notes by dr Claudio Italiano
The information contained in this page is not intended to give any knowledge about the real treatment of a patient who is always a medical act, decided from time to time on the patient's clinical condition and is a very delicate moment. It's about personal therapeutic reflections
Atrial fibrillation (AF) is the most commonly reported arrhythmia in clinical practice: 5% in the
population over 65 in the Cardiovascul Health Study. The prevalence and
incidence of AF increase progressively with age, to reach a percentage of 8.8%
of subjects aged over 80 years. Structural cardiopathy and arterial
hypertension is present in 80-90% of cases. Moreover it correlates generally
with the enlargement of the left atrium, so it is associated with rheumatic
valvulopathy.
It is still associated with the following pathologies:
— Hyperthyroidism by action of hormones on the specific myocardium
— Rheumatic and non-rheumatic valvulopathy, especially v. mitral
— Hypertension
— Cerebral vasculopathy (ictus cerebri)
— Diabetes mellitus
The classification of F.A. it is the so-called temporal one, proposed by
Gallagher and Camm in 1988. It allows to distinguish:
FA paroxysmal, which means episodes of fibrillation that occur suddenly and
regress in 24-48 hours
FA persistent (interruption only with therapeutic interventions
FA permanent or chronic (where cardioversion operations at sinus rhythm (ecg)
have failed and are not indicated at all?
But which therapy to implement in a fibrillating patient?
Is it necessary to treat it or not?
The question arises spontaneously but the answer is complex because the doctor
needs to know:
— The age of the patient and his condition
— The duration of arrhythmia, the onset of the first episode and when it
occurred
— If the FA form is paroxysmal, persistent or chronic
— If the FA responds to anti-arrhythmic drugs
— The coexistence of a heart disease
— If the patient is hyperthyroid (hyperthyroidism) or alcohol abuse (alcohol
addiction)
At this point the patient must be followed and monitored or, at least, must perform an ecg, and must be studied P waves and fibrillation waves, the possible presence of left ventricular hypertrophy marks, if there is a left bundle branch block (ecg2), if there is a pre-excitation, if there has been a previous heart attack and if the heart rate is high, in which case we must also intervene in this sense, that is to reduce it. Finally, the QRS complexes and the QT interval at the track during treatment should be monitored. It is also indicated to perform a standard chest X-ray examination (chest x-ray) to evaluate whether there is a pulmonary parenchyma injury or a circulatory overload. An echocardiographic investigation to evaluate atrial wall hypertrophy, atrial valvulopathy, atrial thrombosis (see tao and thromboembolic disease). In addition, thyroid function tests give us an idea of any problems related to the situation of hyperthyroidism (hyperthyroidism), where the frequency of the ventricle is difficult to control in these situations and the arrhythmia (arrhythmias) occurs frequently.
So, in summary, what to do?
Treatment of an AF uses first of all the control of thromboembolic risk (cf.
tao and thromboembolic risk) and the restoration of sinus rhythm (ecg) which
is not always indicated. In fact, if it is often correct for a patient to
maintain sinus rhythm it is also true that if a patient enters and exits this
arrhythmia, he risks thromboembolism and, therefore, the stroke more than if
it remains in atrial fibrillation. This is due to the fact that when the
atrium starts functioning again, ie during the restoration of sinus rhythm, it
happens that the coagulated blood contained within the left atrial
appendage can be put
back into circulation and sent to the brain. Because? Because in the FA it is
as if the atria were paralyzed and the blood therefore stagnating in the
left atrial appendage, which are like some sort of "pockets" in the atrium wall, in fact it
becomes coagulated.
