Download AF –pathophysiology and medical management

AF –pathophysiology and
medical management
Dipin.S
Junior resident
medicine
• Supraventricular tachy arrythmia
charecterised by uncoordinated atrial
activation and consequent deterioration of
atrial mechanical function.
• ECG -rapid fibrillatory waves with changing
morphology and rate and a ventricular rhythm
that is irregularly irregular
• Usually originates near the pulmonary veins
Classification of AF
Diagnosis
of AF
New
Onset AF
Paroxysmal
Up to 7 d
Persistent
> 7 days
Permanent
CV failed
Types of Atrial Fibrillation
• Paroxysmal AF: if it terminates spontaneously in fewer
than 7 days (often in <24 h).
• Persistent AF: when it terminates either spontaneously
after 7 days or following cardio version.
• Permanent AF: cardio version has failed or not attempted
• Recurrent : after 2 or more episodes
• developed world- the most common causes
are hypertension and coronary artery disease
• developing countries -hypertension,
rheumatic valvular heart disease, and
congenital heart disease are the most causes
• Presence of CHF markedly increases risk of AF
factors
• Factors that trigger
• Factors that perpetuate
• Triggering foci of rapidly firing cells within the
sleeve of atrial myocytes extending into the
pulmonary veins - shown to be the underlying
mechanism of most paroxysmal AF
• The pulmonary veins of patients with paroxysmal AF
demonstrate abnormal properties of conduction
• Markedly reduced effective refractory period within
the pulmonary veins
• Progressive conduction delay within the pulmonary
vein in response to rapid pacing or programmed
stimulation
• Conduction block between the pulmonary vein and the
LA
• Heterogeneity of conduction promotes reentry within
PV
• Other foci- the superior vena cava, the ligament
of Marshall, the musculature of the coronary
sinus, left atrial wall, crista terminalis of right atria
• Prior to initiation-Primary increase in adrenergic
tone followed by a marked vagal predominance
(paroxysmal AF)
• Vagal stimulation shortens the refractory period
of atrial myocardium with a nonuniform
distribution .
perpetuation
• The multiple wavelet hypothesis(More and
colleagues)
• Fractionation of wavefronts traversing the
atria into daughter wavelets.
• The number of wavelets at any moment
depends on the refractory period, conduction
velocity, and anatomic obstacles in different
portions of the atria.
• Interstitial fibrosis predisposes to intraatrial
reentry and AF(Li and colleagues)
• Delayed interatrial conduction and
inhomogeneous dispersion of atrial refractory
periods
• Long-standing AF -loss of myofibrils,
accumulation of glycogen granules, disruption
in cell-to-cell coupling at gap junctions,and
organelle aggregates
• AF itself produces alterations of atrial
architecture that further contribute to atrial
remodeling, mechanical dysfunction, and
perpetuation of fibrillation.
• Myocardial stretch is an important mechanism
of AF in the elderly.
• Altered stretch on atrial myocytes results in
opening of stretch-activated channels.(L type
Ca)
• AF produces electrical remodeling that
promotes further AF.
haemodynamics
• Loss of atrial contraction
• A rapid ventricular rate
• An irregular ventricular rhythm
• Loss of mechanical AV synchrony affects
ventricular filling esp. when left ventricle has
reduced compliance.
• The loss of AV synchrony results in a decrease
in LVEDP (as the loading effect of atrial
contraction is lost)
• Stroke volume and LV contractility are reduced
(Frank starlings principle)
• Although there is a reduction in the LVEDP,
there is an increase in the left atrial mean
diastolic pressure
• Patients with restrictive physiology- pulmonary
edema and hypotension may occur with AF
• In dilated cardiomyopathy – min. hemodynamic
compromise if LV compliance is not affected .
• Patients with heart failure do worse when in AF
• 1st clinical manifestation of AF may be CHF
related to a tachycardia-induced cardiomyopathy.
thromboembolism
• Thrombi mostly arise within the left atrial
appendage
• Flow velocity in left atrial appendage is reduced
during AF
• Nitric oxide (NO) production in the left atrial
endocardium is reduced
• Increase in levels of the prothrombotic protein
plasminogen activator inhibitor 1
Objectives of Treatment
Relief of Symptoms & Prevent recurrencecorrection of rhythm disturbance
Prevention of Systemic Thromboembolism
Tachycardia induced Myocardial Remodeling-rate
control
CHADS2 Scoring
One Point
• Cardiac Failure
One Point
• Hypertension
One Point
• Age more than 75
One Point
• Diabetes
Two Points
• Stroke or TIA, STE
CHADS based Stroke Incidence
CHADS2 Score
(points)
Adjusted Stroke Incidence % per
year
0
1.9
1
2.8
2
4.0
3
5.9
4
8.5
5
12.5
6
18.2
Non valvular Atrial Fibrillation Rx with
anticoagulation
Risk Stratification
Risk Factor
Stratification
Risk Factors to be
Ascertained
High Risk Factors
Prior Stroke/TIA or STE Event
Mitral stenosis , prosthetic
valve
Moderate Risk Factors
Age >75, HF, HT, EF <35%, DM
Weaker Risk Factors
Female, CAD,  Thyroid, 6574 yrs
Antithrombotic Therapy for Patients With Atrial
Fibrillation
• 68% risk reduction with warfarin compared to
placebo
• Target INR 2.5(2-3)
• Not only reduces frequency but severity and risk
of death also.
