Download A5 Ventricular Arrhythmia

Chronic Ventricular Arrhythmias
Objectives - 3
• Differentiate between the major types of ventricular arrhythmias
• Describe the pathophysiology of each major ventricular arrhythmia
• Outline pharmacologic therapies for the treatment of ventricular arrhythmias
• Discuss the role of non-pharmacological therapies (e.g. radiofrequency catheter ablation, implantable
cardioverter / defibrillators) for the treatment of arrhythmias
• List appropriate monitoring to ensure safety of certain antiarrhythmics
Introduction - 4
• Heart failure with reduced ejection fraction (HFrEF) ≤ 40% puts patients at a high risk for ventricular
arrhythmias
• Sustained ventricular arrhythmias are an important cause of morbidity and the most common cause
of sudden cardiac death that account for 75 - 80% of cases
• A Ventricular scar is the basis for the arrhythmia in the majority of patients.
• This most commonly occurs from an MI that causes cell death, or remodeling of the heart
• The term “ventricular arrhythmias” incorporates a wide spectrum of abnormal cardiac rhythms
including:
• Premature ventricular complexes (PVCs), Non-sustained monomorphic ventricular tachycardia
(NSVT), Sustained monomorphic VT, Polymorphic VT, and Ventricular fibrillation
Premature Ventricular Contractions (PVCs) - 5
• Ventricular depolarization NOT preceded by a P-wave
• A.k.a. Ventricular Premature Beats
• The wave before the PVC is a T-wave from the preceding QRS
• May indicate an underlying structural heart disease (SHD), myocardial
ischemia, hypoxia, or electrolyte abnormalities (low or high potassium /
magnesium).
• Common to see PVCs in patients with reduced EF or patients with a normal ejection fraction with
coronary artery disease (CAD)
• PVCs are markers for increased mortality meaning the more a patient has the higher the risk of sudden
cardiac death
• Pharmacological suppression of these have not been proven to reduce sudden death
Non-sustained VT (NSVT) 6
★ Three or more repetitive ventricular beats in a row lasting ≤ 30 seconds in duration at a rate > 100 bpm
• Very similar to PVCs in terms of risk stratification
★ Monomorphic VT that self-converts back to normal sinus rhythm (NSR)
• Unlikely associated with hemodynamic compromise
• May indicate worsening SHD, myocardial ischemia, hypoxia, or electrolyte abnormalities.
• Common in patients with reduced EF
• NSVT is a marker (Holter, or event monitoring, or pacemaker
interrogation) for increased mortality or sudden cardiac death
• Pharmacological suppression of these have not been proven to
reduce sudden death
Patients Case #1 - 7
• FO is a 70 yo male with a history of HFrEF (NICM, EF now 45-49%, was 35-39%), mild COPD,
HPLD, DM type 2 and complex sleep apnea.
• He has stable NYHA class III symptoms, A1C and lipids are below goals. Renal function is stable and
electrolytes are WNL.
• Vitals - BP: 108/72 HR: 69 bpm
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Patient presents to HF clinic with new symptom of dizziness.
Medications: Toprol XL 100 mg, lisinopril 10 mg at bedtime, furosemide 20 mg qam prn, metformin
500 mg bid, simvastatin 10 mg qhs, ASA 81 mg
• 24 hour Holter Monitor (mobile ECG) – Event monitors can be worn for a month
• This patient’s Holter monitor showed Sinus rhythm, first degree AV block, Right bundle branch
block (RBBB) at baseline
• Sinus throughout tracing with occasional PVC's, rare premature atrial contractions (PACs), and
PAC pairs. No further arrhythmias noted.
• PVCs are associated with the symptoms
What are common symptoms associated with PVCs Dizziness, Syncope, Sudden cardiac death, or
Palpitations?
• The most common are dizziness and palpitations.
• Syncope and sudden cardiac death would not be associated with PVCs, but are associated with
sustained ventricular arrhythmias.
