Abstract

This study hypothesized that paroxysmal atrial fibrillation (PAF) reflects the presence of a more severe cardiac hypertrophic cardiomyopathy (HCM) phenotype. HCM is characterized by myocyte hypertrophy, fibrosis, and a high prevalence of PAF. It is currently unresolved whether atrial fibrillation (AF) is a marker or a mediator of adverse outcomes in HCM. This study retrospectively examined 45 HCM patients who underwent cardiovascular magnetic resonance (CMR) imaging in sinus rhythm. The function of all 4 cardiac chambers was assessed, as well as late gadolinium enhancement (LGE) in the left atrium (LA) and left ventricle (LV), as indicators of fibrosis. A fat-saturated, 3-dimensional inversion recovery-prepared, fast-spoiled, gradient-recalled echo sequence, and the image intensity ratio method wereused to measure LA-LGE; LGE in the LV was quantified using a semi-automated threshold technique. HCM patients (n= 45) were divided into 2 groups (PAF, no AF) based on history of PAF. All HCM patients hadLGE in the LA posterior wall. The PAF group (n= 18) had higher LA volume, a lower LA ejection fraction, a lower global peak longitudinal LA strain (PLAS), and a higher amount of LA-LGE compared with the no AF group (n= 27). Amodest inverse association was noted between the LA ejection fraction, PLAS, and LA-LGE; a positive association was present between LV-LGE and LA-LGE. The PAF group had lower ejection fractions in the LV, right atrium, and right ventricle compared with those in the no AF group. PAF is associated with a greater degree of structural LA remodeling and global myopathy, whichsuggests a more severe cardiac HCM phenotype.

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