EP Symposium 2013 - Camenae Group Symposium 2013 Pulling Back the ... • Edrophonium, TNG, Adenosine. Head Upright Tilt Table Testing ... – Midodrine HCL (ProAmatine) 2.5 ‐10

EP Symposium 2013

Pulling Back the Curtain: Demystifying the World of Pacing and Electrophysiology

oror

“Poisons and Torture”

Jay Olen Franklin, MD, FACC, FHRS

Cardiology Consultants of Texas, HTPN

Question 1

• What is the most common reason/indication for ICD implantation in 2013?

– A. Out of hospital cardiac arrest

B Sustained ventricular tachycardia– B. Sustained ventricular tachycardia

– C. Cardiomyopathy with persistantly low EF and increased risk of sudden cardiac death

– D. Severe congestive heart failure

– E. Rapid atrial fibrillation with syncope

Question 2

• A patient post atrial fibrillation ablation begins to bleed from the right femoral puncture site. The best treatment option for femoral bleeding includes:– A. Direct pressure directly on the skin puncture A. irect pressure directly on the skin puncturesites for 15 minutes

– B. Direct pressure 2‐4 cm above (cephalad) to the skin puncture sites for 15 minutes.

– C. Place a sandbag over the femoral puncture site– D. Call for a vascular surgery consult– E. Place a C clamp directly on the skin puncture sites for 60 minutes

Question 3

• What is the most effective and cost‐effective treatment for symptomatic SVT (AV nodal reentry SVT)?– A. Beta blocker

– B. Flecainide 100 mg BID

– C. Catheter ablation

– D. Pacemaker implantation

– E. ER visits for sustained SVT termination with adenosine

Question 4

• What is the most effective treatment for recurrent vasovagal syncope “the malignant vapors”?

– A Beta blockers– A. Beta blockers

– B. Zoloft

– C. Pacemaker implantation

– D. Education

– E. Proamatine

Question 5

• What is the most accurate statement regarding the anticipated beneficial effects of atrial fibrillation ablation?– A. Eliminates need for anticoagulant therapy

– B. Decreases frequency and severity of symptomatic AF episodes.

– C. Cures atrial fibrillation

– D. Eliminates need for antiarrythmic drug therapy

– E. All of the above

Drugs

• All anti‐arrhythmic drugs are poisons

• May or may not require in‐hospital telemetry

• In general are less effective than ablation for suppression of arrhythmias of all kindssuppression of arrhythmias of all kinds

• Appropriate and effective therapy– Primary treatment for most non life‐threatening arrhythmias

– Secondary or adjunctive therapy for all arrhythmias

Syncope

• Transient loss of consciousness and postural tone

– commoncommon

• 3% of ER visits, 6% of hospital admissions

– may be only warning prior to sudden cardiac death

– tremendous psychological burden and source of anxiety for patients and their families

– etiology may be benign, consequences serious

Evaluation of Syncope

• Non‐invasive– Glucose tolerance testing– Holter monitoring / Event recorder monitoring– Echocardiography– Exercise treadmill testingExercise treadmill testing– Nuclear cardiac evaluation– SAECG / T wave alternans– Electroencephalography– CT & MRI scanning– Carotid ultrasonography– History and physical examination


• Invasive or Outpatient Admission

– Cardiac catheterization

– Electrophysiology testing

Head upright tilt table testing– Head‐upright tilt table testing

– Insertable looped event recorder


• Costs

– up to $16,000 per patient

– $800 million per year in US alone

etiology of syncope identified in less than 40%– etiology of syncope identified in less than 40%

Head Upright Tilt Table Testing

• Indication:

– Syncope/Presyncope

• Confirm Dx of “the vapors” (neurocardiogenic or vasovagal syncope – plain old fainting spells)

• Teach patients about their initial symptoms preceding or precipitating syncope

• Evaluate for other forms of cardiovascular syncope not associated with arrhythmias


• Advantages

– remarkable ability to reproduce syncope

– safe and effective method to identify patients predisposed to hypotensive eventspredisposed to hypotensive events

– direct observation of syncope provides understanding of specific pathophysiology

– teaches patient about “triggers” and individual characteristics of syncope ‐ “desensitization”


• Procedure– Overnight fast– No sedation or premedication– Supine on table with weight‐bearing footboard with safety restraints

– IV accessIV access– Continuous ECG monitoring, non‐invasive blood pressure monitoring every 3 minutes

– HUT 70o to 85o for 20‐30 minutes or until abnormal response occurs.

