Antiarrhythmic therapy for supraventricular arrhythmias

ANTI-ARRHYTHMIC THERAPY IN
SUPRA-VENTRICULAR ARRHYTHMIAS
Prof. Kyaw Soe Win
Department of Cardiovascular Medicine
Mandalay General Hospital
Hotel Marvel, 19th May 2018

LECTURE’S OUTLINE:
• Electrophysiology of the heart
• Arrhythmia: definition, mechanisms, types
• Antiarrhythmic Drugs classes: I, II, III, IV
• Guide to treat some types of supraventricular
tachyarrhythmia
• Guide to treat atrial fibrillation

Normal conduction pathway:
1- SA node generates
action potential and
delivers it to the atria
and the AV node
2- The AV node
delivers the impulse
to purkinje fibers
3- purkinje fibers
conduct the impulse
to the ventricles
Other types of
conduction that
occurs between
myocardial cells:
When a cell is
depolarized 
adjacent cell
depolarizes along

HEART RATE DURING ARRHYTHMIA
TACHYARRYTHMIA
Simple : 100-150 Beat/min
it may be due to the abnormality of SA node then it will be called
as Sinus tachyarrhythmia
Paroxysmal: 150-250 Beat/min
If nodal rhythm occurs very fast its called nodal paroxysmal
tachyarrhythmia
Flutters: 250-350 Beat/min
Similarly it may be atrial or ventricular tachyarrythmia
Fibrillation: >350Beat/min
Similarly it may be atrial or ventricular tachyarrythmia

Action potential of the heart:
In the atria, purkinje, and
ventricles the AP curve consists
of 5 phases
In the SA node and AV node,
AP curve consists of 3
phases

Non-pacemaker action
potential
Phase 0: fast
upstroke
Due to Na+
influx Phase 3:
repolarization
Due to K+ efflux
Phase 4: resting
membrane potential
Phase 2: plateu
Due to Ca++
influx
Phase 1: partial
repolarization
Due to rapid efflux of K+
N.B. The slope of phase 0 = conduction velocity
Also the peak of phase 0 = Vmax

Pacemaker
AP
Phase 4: pacemaker
potential
Na influx and K efflux
and Ca influx until the
cell reaches threshold
and then turns into
phase 0
Phase 0: upstroke:
Due to Ca++ influx
Phase 3:
repolarization:
Due to K+ efflux
Pacemaker cells (automatic cells) have unstable membrane potential so they can
generate AP spontaneously

Effective refractory period
(ERP)
It is also called absolute refractory period (ARP)
:
•In this period the cell can’t be excited
•Takes place between phase 0 and 3

ARRHYTHMIA
Definition:
– Disturbances in the heart rate, rhythm, impulse generation or
conduction of electrical impulses responsible for membrane
depolarization
– These disturbances can lead to alterations in overall cardiac
function that can be life threatening.
• Antiarrhythmic drugs:
– Compounds used to prevent or treat cardiac arrhythmias

ARRHYTHMIAS
If the arrhythmia
arises from atria, SA
node, or AV node it is
called
supraventricular
arrhythmia
If the arrhythmia
arises from the
ventricles it is called
ventricular
arrhythmia
Causes of
arrhythmia
arterioscl
erosis
Coronary
artery
spasm
Heart
block
Myocardi
al
ischemia

MECHANISM OF ARRHYTHMIAS
Disturbances in impulse generation may be due to
– Abnormal automaticity
– Delayed after depolarizations
Disturbances of impulse conduction
– The impulse may recirculate in heart causing repeated activation (re-
entry)
– Conduction blocks

MECHANISMS OF ARRHYTHMOGENESIS
1- Abnormal impulse
generation
Automatic
rhythms
Ectopic focus
Enhanced
normal
automaticity
Triggered
rhythms
Delayed
afterdepolarization
Early
afterdepolarization
↑AP from SA node
AP arises from sites
other than SA node

2-
Abnormal
conductio
n
Conductio
n block
1st degree 2nd degree 3rd degree
Reentry
Circus
movement
Reflection
This is when the
impulse is not
conducted from
the atria to the
ventricles
1-This
pathway is
blocked
2-The impulse
from this pathway
travels in a
retrograde fashion
(backward)
3-So the cells here will
be reexcited (first by the
original pathway and the
other from the
retrograde)

