Atrial Electrical and Structural Changes Associated with Longstanding Hypertension in Humans: Implications for the Substrate for Atrial Fibrillation

Authors

  • CAROLINE MEDI B.MeD.,

    1. the Department of Cardiology, Alfred Hospital and Baker IDI, Melbourne, Australia
    2. Department of Cardiology, Royal Melbourne Hospital, Melbourne, Australia
    3. Department of Medicine, University of Melbourne, Melbourne, Australia
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  • JONATHAN M. KALMAN M.B.B.S., Ph.D., F.A.C.C.,

    1. Department of Cardiology, Royal Melbourne Hospital, Melbourne, Australia
    2. Department of Medicine, University of Melbourne, Melbourne, Australia
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  • STEVEN J. SPENCE A.C.C.T.,

    1. Department of Cardiology, Royal Melbourne Hospital, Melbourne, Australia
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  • ANDREW W. TEH M.B.B.S.,

    1. the Department of Cardiology, Alfred Hospital and Baker IDI, Melbourne, Australia
    2. Department of Cardiology, Royal Melbourne Hospital, Melbourne, Australia
    3. Department of Medicine, University of Melbourne, Melbourne, Australia
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  • GEOFFREY LEE M.B., Ch.B.,

    1. the Department of Cardiology, Alfred Hospital and Baker IDI, Melbourne, Australia
    2. Department of Cardiology, Royal Melbourne Hospital, Melbourne, Australia
    3. Department of Medicine, University of Melbourne, Melbourne, Australia
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  • ILONA BADER R.N.,

    1. the Department of Cardiology, Alfred Hospital and Baker IDI, Melbourne, Australia
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  • DAVID M. KAYE M.D., Ph.D.,

    1. the Department of Cardiology, Alfred Hospital and Baker IDI, Melbourne, Australia
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  • PETER M. KISTLER M.B.B.S., Ph.D.

    1. the Department of Cardiology, Alfred Hospital and Baker IDI, Melbourne, Australia
    2. Department of Cardiology, Royal Melbourne Hospital, Melbourne, Australia
    3. Department of Medicine, University of Melbourne, Melbourne, Australia
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  • This study was supported by a grant in aid from the National Heart Foundation. Dr. Medi is supported by a medical postgraduate scholarship from the National Heart Foundation of Australia (NHFA). Dr. Teh is supported by a medical postgraduate scholarship from the National Health and Medical Research Council (NHMRC) of Australia. Prof. Kistler is supported by Research Investigatorship from the Cardiac Society of Australia and New Zealand.

  • Dr. Teh is the recipient of a cardiovascular and lipid research grant from Pfizer. Other authors: No disclosures.

Peter Kistler, M.B.B.S., Ph.D., F.R.A.C.P., Baker IDI Heart & Diabetes Institute, 75 Commercial Road, Melbourne, VIC 3004. Fax: 61-03-9076-2461; E-mail: peter.kistler@bakeridi.edu.au

Abstract

Atrial Remodeling in Human HypertensionIntroduction: Hypertension (HT) is the most common modifiable risk factor for atrial fibrillation (AF), yet little is known of the atrial effects of chronic HT in humans. We aimed to characterize the electrophysiologic (EP) and electroanatomic (EA) remodeling of the right atrium (RA) in patients with chronically treated systemic HT and left ventricular hypertrophy (LVH) without a history of AF.

Methods and Results: Twenty patients with (systolic BP 145 ± 10 mmHg) and without (BP 119 ± 11 mmHg, P < 0.01) systemic HT underwent detailed conventional EP and EA voltage and activation mapping. We measured RA refractoriness at the coronary sinus and high septum at cycle lengths (CLs) 600 and 450 ms, and RA conduction velocities, activation times, and voltages at a global and regional level at CLs 600 ms and 300 ms. HT was associated with slowing of global (73 ± 17 cm/s vs 96 ± 12 cm/s in controls, P < 0.01) and regional conduction velocity particularly in the posterior RA (70 ± 17 cm/s vs 96 ± 12 cm/s in controls, P < 0.01) at the crista terminalis (fractionation and double potentials in HT 72%± 4 vs 43%± 23 in controls, P = 0.04). Mean RA voltage was similar between the 2 groups, however HT was associated with an increase in areas of low voltage (<0.5 mV; HT 13% vs controls 9%, P = 0.04). Sustained AF was induced in 30% HT patients and no controls.

Conclusion: Chronically treated systemic HT with LVH is accompanied by atrial remodeling characterized by: (i) global conduction slowing, (ii) regional conduction delay particularly at the crista terminalis, and (iii) increased AF inducibility. These changes may in part be responsible for the increased propensity to AF associated with systemic HT. (J Cardiovasc Electrophysiol, Vol. 22, pp. 1317-1324, December 2011)

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