– No response ‐ supine isoproterenol infusion to achieve 20% increase of baseline heart rate and repeat 20 minutes of HUT (usually 1‐3 mcg/minute

– Crash cart resuscitative equipment available


• Methods

– HUT (gravity only)

• 90% specificity

– HUT (with isoproterenol)HUT (with isoproterenol)

• 80% ‐ 90% specificity

• increases sensitivity

– HUT (with other provocative agents)

• Edrophonium, TNG, Adenosine


• Abnormal Responses– Classic neurocardiogenic response

• Sudden drop in BP followed by decrease in HR

• Few medical complaints between syncopal spells

• Prodromal symptoms: yawning, nausea, sweating, warmth, di i l d f ti tdizziness, prolonged fatigue post syncope

• “Church Syncope” almost always vasovagal in etiology

• Junctional escape rhythm, long sinus pauses, and AV block may occur

• Rapid return to supine position results in resolution of symptoms

• Patients almost always tell us that they feel “bad” prior to syncope and beg to be put down! (yet deny prodromal symptoms)


• Risks / Disadvantages– No real risks (strapped to table so cannot fall)

– Hated by patients and staff• Long procedures

• Poor reimbursement for time spentPoor reimbursement for time spent

• “Torture” to patients

• Requires outpatient admission and paperwork

• Usually performed with non‐diagnostic EP study (to improve reimbursement)

– Repeat testing on therapy does not confirm treatment efficacy

– Testing rarely alters prescribed treatment

Neurocardiogenic Syncope

• Treatment Options– Volume (2 ‐ 3 liters/day) and sodium loading– Elastic support garment

• Waist high• Jobst style (30 mmHg ankle counter pressure)

– Hydrofludrocortisone (Florinef) 0.1 mg qD or BID– Beta blockers ‐ metoprolol, atenolol, nadolol,pindolol– Disopyramide (Norpace CR) 150 ‐ 200 mg BID– Theophylline 200 mg BID

Neurocardiogenic Syncope

• Treatment Options (continued)– Pseudoephedrine 60 mg QID– Methylphenidate HCL (Ritalin) 5 ‐ 15 mg TID– Midodrine HCL (ProAmatine) 2.5 ‐ 10 mg TID

• Alpha‐agonist– Serotonin Reuptake InhibitorsSerotonin Reuptake Inhibitors

• Sertraline (Zoloft) 25 ‐ 100 mg qD• Nefazadone (Serzone) 100 ‐ 150 mg BID• Prozac

– Permanent Pacemaker Implantation• Sleep mode• DDD or DDI• Rate drop response

– Patient education is key (and only thing that works) – None of the other treatment options have ever shown significant efficacy

Cardiac Electrophysiology

• Goals of EP Study

– Diagnosis of arrhythmia

– Assessment of risk

Treatment– Treatment

– Provide job for electrophysiologist and market for pacemaker / ICD sales force


• Electrophysiology Study

– Recording and pacing from multiple intracardiac sites

– Examine specific parts of conduction systemExamine specific parts of conduction system

– Evaluate induction, termination, and mechanism of arrhythmias


• Indications for Electrophysiology Study

– Recurrent syncope

– Sinus node dysfunction

– AV block

– Paroxysmal supraventricular tachycardia

– Wide complex tachycardia

– Sustained ventricular tachycardia

– Electropharmacologic testing

– Out of hospital cardiac arrest

EP Procedure (continued)

• Electrophysiologist

– Local anesthesia (lidocaine) achieved

– Percutaneous vascular access obtained

• Venous sheaths (2‐5; 5F – 8F size)

• Arterial cannulation may be used (4F‐8F size)

– Catheters placed and manipulated under fluroscopy to appropriate locations in heart

– Catheters are connected to a junction box that delivers a signal to a computerized sense amplifier and stimulator

– Pacing thresholds are checked and pacing stimuli are delivered

– EP sits down and programmed stimulation performed

Vascular Access Sites for EP Study

• Femoral vein and/or artery

– Usually right side

• Internal jugular vein

• Subclavian

Catheter Placement for EP Study

• High Right Atrium (HRA)

• His Bundle (His)

• Right Ventricular Apex (RVA)(RVA)

• Coronary Sinus (CS)

• Alternative Sites:– RVOT

– LV

– LA

– Tricuspid annulus (halo)

– RA Crista region

EP StudyRisks/Complications

Less than 1%• Bleeding• Bruising• Infection

Less than 1 in 1500

• Stroke (1‐2% AF ablation)

• MI• Hemothorax• Pneumothorax• Puncture of heart• Pericarditis/pleuritis• Allergy• Anesthesia‐related• AV block