Here is an
accessory pathway
in the heart called
Bundle of Kent
•Present only in small populations
•Lead to reexcitation  Wolf-
Parkinson-White Syndrome (WPW)
Abnormal anatomic conduction

ACTION OF DRUGS
In case of abnormal
generation:
In case of abnormal
conduction:
Decrease of phase 4
slope (in pacemaker
cells)
Raises the
threshold
↓conduction
velocity
(remember phase
0)
↑ERP
(so the cell
won’t be re-
excited again)

Pharmacologic Rationale & Goals
 The ultimate goal of antiarrhythmic drug therapy:
o Restore normal sinus rhythm and conduction
o Prevent more serious and possibly lethal arrhythmias from
occurring.
 Antiarrhythmic drugs are used to:
 decrease conduction velocity
 change the duration of the effective refractory period (ERP)
 suppress abnormal automaticity

ANTYARRHYTHMIC DRUGS
•Most antiarrhythmic drugs are pro-arrhythmic (promote arrhythmia)
•They are classified according to Vaughan William into four classes according to
their effects on the cardiac action potential
class mechanism action notes
I Na+ channel blocker Change the slope of phase 0
Can abolish
tachyarrhythmia caused
by reentry circuit
II β blocker
↓heart rate and conduction
velocity
Can indirectly alter K and
Ca conductance
III K+ channel blocker
1. ↑action potential duration
(APD) or effective
refractory period (ERP).
2. Delay repolarization.
Inhibit reentry tachycardia
IV Ca++ channel blocker
Slowing the rate of rise in
phase 4 of SA node(slide 12)
↓conduction velocity in
SA and AV node

CLASS I: SODIUM CHANNEL BLOCKERS
• IA: Prolong repolarization
– Quinidine, procainamide, disopyramide, morcizine
• IB: Shorten repolarization
– Lignocaine, mexiletine, phenytoin
• 1C: Little effect on repolarization
– Encainide, flecainide, propafenone

Class I
IA IB IC
They ↓ conduction velocity in non-nodal
tissues (atria, ventricles, and purkinje fibers)They act on open
Na+ channels or
inactivated only
Have moderate K+
channel blockade
So they are used
when many Na+
channels are opened
or inactivated (in
tachycardia only)
because in normal
rhythm the channels
will be at rest state
so the drugs won’t
work
CLASS I DRUGS
Class I: Sodium channel blockers

 Slowing of the rate of rise in
phase 0  ↓conduction velocity
 ↓of Vmax of the cardiac action
potential
 They prolong muscle action
potential & ventricular (ERP)
 They ↓ the slope of Phase 4
spontaneous depolarization (SA
node)  decrease enhanced normal
automaticity
Class
IA
Quinidine
Procainami
de
They make the slope more horizontal

CLASS IA DRUGS USES
 Supraventricular and ventricular arrhythmias
 Quinidine is rarely used for supraventricular arrhythmias
 Oral quinidine/procainamide are used with class III drugs in
refractory ventricular tachycardia patients with implantable
defibrillator
 IV procainamide used for hemodynamically stable ventricular
tachycardia
 IV procainamide is used for acute conversion of atrial fibrillation
including Wolff-Parkinson-White Syndrome (WPWS)
defibrillator

quinidine
AV block
Torsades de
pointes
arrhythmia
because it ↑ ERP
(QT interval)
Shortens A-V
nodal
refractoriness (↑AV
conduction) by
antimuscarinic like
effect
↑digoxin
concentration by :
1- displace from
tissue binding sites
2- ↓renal clearance
Ventricular
tachycardia
procainamide
Asystole or
ventricular
arrhythmia
Hypersensitivity
: fever,
agranulocytosis
Systemic lupus erythromatosus (SLE)-like
symptoms: arthralgia, fever, pleural-
pericardial inflammation.
Symptoms are dose and time dependent
Common in patients with slow hepatic
acetylation
CLASS IA DRUGS TOXICITY

CLASS IB DRUGS
 They shorten Phase 3 repolarization
 ↓ the duration of the cardiac action potential
 They suppress arrhythmias caused by
abnormal automaticity
 They show rapid association &
dissociation (weak effect) with Na+
channels with appreciable degree of use-
dependence
 No effect on conduction velocity
Class IB
lidocaine mexiletine tocainide

