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Heart failure with preserved ejection fraction (HFpEF) is not one single disease but a syndrome composed of multiple pathophysiologic mechanisms.1,2 The assortment of underlying causes of HFpEF and its consequential phenotypic diversity is what makes this syndrome so unique and, unfortunately, so difficult to treat. Despite the heterogeneity of HFpEF, a common thread exists. Regardless of the predominate subtype of HFpEF, the left atrium (LA) plays a central role in the underlying disease process and the symptoms that result from it.See Article by von Roeder et al Multiple studies have shown the diagnostic and prognostic importance of LA size and pressure in HFpEF.3–6 Beyond these parameters, echocardiographic speckle-tracking strain has made it possible to noninvasively measure the functional components of the LA, including reservoir, conduit, and contractile (booster) strain. LA reservoir strain, in particular, has strong prognostic value in HFpEF, and outperforms left ventricular (LV) and right ventricular longitudinal strain in this regard.7 The mechanistic insight gained from evaluating LA mechanics in patients with HFpEF has created a paradigm shift in our thinking of this chamber. It appears that the LA is not simply being a passive marker of disease severity—it is a critical, active component of the HFpEF syndrome. Indeed, in the setting of HFpEF, reduced LA strain (indicative of intrinsic LA mechanical dysfunction) is a major driver of both elevated pulmonary vascular resistance and decreased peak oxygen consumption (Vo2) on cardiopulmonary exercise testing, which leads to exercise intolerance and adverse outcomes (Figure 1).7Figure 1. The central role of the left atrium (LA) in the pathogenesis of heart failure with preserved ejection fraction (HFpEF). Left ventricular (LV) diastolic dysfunction, LA fibrosis, atrial fibrillation, and primary LA myopathy can all contribute to abnormal LA mechanics in HFpEF, which can …

Stepping Out of the Left Ventricle’s Shadow