What would be an appropriate change or addition to patient’s medication regimen to reduce
symptomatic PVCs?
• Add digoxin 0.125 mg daily
- Will not suppress PVCs and potentially worsen the arrhythmia
• Add diltiazem 120 mg daily
- Inappropriate in a patient with reduced ejection fraction (EF)
• Add sotalol 40 mg bid
- Not appropriate at this time, because of safer options
• Increase metoprolol succinate to 200 mg daily (Target Dose!)
★ Beta blockers have been shown to suppress PVCs, and cause patient to become asymptomatic
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Patient Case #2
• MB is a 64 yo AAM with a history of a severe ICM with an EF < 20% s/p ICD, severe diastolic
dysfunction, CAD, s/p 4V CABG 2009,HTN, obstructive sleep apnea (OSA), and obesity.
• Vitals: HR 65 bpm, BP 135/83 mm Hg, weight 300 pounds
• Medications: Carvedilol 25 mg bid, Valsartan 160 mg bid, spironolactone 25 mg daily, BiDil 1 tab tid,
simvastatin 40 mg qhs, furosemide 20 mg bid, ASA 81 mg daily
• Dual chamber Medtronic Virtuoso with leads and device implanted 9 months after CABG.
• Device is programmed (backup pace) DDI 60 bpm
• 6.0% right atrium (RA) paced, 6.1%, right ventricle (RV) paced
• Episodes (since last device interrogation 6 months ago):
• Atrial mode switching (AMS) (atrial arrhythmias): 0, VF: 0, VT: 0
★ Non-sustained Ventricular Tachycardia (NSVT)
- 8 episodes range from 6-22 beats, at a rate of 200 bpm
Optivol
(device which assesses volume excess) findings do not suggest fluid retention.
•
★ Underlying rhythm: NSR at 65 bpm with occasional PVCs.
• This patient is have both PVCs and NSVT
What would be an appropriate change or addition to patient’s medication regimen to reduce
asymptomatic NSVT?
• Continue to monitor – which could be an option
• Increase carvedilol to 50 mg BID
• This would be considered the target dose based on the patient’s weight. Most often carvedilol 25
mg BID is target dose, BUT if the patient is having PVCs or NSVT it would be reasonable for the
target dose to be increased to 50 mg BID as tolerable
• Add flecainide 100 mg BID
• Add amiodarone 200 mg daily
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On next pacemaker interrogation, patient had 12 new episodes of NSVT. The longest was 18 seconds. One
episode resulted in near syncope, but with no ICD firing. The QTC was 432 ms (relatively short). What
would be the treatment?
• Add digoxin 0.125 mg daily
• Not an option to reduce ventricular episodes
• Stop carvedilol; add amiodarone
• Not in a patient with reduced EF. This could worsen arrhythmia
• Add dofetilide 500 µg BID
• Add amiodarone 200 mg daily
• Reasonable addition in this patient’s therapy, because he is symptomatic. If this patient was
asymptomatic then simply monitoring patient would be okay.
• The ICD did not fire and amiodarone LOAD is NOT necessary
CAST trial - 11
• Famous trial to those who follow ventricular arrhythmias
• PVCs show that patients are at higher risk for sudden cardiac death which lead to the CAST trial that
was developed in the 1980s
• This is a post-MI trial with patients who had a certain number of PVCs (e.g. 6 per hour) they were
randomized to an antiarrhythmic (Class 1C flecainide) versus placebo.
★ Results showed patients started on Class 1C antiarrhythmic to reduce the PVCs lead to reduced survival
and increased mortality. The use of Class 1C antiarrhythmics are not used in a patient who has CAD
and post-MI to reduce PVCs.