CLASS IB DRUGS
Lidocaine
 Used IV because of extensive 1st
pass metabolism
 Lidocaine is the drug of choice in
emergency treatment of ventricular
arrhythmias
 Has CNS effects: drowsiness,
numbness, convulstion, and
nystagmus
Mexiletine
 These are the oral analogs of lidocaine
 Mexiletine is used for chronic
treatment of ventricular arrhythmias
associated with previous myocardial
infarction
Adverse effects:
1- neurological effects
2- negative inotropic activity
Uses
They are used in the treatment of ventricular arrhythmias arising during myocardial
ischemia or due to digoxin toxicity
They have little effect on atrial or AV junction arrhythmias (because they don’t act on
conduction velocity)

CLASS IC DRUGS
 They markedly slow Phase 0 fast
depolarization
 They markedly slow conduction in the
myocardial tissue
 They possess slow rate of association and
dissociation (strong effect) with sodium
channels
 They only have minor effects on the duration
of action potential and refractoriness
 They reduce automaticity by increasing the
threshold potential rather than decreasing the
slope of Phase 4 spontaneous depolarization.
Class IC
flecainide propafenone

Uses:
 Refractory ventricular arrhythmias.
 Flecainide is a particularly potent suppressant of premature ventricular
contractions (beats)
Toxicity and Cautions for Class IC Drugs:
 They are severe proarrhythmogenic drugs causing:
1. severe worsening of a preexisting arrhythmia
2. de novo occurrence of life-threatening ventricular tachycardia
 In patients with frequent premature ventricular contraction (PVC) following
MI, flecainide increased mortality compared to placebo.
Notice: Class 1C drugs are particularly of low safety and have shown
even increase mortality when used chronically after MI
CLASS IC DRUGS

Compare between class IA, IB, and IC drugs as regards
effect on Na+ channel & ERP
 Sodium channel blockade:
IC > IA > IB
 Increasing the ERP:
IA>IC>IB (lowered)
Because of
K+
blockade

Class II ANTIARRHYTHMIC DRUGS
(β-adrenergic blockers)
Mechanism of action
 Negative inotropic and
chronotropic action.
 Prolong AV conduction (delay)
 Diminish phase 4
depolarization  suppressing
automaticity(of ectopic focus)
Uses
 Treatment of increased sympathetic
activity-induced arrhythmias such as
stress- and exercise-induced
arrhythmias
 Atrial flutter and fibrillation.
 AV nodal tachycardia.
 Reduce mortality in post-myocardial
infarction patients
 Protection against sudden cardiac
death

CLASS II ANTIARRHYTHMIC DRUGS
Propranolol (nonselective): was proved to reduce the incidence of sudden
arrhythmatic death after myocardial infarction
Metoprolol
Bisoprolol
reduce the risk of bronchospasm
Esmolol:
Esmolol is a very short-acting β1-adrenergic blocker that is used by
intravenous route in acute arrhythmias occurring during surgery or
emergencies
selective

CLASS III ANTIARRHYTHMIC DRUGS
K+ BLOCKERS
 Prolongation of phase 3
repolarization without altering phase
0 upstroke or the resting membrane
potential
 They prolong both the duration of
the action potential and ERP
 Their mechanism of action is still not
clear but it is thought that they block
potassium channels

Class III
sotalol amiodarone ibutilide
Uses:
Ventricular arrhythmias, especially ventricular fibrillation or
tachycardia
Supra-ventricular tachycardia
Amiodarone usage is limited due to its wide range of side effects

SOTALOL
 Sotalol also prolongs the duration of action potential and refractoriness in all
cardiac tissues (by action of K+ blockade)
 Sotalol suppresses Phase 4 spontaneous depolarization and possibly
producing severe sinus bradycardia (by β blockade action)
 The β-adrenergic blockade combined with prolonged action potential duration
may be of special efficacy in prevention of sustained ventricular tachycardia
 It may induce the polymorphic torsades de pointes ventricular tachycardia
(because it increases ERP)
Ibutilide
Used in atrial fibrillation or flutter
IV administration
May lead to torsade de pointes
Only drug in class three that possess pure K+ blockade

AMIODARONE (CORDARONE)
 Amiodarone is a drug of multiple actions and is still not well understood
 It is extensively taken up by tissues, especially fatty tissues (extensive distribution)
 t1/2 = 60 days
 Potent P450 inhibitor
 Amiodarone antiarrhythmic effect is complex comprising class I, II, III, and IV actions
• Dominant effect: Prolongation of action potential duration and refractoriness
• It slows cardiac conduction, works as Ca2+ channel blocker, and as a weak β-adrenergic
blocker
Toxicity
 Most common include GI intolerance, tremors, ataxia, dizziness, and hyper-or hypothyrodism
 Corneal microdeposits may be accompanied with disturbed night vision
 Others: liver toxicity, photosensitivity, gray facial discoloration, neuropathy, muscle weakness,
and weight loss
 The most dangerous side effect is pulmonary fibrosis which occurs in 2-5% of the patients

