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C-reactive protein and P-wave in hypertensive patients after conversion of atrial fibrillation

Andrea Mazza1, Maria G Bendini, Marco Cristofori

  • 1Cardiology Division, Santa Maria della Stella Hospital, Orvieto, Italy.

Journal of Cardiovascular Medicine (Hagerstown, Md.)
|March 24, 2012
PubMed

Insights

High-sensitivity C-reactive protein (hs-C-reactive protein) is linked to prolonged P-wave duration and dispersion in hypertensive patients post-atrial fibrillation conversion. This suggests subclinical inflammation may impact atrial activation.

Area of Science:

  • Cardiology
  • Electrophysiology
  • Inflammation Markers

Background:

  • Atrial fibrillation recurrence is a clinical concern.
  • P-wave duration and dispersion are ECG markers of atrial activation.
  • High-sensitivity C-reactive protein (hs-C-reactive protein) is an inflammation marker.

Purpose of the Study:

  • To investigate the association between hs-C-reactive protein and P-wave parameters (P maximum/P dispersion) in hypertensive patients after atrial fibrillation conversion.
  • To determine if hs-C-reactive protein can predict delayed or inhomogeneous atrial activation.

Main Methods:

  • 92 hypertensive patients undergoing cardioversion for atrial fibrillation were enrolled.
  • Hs-C-reactive protein levels were measured before cardioversion.
  • 12-lead ECGs were recorded immediately after sinus rhythm restoration to assess P-wave duration and dispersion.

Main Results:

  • Elevated hs-C-reactive protein (>0.30 mg/dl) was significantly associated with increased P maximum (>120 ms) and P dispersion (>40 ms) in univariate and multivariate analyses.
  • Male sex was also associated with increased P maximum.
  • Hs-C-reactive protein was the sole predictor for increased P dispersion in multivariate analysis.

Conclusions:

  • Hs-C-reactive protein is associated with prolonged P-wave duration and dispersion in hypertensive patients post-atrial fibrillation conversion.
  • Subclinical inflammation, indicated by hs-C-reactive protein, may contribute to delayed and inhomogeneous atrial activation in these patients.
  • These findings highlight the potential role of inflammation in atrial remodeling and dysfunction.
Abstract

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