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Arrhythmias -

Medical Therapy

David Luria, Sheba Medical Center


Antiarrhythmic medications
 1st class (Na channel blockers)
 1A
 Quinidine
 Procainamide
 Disopyramide (Rithmical)
 Giluritmal
 1B
 Lidocaine
 Mexiletine (mexillene)
 1C
 Propapfenone (rythmex)
 Flecainide (tambocor)
)Antiarrhythmic medications (2

 2nd class
 Beta blockers
 3rd class (K channel blockers)
 Amiodarone (Procor)
 Sotalol
 Dofetilide

 4th class (Ca channels blockers)


 Verapamil
SVT - Medical therapy

 Termination
 adenosin, verapamil, beta blockers IV
 “pill in the pocket” (1c drugs)

 Prevention
 any antiarrhythmic drug
 first choice are beta blockers &

Ca++ channels blockers


VT - medical therapy
 Ischemic VT
 No AAD prevents SCD
 CAST study
 Termination (IV)
 Lidocaine
 Amiodarone
 Procainamide
 Prevention
 Amiodarone
 Mexilletine
 Sotalol
 1A drugs
)VT - medical therapy (2

 Non-ischemic cardiomyopathy
(ARVD, DCM, HCM)
 Sotalol
 Amiodarone
 Disopyramide (HOCM)

 Idiopathic VT
 RVOT VT (beta-blockers, AAD)
 Fascicular VT (Verapamil, AAD)
AF - medical therapy
Rate Control
Beta Blockers
Verapamil
Digoxin
)Antiarrhythmic therapy (guidelines
Proarrhythmia

 Torsade de pointes
 Sustained VT
 1:1 flutter

- start of the therapy


- drug interactions
(diuretics, antidepressants)
- concomitant medical
conditions
Nattel S, Am Heart J 1995
Total mortality with Quinidine
RCT n
Boissel 212

Byrne-Quinn 92

Hartel 175

Hillestad 100

Lloyd 53

Sodermark 176

ALL STUDIES N = 808


Circulation 1990
0 1 2 3 4 5 6 7 8 9 10 11 12
Quinidine Better Quinidine Worse
?Recent Quinidine rehabilitation

 PAFAC & SOPAT European trials


 Combine therapy of Quinidine (480/d) and
Verapamil (240/day) vs Sotalol (320/day)
 Persistent/paroxysmal AF
 Same efficacy (about 50% 1 y)
 Same rate of combine
death/syncope/TdP/NSVT (about 5% during 2y)
 TdP only in SOTALOL group

EHJ, 2004
Side effects

 CHF exacerbation
 Pulmonary toxicity
20-30 % of pts stop
 GE symptoms antiarrhythmics
 Thyroid dysfunction due to side effects
 Hepatic dysfunction
 Blood dyscrasias
 Sleep disturbances
)Antiarrhythmic therapy (guidelines

 1C drug up to QRS widening 150%

 1A and Sotalol up to QTc 520 msec

 Before DC (to enhance conversion and


prevent IRAF): 1C and III
Start antiarrhythmic therapy

 In hospital Outpatient
- IA drugs (QT monitoring)
- Lone AF (1C, III)
- 1C drug in pts with heart disease
(QRS/VT monitoring) - Amiodarone
- Sotalol in pts with heart disease
(QT monitoring)
Antithrombotic therapy

Antithrombotic therapy to prevent thromboembolism is


recommended for all patients with AF, except those with
lone AF or contraindications. (Level of Evidence: A)

For patients without mechanical heart valves at high


risk of stroke…to achieve the target intensity
international normalized ratio (INR) of 2.0 to 3.0, unless
contraindicated.
Risk factors for Stroke

 High (one enough for COUMADIN)


 Previous embolic event

 Rheumatic MS

 Mechanical prosthetic valves


Risk factors for Stroke

 “Moderate validated”
(two required COUMADIN,
one - ASPIRIN)
 Age >75
 HTN
 Heart failure
 Low EF (<35%)
 Diabetes
Risk factors for Stroke

“Moderate, less well validated”


(one or more could be managed with
COUMADIN or ASPIRIN)
 Age 65-75
 Female gender
 Coronary artery Disease
Interruption of anticoagulation

In patients with AF who do not have mechanical


prosthetic heart valves, it is reasonable to interrupt
anticoagulation for up to 1 wk without substituting
heparin for surgical or diagnostic procedures that
carry a risk of bleeding. (Level
of Evidence: C)
Cardioversion -
Anticoagulation therapy

Before cardioversion of AF (ALL TYPES):