CLASS IV ANTIARRHYTHMIC DRUGS
(CALCIUM CHANNEL BLOCKERS)
 Calcium channel blockers decrease inward Ca2+ currents resulting
in a decrease of phase 4 spontaneous depolarization (SA node)
 They slow conductance in Ca2+ current-dependent tissues like AV
node.
 Examples: verapamil & diltiazem because they act on the heart
only and not on blood vessels.
 Dihydropyridine family are not used because they only act on
blood vessels
More effective in treatment of atrial than ventricular arrhythmias.
Treatment of supra-ventricular tachycardia preventing the
occurrence of ventricular arrhythmias
Treatment of atrial flutter and fibrillation
contraindication
 Contraindicated in patients with pre-existing depressed heart
function because of their negative inotropic activity

MISCELLANEOUS ANTIARRHYTHMIC DRUGS
Adenosine
oAdenosine activates A1-purinergic receptors decreasing the SA nodal firing
and automaticity, reducing conduction velocity, prolonging effective refractory
period, and depressing AV nodal conductivity.
oIt is the drug of choice in the treatment of paroxysmal supra-ventricular
tachycardia.
oIt is used only by slow intravenous bolus.
oIt only has a low-profile toxicity (lead to bronchospasm) being extremly short
acting for 15 seconds only

class ECG QT Conduction velocity Refractory period
IA ++ ↓ ↑
IB 0 no ↓
IC + ↓ no
II 0 ↓In SAN and AVN ↑ in SAN and AVN
III ++ No ↑
IV 0 ↓ in SAN and AVN ↑ in SAN and AVN

Types of Arrhythmia
Supraventricular Arrhythmias
Sinus Tachycardia:
Atrial Tachycardia
Paroxysmal Atrial Tachycardia (PAT):
Paroxysmal SVT
Atrial Flutter:
Atrial Fibrillation:
AV blocks
 First degree AVB
 Second degree AVB
 Third degree AVB
ventricular Arrhythmias
Ventricular Premature Beats (VPBs):
Ventricular Tachycardia (VT):
Ventricular Flutter
Ventricular Fibrillation

PRESENTATIONS OF TACHYARRHYTHMIAS
 Palpitation
 Dizziness
 Syncope
 Chest pain
 Sudden death ( ventricular arrhythmia )

DIAGNOSTIC TESTING FOR TACHYARRHYTHMIAS
 Resting ECG (if you’re lucky!)
 Continuous ambulatory ECG (24-48hrs)
 Event recorders: triggered by patient
 Implantable loop recorder (up to 3 years battery life)
Others to consider:
 TTE to evaluate for structure heart disease
 Ischemia evaluation if life-threatening arrhythmia
 EP testing to provoke arrhythmia and potentially ablate

FIRST STEP FOR TREATING TACHYARRHYTHMIAS
 STABLE or UNSTABLE?
 Acute altered mental status,
 Ischemic chest discomfort,
 Acute heart failure,
 Hypotension, or
 Other signs of shock suspected to
be due to a tachyarrhythmia

UNSTABLE SYNCHRONIZED CARDIOVERSION
due to a tachyarrhythmia, proceed to immediate synchronized cardioversion
 If possible,
 establish IV access before cardioversion
 administer sedation if the patient is conscious.
 Do not delay cardioversion if the patient is
extremely unstable
Synchronized
 This synchronization avoids shock delivery
during the relative refractory period of the
cardiac cycle when a shock could produce VF

STABLE VAGOTONIC MANEUVERS
• Valsalva maneuver
• Facial ice pack (“diving reflex” for kids)
• Carotid sinus massage
VALSALVA MANEUVER
The Valsalva maneuver performed in the supine position appears to be the most
effective vagal maneuver for the conversion of reentrant SVT.
For maximal effectiveness the strain phase must be adequate (usually at least l0
seconds), with slowing or conversion seen during the release phase
FACIAL ICE PACK (“DIVING REFLEX”)
Placing an ice pack on the face or facial immersion in cold water is usually
reserved for infants and is done for 6 to 7 seconds with the nostrils held
closed (diving reflex)

CAROTID SINUS MASSAGE
Stimulation of carotid sinus Triggers
baroreceptor reflex and increased vagal tone,
affecting SA and AV nodes
Check for carotid bruit before massage.
At the level of cricoid cartilage,at the angle of
mandible the carotid sinus is situated.
 ECG recording to be present.
 Pressure on the carotid sinus and Baroreceptors.
 Carotid massage should be done for 10 seconds
at a time, first on the side of the nondominant
cerebral hemisphere,
 never simultaneously on both sides.

