Background: Atrial cardiomyopathy (AtCM) is associated with new-onset atrial fibrillation (AF) and progression from paroxysmal to persistent AF. Histology is the gold standard for diagnosing AtCM but is not routinely performed in clinical practice because of its invasiveness and complication risk. Electroanatomical mapping and cardiac MRI are valuable for AtCM assessment, yet their applicability for large scale quantification is limited. We therefore aimed to investigate various non invasive markers of AtCM with respect to their ability to differentiate paroxysmal from persistent AF.
Methods: We analyzed 144 consecutively enrolled patients with paroxysmal or persistent AF admitted to the University Heart Center Freiburg‑Bad Krozingen in sinus rhythm. All patients underwent standardized workup including a digital 12‑lead resting ECG for amplified P‑wave duration (APWD) analysis, transthoracic echocardiography to quantify LA diameter and LA volume index, and blood sampling for biomarkers to measure NT‑proBNP, high‑sensitivity troponin T and C‑reactive protein. Clinical covariates (age, sex, BMI, CHA2DS2‑VASc) were recorded. Normality was assessed by the Shapiro-Wilk test; group comparisons used t‑test or Mann-Whitney U for continuous variables as appropriate and Fisher’s exact test for categorical variables. Variables with p < 0.10 in univariate logistic regression were considered for multivariable modeling. As none of the clinical covariates reached p < 0.10, the multivariable logistic model was adjusted for CHA2DS2‑VASc score and BMI; age and sex were not entered separately to avoid double counting components of the CHA2DS2‑VASc score. Spearman and partial Spearman correlations (age/sex adjusted) assessed relations among non‑invasive parameters.
Results: Of 144 evaluable patients (67.2 ± 9.1 years; 68.1% male), 95 had paroxysmal and 49 persistent AF. Clinical factors (age, sex, BMI, CHA2DS2‑VASc) did not differ between groups. Among non‑invasive AtCM markers only APWD differed significantly: median 139 ms (25th–75th: 130.5–148.5) vs 146 ms (140–163), p < 0.001 (Cliff’s δ = −0.36, 95% CI −0.52 to −0.17). LA diameter medians were 43 mm (25th–75th: 38–46.5) vs 43 mm (41–46), p = 0.67. LA volume index medians were 40 ml/m² (25th–75th: 30–47) vs 42 ml/m² (36–48), p = 0.32. Blood‑based biomarker medians (paroxysmal vs persistent) were NT‑proBNP 714 (25th–75th: 284.25–1445.5) vs 472 (192.25–1704.5) pg/ml, p = 0.59; troponin T 101 (65.5–161.5) vs 120 (88–179) ng/l, p = 0.12; CRP 1.5 (0.8–3.5) vs 1.7 (1–2.5) mg/l, p = 0.99.
In univariate analyses APWD was the only non‑invasive predictor meeting the selection threshold. In the adjusted multivariable logistic model (adjusted for CHA2DS2‑VASc and BMI; complete cases n = 143) APWD remained independently associated with persistent AF (adjusted OR per 1 ms = 1.0426; 95% CI 1.019–1.069; p = 5.9×10−4; adjusted OR per 10 ms = 1.517; 95% CI 1.211–1.954). CHA2DS2‑VASc and BMI were not significant. Partial Spearman correlations (age/sex adjusted) showed a modest association between APWD and LA diameter (rho = 0.224, p = 0.0076). NT‑proBNP correlated more strongly with LA volume index than with APWD (Spearman rho = 0.348, p < 0.001 vs rho = 0.181, p = 0.039).
Conclusions: In this prospective cohort, APWD was the only non invasive AtCM marker that differentiated persistent from paroxysmal AF and remained significant after adjustment for CHA2DS2 VASc-Score and BMI. APWD correlated with LA enlargement, whereas NT proBNP primarily correlated with LA enlargement. These complementary, non invasive measures may help to identify atrial remodeling in AF patients and support refined risk stratification for disease progression and prevention of adverse outcomes.