Pharmacotherapy of PVCs and NSVT - 12
• PVCs
• No therapy indicated for asymptomatic PVCs in otherwise healthy individual
★ Beta-blockers preferred if patient is symptomatic
★ PVCs with SHD – already strong indication for beta blocker
- Initiate or increase dose
NSVT
•
• No therapy indicated for asymptomatic NSVT if infrequent
- If SHD, initiate or increase dose of beta-blocker
• Beta-blockers preferred if patient is symptomatic
• May consider Class III antiarrhythmic if symptomatic or frequent with a beta-blocker
- May consider amiodarone or sotalol in patients with good renal function
Monomorphic VT - 13
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A repetitive sequence of ventricular activation with a > 30 seconds duration
QRS morphology that does not change from beat to beat
This pattern can indicate a single focus that initiates ventricular activation, or a stable substrate capable
of supporting a reentrant circuit
• Reentrant Circuit – a signal comes down through the AV node or a ventricular substrate has become
fibrosed. This hits refractory tissue going through a slow conduction pathway and comes up
retrograde through a fast conducting pathway creating a reentrant circuit which creates a ventricular
arrhythmia. This may be precipitated by a PVC or early after depolarization.
May occur with or without CAD. This includes idiopathic and VT due to SHD
ECG Changes in VT - 14
• Atrioventricular dissociation
• Fusion or capture beats
• QRS width (LBBB >160 ms, RBBB >140 ms)
• Northwest axis
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• Concordance – deflection is in the same direction in the precordial leads
• LBBB morphology with right axis deviation
• Absence of RS complexes in precordial leads
One or multiple ECG changes indicates a Ventricular tachycardia
Idiopathic VT (subtype of a monomorphic VT) - 15
• VT without SHD, inherited disorder, or electrolyte abnormalities
• If the patient has a K+ = 2 and is in VT. This would be considered idiopathic VT
• Rarely life-threatening, but may be associated with hemodynamic compromise and syncope
TWO subtypes of idiopathic VTs are:
• Focal VT
• Most originate from the right ventricular outflow tract (RVOT)
• Originates from a focus with automaticity mediated by cAMP triggered activity of Calcium
overload
• VTs may be sustained or may present as repetitive runs of NSVTs
• Fascicular VT
• Reentry involving the fascicles of the left bundle branch
• Amendable to catheterization, but with multi-foci drug therapy may be first-line option
Therapy of Idiopathic VT - 16
• Focal VT – treatment depends on the severity of symptoms
• Beta-blockers OR nonDHP CCBs (diltiazem or verapamil) – considered if patient had dizziness or
palpitations
• Catheter ablation – first-line option if patient was symptomatic with syncope
• May consider Class I or Class III antiarrhythmic if above treatments are not effective
• Fascicular VT
• Beta-blockers or nonDHP CCBs (most sensitive to verapamil) – First-line option
• Catheter ablation – reasonable option
• May consider Class I or Class III antiarrhythmic if above treatments are not effective
Ventricular Arrhythmias due to structural heart disease (SHD) - 17
• Sudden death accounts for > half of all cardiac deaths and up to 15% of total mortality
• Frequently due to VT degenerating into a ventricular fibrillation (VF)
• Mechanism:
• Most commonly a result of reentry involving a region of myocardial scar
• Most common cause of a scar is an old infarct
• This type of VT occurs without having acute ischemia.
Risk Stratification of Sudden Cardiac Death (SCD) due to VT/VF in SHD - 18
• Risk factors for sudden cardiac death (SCD) in those with structural heart disease (SHD)
• Structural heart disease is defined as having a low ejection fraction or ACS post-MI
• Men > women (3 to 5 times)
• Patients who survive an MI
• Depressed left ventricular ejection fraction (LVEF)
• Inducible VT during invasive EP study with programmed ventricular stimulation
• Other less validated risk factors
• Abnormal heart rate variability – GOOD if there is variability in HR (e.g. Exercise)
• Microvolt T-wave alternans – observing T waves differences and amplitude (not used much
anymore)
• Ambient ventricular arrhythmias – occasional NSVT or frequent PVCs
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Internal Cardioverter – Defibrillator (ICD) - 19
• Patients at risk should consider a ICD
• Single chamber pacemaker is put in the left side of the chest underneath the skin which is usually the
opposite arm of the dominant hand. (vice versa if the patient is left-handed)
• A coil is associated with a lead that is implanted into the right ventricle
• When the pacemaker detects an abnormal arrhythmia then 2 options are available. It can pace the patient
out of it OR deliver a shock to the patient. Delivering a shock is what most often happens.