APPROACH TO NARROW COMPLEX TACHYCARDIA

MULTIFOCAL ATRIAL TACHYCARDIA
At least three consequtive p waves with different morphologies with
a rate > 100 bpm to be present.
Isoelectric baseline between p waves.
Also called as choatic atrial tachycardia
Mostly seen in COPD ,electrolyte abn,theophylline
Rate usually does not exceed 130-140 bpm.

WPW SYNDROME
Two types
 Orthodromic
 Antidromic
 Antidromic is wide complex tachycardia
 In NSR detected by delta wave.
 Can ppt into AF and VF on use of AV nodal blockers
 MEMBRANE ACTIVE ANTIARRHTYHMIC DRUGS are safe.
 CONCEALED WPW syndrome – no delta wave .less risk of AF

JUNCTIONAL TACHYCARDIA
Non paroxysmal – accelerated junctional rhythm
• Rate < 100 bpm Usually junctional node 40-60 bpm
• Paroxysmal or focal junctional tachycardia is rare –automaticity.
• 110-250bpm.
• P waves may be before or after QRS complex
• Infrequent and nonsustained episodes –no treatment
• Acute termination of SVT and establish the mechanism of SVT in case of acute
setting.
• Long term goal is abolishing the arryhthmia substrate.
• Precipitating factors – electrolyte imbalance,hypoxia,ischemia,hyperthyroidism
to be sought out.

If SVT is suspected to be AVNode dependent – drug of choice
is adenosine and CCBs verapamil and diltiazem.
 Useful for sustained cases of AV node independent
tachycardias.
 But digoxin, BBs, CCBs better control of ventricular response
in atrial tachycardias
Class I agents to be combined with AV nodal blocking
drugs – to eliminate 1:1 conduction of atrial to ventricles.

CATHETER ABLATION
 Radiofrequency is delivered at the site of
earlier activation
 90-98% success in AV node dependent
 60-80% in case of AV node independent.
 Cryoablation more useful…

In case of WPW syndrome, symptomatic
concealed or manifested ..and evidence of pre-
excitation on NSR …
Send the patient for catheter ablation…

PHARMACOLOGICAL CARDIOVERSION FOR STABLE PATIENTS
C
A
R
D
I
O
V
E
R
S
I
O
N
A
B
L
A
T
I
O
N

www.HRSonline.org
Classification of AF
ACC/AHA/ESC Guidelines
Fuster et al. J Am Coll Cardiol. 2006;48:854-906.
Persistent
(Not self-terminating)
Paroxysmal
(Self-terminating)
First
Detected
Permanent

www.HRSonline.org
Pharmacologic Management of Patients With Newly Discovered AF
Newly Discovered AF
Paroxysmal
No therapy needed,
unless severe symptoms
(eg, hypotension, HF,
angina pectoris)
Persistent
Accept permanent AF
Anticoagulation
and rate control,
as needed
Rate control and
anticoagulation,
as needed
Consider antiarrhythmic
drug therapy
Long-term drug
prevention unnecessary
Anticoagulation,
as needed
Cardioversion

www.HRSonline.org
Recurrent Paroxysmal AF
Newly Discovered AF
Paroxysmal
No therapy needed,
angina pectoris)
Persistent
Accept permanent AF
Anticoagulation
and rate control,
as needed
Rate control and
anticoagulation,
as needed
drug therapy
Long-term drug
Anticoagulation,
as needed
Cardioversion

www.HRSonline.org
Rate Control vs Rhythm control
Newly Discovered AF
Paroxysmal
No therapy needed,
angina pectoris)
Persistent
Accept permanent AF
Anticoagulation
and rate control,
as needed
Rate control and
anticoagulation,
as needed
drug therapy
Long-term drug
Anticoagulation,
as needed
Cardioversion

www.HRSonline.org
Newly Discovered AF
Paroxysmal
No therapy needed,
unless severe
symptoms
angina pectoris)
Persistent
Accept permanent AF
Anticoagulation
and rate control,
as needed
Rate control and
anticoagulation,
as needed
drug therapy
Long-term drug
Anticoagulation,
as needed
Cardioversion