• Relative risk reduction of 22% with aspirin
compared to placebo
• No difference in the indications for
antithrombotic therapy between paroxysmal,
persistent or permanent AF.
Cardioversion
• antiarrhythmic drugs
or
• the direct-current approach
• AF of <48 hours can be cardioverted without
prior anticoagulation
• anticoagulation therapy is recommended for
AF of uncertain duration.
2 strategies
• Oral warfarin with a therapeutic INR (2–3) for 3 to
4 weeks before cardioversion followed by
continued warfarin thereafter
• Transesophageal echocardiography (TEE) and
heparin immediately before cardioversion
followed by oral warfarin thereafter.
• Left atria – stunning effect. So anticoagulation is
to be continued for 4 wks
Direct current cardioversion
• Anteriorly and posteriorly placed electrodes
• Synchronized to QRS complex
• Initial shock energy of 200J preferred ( higher
energy less chance of VF)
• In AF> 3 mnths antiarrythmic drug started
before cardioversion to prevent immediate or
early reccurance
• AF lasting <1 wk – cardioversion -using oral
flecainide, propafenone, dofetilide, and
intravenous ibutilide.
• For longer duration- iv dofetilide( also
amiodarone and ibutilide may be useful)
• Single oral dose of propafenone or flecainide –
in recent onset AF (pill in the pocket)
Rate control vs rhythm control
The choice of strategy is determined by :
• paroxysmal or persistent AF
• severity and type of symptoms
• associated cardiac and other medical diseases
• age of patient
• short- and long-term treatment goals
• choice of pharmacologic or nonpharmacologic therapy
• Try and maintain sinus rhythm in younger patients with AF
• In the elderly, if symptoms can be controlled with a rate strategy, it
is preferred.
• Anticoagulation is needed in patients at high risk for stroke
regardless of whether a rate or rhythm strategy is chosen.
Major Trials Comparing Rhythm Strategy and Rate
Strategy
Major trials include:
– AFFIRM (Atrial Fibrillation Follow-Up Investigation of Rhythm Management )
– RACE (rate control versus electrical cardioversion)
– PIAF (pharmacological intervention in AF)
– AF-CHF
Major overall findings:
– Rhythm-control strategy was not superior to rate-control strategy in terms of
morbidity/mortality
– Appropriate choice of therapy should be based on each patient’s symptoms and
disease
– rate control, prevention of thromboembolism, and correction of the rhythm
disturbance - these strategies are not mutually exclusive
1. The AFFIRM Investigators. N Engl J Med. 2002;347:1825-1833;
2. Van Gelder IC, et al. N Engl J Med. 2002;347:1834-1840;
3. Hohnloser SH, et al. Lancet. 2000;356:1789-1794;
4. Carlsson J, et al. J Am Coll Cardiol. 2003;41:1690-1696;
5. Opolski G, et al. Chest. 2004;126:476-486;
6. Roy D, et al. N Engl J Med. 2008;358:2667-2677;
7. Fuster V, et al. Circulation. 2006;114:e257-e354.
Control of ventricular rate
• In the acute phase, iv diltiazem, metoprolol,
esmolol, or verapamil (slowing of AV nodal
conduction within 5 minutes)
• Iv digoxin is less useful
• In chronic phase- digoxin gives good control of
resting heart rate
• Beta blockers and CCBs during exercise.
• Chronically elevated vent. Rates despite drug
therapy- AV nodal ablation
Maintenance of sinus rythm
• Avoidance of inciting factor
• Safety first principle in selecting
antiarrythmics
• Class Ic drugs are to combined with AV nodal
blockers
• Monitor QRS duration with class Ic(150%
increase-reduce drug)
• Monitor QT interval with sotalol and
amiodarone
Antiarrhythmic drug therapy to maintain sinus rhythm in patients with recurrent
paroxysmal or persistent atrial fibrillation
Other drugs
• ACE inhibitors ARBs
• Reduce atrial fibrosis and promote favourable
hemodynamics
Pharmacological management of patients with newly discovered atrial fibrillation AF
Pharmacological management of patients with recurrent paroxysmal atrial fibrillation (AF)
Pharmacological management of patients with recurrent persistent or permanent atrial
fibrillation (AF)