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Does cardiac resynchronization therapy restore peripheral circulatory homeostasis?

Chukwudiebube N Ajaero1,2,3, Cher-Rin Chong4,5, Nathan E K Procter6

  • 1The Queen Elizabeth Hospital, Adelaide, Australia.

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|October 15, 2017
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Summary

Cardiac resynchronization therapy (CRT) improves heart function, but not through changes in nitric oxide (NO) signaling. However, reduced inflammation after CRT predicts better clinical outcomes in heart failure patients.

Keywords:
Augmentation index (AIX)Cardiac resynchronisation therapy (CRT)Left ventricular dyssynchronyNitric oxide (NO) signallingSymmetric dimethylarginine (SDMA)Thioredoxin-interacting protein (TXNIP)

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Area of Science:

  • Cardiology
  • Vascular Biology
  • Heart Failure Management

Background:

  • Cardiac resynchronization therapy (CRT) is a treatment for heart failure.
  • Peripheral circulatory remodeling and nitric oxide (NO) signaling are potential mechanisms for CRT response.
  • Understanding these mechanisms can optimize CRT efficacy.

Purpose of the Study:

  • To investigate if peripheral circulatory remodeling, specifically vascular compliance and NO signaling markers, influences patient response to CRT.
  • To evaluate changes in various physiological and biochemical markers before and after CRT.

Main Methods:

  • Assessed clinical parameters (peak oxygen consumption, 6-minute walk distance, NYHA class, quality of life) and echocardiographic data in 33 patients pre- and 6-months post-CRT.
  • Measured augmentation index, platelet NO responsiveness, thioredoxin-interacting protein, N-terminal proBNP, SDMA, hs-CRP, catecholamines, and MMPs.

Main Results:

  • CRT significantly improved clinical and echocardiographic parameters.
  • No significant changes were observed in augmentation index, platelet NO response, or thioredoxin-interacting protein.
  • N-terminal proBNP and SDMA levels decreased significantly post-CRT.
  • Reduced SDMA correlated with decreased hs-CRP and increased peak oxygen consumption.

Conclusions:

  • The beneficial effects of CRT are not mediated by changes in peripheral NO-related signaling.
  • CRT leads to suppression of inflammation, and the extent of this suppression predicts clinical improvement.
  • Peripheral vascular remodeling does not appear to be the primary driver of CRT benefits.