I- Introduction :
Atrial fibrillation is the arrhythmia most common sustained.
It is estimated that approximately 2,2 million patients in the US and 6 million EU had presented a paroxysmal and persistent AF.
It represents Ie third of hospitalizations for arrhythmia.
It is aujourd & rsquo; hui genuine hugely expensive public health problem in developed countries.
II- Definition and classification :
III- Epidemiology :
Ago in population overview :
The prevalence of AF is the & rsquo; order 0,4 % at 1% It increases exponentially with the & rsquo; age :
Rare in young
< 1 % subjects under 60 years
5% > from 65 years and beyond 8% > from 80 years.
Pathology of the elderly :
70% patients with an age between 65 and 85 years
It increases in the presence of & rsquo; heart disease or d & rsquo; valvular damage associated
Absence of heart disease : 0,04% [HISS]
Presence of ischemic heart disease x10 : 0,6% [CASS]
In general medicine :
3,5% between 65 at 74 years (Hill and partnership.)
5% (Kitchin et Milne)
In hospitals :
7% service & rsquo; e Medical Emergency [Lip].
15%. Cardiology service (Levy et al)
It increases especially with the severity of I has underlying heart disease.
IV- PATHOPHYSIOLOGY :
Mechanisms of atrial fibrillation :
The pathogenesis of AF is complex, three main theories are involved in the onset of AF:
– The circuits of reentry
– L & rsquo; increase in & rsquo; automaticity
– Circuit single reentrant conduction with a fibrillar
L & rsquo; initiation and maintenance of atrial fibrillation involves the & rsquo; interaction 3 factors :
– A trigger : THAT, TS, flutter.
– The anatomical arrhythmogenic substrate : All d & rsquo; anatomical abnormalities : Dilatation, interstitial fibrosis, inflammation or cell degeneration l & rsquo; headset
– Factors m ripple : sympathetic and parasympathetic
V- ETIOLOGY :
The FA often secondary to pathological situations :
– Extracardiaques that & rsquo; we must know search systematically for, they condition treatment.
In some cases, FA appears isolated without detectable etiology.
Among the secondary causes :
– Acute because, transient and reversible.
– A permanent cause.
acute causes :
– immediate aftermath of cardiac and thoracic surgery,
– Myocardial infarction in acute phase.
– Acute peri carditis.
– Myocardite aigue.
– Pulmonary embolism.
– An infectious disease (pulmonary or urinary particularly acute in the elderly),
– other lung disease (Acute respiratory failure, lung cancer or mediastinal).
extra cardiac causes :
– Syndrome & rsquo; sleep apnea.
– Infectious disease (pulmonary or urinary particularly acute in the elderly).
– Other lung disease (Acute respiratory failure, BPCO, lung cancer or mediastinal).
s permanent causes heart :
serious complication : rise beyond morbidity and mortality : Secondary stroke with AF are more severe with higher mortality (25% vs 14%) / Other ischemic stroke
They s & rsquo; especially observed in the FA d & rsquo; recent installation and after restoration of sinus rhythm spontaneously or with medication or electrical cardioversion.
WE- CLINIQUE :
Circumstances of discovery :
Highly variable dependent paroxysmal or permanent nature of the & rsquo; arrhythmia, ventricular rate, the patient's age, of physical activity, l & rsquo; whether or not there & rsquo; in heart disease- core.
Most often it is the functional symptoms that lead the patient to consult :
– irregular palpitations
– Asthenia more or less tolerated at rest but that s & rsquo; & rsquo to accentuate, stress.
Sometimes, F A is manifested by signs of more serious type :
– functional angor
In other cases, F A can be revealed by a complication :
IC, O 4P, embolism (AVC or AJ T), State of shock FA may be asymptomatic in 1/3 cases
paraclinical examinations :
Allow to :
– Diagnosing FA
– Documenting a paroxysmal AF in patients seen in sinus rhythm,
– Search aetiology
– I evaluate the consequences of a FA
– Assessing the risk of thromboembolism
Any patient with & rsquo; AF must be the & rsquo; & rsquo subject, including a minimum balance :
BIOLOGY : Glucose Creatinine, kaliémie, hémogramme, platelets, prothrombin time for the prescription of & rsquo; anticoagulant therapy (AVK)
The thyroid function tests (TSH) must be systematic in particular when the FA seems isolated OTHER : TV thorax, ETO, OF, Holter ECG, electrophysiological exploration.