• The pacing out of an arrhythmia will work only sometimes mostly for monomorphic VT and not
necessarily with a polymorphic VT
• There are dual chamber pacemakers with a ICD function which have a right ventricular and atrial
lead.
• Having the additional lead in the right atrium can detect a patient in atrial fibrillation / flutter that has a
fast rate which can often cause a ICD shock distinguishing it from a ventricular arrhythmia.
Who do we give these ICD to? – VT: Primary Prevention SHD - 20
• Ischemic heart disease – Is the most common reason
• ICDs reduce mortality of about 25%
• LVEF 35%, documented prior MI, at least 40 days status post-MI, NYHA class II and III
• LVEF < 30%, at least 40 days post-MI and NYHA class I
• NSVT caused by MI, LVEF < 40%, and inducible VF or SVT at EPS
• Non-ischemic heart disease
• NIDCM, NYHA class II and III, LVEF ≤ 35%
• SVT and normal or near normal ventricular function
• SHD and spontaneous SVT, regardless of symptoms
• Patients receiving CRT for NYHA class III or IV symptoms despite optimal medical therapy
• Non-hospitalized patients awaiting cardiac transplantation
• Contraindications
• CABG or PTCA within 3 months or MI within 40 days
• Irreversible brain damage
• Any other disease associated with a likelihood of survival of < 1 year
• Psychiatric history that may be irritated by ICD
Patient Case #3 - 21
• AF is a 44 yo WM who was admitted 2 weeks ago due to A. Fib with rapid ventricular response (RVR).
• TTE showed an EF of < 20%
• Patient also has a history of HTN and alcoholism. He presents to clinic today for the first time feeling
well. He is abstaining from alcohol. GOOD alcohol is considered cardiotoxic in this patient.
• Vitals: BP 110/74 mm Hg and HR 62 bpm
• Medications: Metoprolol succinate 75 mg daily, bumetanide 0.5 mg qam, digoxin 0.125 mg qam.
What additional testing would likely be done in this patient with a newly reduced EF?
• Left/right heart Cath. (L/RHC) – not reasonable, because patient is not having chest pains
• Myocardial perfusion study (MPS) – this would be appropriate or a stress test to see if patient is
having underlying ischemia causing the reduced ejection fraction.
• Nothing – this would NOT be appropriate. Need to find why patient has reduced ejection fraction
• Cardiac MRI
When would be the most appropriate time to consider placement of a ICD?
• 3 month – re-echo the patient at 3 months and consider a ICD if the patient’s ejection fraction is still
low and the patient prefers
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What medications should be added for primary prevention of SCD?
• Ace inhibitor – shown to reduce sudden cardiac death, AND this patient is not currently on this
class of medication. (patient is already on a beta blocker, loop diuretic, and digoxin)
• Non-DHP Calcium channel blocker (e.g. Diltiazem)
• Amiodarone
• Spironolactone
ICD is probably the most important device for patients to get who are at risk for a ventricular arrhythmias
OR who have already had one. However, medications will also prevent arrhythmias.
Non-antiarrhythmic Pharmacotherapy for Primary Prevention of SCD in SHD - 23
• Beta-blockers – have been proven to reduce sudden cardiac death
• Metoprolol succinate (MERIT-HF)
• Carvedilol (COPERNICUS) (CAPRICORN)
• Bisoprolol (CIBIS-II)
• ACE inhibitors – in the post-MI population also reduces sudden cardiac death
• Trandolapril (TRACE)
• Ramipril (AIRE) (HOPE)
• Aldosterone antagonist – also reduces sudden cardiac death
• Spironolactone (RALES)
• Eplerenone (EPHESUS)
• Statins – associated with reduced sudden cardiac death
• N-3 Polyunsaturated Fatty Acids (a.k.a. Fish oils) is questionable. Not recommended to prevent VT
Antiarrhythmic Pharmacotherapy for primary Prevention of SCD in SHD - 24
• Amiodarone
• Potential benefit in post-MI patients (CAMIAT)(EMIAT)
• Sotalol
• Reduced mortality and ICD shocks in patients with previous VT/VF.