Hence the categorical need to carry out a therapy with low molecular weight
heparins, or at least an antiplatelet therapy (aspirin) but there isn't
evidence for this treatment into prevention of cardioembolic risk. For this
reason it's better to use the
therapy with oral anticoagulants (tao). Before deciding whether to restore and
then maintain the Sinus Rhythm, ie that of the sinus node, the physiological
one, it is important to know whether there is any chance of success in
maintaining this rhythm, with antiarrhythmic prophylaxis and patient
compliance. The predictors of relapse are the following:
• Subjects already treated in electrical cardioversion with FA recurrence
• Subjects in atrial fibrillation for more than 36 months
• Subjects in NYHA class III or IV,
• Subjects with left atrial dilatation> 60 mm
• Subjects with mitral valvulopathy and cardiomegaly
• Subjects NOT responsive to antiarrhythmic therapy
• Subjects who have more than 12 episodes / year
• Subjects in fibrillation for more than 4 years•
Another point to eviscerate is if it is correct to restore the rhythm in each
case or not; recent studies have shown that it is not necessary to restore it
anyway (AFFIRM study)• However, in any case, in the young patient with an
episode of paroxysmal fibrillation it is good to intervene with arrhythmia
control therapy, but if the repetition does not seem necessary to prescribe
any antiarrhythmic drug (ACC / AHA / ESC guidelines) even if the common sense
believes that it is appropriate in all young people to take all measures to
restore sinus rhythm, including electrical cardioversion and radio-ablation of
the conduction bundle that generates the mechanism of re-entry, the mechanism
by which a stimulus "turns" to infinity in the conduction tissue and excites
the ventricles in a chaotic manner• For subjects with chronic atrial
fibrillation, the control of only the heart rate is indicated and sufficient,
with drugs such as non-dihydropyridine calcium antagonists and beta-blockers
as well as digital• However, the use of amiodarone, again in non-thyreopathic
subjects, is indicated in the restoration of sinus rhythm, as is
hydroquinidine•
The treatment of acute AF within 48 hours includes:
Cardioversion with propafenone and flecainide, antiarrhythmics class IC, which
is very effective therapy, both intravenously and orally and is ALWAYS
contraindicated, however, in the patient with ventricular dysfunction (heart
failure) due to the negative inotropic effect of the drug that aggravates pump
failure and the same applies to subjects with bradycardia or with BAV II and
BAV III or sinus node disease• Furthermore there is a risk that a F•A• turn
into atrial flutter, far more dangerous for high ventricular response• Some
authors believe that oral loading of 300 mg single dose phycoinide or
propafenone 600 mg single dose is sufficient to restore sinus rhythm• The
quinidine, once very used, antiarrhythmic class IA, in patients with FA of
recent onset, at the dosage of 200 mg every 2 hours up to a maximum of 1200 mg
causes slowing of the conduction speed but is associated with the phenomenon
of long QT which can generate an ugly arrhythmia called "tip torsion", ie real
episodes of ventricular tachycardia• Therefore today it is almost abandoned in
use• Amiodarone, antiarrhythm in class III, is used in FA recently onset at a
dosage of 150 mg iv in 10 minutes followed by 360 mg in 6 hours plus 540 in
the following 24 hours• Sotalol, on the other hand, was less effective•
Digital and calcionatagonists (diltiazem and verapamil) are used only to
correct the frequency•
Treatment of AF: the reported dosages are intended as guidelines and always
under the supervision and responsibility of the doctor who practices them and
is reduced in the case of particularly sensitive or underweight patients•
Medication e•v• - Bolus - maintenance speed - effectiveness in%
Propafenone: 1•5-2 mg / kg in 10-20 '- maintenance at 2 mg / min - 80-90%
Flecainide: 1•5-3 mg / kg in 10 '- maintenance 0•15-0•25 mg / kg / h - 80-90%
Amiodarone: 150 mg in 10 '- maintenance at 360 mg / 6 hours - 540 mg / 18 -
900 mg / 24 hours - 42-92%
Drug for os
Propafenone: 500 mg single dose - maintenance at 400-600 mg / day - 75%
Flecainide: 300 mg single dose - 150-300 mg / day - 75%
Other therapy
Left atrial appendage occlusion (LAAO), also referred to as Left atrial
appendage closure (LAAC) is a treatment strategy to reduce the risk of left
atrial appendage blood clots from entering the bloodstream and causing a stroke
in patients with non-valvular atrial fibrillation (AF)•
In non-valvular AF, over 90% of stroke-causing clots that come from the heart
are formed in the left atrial appendage• The most common treatment for AF stroke
risk is treatment with blood-thinning medications, also called oral
anticoagulants, which reduce the chance for blood clots to form• These
medications (which include warfarin, and other newer approved blood thinners)
are very effective in lowering the risk of stroke in AF patients• Most patients
can safely take these medications for years (and even decades) without serious
side effects•
However, some patients find that blood thinning medications can be difficult to
tolerate or are risky• Because they prevent blood clots by thinning the blood,
blood thinners can increase the risk of bleeding problems• In select patients,
physicians determine that an alternative to blood thinners is needed to reduce
AF stroke risk• Approximately 45% of patients who are eligible for warfarin are
not being treated, due to tolerance or adherence issues•[2] This applies
particularly to the elderly, although studies have indicated that they can also
benefit from anticoagulants•
Left atrial appendage closure is an implant-based alternative to blood thinners•
Like blood thinning medications, an LAAC implant does not cure AF• A stroke can
be due to factors not related to a clot traveling to the brain from the left
atrium• Other causes of stroke can include high blood pressure and narrowing of
the blood vessels to the brain• An LAAC implant will not prevent these other
causes of stroke•