Biomedical Engineering Reference
In-Depth Information
3.1.2.2
Atrial Activity Extraction in Atrial Fibrillation
Atrial fibrillation (AF) is the sustained cardiac arrhythmia most often encountered in
clinical practice. Its incidence increases with age, and about 10 % of the population
over 70 years old is affected by the condition; this amounts to more than six
million people in Europe and the United States alone. AF accounts for about two
thirds of hospitalizations related to cardiac disturbances, and its cost to health-care
providers is estimated to around 3,000 euros per patient per year in the Western
world. AF patients usually complain of relatively minor symptoms like palpitations,
tiredness, dizziness or lack of breath, but the condition can also entail more serious
complications such as thrombo-embolic disorders. Indeed, AF is held responsible
for up to 20 % of cerebral vascular accidents (brain strokes), which often lead to
major impairment and even death [
11
].
Despite its incidence and risks of serious complications, the causes of AF are not
yet fully understood. Ectopic foci located around the pulmonary veins and reentrant
electrical pathways in the atrial myocardium due to the progressive shortening of
the atrial myocytes' refractory period are two of the most generally acknowledged
mechanisms behind the genesis and perpetuation of the disease. These mechanisms
result in several electrical depolarization wavefronts propagating in a disorganized
manner across the atria. This phenomenon is illustrated in Fig.
3.5
a, which shows
a 5-s segment recorded by a catheter-tip electrode on the atrial wall of a persistent
AF patient (data recorded at the Cardiology Department of Princess Grace Hospital,
Monaco). Such a catheter is typically inserted under sedation or general anesthesia
through the patient's femoral vein up to the right atrium prior to the ablation of atrial
tissue with radiofrequency energy [
12
]. Whereas endocardial bipolar recordings
in sinus rhythm are characterized by very short impulses synchronized with the
ventricular rate (Sect.
3.1.1
), local activations during AF spread out in time and are
no longer synchronized with the heartbeat, represented by the QRS complexes in the
ECG plot of Fig.
3.5
b. This disorganized electrical activation causes an inefficient
atrial contraction, so that the atria are said to quiver or fibrillate rather than beat. As
a result, blood ejection towards the ventricles is incomplete and stagnation in the
atria can easily generate thrombi.
Compared with endocardial recordings, the ECG presents the obvious advantage
of not requiring a catheter, and is thus a much more efficient procedure in terms of
time and cost, with practically no complications for the patient. Figure
3.5
bshows
the surface ECG signal recorded simultaneously in lead V1 from our persistent AF
patient. With an electrode very close to the right atrium (Fig.
3.2
), this lead records
atrial activity quite clearly. AF is characterized by the absence of P wave and the
presence of fibrillatory waves, or f waves, at about 200-500 cycles per minute
(around 3-9 Hz). The fibrillatory waves are visible in the TQ segments between
consecutive beats, as illustrated by the plot. This atrial activity signal is of particular
interest to cardiologists as it can provide useful noninvasive information about
the state and evolution of the disease. For instance, the dominant atrial frequency
(the inverse of the atrial cycle length) has been shown to correlate with the atrial
myocytes' refractory period and the probability of spontaneous cardioversion [
2
].
Unfortunately, the atrial signal is masked in both time and frequency domains by the
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