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Volume 23, Issue 5, Pages 538-544 (May 2010)


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Left Atrial Phasic Volumes Are Modulated by the Type Rather Than the Extent of Left Ventricular Hypertrophy

Suzanne Eshoo, MDaCorresponding Author Informationemail address, Chris Semsarian, MD, PhDbcd, David L. Ross, MDa, Liza Thomas, MD, PhDe

published online 12 March 2010.

Background

The aim of this study was to evaluate whether maximal left atrial (LA) volume and phasic atrial function would be further altered in patients with hypertrophic cardiomyopathy (HCM) compared with patients with systemic hypertension (HT) with similar left ventricular (LV) mass. LA enlargement on echocardiography has been documented in HCM and moderate or severe HT, both conditions causing LV hypertrophy.

Methods

Thirty-five patients with HCM were compared with patients with HT matched for LV mass and normal controls matched for age and gender. Maximal, minimal, and pre-“p” LA biplane and real-time 3-dimensional volumes and LA phasic function were evaluated. Atrial function was estimated by LA ejection force, atrial fraction, and A′ velocity.

Results

Maximal, minimal, and pre-“p” LA volumes were significantly increased in the HCM group compared with the HT group and controls. Additionally, LA phasic volumes demonstrated that conduit volume and total, passive, and active emptying fractions were decreased in the HCM group. Despite similar LV mass, the HCM group had a higher incidence of abnormal diastolic filling (60% vs 34%, P = .001).

Conclusions

Patients with HCM appeared to have larger LA volumes, poorer LA function, and greater severity of diastolic dysfunction compared with those with HT having comparable LV mass. LA changes may be due to coexistent atrial myopathy associated with other pathophysiologic aspects of HCM, including outflow obstruction, mitral regurgitation, and myocardial fibrosis in HCM.

a Westmead Hospital, University of Sydney, Sydney, Australia

b Faculty of Medicine, University of Sydney, Sydney, Australia

c Agnes Ginges Centre for Molecular Cardiology, Centenary Institute, Sydney, Australia

d Department of Cardiology, Royal Prince Alfred Hospital, Sydney, Australia

e Liverpool Hospital, University of New South Wales, Sydney, Australia

Corresponding Author InformationReprint requests: Suzanne Eshoo, MD, Westmead Hospital, Department of Cardiology, Darcy Road, Westmead, 2145, NSW, Australia.

PII: S0894-7317(10)00094-5

doi:10.1016/j.echo.2010.01.022


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