VII- COMPLICATIONS :
L & rsquo; heart failure and AF are frequently associated AF can be a cause as a consequence of the & rsquo; IC FA because of the & rsquo; heart failure : rhythmic cardiomyopathy :
Mentioned from Philips 1949, ventricular dysfunction induced by the only recently validated FA (CMD).
– The risk & rsquo; heart failure is X 3,4
– It is estimated that 42% FA patients develop during their lifetime IC.
– The diagnosis is difficult to ask for certain
– Slowing the heart rate or the restoration of sinus rhythm —> improving LV function
– Cooldowns > first month.
– The risk of recurrence can : interest to maintain sinus rhythm.
FA consequence of & rsquo; an IC :
– L & rsquo; X heart failure risk by FA 4,5 at(FHS)
– More than 45% in heart failure patients had intermittent or permanent AF (E HFS)
The passage in atrial fibrillation can lead to heart failure during the & rsquo; evolution & rsquo; heart disease up & rsquo; here well tolerated and may aggravate preexisting heart failure.
VIII- AVC :
– AF is an independent factor & rsquo; embolism : Stroke and cerebral embolism devices (including stroke)
Cerebral embolism : The most common location 3/4 cases
– FA : leading cause of & rsquo; cardioembolic stroke : 50 % cases, 25% ischemic strokes are secondary to the FA.
– In patients with AF not anti coagulated l & rsquo; incidence of embolic events is 5% per year (7% year & if rsquo; there are silent ischemic stroke and TIA)
– d & rsquo risk; stroke increases with : (thromboembolic risk)
Age : interest AVK elderly TRT The type of underlying heart disease :
Risk : by X 5,6 in the & rsquo; X17,5 absence of heart disease in case of & rsquo; rheumatic valvular.
The character of atrial fibrillation : d & rsquo risk, stroke is the same regardless of the type AF :
paroxysmal, persistent or permanent
– some studies : significantly lower risk in case of paroxysmal AF : 2 at 3% par an vs 6% per year.
– On healthy heart : risk three times less with paroxysmal AF / permanent.
– d & rsquo risk; stroke varies 1 at 15 % per year depending on associated risk factors :
L & rsquo; age, l & rsquo; hypertension, the history of & rsquo; transient ischemic attack or d & rsquo; stroke, diabetes and & rsquo; heart failure, are independent risk factors
Individual risk stratification that is based only on those elements (CHADS 2, CHADS2vasc)
FA – independent risk factor for mortality and d & rsquo; cardio vascular events.
Mortality : X2
especially cardiovascular : the 2/3 of cardiovascular death : sudden death, IC and stroke (FHS, CASS, ALFA)
Excess mortality associated depends on the :
Underlying cardiac disease: RR 2 at 8 (FHS, PP)
Severity ++++ of the underlying heart disease (Val-HeFT SOLVD : 34% vs 23%)
IX- TREATMENT :
OBJECTIVES OF TREATMENT : The management of AF has three basic principles :
1- Treatment of rhythm disorder : both strategies :
+ rhythm control strategy : restore sinus rhythm with electrical or drug cardioversion and maintain sinus rhythm by antiarrhythmic therapy to prevent recurrences
+ heart rate control strategy : (respect of the FA) : freinateurs by the AV node : BB, calcium channel blockers or digoxin
2- anticoagulant therapy : to prevent embolic events
3- Treatment of the cause : if possible
1- Processing disturb the rhythm :
+ rhythm control strategy :
it is to reduce the FA by cardioversion. This strategy is proposed to restore sinus rhythm in patients with paroxysmal AF and well tolerated in patients with persistent AF d & rsquo; recent installation.
When this treatment strategy is proposed. There are two options appropriate cardioversion : Electrical cardioversion or pharmacologic cardioversion.
– Electrical cardioversion :
Electrical cardioversion is probably the most effective way (Success EEC = 90%) superior to antiarrhythmic.
It is proposed when the FA is poorly tolerated (OAP, State of shock, Angor or IDM, WPW), the external electric shock is performed immediately (immediate cardioversion) or after failure of the drug cardioversion.
– The drug cardioversion:
Drug cardioversion is probably less effective than electrical cardioversion
Many factors influence the & rsquo; treatment efficacy, in particular the duration of AF, the presence of & rsquo; an underlying heart disease, the circumstances d & rsquo; emergence of & rsquo; arrhythmia.
the highest conversion rates are usually reported in patients without heart disease, presenting an episode of short duration.
