Role of inflammation in atrial fibrillation: specific biomarkers of tissue damage, atrial remodelling and dysregulation of angiogenesis

The relationship between inflammation and atrial fibrillation (AF) has been poorly studied with common inflammatory markers and limited to analysing one or two markers. Given the large number of pathways in the inflammatory process and the complexity of their relationship with AF, we set out to study a broad panel of more specific biomarkers that attempt to cover as many inflammatory interactions and mechanisms as possible.

Our objetive was to evaluate which biomarkers were elevated in AF patients compared to the general population.

We studied 74 patients who were to undergo an ablation procedure (53 with AF and 21 controls -microscopic substrates-), drawing a blood sample before the procedure.

Exclusion criteria were: cancer, inflammatory diseases, heart failure or major echocardiographic alterations including mild ventricular hypertrophy.

Baseline characteristics, basic analytical parameters and levels of 20 specific inflammatory biomarkers were collected and compared in patients with and without AF.

Figure 1 shows the baseline characteristics of the sample. The usual analytical parameters in clinical practice showed no relevant differences between the two groups.

Of the 20 specific inflammatory parameters, significant differences were found in 4: biomarkers of cardiomyocyte damage (NT-proBNP: (AF)130.8 +- 208.0 pg/mL vs (control) 80.3 +- 66.5 pg/mL; p=0.041), of atrial remodelling (Endostatin: 95.0 +- 28.8 ng/mL vs 80.1 +- 17.2 ng/mL; p<0.01), angiogenesis dysregulation (MCAM: 241.8 +- 51.9 ng/mL vs 197.1 +- 96.4 ng/mL; 0.033) and hepato-inflammatory cardiovascular risk markers (SAP; 7426.6 ± 2641.0 ng/mL vs 9406.9 ± 3904.1 ng/mL; p<0.011).

In addition to these individual differences, multiple correspondance analysis (figure 2) allowed grouping most of the patients without arrhythmia using information from the biomarker set.

In patients with AF, several specific parameters of inflammation are elevated compared to controls, supporting the presence of an activation of inflammation in these patients.

Due to the large number of factors involved in the inflammatory process and the variability with which they can be activated, future research evaluating the clinical implication of these findings is essential.

Baseline Characteristics