• MI

• Death

• Tamponade

EP StudyDischarge Instructions

• Encourage ambulation• A small “knot” at insertion site is normal (dime to quarter size)• Bleeding at the access site unusual

– Venous requires simple pressure– Arterial requires firm pressure and return to ER/Office

• Infection uncommon – call if occurs may need antibiotic• Infection uncommon – call if occurs, may need antibiotic• No driving or other high risk activities for 12 hrs after receiving sedation

agents• Lifting (>20 lbs) and vigorous exercise restrictions

– Venous: 2 days– Arterial:

• 4F for BP monitoring only ‐ 2 days• Left heart retrograde catheterization 6F to 8F – 7 days

• Return to work next day

Catheter Ablation

• The removal or destruction of tissue.

• To eliminate the site of origin of a tachycardia or to interrupt a portion of the arrhythmia circuit.

• Energy sources:

– Direct current shocks (historical)

– Surgical – scalpel, cryoablation, cautery, laser

– Radiofrequency (modified cautery, current standard)

– Cryoballoon or cryocatheter

Catheter Ablation

• Indications

– Cure of SVT (WPW, AVNRT, Concealed AP, AFl, AT, AF?)

– Cure of specific VTs

• RVOT VT

• Idiopathic repetitive monomorphic LV VT

• Bundle‐branch reentry VT

• Rarely, ischemic VT (slow, monomorphic, drug‐refractory

– Palliation of SVT • AVJ ablation with PPM implantation for AF

– Palliate symptoms from palpitations (APCs, VPCs)

AV Nodal Reentry SVT

• Classic paroxysmal supraventricular tachycardia ‐ (AVNRT) ‐ 60‐65% of SVT

• Rapid, narrow QRS rhythm ‐ no visible P wave on ECG ‐ 150‐220 bpmp

• Abrupt onset & offset ‐ symptomatic, but non‐life threatening ‐ major nuisance

• Dizziness, palpitations, syncope, chest pain, anxiety, dyspnea


• Congenital ‐ patient is born with an extra pathway near the AV node

• Historically felt to be reentry within the AV node Reentry actually involves “fast”node. Reentry actually involves fast pathway (AV node) retrograde, with antegrade conduction via the “slow” pathway along the tricuspid annulus near the os of the coronary sinus


• Treatment Options– Drug Therapy: almost never renders patient completely free of SVT episodes

• AV nodal blockers

• Potent antiarrhythmics

– Antitachycardia pacing therapy

– Surgical Ablation (curative)

– Ablate & Pace (curative ‐ not optimal)

– RF or Cryo Catheter Ablation (curative)


• Treatment Options– Radiofrequency Catheter Ablation

• Ablate (eliminate conduction) by means of a radiofrequency burn via specialized electrode catheter

• Modify “slow” (preferred) or “fast” (old) pathway y (p ) ( ) p yconduction selectively ‐ leaves conduction intact ‐does not require pacemaker

• Curative in > 95% of cases ‐ does not eliminate palpitations

• Two to six hour same‐day elective procedure ‐ may require overnight telemetry observation

• Primary, preferred therapy for AVNRT• Cryo catheter study ongoing – may be safer

Wolff‐Parkinson‐White Syndrome

• WPW

– Antegrade and retrograde conduction via an accessory pathway

– Accessory pathways connect the atrium and ventricle electrically at site other than the AV node

– “Delta wave” present on the resting ECG ‐ at the initial part of the QRS

– Preexcitation: excitation of the ventricle via the accessory pathway earlier than the ventricle would have been excited via the AVN


• WPW

– AVRT: AV reentry supraventricular tachycardia• Orthodromic: antegrade via AVN, retrograde via AP ‐ 95% of SVT

i APusing AP

• Antidromic: antegrade via AP, retrograde via AVN

– Atrial flutter / fibrillation: potentially life‐threatening

• “Concealed” accessory pathways:

– orthodromic SVT identical to that in WPW

– no “delta wave” on ECG (“concealed”)


• Rapid, narrow QRS supraventricular tachycardia ‐ visible retrograde P wave

• 150‐250 bpmp

• Abrupt onset & offset ‐ typically terminated with vagal maneuvers, adenosine, verapamil*

• Dizziness, palpitations, syncope, chest pain, dyspnea, sudden cardiac death

• Congenital ‐ 1 of 1000 live births have APs


• Treatment Options

– Drug Therapy: almost never renders patient completely free of SVT episodes

• AV nodal blockersAV nodal blockers

• Potent antiarrhythmics

– Surgical Ablation: historical

– Ablate & Pace

– RF Catheter Ablation (curative)


