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Published on: September 17, 2014
Inflammation and Atrial Electrical Remodelling in Patients With Embolic Strokes of Undetermined Source
Maurizio Acampa1, Pietro Enea Lazzerini2, Francesca Guideri1
1Stroke Unit, Department of Neurological and Sensorineural Sciences, Azienda Ospedaliera Universitaria Senese, "Santa Maria alle Scotte" General Hospital, Siena, Italy.
Insights
Systemic inflammation, indicated by high-sensitive C-reactive protein (hsCRP), is linked to increased P wave dispersion (PWD) in patients with embolic strokes of undetermined source (ESUS). This suggests inflammation may contribute to atrial electrical remodeling and elevate atrial fibrillation risk.
Area of Science:
- Cardiology
- Neurology
- Biochemistry
Background:
- Embolic strokes of undetermined source (ESUS) constitute approximately one-third of all ischemic strokes.
- Silent atrial fibrillation (AF) is a potential cause of ESUS, with P wave dispersion (PWD) on ECG as a predictor of paroxysmal AF.
- Inflammation, measured by high-sensitive C-reactive protein (hsCRP), is associated with AF development and persistence, potentially through atrial remodeling.
Purpose of the Study:
- To investigate the relationship between P wave dispersion (PWD) and high-sensitive C-reactive protein (hsCRP) in patients diagnosed with ESUS.
- To explore the potential role of inflammation in atrial electrical remodeling that predisposes to AF in ESUS patients.
Main Methods:
- 174 patients with ESUS underwent neuroimaging, arterial ultrasound, echocardiography, and ECG.
- P wave dispersion (PWD) and hsCRP levels were measured in all participants.
- Statistical analysis, including Spearman correlation, was used to assess the relationship between hsCRP and PWD.
Main Results:
- A significant positive correlation was observed between hsCRP and PWD (Spearman r: 0.35, p<0.0001).
- Patients with high PWD (>40 msec) exhibited hsCRP levels three-fold higher than those with normal PWD (≤40 msec).
- Elevated hsCRP was significantly associated with higher PWD in the ESUS cohort (1.57±2.9 mg/dl vs 0.42±0.4 mg/dl, p=0.0005).
Conclusions:
- The study found elevated hsCRP levels in ESUS patients with high PWD, indicating a link between inflammation and atrial electrical changes.
- These findings support the hypothesis that systemic inflammation contributes to atrial electrical remodeling in a subset of ESUS patients.
- This inflammatory pathway may increase the risk of developing AF in patients with embolic strokes of undetermined source.
Background:
About one third of ischaemic strokes are classified as embolic strokes of undetermined source (ESUS). A silent atrial fibrillation (AF) may play a pathogenic role in these strokes and P wave dispersion (PWD), representing an electrocardiographic (ECG) predictor for paroxysmal AF, thereby a potential marker of covert cardioembolism, was found to be increased in cryptogenic stroke. Furthermore, current evidence links AF to inflammation: inflammatory markers, such as high-sensitive C-reactive protein (hsCRP), have been related to the development and persistence of AF, possibly by promoting atrial remodelling. The aim of this study was to evaluate whether a relationship between PWD and hsCRP in patients with ESUS exists, in order to highlight a possible role for inflammation in the atrial electric remodelling, that predisposes to AF.
Methods:
We enrolled 174 patients (91 males, 83 females; mean age 69±13years) with ESUS. All patients underwent neuroimaging examination, arterial ultrasound examination, echocardiography and ECG. P wave dispersion and hsCRP were measured in all subjects.
Results:
A significant positive correlation was found between hsCRP and PWD (Spearman r: 0.35, p<0.0001). In patients with high PWD (>40 msec; n=102), hsCRP was three-fold higher than in patients with normal PWD (≤40 msec; n=72)(1.57±2.9 vs 0.42±0.4mg/dl, p=0.0005).
Conclusions:
Our results show increased hsCRP levels in cryptogenic stroke patients with high PWD. These findings provide support for the hypothesis that systemic inflammation plays a role in a fraction of patients with ESUS, by increasing AF risk via atrial electric remodelling.
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