– anticoagulation framing cardioversion ;
The risk & rsquo; thromboembolism after cardioversion 7-11%; d & rsquo; hence the need & rsquo; an anticoagulant effective dose trt (INR 2 at 3) regardless of the type used for any cardiversion FA whose duration > 43 hours, or age of the unknown FA :
delayed cardioversion : trt AVK at least 3 weeks before
rapid cardioversion heparin after checking the & rsquo; absence of left atrial thrombus intra TEE
If the FA duration is < 43 hours : AVK need according & rsquo; patient risk assessment.
In the 2 case, continuing VKA 4 weeks after the FA reduction regardless of the method used (electrical or pharmacological).
– Choice of method cardioversion :
The choice between these 2 methods depends on clinical considerations, techniques and patient preferences:
In case of poorly tolerated AF (OAP, State of shock, Angor or IDM, WPW), the external electric shock is performed immediately. (immediate cardioversion)
Outside of & rsquo; emergency, instead and I es m odali tees cardioversion can be individualized (delayed cardioversion)
Generally the two techniques are combined, drug cardioversion is initiated, followed in case of & rsquo; failure by electrical cardioversion after effective anticoagulation 3 weeks.
– Maintain sinus rhythm after cardioversion :
after cardioversion, antiarrhythmic therapy should be continued because I e risk of recurrence is high (> 5 0 % in 1AN). The most common factors associated with recurrence being functional class and & rsquo; seniority FA
The choice among the various drugs must be based on an individualized assessment of the risks and benefits of treatment, and should be reassessed according to the & rsquo; efficiency.
Prescribing & rsquo; antiarrhythmic n & rsquo treatment is not mandatory s & rsquo; s it & rsquo; d & rsquo acts; a first crisis, quick resolution, with correct tolerance and & rsquo; absence of underlying heart disease.
+ Strategy Heart Rate Control :
The FC control is the recommended strategy for the majority of patients in permanent or persistent AF :
– If the reduction of the FA n & rsquo; is not possible.
– If antiarrhythmic therapy involves risk.
The pharmacological agents used as first line to control heart rate are beta blockers (metoprolol, propranol, etc.), calcium channel blockers bradycardic (diltiazem, verapamil) and digitalis. Used IV (FA hemodynamically stable rapid symptomatic) or oral (FA asymptomatic) as monotherapy or in combination in the case of & rsquo; failure of monotherapy
The choice of the molecule recognizes symptoms, lifestyle and heart disease in- core.
optimal control of CF :
A heart rate 80 at 100 per minute recommended for little or asymptomatic patients
A strict control of heart rate FC < 80 c / m s & rsquo they remain symptomatic
2- Prophylactic antithrombotic treatment :
The continuation of & rsquo; anticoagulation beyond the period of four weeks after cardioversion is proposed for chronic AF, persistent, permanent, or recurrent, When & rsquo; it is associated with a significant risk of embolic complications.
The frequency of AF recurrence after cardioversion, including sub antiarrhythmic treatment (AFFIRM) remains high
The difficulty lies in the & rsquo; establishing proof of the final maintenance of sinus rhythm, allowing the & rsquo; s final judgment of & rsquo; anticoagulation (FA intermittent forms, which are often asymptomatic, difficult to detect, which are associated with the same embolic risk that persistent or permanent forms.
If in doubt, maintaining & rsquo; anticoagulation in the long term, even permanent, is justified.
therapeutic classes used in thromboprophvlaxie :
– Read THE K :
The most effective to prevent stroke, recommended for most patients, even when the patient's thrombotic risk is low (but not zero)
– The new anticoagulants :
dabigatran, rivaroxaban, endoxaban…: At least as effective if not more than AVK. To replace the AVK. Without biological control of coagulation. Used in non-valvular AF
– Unfractionated heparin and LMWH :
They are recommended in case of & rsquo; anticoagulation during acute & rsquo; immediate cardioversion or during the relay in case of & rsquo; surgery or invasive procedure inducing bleeding risk (denture wearers).
– Antiplatelet agents :
limited space, offered if the risk almost zero but preferably not give.
Indication de la thromboproohylaxie :
Absolute Risk & rsquo; n & rsquo stroke, is not the same in all patients with AF, it ranges between 1 and 12% depending on the number of risk factors present in the patient
The decision of & rsquo; antithrombotic therapy and the choice of & rsquo; antithrombotic based on :
– the thromboembolic risk level : embolic risk stratification based on the score CFIADS 2 now changed CHADS2 score VASC
– Benefit / risk of bleeding : Evaluate the thromboembolic risk against risk of bleeding induced by anticoagulants.