• Good option if patient has had a ICD device firing. Patient must have GOOD renal function.
• Dofetilide
• No benefit over placebo (DIAMOND-MI) (DIAMOND-CHF)
• Digoxin
• Potential harm (DIG)
• Dronedarone
• No data, and inappropriate at this time due to lack of evidence.
Placebo versus Amiodarone versus ICD - 25
• This study looked at patients who were post-MI with reduced
ejection fraction and symptoms to prevent ventricular arrhythmias
and sudden cardiac death
★ Results: ICD therapy was the best in reducing mortality rate, and
there was no difference between amiodarone and placebo.
• The ICD therapy is the best modality to prevent sudden cardiac death and ventricular arrhythmias.
However, to suppress arrhythmias so the patient does not get shocked we can potentially use
amiodarone to suppress ICD shocks and improve quality of life
Polymorphic VT - 26
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QRS morphology is continuously changing
• Beat-to-beat alterations in ventricular activation.
May occur in patients without structural heart disease who have genetically based ion channel
disorders such as:
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Long QT syndromes, Brugada syndrome, Catecholaminergic polymorphic VT syndrome, or
Idiopathic ventricular fibrillation.
• Myocardial ischemia is the most common underlying etiology for a polymorphic VT
• Cardiac myocyte death results in K+ leakage
• Increased extracellular K+ depolarizes myocytes in ischemic border
• Provides substrate for reentry
Polymorphic VT: Inherited Disorders - 27
• Long QT syndrome
• Most often due to genetic abnormalities of either K+ or Na+ channels
• Associated with Syncope and sudden death as a result of torsades de pointes (TdP)
• Brugada syndrome
• Abnormal Na+ channels in 25% of cases
• Syncope and sudden death result from PVT, tend to occur during sleep, and can be precipitated by
fever. Most cases this is detected early in life.
• Catecholaminergic polymorphic VT
• Abnormal calcium processing causes exercise-induced PVT
• Most patients present during childhood with syncope or cardiac arrest
• May have sequence variations in the cardiac ryanodine receptor or calsequestrin
• Arrhythmogenic right ventricular dysplasia (ARVD)
• Associated with fibrofatty replacement of the right ventricle
• May present with monomorphic or polymorphic VT
• Class IIA indication for primary prevention with a ICD
Polymorphic VT: Torsades de Pointes (TdP) - 28
• Rapid form of PVT associated with delayed ventricular depolarization
• Prolonged QT interval
• An insult delays repolarization most commonly by blocking K+ channels (usually drug-related)
• Provokes EADs that may trigger reentry and TdP
• Many risk factors (e.g female gender, electrolyte abnormalities)
• Class 1A and Class III antiarrhythmics most commonly associated
• Many more drugs: www.qtdrugs.org
• Do not use QTc prolonging drugs with baseline QTc > 450 ms
• Stop or reduce offending agent if QTc > 500 or 550 ms (if wide QRS)
Ventricular Fibrillation (VF) - 29
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Absence of organized ventricular rhythm
Common cause of sudden cardiac death (SCD)
VF without MI = high risk of recurrence
VF with ACS = lower risk of recurrence
Causes the Most common is SHD
• Others: MVP, WPW and inherited disorders
VT/VF: Secondary Prevention - 30
• ICD is the secondary Prevention in a patient who has VT/VF
• Survivors of cardiac arrest caused by VF or hemodynamically unstable sustained VT after evaluation to
diagnose cause of event and to exclude completely reversible causes
• Syncope of undetermined etiology with clinically relevant, hemodynamically significant sustained VT
or VF induced at EP study
• Unexplained syncope, significant left ventricular dysfunction, and non-ischemic dilated cardiomyopathy
• Contraindications
• Candidate for revascularization
• Irreversible brain damage
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• Any other disease associated with a likelihood of survival of <1 year
Patient case #5
• MB is a 60 yo WM with a hx of HFrEF (< 20%), 3VCABG, most recent LHC showed only LIMA graft
patent. Maximal medical management recommended. BiV-ICD implanted 2 years ago. ACEi or ARB
intolerant.
