[Atrail fibrillation and heart failure: a complex relationship].
Atrial fibrillation (AF) and heart failure (HF) often coexist in the same patient, not only because they can result from the same heart disease, but also because each of them can directly lead to the other. In the genesis of AF, structural, electrical and functional factors share a key role, but the importance of any of them is variable, according to the different clinical situations. AF causes atrial changes, electrical, anatomical or both, that can result in maintenance, recurrence and even irreversibility of the arrhythmia. In addition, AF affects the ventricular function by: a) loss of atrioventricular synchrony; b) irregular ventricular response; c) rapid ventricular response, possibly leading to tachycardia-induced cardiomyopathy. AF, thus, can "beget" HF, even in subjects with a previously normal heart. On the other hand, HF often "begets" AF. The prevalence of AF in patients with HF, indeed, increases from 5% (NYHA class I) to 50% (NYHA class IV). The mechanisms of HF-induced AF, include: a) increase of "critical atrial mass"; b) atrial stretch, with mechanoelectrical feedback; c) neuroendocrine changes; and d) extracellular matrix fibrosis. In brief, there is an important association between HF and development of AF and vice versa. AF-induced prognosis worsening of HF patients is not always true: in advanced HF, thus, no evidence has been obtained that the arrhythmia is associated with a decreased survival. This observation, as well as the lesson from "rhythm" versus "rate" control clinical trials, can help the management of AF in HF. The so-called "non channel target therapy" could be of value in this context.
Costantini
Marcello
M
U.O. di Cardiologia, Ospedale S. Caterina Novella, Azienda USL LE/1, Galatina (LE). marcellocostantini@virgilio.it
Ranieri
Anna Teresa
AT
Fachechi
Claudio
C
Tritto
Cristina
C
Sticchi
Gianni
G
D001281:Atrial Fibrillation / Q000150:complications* / Q000209:etiology; D006333:Heart Failure / Q000150:complications* / Q000209:etiology; D006801:Humans; D011379:Prognosis