• Treatment Options

– Radiofrequency Catheter Ablation• Ablate (eliminate conduction) along the AP using RF energy burn via a specialized electrode catheter

• Selectively eliminate conduction in AP ‐ leaves AVN intact ‐does not require pacemaker

• Curative in > 95% patients with accessory pathway mediated SVT

• Prevents SVT ‐ does not eliminate palpitations

• Two to six hour elective same‐day procedure, may require overnight telemetry observation

• Primary, preferred therapy for WPW / concealed APs

ATRIAL FLUTTER

Radiofrequency Catheter Ablation

• Criteria for successful ablation– Termination of atrial flutter during RF energyTermination of atrial flutter during RF energy application

– Not reinducible into atrial flutter

– Confirmation of bi‐directional conduction block in the TV‐IVC isthmus with pace‐mapping

• Repeat mapping and RF energy application until ablation success achieved

ATRIAL FLUTTER

Radiofrequency Catheter Ablation• Initial ablation success now > 90%• Recurrence rates 25‐35% in early studies, but using bi‐directional block as endpoint may reduce recurrence rates to < 10%recurrence rates to < 10%

• First line therapy for type I atrial flutter• Procedure endpoints of noninducibility and bi‐directional TV‐IVC isthmus conduction block

• Future advances: – Super‐long ablation electrodes– High output RF generators

Classification of AF

Gallagher MM, Camm AJ. Classification of atrial fibrillation. PACE. 1992;20:1603‐1605

Progression from Paroxysmal to Persistent/Permanent AF: 8% at 1 year, 20% at 3 years

HRS Consensus Classification of AF

• Paroxysmal AF is recurrent AF that terminates spontaneously within seven days.

• Persistent AF is sustained beyond seven days or may have occurred less than seven days but requires chemical or electrical cardioversionchemical or electrical cardioversion.

• Longstanding persistent AF is AF lasting longer than one year.

• Permanent AF is typically used to describe the patients’ or doctors’ decision not to undergo treatment to terminate AF and attempt to maintain sinus rhythm.

Source: Calkins HG, et al. Heart Rhythm 4;6:816-861.

AFib Treatment Options

Patient/PhysicianChoices

Surgery

Open ‐ MAZEMinimally‐Invasive

RXAntiarrhythmic &Rate‐Control Drugs+ Anticoagulants

Cardioversion

Non‐Surgical

Catheter Ablation

Medical Therapy for AFThree Tier Approach

• Antiarrhythmic Medications– Maintain normal sinus rhythm

• Rate Control–Drugs

–AV junction ablation

• Anticoagulation

Rx – Antiarrhythmics/Rate Control

Do not cure AF, but try to control / treat symptoms of irregular rhythm

Less than ½ of patients using them for at least a year are able to maintain normal sinus rhythm

Side effects may include dizziness, new types of irregular heartbeat, chest pains, shortness of breath, and visionheartbeat, chest pains, shortness of breath, and vision problems

Amiodarone (Cordarone) is the most effective, but has additional, more serious side effects including heart block and toxicity in the lungs and/or liver

Rate control drugs (beta blockers and calcium channel blockers) slow the heart rate but rarely return the heart to normal sinus rhythm

Medical Management of AF

• Problems with medical approach– High complication rate from anticoagulants

• Coumadin™ (warfarin) / dabigatran / rivaroxaban / apixaban

• Risk is additive over lifetime

• Anticoagulation decision based on CHADS or CHADS‐Vasc score

– Anti‐arrhythmic drugs are not benign

• Own set of complications that may be worse than AF

• Rhythm control

– Amiodarone, sotalol, propafenone, flecainide, dronaderone, dofetilide, ?anticoagulant

• Rate control

– Digoxin, beta blocker, Ca++ Blocker, ?anticoagulant

Rx – Anticoagulants or Blood Thinners

For stroke prevention, most patients with AF are prescribed an anticoagulant like warfarin (Coumadin) to prevent the formation of blood clots caused by the pooling of blood in the quivering atria – left atrial appendage Dabigatran (Pradaxa)

Rivaroxaban (Xarelto)

Apixaban (Eliquis)

Aspirin is much less effective and only used in patients at low risk of stroke

New anticoagulants are all equivalent to coumadinand demonstrate equal risks of bleeding and stroke prevention in AF – convenience is significant

stroke

In studies, warfarin reduced the risk of stroke by 68% compared to no treatment at all

