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Valvular heart disease
Original research article
Higher left ventricular mass–wall stress–heart rate product and outcome in aortic valve stenosis
  1. Eva Gerdts1,
  2. Sahrai Saeed2,
  3. Helga Midtbø2,
  4. Anne Rossebø3,
  5. John Boyd Chambers4,
  6. Eigir Einarsen5,
  7. Edda Bahlmann6,
  8. Richard Devereux7
  1. 1 Department of Clinical Science, University of Bergen, Bergen, Norway
  2. 2 Department of Heart Disease, Haukeland Universitetssjukehus, Bergen, Norway
  3. 3 Cardiology Department, Oslo University Hospital, Ullevål, Norway
  4. 4 Guys and St Thomas Hospital, London, UK
  5. 5 Department of Clinical Science, University of Bergen, Bergen, Hordaland, Norway
  6. 6 Cardiology, Asklepios Clinic St. Georg, Hamburg, Germany
  7. 7 NewYork-Presbyterian Hospital/Weill Cornell Medical Center, New York, New York, USA
  1. Correspondence to Professor Eva Gerdts, Department of Clinical Science, University of Bergen, Bergen 5020, Norway; Eva.Gerdts{at}med.uib.no

Abstract

Objective Whether increased myocardial oxygen demand could help explain the association of left ventricular (LV) hypertrophy with higher adverse event rate in patients with aortic valve stenosis (AS) is unknown.

Methods Data from 1522 patients with asymptomatic mostly moderate AS participating in the Simvastatin-Ezetimibe in AS study followed for a median of 4.3 years was used. High LV mass–wall stress–heart rate product was identified as >upper 95% CI limit in normal subjects. The association of higher LV mass–wall stress–heart rate product with major cardiovascular (CV) events, combined CV death and hospitalised heart failure and all-cause mortality was tested in Cox regression analyses, and reported as HR and 95% CI.

Results High LV mass–wall stress–heart rate product was found in 19% at baseline, and associated with male sex, higher body mass index, hypertension, LV hypertrophy, more severe AS and lower LV ejection fraction (all p<0.01). Adjusting for these confounders in time-varying Cox regression analysis, 1 SD higher LV mass–wall stress–heart rate product was associated with higher HR of major CV events (HR 1.16(95% CI 1.06 to 1.29)), combined CV death and hospitalised heart failure (HR 1.29(95% CI 1.09 to 1.54)) and all-cause mortality (HR 1.34(95% CI 1.13 to 1.58), all p<0.01).

Conclusion In patients with initially mild–moderate AS, higher LV mass–wall stress–heart rate product was associated with higher mortality and heart failure hospitalisation. Our results suggest that higher myocardial oxygen demand is contributing to the higher adverse event rate reported in AS patients with LV hypertrophy.

Trial registration number NCT000092677;Post-results.

  • aortic stenosis
  • hypertension
  • echocardiography

This is an open access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited, appropriate credit is given, any changes made indicated, and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/.

https://doi.org/10.1136/heartjnl-2018-314462

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    Footnotes

    • Contributors EG and RD contributed to the conception and design of the work, analysis and interpretation of data and drafting and critical revision of the work. SS, HM, AR, JBC, EE and EB contributed to data collection and critical revision of the work. All authors gave final approval of the version published and agree to be accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved.

    • Funding The SEAS echocardiography core laboratory was supported by the MSP Singapore Company, LLC, Singapore, a partnership between Merck & Co., and the Schering-Plough Corporation during study conduct from 2002 to 2008.

    • Competing interests None declared.

    • Ethics approval The SEAS study was approved by ethical committees in all study centres.

    • Provenance and peer review Not commissioned; externally peer reviewed.

    • Patient consent for publication Not required.