Metabolism - Clinical and Experimental
Volume 59, Issue 2 , Pages 159-165, February 2010

Increased left ventricular arrhythmogenicity in metabolic syndrome and relationship with myocardial performance, risk factors for atherosclerosis, and low-grade inflammation

  • Christina Voulgari

      Affiliations

    • First Department of Propaedeutic Medicine, Laiko General Hospital, Athens University Medical School, Athens 115 27, Greece
  • ,
  • Nicholas Tentolouris

      Affiliations

    • First Department of Propaedeutic Medicine, Laiko General Hospital, Athens University Medical School, Athens 115 27, Greece
    • Corresponding Author InformationCorresponding author. Tel.: +30 210 745 6448; fax: +30 210 746 2640.
  • ,
  • Dimitrios Papadogiannis

      Affiliations

    • First Department of Propaedeutic Medicine, Laiko General Hospital, Athens University Medical School, Athens 115 27, Greece
  • ,
  • Ioannis Moyssakis

      Affiliations

    • Cardiology Department, Laiko General Hospital, Athens 115 27, Greece
  • ,
  • Despoina Perrea

      Affiliations

    • Laboratory for Experimental Surgery and Surgical Research, Athens University Medical School, Athens 115 27, Greece
  • ,
  • Despoina Kyriaki

      Affiliations

    • First Department of Propaedeutic Medicine, Laiko General Hospital, Athens University Medical School, Athens 115 27, Greece
  • ,
  • Nicholas Katsilambros

      Affiliations

    • First Department of Propaedeutic Medicine, Laiko General Hospital, Athens University Medical School, Athens 115 27, Greece

Received 24 November 2008; accepted 19 June 2009. published online 22 September 2009.

Abstract 

Metabolic syndrome (MetS) is a clustering of cardiovascular risk factors recently associated with left ventricular dysfunction. Limited data exist on the association between MetS and ventricular arrhythmogenicity. This study examined differences in ventricular arrhythmogenicity assessed by classic (QT interval) and newer (spatial QRS-T angle [spQRS-Ta]) electrocardiographic markers in subjects with and without MetS. A total of 306 subjects, 153 with and 153 without MetS, matched for sex and age were examined. The spQRS-Ta, which vectorcardiographically quantifies the deviation between the directions of ventricular depolarization and repolarization, was measured using a computer-based electrocardiograph. Left ventricular mass index and myocardial performance were evaluated echocardiographically. The spQRS-Ta was significantly higher in subjects with in comparison with those without MetS. Left ventricular mass index, QT interval, and its dispersion were not different between the 2 groups. Left ventricular myocardial performance was worse in subjects with MetS and was associated with higher values of the spQRS-Ta. Multivariate linear regression analysis demonstrated MetS status as the strongest predictor of ventricular arrhythmogenicity. Addition of the high-sensitivity C-reactive protein in the model increased the explained variance of the spQRS-Ta by 11%. In conclusion, ventricular arrhythmogenicity is present in MetS and is associated with myocardial dysfunction, risk factors for atherosclerosis, and low-grade inflammation. The independent association between the spQRS-Ta and MetS implies that the clustering of the metabolic disturbances has additional prognostic information than its individual components in terms of ventricular arrhythmogenicity and may explain in part the excess cardiovascular risk in subjects with MetS.

To access this article, please choose from the options below

Login to an existing account or Register a new account.

  • Purchase this article for 31.50 USD (You must login/register to purchase this article)

    Online access for 24 hours. The PDF version can be downloaded as your permanent record.

  • Subscribe to this title

    Get unlimited online access to this article and all other articles in this title 24/7 for one year.

  • Claim access now

    For current subscribers with Society Membership or Account Number.

  • Visit SciVerse ScienceDirect to see if you have access via your institution.
 

PII: S0026-0495(09)00298-4

doi:10.1016/j.metabol.2009.06.028

Metabolism - Clinical and Experimental
Volume 59, Issue 2 , Pages 159-165, February 2010