Warfarin requires careful monitoring of INR (every 4 weeks) to ensure correct blood levels as too low an INR doesn’t prevent clots from forming & too high an INR can cause internal bleeding

Consistent use is absolutely critical, activity limitations accepted, dietary restrictions must be followed, and the patient’s doctor must be made aware of all other drugs and dietary supplements being taken as there are many that can either increase or decrease warfarin’s effectiveness

Doesn’t treat AF symptoms or causes but can help reduce incidence of stroke

Cardioversion

Electrical shock delivered to heart so it beats regularlyagain

Often performed in earlystages of AFstages of AF

Does not cure AF – restores normal rhythm, does not maintain normal rhythm

Usually followed up with amedication regimen (bloodthinner and/or rhythm management drug)

ATRIAL FIBRILLATION

AF Hospital Admissions and Costs• Hospital days

– > 1/3 of all hospital days with arrhythmia as the principal diagnosis (> 1 million hospital days)hospital days)

• Average length of stay and costs– 4.2 days– Costs: $6,334 + $7,369– > $1 billion annually

Bialy et al. JACC, 1992; Nattel. AHJ, 1995; Gersh. “Atrial Arrhythmias State of the Art”, 1995.

ATRIAL FIBRILLATION

AVJ Ablation and Pacemaker Implantation

• Permanent AF (perhaps for paroxysmal or persistent)

• Creates complete AV block

• Permanent pacemaker dependence

• Eliminates need for rate‐controlling drugs

• May still require medication to maintain sinus

• Most patients receive chronic anticoagulation

ATRIAL FIBRILLATION

AVJ Ablation and Pacemaker Implantation• Benefits

– Reversal and prevention of tachycardia‐induced cardiomyopathyImproved quality of life– Improved quality of life

• Activities of daily living easier• Physician visits less frequent• ER visits and hospital admissions decreased• Fewer drug trials• Fewer CHF episodes

– Improved exercise tolerance

Catheter Ablation of AF

Small catheters (wires inside long sheaths) are threaded through a vein in the leg and up to the heart and across the atrial septum into the left atrium

Electrodes at end of catheter detectfaulty electrical firing sites

Energy is used to scar these sites

Scars block electrical impulses causing AF

Success rates for curing AF vary (70% ‐80%) and follow‐up procedures are sometimes necessary (20%) Requires an overnight hospital stay

Interventional Treatment Options for AF

• Electrophysiological catheter based therapies

• Pulmonary vein isolation (PVI)

• Radiofrequency (RF ‐ heating) and• Radiofrequency (RF ‐ heating) and

cyrothermic(freezing) energy sources

• PVI “plus” – additional linear and focal

ablations of atrial tissue and ganglionic plexi

Pulmonary Veins as Triggers of AF

• Intrinsic pacemaker function

• Shorter refractory periods

• Fewer cell‐cell interactions

M ibl• More susceptible to stretch and fibrosis

• Amenable to focal, triggered and re‐entrant arrhythmia

PV Anatomy

PV Isolation

PV Isolation

“En Bloc” PV Isolation

Dissociated PV Activity

IFV1

PV

CSp

CSd

PV Exit Block

IFV1

PV

CSp

CSd

Balloon Catheters for AF

Balloons to Achieve PV Isolation

• Minimize energy delivery

• Simplify energy delivery

• Enhance efficacy

• Minimize complications

• Great variation in PV anatomy

• Need to deliver energy to PV antral region

Balloon Concept for PV Isolation

• Laser

• High‐intensity, focused ultrasound

• Cryo

– Effective lesion

– No thrombus

– Preservation of basement membrane

– Orientation independant

Cryoballoon Lesion Formation

Cryo‐Balloon Postioning

Left Upper Pulmonary Vein: RAO View

Ideal Candidates for Catheter Ablation of AF

• Lone Paroxysmal Atrial Fibrillation

• Frequent symptomatic episodes

• Failure of at least one AA drugg

• LA size < 5 cm

• Preserved EF

• No comorbid lung disease

Less Ideal Patients

• Persistent/Permanent AF

• Unclear Symptoms– Amiodarone challenge

• Large LA• Large LA

• Depressed EF

• Comorbid lung disease/obesity

• “I want to get off coumadin”

• New Complication: Atrial Flutter

Success Rates

• Definition of Success–No AF–No AF on a previously failed medication–Marked reduction in episodes and/or p /symptoms

• In ideal patients, 70‐80%– Early recurrence common and insignificant

–Persistent or long‐term persistent may be only 50% success

Failure of PVI for Paroxysmal AF

• Success rate of PVI 70‐80%– AA drugs < 50%

• Pulmonary Vein reconnection.