COUMADIN if AF ≥ 48 h
(1 mo before and 3 after)
TEE-guided cardioversion

 As good as Coumadin to prevent embolism


 Dense “spontaneous ECHO contrast” is a risk
factor for embolism – contraindication to
cardioversion
 Absence of thrombus/”smoke” is not
guarantee for post cardioversion thrombus
formation: need anticoagulation post CV
Cardioversion: role of drugs

 Flecainide, Amiodarone and Ibutilide


decrease atrial DFT
 Any antiarrhythmics can prevent immediate
recurrence
 Risk of SSS aggravation by drugs
?Stop anticoagulation after DC

 NO
 Risk for embolism is the same during
“successful rhythm control” in PAF pts
 Asymptomatic AF is potential explanation
(in PAFAC –
70%, in SOPAT – 50% by daily ECG
transmission)
 Drugs can mitigate symptoms
 Particular cases could be of exception…
Pill in the pocket” strategy“

 Oral 1C drugs in ER effective (up to 85%)


and safe in termination of PAF.
J Am Coll Cardiol 2001
 Outpatient self use of single loading dose:
165 pts, 569 AF episodes, 95 % terminated
successfully without need in ER

NEJM 2005
Pill in the pocket” strategy“

Potential side effects:


 Hypotension
 QRS widening
 Proarrhythmia:
- VT
- atrial flutter with 1:1 conduction,
- bradicardia /pauses (during conversion)
Antiarrhythmic therapy
)AFFIRM substudy (JACC, 2003

 Stop drug due to adverse events (one year):


Amio-12.3 % Sotalol- 11.1 % Class I – 28.1%
 After 5 years only half pts are in sinus
Angiotensin system blockade
for AF therapy

 ACE inhibitors (SOLVD)  Angiotensin receptor


blockers

Circ 2003
Circ 2002
Beta blocker vs. A II blocker

LIFE study, JACC 2005


Mechanism of ACE blocker effect
 Improve of hemodynamic parameters and
atrial stretch
 Attenuation of hypokalemia
(diuretics therapy)
 Reduce atrial arrhythmogenic remodeling
- fibrosis
- conduction abnormalities
Drugs on the way: Ibutilide

 Class III drug, IV for cardioversion

 4% of TdP (women 5.6% vs men 3%)

 Contraindicated to low EF due to


proarrhythmia

 Adverse effect - hypotension


Dofetilide

 Class III drug: selective IKr blocker


 SAFIRE-D: 87% conversion to SR within 30 h;
58 % in SR after 1 year
 DIAMOND
- patients with decreased LV function
- 79% maintain SR
- 0.8 % had TdP within first 3 days
Drugs under investigation
 Azimilide: group III Na and K channel
blocker, good for CHF pts, low toxicity

 Dronedarone: noniodinated amiodarone

 Atrioselective agents: I kur blockers –


only atrial antiarrhythmic effect
(no pro- arrhythmia)
Torsade de pointes – emergency therapy

 Magnesium IV – 2.0 g (x 2), up to 10 g during 24


hours (3-10mg/min IV)
(CAUTION: RF, knee reflex, lethargy)
 Potassium supplementation (up to 4.5 mmol/l)
 Pacing (100-140/min) or Isoproterenol (not for
congenital LQTS)

NOTE: danger from antiarrhythmic drugs (lidocaine help


in 50%)
Brugada Syndrome
cellular basis

)I TO (K

Na
Medical therapy

 Ito blockers: Quinidine and Tedisamil

 Normalization ECG (both)


 “Electrical storm” (both)
 Efficacy was shone in experimental work to
normalize epicardial dome, ECG and prevent faze
II re-entry (only Quinidin)
 Long term efficacy (only Quinidin)
 25pts with Brugada ECG
and inducible VF (7 after
CA, 8- syncope)
 Quinidin 1200-1500 mg
 Non-inducibility 88%
 F/u for 6 mo to 22 years
 No arrhythmic events
CIRCULATION 1981
Isoproterenol therapy
CIRCULATION 1988
Pregnancy
Medical therapy

 No entirely safe drugs:


use as less as possible !
 Acute setting
 Adenosine for SVT (Verapamil IV - second
choice, care with hypotension)
 Lidocaine for VT (organic)
 Metopralol for idiopathic VT (adenosine)
 DC for PAF/flutter or any unstable arrhythmia
)Medical therapy (cont
 Preventive therapy
 1st choice: Cardio-selective beta blockers
 2nd choice: Sotalol
 3rd choice: Quinidine, Flecainide
 Anticoagulation (AF,
standard indications)
 All type carry risk of retro-placental bleeding
 Coumadin is contraindicated first 8-10 weeks and
before delivery: substitution by Heparin / Enoxaparin