Despite all efforts to prevent AF in hypertensive patients, structural heart disease and atrial cardiomyopathy in this setting would nonetheless cause progressive atrial derangement and electrical vulnerability, thus promoting a vicious cycle known as “atrial failure”, which is intimately connected with AF development [105].

It is well known that AF is a potentially life-threatening cause of cerebral thromboembolism, and clinically silent forms might wreak even greater havoc if not recognised in a timely manner. For these reasons, hypertensive patients with an uncertain history of AF and evidence of prior cerebrovascular events should be accurately studied to differentiate strokes of cardioembolic origin from those secondary to atherosclerotic disease or cerebral haemorrhage [106]. In these cases, ECG monitoring can be helpful to identify patients with clinically silent AF [107,108], and, in the case of cryptogenic stroke, an implantable cardiac monitor (ICM) should be considered [10]. Over the last decade, cardiac implantable electronic devices (CIEDs) [109], ICM included [110], have proved extremely helpful in the early detection of subclinical AF episodes, but it is still debated which arrhythmic burden should prompt immediate oral anticoagulation in these patients. For the sake of clarity, clinically silent AF is defined for asymptomatic arrhythmia episodes detected on 12-lead ECG or an ECG strip; conversely, subclinical AF is represented by arrhythmia detected by CIEDs [10]. However, differentiating clinical from subclinical AF is not a matter of mere speculation. In fact, subclinical AF seems to portend a lower thromboembolic risk compared with clinical AF [111], and no clear cause–effect relationship between subclinical AF and ischemic stroke has been clearly proven in this setting [109]. However, the longer the duration of subclinical AF episodes, the greater their association with thromboembolic events [112]. For this reason, a recent European Heart Rhythm Association (EHRA) consensus document suggested oral anticoagulation administration for subclinical AF episodes longer than 5.5 h/day only when a significant risk of cerebral thromboembolism is established (i.e, CHA2DS2Vasc scores ≥ 2 and 3 in men and women, respectively) [111]. Whether this strategy pays off in terms of better clinical outcome is unclear. In fact, by randomising elderly patients with stroke risk factors and no AF history to the ICM strategy or usual care, the LOOP study did not prove the superiority of ICM over controls in terms of better clinical outcome after early AF detection [110]. Several issues raised by the same investigators might explain the overall negative results of this trial, such as the inadequate estimate of the primary outcome event rate, the relatively short duration of follow-up, and the initiation of oral anticoagulation for subclinical episodes lasting as low as 6 min. In keeping with prior observations [112], these results would suggest that not all subclinical AF episodes may benefit from early anticoagulation, and two ongoing randomized controlled trials might provide clearer answers in patients with CIEDs [113,114].

Moreover, in this already hazy scenario, it is all but crystal-clear which hypertensive patients with neither stroke history nor CIEDs/ICM should be screened for silent AF, and, not least, through which modality. On the one hand, the burden of cardiovascular comorbidities and blood biomarkers might play an important role in identifying people at a sufficient risk to warrant AF screening [115]. The thorough assessment of the P wave morphology on surface ECG may also be useful in identifying potential risk markers for AF, such as prolonged P wave duration, left atrial enlargement, and advanced interatrial (i.e., Bachmann bundle) block. [116]. Similar observation can be made for LVH, diastolic dysfunction, and left atrial enlargement as assessed on transthoracic echocardiogram [116]. However, what would be the best approach for AF screening in high-risk patients? On one side of the spectrum of the available modalities for AF screening, on account of the low cost and the great sensitivity yield, radial pulse taking should be regarded as the first option to be offered in patients aged ≥65 years and deemed at high risk of developing AF. Surface ECG analysis in the case of arrhythmic pulse is therefore warranted, and, if clinical AF is confirmed, oral anticoagulation should be promptly administered according to the patient’s thromboembolic risk profile [10]. Furthermore, a variety of screening technologies have been developed over the years and with progressively better AF detection accuracy [117], but no comparative trials have been carried out so far with any of these devices. Accordingly, European guidelines on AF diagnosis and management [10] strongly recommend a single-lead ECG tracing of ≥30 s or 12-lead ECG to confirm a diagnosis of clinical AF when detected by screening tools. Although similar observation can be applied to the use of ICM in the same setting, the positive clinical interaction observed in the LOOP trial between high blood pressure values and better clinical outcome in early anticoagulated patients in the ICM arm may prompt the use of an implantable loop recorder (ILR) as a screening tool in selected patients with HTN.

In conclusion, AF detection in its early stage is paramount, and an appropriate therapy might eschew severe complications potentially leading to disability and death in the affected patients. However, it should be ascertained which patients portend a greater risk of AF and thereby who should be screened for this arrhythmia and by which modality. While waiting for sounder results from ongoing clinical trials, Figure 2 provides a proposed algorithm for silent/subclinical AF detection and management in hypertensive patients.