Abstract
> Form follows function—this has been misunderstood. Form and function should be one, joined in a spiritual union. > > —Frank Lloyd Wright Left atrial (LA) remodeling refers to the spectrum of pathophysiological changes in atrial structure and mechanical function and the electric, ionic, and molecular milieu of the LA that most often occurs in response to stresses imposed by conditions such as hypertension, heart failure, diabetes mellitus, and obesity. Remodeling is initially adaptive, but when it occurs in response to a chronic pathological stimulus (as opposed to remodeling of the athlete’s heart), it often becomes maladaptive and associated with an increased risk of cardiovascular events and mortality.1 Remodeling forms the basis of atrial cardiomyopathy, defined recently by a multisociety, expert consensus statement as any complex of structural, architectural, contractile, or electrophysiological changes affecting the atria with the potential to produce clinically relevant manifestations.2 See Article by Oliver et al LA structural remodeling is the complex phenotypic expression that results from changes in LA size, shape,3 and architecture and alterations in the cardiomyocyte, fibroblast, and noncollagen infiltrative compartments of the atrium.2 LA enlargement, which is simple to measure, is the default clinical hallmark of structural remodeling that occurs most often in response to LA pressure and volume overload; in the absence of atrial fibrillation, mitral valvular disease, and high cardiac output states, it is an excellent biomarker for the presence and severity of left ventricular (LV) diastolic dysfunction.4 Moreover, LA enlargement portends a poor prognosis in a variety of cardiovascular diseases.1 Indices of LA size are also markers of cardiovascular risk in the general population.5,6 The strength of the association between atrial remodeling as determined by increased maximal indexed LA volume (LAVi) and cardiovascular risk reported in the literature is influenced by the nature …
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