• Vitals: BP 98/62 mm Hg, HR 60 bpm
• Medications: Carvedilol 25 mg bid, spironolactone 25 mg daily, torsemide 60 mg bid, ASA 81 mg
daily, Atorvastatin 80 mg daily
• Patient experienced a ICD shock today. He is asymptomatic. What should you recommend regarding
evaluation?
• Call 911 – IF patient has one shock with symptoms or > 1 shock
• Drive to ED
• Return to clinic within 1 week
• Scheduled to clinic today or tomorrow (preferred by instructor and check electrolytes)
ICD firing: what next? - 32
Patient case# 5 continued - 33
• Patient returns to clinic the next day with labs: SCr 1.5 mg/dL, K+ 2.6 mmol/L, MG++ 1.5,
• PM check showed appropriate shock for VF. What is the most appropriate change to patient’s therapy?
• Replace electrolytes – before anything else
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•
• Start Amiodarone 400 mg PO TID
• Admit for sotalol load 80 mg PO b.i.d.
• Increase carvedilol to 50 mg b.i.d.
If patient had electrolytes replaced and had another appropriate ICD shock one month later, what would
be the most appropriate change to therapy to prevent futureVT/VF episodes?
• Add amiodarone 400 mg PO TID – because this patient has had 2 episodes, AND this ICD shock
needs to be suppressed
• Increase carvedilol to 50 mg BID – not appropriate
• Add quinidine 324 mg BID – more pro-arrhythmic
• Add dronedarone 400 mg PO BID – no studies in this population (however it is often used)
Patient case #6
• A 48 yo WF presents to the ED due to ICD storm. Patient has a history of VF/VT due to an unknown
cause. It was determined to be idiopathic VT years ago on EP study; likely fascicular VT. She has had
multiple VT ablations. Until now, she has been VT/VF free for 1.5 years. Other PMH is
hypothyroidism, Vitamin D deficiency, and GERD.
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Home medications: amiodarone 400 mg daily, metoprolol tartrate 100 mg bid, levothyroxine 200 mcg
daily, ergocalciferol 600 units daily, ranitidine 150 mg bid.
Patient adequately treated with lidocaine infusion to stop VF. The hospital team will transition her to a
maintenance antiarrhythmic therapy tomorrow AM.
What is the most appropriate change to patient’s therapy?
• No change
• Increase amiodarone to 800 mg daily – patient is already on the appropriate dose of amiodarone
• Initiate mexiletine 250 mg PO tid – lidocaine was effective and this drug is the oral equivalent
- Usually, patients need a PPI because this drug causes GERD. Take with food!
• Initiate quinidine 324 mg PO tid
Catheter Ablation with any VT is an option - 35
• Catheter inserted into venous circulation and threaded to heart
• Radiofrequency “burns” tissue surrounding arrhythmogenic substrate
• More effective for arrhythmias with single foci (focal VT, aflutter)
• Can be considered second-line therapy for idiopathic VT and second or third-line therapy in PVT/VF
Amiodarone safety monitoring - 36
Amiodarone is a toxic drug!
• Ocular – corneal deposits, optic neuritis
• Cardiovascular – bradycardia, orthostatic hypotension, TdP (<1%), phlebitis (IV)
• Pulmonary toxicity – Are the most serious toxicities which include: pulmonary fibrosis,
hypersensitivity pneumonitis. These can be monitored through symptoms.