• Drivers from outside the “LA‐PV” junction

• Non‐Pulmonary Vein fociNon Pulmonary Vein foci– 28% of patients with Paroxysmal AF had non‐PV sources of ectopy

– Locations:• Posterior LA (border of PV and LA)

• Crista Terminalis

• Ligament of Marshall

• SVC

• CS ostium

Chen, Circulation, 2003

Complications with RF Energy

• Pulmonary vein stenosis

• Perforation/tamponade

• Thromboembolic events

• LA‐Esophageal fistula

– 10% incidence of esophageal ulcers

– 1/5000 LA‐Esophageal fistulae: LETHAL

• Time consuming

• Exhausting

Complications of Antral Isolation

Ventricular Tachycardia

VT: Treatment Options

• Drug therapy

– Guided by EP testing

– Guided by non‐invasive monitoring

Empiric– Empiric

• Surgical ablative therapy

• Catheter ablation

• ICD therapy

RVOT VT Ablation

RVOT VT Ablation

Clinical VT Pace Map at VT Site

RVOT VT Ablation

Catheter AblationPost Op Care

• Conscious sedation: patient returns directly to the room after the procedure– May be used for AVJ ablation and pacemaker implantation

– Historically used for all ablations – very “heavy” conscious sedation

• General anesthesia: patient goes to a recovery area before returning to the room (30‐60 minutes)

– Used for most ablations

– Safer and easier for patient due to length of procedure

Standard endotracheal tube or laryngeal mask airway– Standard endotracheal tube or laryngeal mask airway

• Bedrest:

– May elevate HOB no more than 30 degrees

– Affected leg straight

• 3 hrs for venous access

• 6 hrs for arterial access

• Medication for pain

• Monitor vital signs at frequent intervals

• Monitor access site for bleeding or hematoma

• Monitor pulses distal to the access site

Catheter AblationDischarge Instructions

• Encourage ambulation• A small “knot” at insertion site is normal (dime to quarter size)• Bleeding at the access site unusual

– Venous requires simple pressure– Arterial requires firm pressure and return to ER/OfficeArterial requires firm pressure and return to ER/Office

• Infection uncommon – call if occurs, may need antibiotic• No driving or other high risk activities for 12 hrs after receiving sedation agents• Lifting (>20 lbs) and vigorous exercise restrictions

– Venous: 2 days– Arterial:

• BP monitoring 4F only ‐ 2 days• Left heart retrograde catheterization 6F to 8F – 7 days

• Return to work next day• Follow‐up visit 4‐8 weeks with ECG

Permanent Pacemaker Implantation

• Indications

– Symptomatic bradycardia (rates < 40 bpm)

– Sick Sinus Syndrome

– Sinus pauses > 3 seconds duration

– Complete AV block

– Carotid Sinus Hypersensitivity

– Syncope with negative evaluation for other causes

– Biventricular Cardiac Resynchronization Therapy for CHF

Permanent Pacemaker Implantation• Local anesthesia and additional IV sedation or general anesthesia• Incision developed into pacemaker pocket

– 4‐6 cm long– Pocket below fat – onto the pectoralis fascia

• Percutaneous puncture into vein or direct cutdown to cephalic vein• Peel‐away sheath placed over guidewire• Lead or leads placed under fluroscopy• Leads tested for capture and sensing thresholds• Leads sutured to pectoralis muscle• Pulse generator attached to leads and placed in pocket• Pocket closed in 2 layers• Bandage of steri‐strips, 4x4, clear dressing or glue

Permanent Pacemaker ImplantationPost Op Care

• Conscious sedation: patient returns directly to the room after the procedure

• General anesthesia: patient goes to a recovery area before returning to the room (30‐60 minutes)

• Bedrest for 2‐3 hours

– May elevate HOB no more than 30 degrees

– No limit of arm motion unless specifically requested (no need for sling or immobilizer)immobilizer)

• Medication for pain

• Monitor vital signs at frequent intervals

• Monitor access site for bleeding or hematoma

• AP portable CXR following procedure

• PA and lateral CXR the morning following implantation if stay overnight

• Pacemaker interrogation and check morning pre‐discharge rarely used unless concerns arise

• Patients are commonly sent home same day unless pacemaker dependent

Permanent Pacemaker Implantation Post Op Care (continued)

• Restricted activities– MRI scans – there are now low level MRI capable pacemaker

systems– Arc welding in dependent patients– Deep heat or ultrasonic massage over device– Radiation therapy directly over pulse generator– Radiation therapy directly over pulse generator

• Acceptable activities– Use of microwave oven, electric hand tools, electric blanket,

magnets in shoes or on back, personal stereo, cellular phone, portable phone, CB radio, etc.

