Independent of left ventricular mass, circulating inflammatory markers rather than pressure load are associated with

Gavin R Norton1, Vernice R Peterson1, Chanel Robinson1

  • 1Cardiovascular Pathophysiology and Genomics Research Unit, School of Physiology, Faculty of Health Sciences, University of the Witwatersrand, Johannesburg, South Africa.

Insights

Concentric left ventricular (LV) remodelling is linked to inflammation, not just blood pressure. This pro-inflammatory state is associated with LV remodelling independent of LV mass.

Area of Science:

  • Cardiology
  • Biomedical Science
  • Inflammation Research

Background:

  • Concentric left ventricular (LV) remodelling predicts cardiovascular outcomes, but the underlying mechanisms independent of LV mass (LVM) remain unclear.
  • This study investigated whether inflammation or pressure load is the primary driver of concentric LV remodelling.

Purpose of the Study:

  • To determine the association between inflammatory markers and concentric LV remodelling, independent of LV mass and blood pressure.
  • To elucidate the relationship between pro-inflammatory markers and cardiac structure.

Main Methods:

  • Assessed inflammatory markers (ELISA) in 764 community participants.
  • Measured LV relative wall thickness (RWT), LV mass index (LVMI), and diastolic function using echocardiography.
  • Analyzed associations between inflammatory markers, RWT, LVMI, and blood pressure, controlling for confounders.

Main Results:

  • Circulating tumor necrosis factor-α (TNF-α) and interleukin-6 were independently associated with LV relative wall thickness (RWT), independent of LV mass index (LVMI) and blood pressure.
  • The impact of TNF-α on RWT was comparable to age and second only to LVMI.
  • Increased TNF-α concentrations were observed in participants with concentric LV remodelling and concentric LV hypertrophy (LVH), but not eccentric LVH.

Conclusions:

  • A pro-inflammatory state, particularly elevated TNF-α, is strongly associated with LV concentric remodelling.
  • This association is independent of LV mass and blood pressure load, suggesting inflammation plays a key role in this cardiac adaptation.
Abstract

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