Maintenance of Sinus Rhythm
No (or minimal)
heart disease
Flecainide
Propafenone
Sotalol
Amiodarone
Dofetilide
Catheter
ablation
Hypertension
Substantial
LVH
No Yes
Flecainide
Propafenone
Sotalol
Amiodarone
Amiodarone
Dofetilide
Catheter
ablation
Catheter
ablation
Catheter
ablation
Catheter
ablation
Amiodarone
Dofetilide
Dofetilide
Sotalol
Coronary artery
disease
Heart
failure
Amiodarone

WHAT IS ADEQUATE RATE CONTROL?
• Adequate rate control is critical to avoid tachycardia-mediated
cardiomyopathy
• 60-80 beats per minute at rest AND
• 90-115 beats per minute with exertion
• Criteria vary with age
• May be evaluated using 24-hour Holter recording

0
2
4
6
8
10
12
14
16
18
20
AFFIRM
RACE
PIAF
STAF
HOT
CAFÉ
AFFIRM
RACE
PIAF
STAF
HOT
CAFÉ
Rate Rhythm
RHYTHM VS RATE CONTROL IN AF EVIDENCE BASE (CONT'D)
Stroke
Death

PILL IN POCKET APPROACH
In whom recurrences are infrequent.
 But sustained.well tolerated hemodynamically.
 Patients who have had only a single episode of SVT..
 100-200mg of flecainide at the onset of SVT is a reasonable
approach…until he reaches the hospital.
 40-160 mg verapamil –without preexcitation,
 Betablockers
 Propafenone 150-450 mg.
 80% cases interrupted with a combination of CCB and BB in 2 hrs…

NEW FORMULATIONS OF AADS
PROPAFENONE RAFT AND ERAFT STUDIES

Faster restoration of Sinus Ryhthm
Propafenone 2.4 hrs
Amiodarone 6.9 hrs
(P=0.05)
Median time to restoration of normal sinus rhythm
•Propafenone shows faster restoration to sinus rhythm within 2.4 hrs
compared to 6.9 hrs of amiodarone
prospective, randomized, multicenter study compares the time to conversion to sinus rhythm in Patients with
recent-onset AF (<2 weeks), without contraindications

Faster restoration of Sinus Ryhthm
prospective, randomized, multicenter study compares the time to conversion to sinus rhythm in Patients with
recent-onset AF (<2 weeks), without contraindications
Propafenone 56%
Amiodarone 47%
% of patients restored to normal sinus rhythm within 24 hrs
•56% of patients on propafenone restored to sinus rhythm within 24 hrs

REMARKABLE SAFETY
0%
5%
10%
15%
20%
25%
Amiodarone Propafenone
% of patients
(who had side effects need to withdraw medication)
23.6%
2.7%
• Meta-analysis 29 RCT trails including 11763 patients on different anti-arrhythmic agents
(dronedarone,amiodarone,flecanide,propafenone,sotalol,placebo) 716 pts on amiodarone & 1,261 pts on propafenone

NEW AAD DEVELOPMENT
• Beta blockers with Class I or III effects
• Amiodarone congeners
• Atrial-selective antiarrhythmic drugs
– IKur- , Ito and IKACh- blocker
– Atrial-selective Na channel blocker
– 5-HT4 receptor antagonist
• Stretch-activated channel blockers
• ACEI/ARB
• NCX (Na/Ca exchanger) inhibitor
• Anti-inflammatories (statins)
• Gap junction conduction facilitation

REFERENCES
1. Evaluation and initial treatment of supraventricular tachycardia, The New England Journal of Medicine;
2012; 367: 1438-48.
2. 2015 ACC/ AHA/HRS Guideline for Management of Adult patients with Supraventricular Tachycardia.
3. Mixed treatment comparison of dronedarone, amiodarone, sotalol, flecainide, and propafenone, for the
management of atrial fibrillation, Europace (2011) 13, 329–345 doi:10.1093
4. 2016 ESC Guidelines for the management of atrial fibrillation developed in collaboration with EACTS

Antiarrhythmic therapy for supraventricular arrhythmias

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