Background and objectives: Atrial fibrillation (AF), the most prevalent sustained arrhythmia, poses a significant public health challenge due to its links with stroke, heart failure, and mortality. Hypertension, a primary modifiable cardiovascular risk factor, is a well-established risk factor for AF that facilitates structural and electrical changes in the atria, including dilation, fibrosis, and pressure overload. Material and Methods: we conducted a literature search regarding the shared mechanisms, risks and treatments of hypertension and atrial fibrillation. Results: The renin–angiotensin–aldosterone system plays a pivotal role in this remodelling and inflammation, increasing AF susceptibility. Uncontrolled hypertension complicates AF management, diminishing the effectiveness of mainstay treatments, including antiarrhythmic drugs, catheter ablation, and cardioversion. Effective blood pressure management, particularly with therapies targeting the renin–angiotensin–aldosterone system (RAAS), can lower the risk of new-onset AF and reduce the incidence of recurrent AF, enhancing the success of rhythm control strategies. These antihypertensive therapies mitigate myocardial hypertrophy and fibrosis and attenuate both atrial pressure strain and the inflammatory response, mitigating the substrates for AF. Conclusion: This review highlights the urgent need for integrated strategies that combine BP control, AF screening, and lifestyle modifications to minimise the burden of AF and its complications. Future research should investigate the specific mechanisms of cellular-level interactions associated with a hypertensive predisposition to AF, including systematic inflammation and the role of genetics, the impact of blood pressure variations on AF risk, and individualised treatment strategies specifically targeting the shared mechanisms, simultaneously propagating hypertension and AF.

Background: Pulmonary vein isolation (PVI) is an effective management method for paroxysmal atrial fibrillation (PAF). The P wave in the 12-lead electrocardiogram (ECG) represents atrial depolarisation. This study aims to utilise the P wave to predict PVI outcomes for PAF. Methods: This single-centre retrospective study aimed to predict PVI outcomes using P wave parameters. It included 211 consecutive patients with first PVI for PAF between 2018 and 2019 and targeted the pulmonary veins (PVs). Procedure success was defined by freedom of ECG-documented AF at 12 months. Digital 12-lead ECGs with 1–50 hertz bandpass filters were monitored before the procedure. Corrected P wave duration (PWDc), P wave amplitude (PWV), P wave dispersion (PWDisp), intra-atrial block (IAB), P wave area (PWA), and P wave terminal force in V1 (PTFV1) were measured before ablation and correlated with the outcomes. Results: Successful PVI occurred in 154 patients (73%). Demographics were similar between both arms. P wave parameters correlated with PVI failure included increased PWDc in all leads except for lead III, aVR, and V3, decreased PWV in lead I (hazard ratio [HR]: 0.7, 95% confidence interval [CI]: 0.53–0.95), lead II (HR: 0.45, 95% CI: 0.22–0.65), aVL (HR: 0.58, 95% CI: 0.22–0.98), and aVF (HR: 0.67, 95% CI: 0.58–0.87), decreased PWA in lead I (HR: 0.55, 95% CI: 0.21–0.76), lead II (HR: 0.48, 95% CI: 0.34–0.87), aVL (HR: 0.65, 95% CI: 0.45–0.96), and aVF (HR: 0.61, 95% CI: 0.32–0.89), and the presence of IAB (HR: 2, 95% CI: 1.4–4.2, p = 0.02). PWDisp and PTFV1 were not correlated with PVI outcome. Conclusions: PWDc, PWA, PWV, and IAB are valuable predictors for PVI outcome for PAF at 12 months.