explanations are on the reverse side of the page.

21

There is:

a. sinus node dysfunction

b. aV block

c. Both a and B

ECG - 1

for correct answer see overleaf

39 yr old obese lady. recurrent low feeling with fatigue


The correct answer is ‘a’ – sinus node dysfunction (snd)

the eCg shows a long sinus arrest of 3.6 seconds. during this, no P wave is seen. otherwise, there is bradycardia. every P wave is connected with a normal Pr interval. Hence, there is no aV block. the symptoms are most likely because of snd. Hence an ‘atrial-based pacemaker’ seems necessary.

a 24-hour Holter and a treadmill stress test are useful for decision-making in borderline cases. figure 1 (a) shows the eCg after a permanent pacemaker. the patient had 1:1 aV conduction when atrium was paced upto 180 bpm. Hence, an aaIr pacemaker was implanted with relief of symptoms.

all the complexes here show a pacing spike prior to the P wave. In one complex, the pacing stimulus is seen only in lead V2 (↓) because of respiratory variation causing difference in pac-ing spike amplitude.

Figure 1 (a)

ECG - 1

23

a. supraventricular tachycardia (sVt) with left bundle branch block (lBBB)

b. Idiopathic Right ventricular outflow tract (RVOT) VT

c. arrhythmogenic right ventricular dysplasia (arVd)

ECG - 2


27 yr old man. 3 episodes of rapid palpitations with near-syncope/syncope. Wide Qrs tachycardia documented. Currently he is on amiodarone and metoprolol.


ECG - 2

The correct answer is ‘c’ – arVd

The ECG above shows a regular wide QRS (QRS=135 ms) tachycardia @ 170 bpm. The marked fluctuation in the T waves in long lead II along with the occasional ‘P’ waves (*) strongly suggest VA dissociation.Moreover, the lBBB like morphology, the negative Qrs in V1 along with right axis deviation (Qrs axis=120°) is another hall-mark of Vt arising from the rVot.

the sinus rhythm eCg is abnormal, with t inversion in V1-V3 and low limb lead voltages. this is consistent with arVd. sinus bradycardia and Pr prolongation could be because of anti-arrhythmic drugs. this patient’s echocardiogram showed a mildly dilated rV with outpouchings. the cardiac MrI confirmed these findings.this patient is at high risk of sudden death and syncope and needs an ICd.

25

the following is not seen:

a. a. sinus bradycardia

b. Complete aV block

c. Atrial fibrillation

d. Inferior and rV MI

ECG - 3


50 yr old man, H/O palpitations; now comes with giddiness


ECG - 3

The correct answer is ‘a’ – sinus bradycardia

no regular normal P waves are seen. the undulating baseline due to af is well seen in long lead II. the isolated apparent P wave in lead III is therefore misleading. The ventricular rate is regular and slow (35 bpm) with narrow Qrs complexes. Hence, there is complete aV block with junctional escape rhythm.

there is st elevation of around 2 mm seen in leads II, III, aVf and V1-V4.

there are also 1 mm st elevation ‘qr’ complexes in leads V4r – V6r. Hence, there is a strong suggestion of an inferior right ventricular MI. a large rV branch crossing anteriorly can give a pseudo-anteroseptal MI pattern in proximal right coronary artery occlusion.

Presumably, the patient was symptomatic previously because of atrial flibrillation and currently because of MI with complete aV block.

27

This ECG shows:

a. atrial and ventricular pacing

b. PVCs

c. fusion complexes

d. Both B and C

ECG - 4


70 yr old lady; H/o pacemaker for sinus node dysfunction; later, episodes of atrial fibrillation


ECG - 4

The correct answer is ‘d’ – Both B and C

all the P waves are preceded by a pacing artifact slowing the presence of an atrial-based pacemaker.

long lead II shows frequent unifocal PVCs.

the fusion complexes are marked by f. during these, the ventricular activation is partly by the PVC conduction and ventricular conduction.

29

a. sVt

b. Vt

c. sVt and Vt

ECG - 5


75 yr old lady with 2 yr H/O recurrent rapid palpitations, occasionally with syncope


ECG - 5

The correct answer is ‘a’ – sVt

Top panel

the upper strip shows onset of tachycardia with a PaC (*) alongwith a prolonged Pr interval. after this during the “tachycardia” (ventricular rate 96 bpm) a P’ wave is seen exactly between 2 Qrs complexes. Note that these QRS complexes have a prominent R’ in the first channel () which is not seen during sinus rhythm. this r’ strongly suggests an additional P wave.

Bottom panel

there is a transition to a faster wide Qrs tachycardia. note that the rr durations are now exactly half. thus, the sVt showed 2:1 aV conduction which changed to 1:1 aV conduction with rate-related bundle branch block.

this sVt is most likely slow-fast aV nodal reentry tachycardia.

the arrowheads are of equal length

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*Life Members : 1. Person should be a Post-Graduate in Medicine/Pediatrics/Anaesthesia/ Physiology or other allied subjects from an University recognised by Medical Council of India, with interest in Cardiology / Electrocardiology.

2. Candidates are requested to submit Xerox copies of the PG Certificate and Medical Council of India Registration Certificate alongwith Application Form.

**Fellowship: 1. Person should be a Member of the Society.

2. He/She should be of atleast 7 years of standing after Post-Graduation.

3. He/She should have minimum 3 publications In Cardiology In Indexed Journals (Not Abstracts)

4. List of Publications to be submitted for the Fellowship.

5.

*Subject to approval of the Executive Body of the Society**Subject to the approval of the Credential Committee of the Society.

Fellowship Fees: Rs.2,000/- (+Rs.100/- for outstation cheque) only. Incase, fellowship not approved by the Credential Committee, the cheque / draft will be returned.

RULES/REGULATIONS OF THE SOCIETY REGARDING ADMISSION OF LIFE MEMBERS/FELLOWSHIP

*Life Members : 1. Person should be a Post-Graduate in Medicine/Pediatrics/Anaesthesia/ Physiology or other allied subjects from an University recognised by Medical Council of India, with interest in Cardiology / Electrocardiology.

2. Candidates are requested to submit Xerox copies of the PG Certificate and Medical Council of India Registration Certificate alongwith Application Form.

**Fellowship: 1. Person should be a Member of the Society.

2. He/She should be of atleast 7 years of standing after Post-Graduation.

3. He/She should have minimum 3 publications In Cardiology In Indexed Journals (Not Abstracts)

4. List of Publications to be submitted for the Fellowship.

5.

*Subject to approval of the Executive Body of the Society**Subject to the approval of the Credential Committee of the Society.

Fellowship Fees: Rs.2,000/- (+Rs.100/- for outstation cheque) only. Incase, fellowship not approved by the Credential Committee, the cheque / draft will be returned.

www.iseindia.orgfor more information

& latest updates

SECRETaRIaTS. B. GUPTA

PRESIDENT ELECT

Indian Society of ElectrocardiologyHead, Department of Medicine and Cardiology, C. Rly, Head Quarters Hospital, Byculla, Mumbai - 400 027.

Phone : 2371 7246 (Ext. 425), 2372 4032 (ICCU), 2373 2911 (Chamber) • Resi: 2262 4556 Fax : 2265 1044 • Mobile : 0 98213 64565 / 0 99876 45403

E-mail : [email protected] • Website : www.iseindia.org

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