– OK to fly – carry ID card and if examined OK to permit magnetic metal detector wand over pulse generator briefly –

– OK to walk through metal detector turnstile or airport imaging system

Sudden Cardiac Death

• 450,000 people experience SCD in the U. S. each year

• Approximately 1 every minute

d f d h i S• Most common mode of death in U. S.

• 90‐150,000 survive (20‐30%)

• Prophylactic ICD implantation may be able to protect some in highest risk groups

ICD Therapy

• Indications: Class I– Cardiac arrest due to VT/VF, not due to a transient or reversible

cause– Spontaneous sustained VT– Syncope of undetermined etiology– Syncope of undetermined etiology

• Clinically relevant, hemodynamically significant sustained VT/VF at EPS• Drug therapy ineffective, not tolerated, not preferred

– Nonsustained VT with CAD, prior MI, LVEF < 40%, inducible sustained VT/VF not suppressible by Class I antiarrhythmic drug (MADIT I criteria)

– CAD, prior MI, LVEF < 35% (without diagnostic EP study) and no MI in less than 40 days, or revascularization less than 90 days

– Dilated cardiomyopathy (no CAD) and EF <35% over 9 months since diagnosis on optimal medical therapy

ICD Therapy

• Indications: Class II b (no class II a)– Cardiac arrest presumed due to VF when EPS precluded by other medical conditions

– Severe symptoms due to sustained VT/VF as a bridge to y p gtransplantation

– Familial/inherited conditions at high‐risk for sudden death (long QT syndrome, hypertrophic cardiomyopathy)

– Nonsustained VT with CAD, prior MI, LVEF < 40%, inducible sustained VT/VF at EPS

– Recurrent syncope of undetermined etiology with LV dysfunction, and inducible sustained VT/VF at EPS when other causes of syncope have been excluded

ICD Therapy

• Indications: Class III (not indicated)– Syncope of undetermined cause and no inducible VT/VF– Incessant VT/VF– VF or VT due to arrhythmias treatable with surgical or catheterVF or VT due to arrhythmias treatable with surgical or catheter

ablation (WPW, RVOT‐VT, idiopathic LV‐VT, fascicular VT)– VT/VF due to transient or reversible disorder– Severe psychiatric illness– Terminal illness with life expectancy < 6 months– CAD, LV dysfunction, prolonged QRS without spontaneous or

inducible VT in patients undergoing CABG– NYHA Class IV drug‐refractory CHF in patients who are not

candidates for cardiac transplantation

ICD Therapy

• Benefits

– Efficacy > 95%

– Automatic

May not need drugs– May not need drugs

ICD Implantation Post Op Care (continued)

• Restricted activities– MRI scans (no MRI capable ICD)– Arc welding– Deep heat or ultrasonic massage over device– Radiation therapy directly over ICD

A bl i i i• Acceptable activities– Use of microwave oven, electric hand tools, electric blanket,

magnets in shoes or on back, personal stereo, cellular phone, portable phone, CB radio, etc.

– OK to fly – carry ID card and if examined OK to permit magnetic metal detector wand over pulse generator briefly

– OK to walk through metal detector turnstile– OK to walk through other airport imaging systems

ICD Therapy

• Limitations– Surgical implantation– Inappropriate shocks

• Sinus tachycardia• Atrial fibrillation• Nonsustained VT

– Painful– Psychological impact– Limited pulse generator longevity– Does not prevent arrhythmia occurrence– Expensive

Tiered Therapy ICD

Antitachycardia Pacing

GEM® III DR ICD with Sprint Quattro™ 6944 Lead

Sprint™ ICD Lead - 6942

Sprint™ Steroid Eluting ICD Lead

ICD Therapy

• Ideal Device– Multi‐programmable decision‐tree– Nonthoracotomy transvenous system– Hemodynamic sensor input– Dual chamber for atrial sensing/pacing and tachycardia

detectiondetection– Event counters / Telemetry / Holter– Telephone telemetry follow‐up capability– Automatic response– Noninvasive electrophysiology testing– Small size– Atrial & ventricular cardioversion, defibrillation,

antitachycardia pacing (universal rhythm control device)• Newest ICD is completely subcutaneous system – no

pacing capability

Cardiac Resynchronization Therapy ‐ Indications

• Symptomatic heart failure (NYHA III‐IV)

• Wide QRS complex (>120 or >130 ms)p ( )

• LV dysfunction (LVEF<35%)

Sinus Sinus nodenode

Intraventricular Activation

•Organized ventricular

Mechanism IIVentricular ResynchronizationVentricular Resynchronization

AVAVnodenode

Organized ventricular activation sequence

• Coordinated septal and freewall contraction

• Improved pumping efficiency

Stimulation Stimulation therapytherapy

Conduction Conduction blockblock

Kass D. New dimensions in device-based therapy for heart failure–mechanisms of stimulation for heart failure. Heart Failure Society of America 1999.

