Sanjay Sivalokanathan1, Tarek Zghaib2, Gabriela V Greenland3, Nestor Vasquez1, Shibani M Kudchadkar1, Effrosyni Kontari1, Dai-Yin Lu1, Ketty Dolores-Cerna4, Rob J van der Geest5, Ihab R Kamel1, Jeffrey E Olgin6, Theodore P Abraham3, Saman Nazarian7, Stefan L Zimmerman8, M Roselle Abraham9. 1. Hypertrophic Cardiomyopathy Center of Excellence, Johns Hopkins University, Baltimore, Maryland. 2. Hypertrophic Cardiomyopathy Center of Excellence, Johns Hopkins University, Baltimore, Maryland; Department of Radiology, Johns Hopkins School of Medicine, Baltimore, Maryland. 3. Hypertrophic Cardiomyopathy Center of Excellence, Johns Hopkins University, Baltimore, Maryland; Division of Cardiology, University of California San Francisco, San Francisco, California. 4. Department of Statistics, Cayetano Heredia University, Lima, Peru. 5. Leiden University Medical Center, Leiden, the Netherlands. 6. Division of Cardiology, University of California San Francisco, San Francisco, California. 7. Division of Cardiology, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania. 8. Department of Radiology, Johns Hopkins School of Medicine, Baltimore, Maryland. 9. Hypertrophic Cardiomyopathy Center of Excellence, Johns Hopkins University, Baltimore, Maryland; Division of Cardiology, University of California San Francisco, San Francisco, California. Electronic address: Roselle.Abraham@ucsf.edu.
Abstract
OBJECTIVES: This study hypothesized that paroxysmal atrial fibrillation (PAF) reflects the presence of a more severe cardiac hypertrophic cardiomyopathy (HCM) phenotype. BACKGROUND: 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. METHODS: 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 were used to measure LA-LGE; LGE in the LV was quantified using a semi-automated threshold technique. RESULTS: HCM patients (n = 45) were divided into 2 groups (PAF, no AF) based on history of PAF. All HCM patients had LGE 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). A modest 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. CONCLUSIONS: PAF is associated with a greater degree of structural LA remodeling and global myopathy, which suggests a more severe cardiac HCM phenotype.
OBJECTIVES: This study hypothesized that paroxysmal atrial fibrillation (PAF) reflects the presence of a more severe cardiac hypertrophic cardiomyopathy (HCM) phenotype. BACKGROUND: 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. METHODS: 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 were used to measure LA-LGE; LGE in the LV was quantified using a semi-automated threshold technique. RESULTS: HCM patients (n = 45) were divided into 2 groups (PAF, no AF) based on history of PAF. All HCM patients had LGE 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). A modest 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. CONCLUSIONS: PAF is associated with a greater degree of structural LA remodeling and global myopathy, which suggests a more severe cardiac HCM phenotype.
Keywords:
cardiovascular magnetic resonance imaging; hypertrophic cardiomyopathy; late gadolinium enhancement in the left atrium; paroxysmal atrial fibrillation
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