Score CHADS2 VASC
Despite their proven efficacy in the prevention of A >C (50 %), they face the risk of bleeding complications (annual incidence ranging from 7 at 22 %). L & rsquo; intracerebral hemorrhage remains I was more serious (death). This risk lim you prescription anti coagulants in partjculier in the elderly. L & rsquo; evaluation of bleeding risk related to the & rsquo; anticoagulation is important before any prescription blood thinners
To assess the risk of bleeding, l’ESC propose
D & rsquo; use HASBLED bleeding risk score based on 7 factors beyond. Thus for each patient the risk of AF & rsquo; stroke must be balanced against the risk of bleeding induced by anticoagulants.
3- Removal of the atrioventricular node ventricufaire radiofrequency (or surgical) with setting up & rsquo; pacemakers :
Therapeutic procedure should be reserved for patients in whom a rhythm control n & rsquo; is not indicated and the pharmacological control of FC, including combination therapy, has failed
Allows an effective control of heart rate in symptomatic patients, refractory to all traiternent anti arrhythmic Iorsque I has rapid response ventricul area remains.
Let persist FA therefore embolic risk prosecution and a requirement under anticoagulant therapy with a bleeding risk.
d & rsquo destruction a useful structure which requires the establishment of & rsquo; a definitive pacemaker and amends & rsquo; ventricular activation
However, the deleterious effects of this non-physiological activation, however, are offset by controlling the heart rate and regularity of the rhythm.
4- L & rsquo; ablation of arrhythmogenic foci :
L & rsquo; surgical removal : myocardial area involved in the genesis and maintenance of & rsquo; arrhythmia is a radical treatment and is used to permanently cure 70% at 95% FA December. Despite this, it n & rsquo; is not performed routinely in & rsquo; now, notably because of its complexity and technical difficulties. It is practiced mainly during concomitant cardiac surgery.
L & rsquo; radiofrequency ablation : Another treatment option for AF tends to replace the & rsquo; surgical removal [311, 312]. high success rate varies according to whether the FA is paroxysmal or persistent between 56% and 87% patients after one to two procedure
These methods involve risks (tamponade, TIA or stroke,pulmonary vein stenosis, fistule oesophago-atrial, even death . C & rsquo; is for this reason that & rsquo; they remain a treatment option for second-line reserved for very specialized centers.
The paroxysmal AF and persistent high life threatening arrhythmias in particular the rebels antiarrhythmic treatment, FA complicated d & rsquo; heart failure when & rsquo; he persists symptoms despite good control of the frequency, symptomatic sinus disease or those which generate high rates ventricular ( WPW) constitute the & rsquo; usual indication
5- Treatment of the cause :
Treating the cause may be immediate (IDM, myocardite, hyperthyroidism, alcohol intoxication, acute pulmonary disease ….) or deferred (intervention valvulopathy, treatment & rsquo; heart failure or d & rsquo; hypertension …)
Treatment d & rsquo; upstream :
Treatment d & rsquo; upstream, to prevent or delay myocardial remodeling associated with hypertension, an IC or inflammation (eg after heart surgery) can prevent the development of & rsquo; a new FA (primary prevention) or, FA being present, its rate of recurrence or progression to permanent AF (secondary prevention). the IEC, the ARA-II, antagonists of the & rsquo; aldosterone, statins and omega-3 polyunsaturated fatty acids are treatments & rsquo; upstream FA
Despite extensive data on the potential of these drugs AAR, clinical data remain controversial.
The most abundant evidence supports primary prevention of AF in & rsquo; IC with ACE inhibitors and ARBs and postoperative AF with statins. At & rsquo; now, it n & rsquo; there is no
robust evidence to justify recommending the & rsquo; use of polyunsaturated fatty acids omega-3 for prevention, primary or secondary, FA.
X- Conclusion :
Atrial fibrillation is a common arrhythmia, whose incidence is steadily increasing. The management should be individualized based on patient characteristics. Clinical practice recommendations can guide the physician in decisions on treatment choice on the overall strategy, the terms cardioversion or thromboembolism prevention.
In complex cases, especially during failure of first-line treatments, the patient must be presented to a specialist (rythmologue).
Dr Bouchair's course – Faculty of Constantine