Step 2: Perform Venograms Varying Patient Anatomy 1,2,3

2. Neri et al. Europace 2000;I :D95 Abstract 88/2

1. Potkin et al. Am J Cardiol 1987;60:1418-1421

3. Hill et al. Europace 2000;I:D238 Abstract 167/2

Photos Courtesy of Dr. Daniel Gras

Venogram Images of Cardiac Venous System

Courtesy of D. Gras M.D.

Implanted LV Epicardial Lead

•• Transvenous LV accessTransvenous LV access

•• Coronary venous placementCoronary venous placement

TherapyTherapy

Final Lead Position

Transvenous Lead Extraction

• Indications– Mandatory

• Infection – Sepsis

E d diti– Endocarditis

• Migration of severed transvenous leads

• Lead complication?– Telectronics Atrial J “Accufix” pacing lead

– St. Jude Riata ICD lead

– Medtronic Sprint Fidelis ICD lead

Pacemaker Site Infection


• Indications

– Necessary

• Infection (local pocket)

Li it d l• Limited vascular access

• Vein thrombosis or occlusion

• Chronic draining sinus

• Lead replacement for failure


• Indications

– Discretionary

• Lead replacement for failure or incompatibility

• Lead complication

– Telectronics Atrial J “Accufix” (no fracture)

• Pain

• Malignancy


• Success rates for transvenous extraction

– Complete extraction 85‐90%

– Partial extraction 5‐8%

Not removed 3 6%– Not removed 3‐6%


• Factors favoring successful extraction

– Physician experience (>20 procedures)

– Shorter implant duration

Active fixation leads– Active fixation leads

– Atrial lead placement

– Left subclavian implant

Access Sites for Lead Extraction

Scar Tissue Locations

Atrial Lead Fibrosis

Ventricular Lead Fibrosis

Counter Traction

Counter Traction

Counter Traction

Laser Sheath Extraction

CVX‐300 Excimer Laser

SLS Distal Tip

Proper Alignment

Improper Alignment

Improper Alignment

Traction ‐ Countertraction

Traction Countertraction

Pulling on the leadmay invert the heartor tear myocardium

Pull the lead, push the outer sheath; localizesshearing force on scar

Countertraction


• Complications: <4%– Hemopericardium/tamponade– Hemothorax– Pulmonary embolism– Migration of lead fragmentBacteremia after failed e traction– Bacteremia after failed extraction

– Stroke– Ventricular tachycardia– Myocardial avulsion without sequelae– Thrombosis– Acute hypotension– Chest wall hematoma


• Preparation for Surgery

– Thorough patient history & physical examination

– Chest X ray / Echo / TEE?

– Type & cross‐match blood

– Prep chest to groin ‐ possible thoracotomy, sternotomy, or femoral approach

– Temporary transvenous pacing (femoral)

– Extensive collection of sheaths, locking stylets, snares, accessory equipment


• Procedure Room– High quality fluroscopy– Pacing equipment– Defibrillator– Pericardiocentesis tray– Anesthesia equipment

• Readily available equipment & personnel– Echocardiography– Cardiopulmonary bypass and chest instruments– Blood products– Cardiothoracic surgeon on standby


Lessons for the Future

• Infected hardware does not heal!

• Erosion = Infection

Ab d ld l d• Abandon or remove old leads

– Do not mutilate or cut

– Cap abandoned leads and sew to fascia

• Consider using active fixation leads


Lessons for the Future

• Meticulous sterile technique for pacemaker implantation/revision procedures– Preoperative antibiotics and Hibiclens scrub– Preoperative antibiotics and Hibiclens scrub– Laminar flow OR/cath lab suite– Steri‐drape and generous sterile field– Limited handling of pulse generator– Hemostatic pocket ‐ surgically evacuate hematoma/seroma promptly

– Do not stick needles in pocket ‐ you can not suck clots through an 18 gauge needle

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