• Subacute cough, dyspnea
• Stop Amiodarone, supportive therapy
• GI – hepatotoxicity, GI upset, anorexia
• Reduce dose, stop if LFTs > 3x ULN
• If GI upset, reduce dose, split dose or take with food
• Neurologic/psych – polyneuropathy, ataxia, tremor, insomnia
• Endocrine – thyroid dysfunction
• ~3 mg iodine bioavailable/100 mg amiodarone, or 40x
RDA
• Hypothyroidism more common, replacement therapy;
Stop or antithyroid treatment if hyperthyroidism
• Dermatologic – skin discoloration (blue-gray), photosensitivity. Stay out of SUN!
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Amiodarone Safety Monitoring at Baseline! - 13
Drug interactions
• Substrate of CYP3A4, 2C8
• Inhibits CYP1A2, 2C9, 2D6, 3A4 and p-glycoprotein
• Digoxin
• Increases Digoxin concentration ~50-100%
• Decrease Digoxin dose 50% (especially if baseline digoxin concentration > 1 ng/ul)
• Warfarin
• Increases Anticoagulant effect of warfarin
• Decrease Warfarin dose ~25-50%
• Beta-blockers and nonDHP CCBs
• Additive negative chronotropic effects
• Simvastatin – maximum 20 mg at night
Dofetilide Safety Monitoring - 39
May cause QT prolongation and TdP
• Requires in-hospital initiation with continuous ECG monitoring for 3 days
Admit to hospital
• Adjust initial dose based on renal function, check baseline ECG (to ensure QT interval < 440 msec)
• 2-3 hours post-dose, check ECG, decrease dose or discontinue if QT interval increased > 15% or is >
500 msec
Drug interactions
• Substrate for CYP3A4
• CI with verapamil
• Renal elimination involves both glomerular filtration as well as active tubular secretion through the
cation transport system
• Contraindicated with cimetidine, ketoconazole, trimethoprim, prochlorperazine, megestrol acetate
• Caution with drugs that complete with active transport – metformin, thiazide diuretic, K-sparing
diuretics
• Amiodarone – must stop for at least 3 months befor initiating dofetilide
• Class I or Class III antiarrhythmics – must be stopped at least 3 half-lives before initiating dofetilide
• ECG and electrolytes / renal function every 3 months
Sotalol safety monitoring - 41 (VERY similar to Dofetilide)
May cause QT prolongation and TdP
• Requires in-hospital initiation with continuous ECG monitoring for 3 days
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Admit to hospital
• Adjust initial dose based on renal function, check baseline ECG (to ensure QTc < 500 msec)
• 2-3 hours post-dose, check ECG, decrease dose or discontinue if QTc > 550 msec
• Increase dose if no effect after 3 days and QTc < 550 ms, continue to double every three days if not
effective; maximum dose 320 mg bid
Drug interactions
• Eliminated renally
• Amiodarone – should stop for at least 3 months before initiating sotalol
• Class I or Class III antiarrhythmics – must be stopped at least 3 half-lives before initiating sotalol
• ECG at least yearly to assess QT and electrolytes at least yearly (preferably every 6 months)
Key Concepts - 43
• There are many different classifications of ventricular arrhythmias
• Ambient arrhythmias (PVCs or NSVT) are benign and often not treated unless symptomatic
• Primary prevention with ICD of ventricular arrhythmias is dependent on underlying risk factors. Those
at high risk receive ICDs and appropriate drug therapy
• Secondary prevention almost always involves a ICD unless contraindicated.
• Adding antiarrhythmics to reduce arrhythmia burden is reasonable if patient has multiple occurrences of
ICD firing and/or is symptomatic (Amiodarone most often use because of CKD in patients)
• Patients with GOOD renal function Sotalol would be an option
• Combination antiarrhythmics in refractory VT/VF often includes mexiletine and amiodarone
• Catheter ablation is more effective at preventing arrhythmias if originating from a single focus
• Monitoring antiarrhythmics is necessary to endure safety
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