Interatrial Conduction Block in an Obstructive Sleep Apnea Patient: An Electrical Premonitor of Atrial Fibrillation.

Obstructive sleep apnea (OSA) is an important sleep disorder and is associated with increased cardiovascular morbidity and mortality. Several recent studies have demonstrated an association OSA and atrial fibrillation (AF). Therefore, it is of great importance understanding the pathophysiological substrate and the interaction between OSA and AF. Moreover, it is well accepted that interatrial block (IAB), evaluated not only by the P-wave duration but also by the P-wave morphology, has the potential to give information about the anatomical substrate predisposing to AF. OSA and AF share many risk factors and comorbidities, including older age, male gender, obesity, hypertension, heart failure, and coronary artery diseases. IAB is defined when the P-wave is ≥120 ms which signifies excessive time for sinus impulses to conduct from the right atrium to the left atrium and may predict future AF events. Accordingly, recent studies have suggested that OSA is associated with atrial functional and structural remodeling which indeed are associated with increased risk of AF. We speculate that IAB, a known factor to predict future AF episodes, may associate with OSA and contribute to the development of arrhythmic events. In the present case, the report presents a woman with OSA and IAB on the surface electrocardiogram (ECG)automatic P-wave analysis and some short episodes of AF in the external event recorder monitoring. Copyright:

INTRODUCTION

Interatrial delay depolarization in many cases is reported as interatrial block (IAB). The last provide valuable information about atrial functional and structural abnormalities and have been used by several studies as a possible predictor of atrial fibrillation (AF). It is well demonstrated that prolonged P-wave duration, which indicates interatrial conduction delay, is associated with increased risk of developing AF.[1] On the other hand, obstructive sleep apnea (OSA) is well known to be associated with AF.

The pathophysiological mechanisms of this association remain unclear. Some hypotheses have been proposed, such as increased sympathetic tone, hypertension, obesity (a comorbidity that is frequent for both conditions), and increased pulmonary pressure.[23] However, the prevalence of IAB, an accepted risk factor for AF, in patients with OSA, has been supported in only a few studies.[4] Diagnosis of IAB is easy to perform using the surface ECG. It is partial when the P-wave duration is ≥120 ms, and advanced if the P-wave presents a biphasic pattern in II, III, and aVF.

IAB is very frequent in the elderly and, particularly in the case of the advanced type, they are associated with AF, and AF recurrences.[5] This association has been recently named Bayés syndrome.[6]

We describe a case of a woman patient with OSA in whom detection of IAB motivated extended cardiac monitoring resulting in the diagnosis of paroxysmal AF.

CASE PRESENTATION

A woman of 52 years old obese patient (BMI 31.8 Kg/m2) with hypertension without treatment, arrived in the cardiology ambulatory complaining of fainting episodes, palpitations, dyspnea, diurnal somnolence, and fatigue after small physical efforts. On the physical examination, blood pressure was 165/100 mmHg. Blood gas analysis revealed normal acid–base status and electrolytes at rest. Some other laboratory results have shown hemoglobin 12.5 g/dl, platelet 202,000, creatinine 0.95 mg/dl, total cholesterol 192 mg/dl, low-density lipoprotein 90 mg/dl, triglycerides 138 mg/dl, thyroid-stimulating hormone 2.960 mU/L, uric acid 5.9 mg/dl, and alanine aminotransferase 10 U/L. Her CHA2DS2-VASc score was 2. A resting bedside ECG was performed with sinus rhythm (72 bpm), P duration 126 ms, PQ 146 ms, and QTc 429 ms [Figures 1 and 2]. A careful observation of the P-wave morphology, duration, and voltage revealed an IAB alteration (duration 126 ms, and the polarity was bimodal in II, III, and aVF leads) with a P-wave, recorded in V1, as a biphasic with a negative terminal force.

Figure 1

Electrocardiogram with calibration 20 mm/mv and paper velocity 25 mm/s shows bifid P-wave in D2, D3, and aVF leads (small arrow). A biphasic P-wave in V1 lead with a huge negative terminal force (small arrow)

Figure 2

P-wave in D2, D3, and aVF and V1 is shown in electrocardiogram with calibration 10 mm/mv and paper velocity 25 mm/s. The automatic analysis of P-wave duration had shown 126 ms

Due to the suspicion of obstructive apnea syndrome (STOP-BANG score 7), the patient was referred to the hospital sleep clinic. The patient underwent a polysomnographic study which diagnosed mild-to-moderate OSA (apnea–hypopnea index >11.6 events/h).

In October 2020, the patient performed an echocardiography which had shown initial left ventricular hypertrophy with normal biventricular global systolic function. Cardiac valves were normal. Left atrial anterior–posterior dimensions increased (43 mm). On Doppler transmitral flow, a diastolic dysfunction type I was also observed.

By applying the simple morphology-voltage-P-wave (MVP) ECG risk score[7] for the prediction of AF, we obtained a score equal to 4 (intermediate probability risk of AF). The above score is a simple electrocardiographic evaluation of P-wave and prediction of AF. Therefore, due to intermediate prediction AF score, we also evaluate P-wave in lead V1 which shows a biphasic morphology with a negative terminal force (Ptf).[8] Moreover, a 7-day ECG registration by an external event EKG recorder was obtained [Figure 3]. After this prolonged time ECG monitoring, we discover multiple but short periods of AF. Because of low CHA2DS2VASc scores, we decided not to initiate anticoagulant therapy in this case.

Figure 3

A strip with episode of paroxysmal atrial fibrillation was recorded in the ECG external event recorder monitoring

DISCUSSION

It is well known that IAB has values in predicting occurrence or recurrence AF. OSA syndrome, an underdiagnosed condition that affects approximately 5% of the general population,[9] is characterized by repeated upper airway obstruction during sleep and symptoms associated with unrefreshing sleep. Several recent studies have underlined the important relationship between AF and OSA, two highly prevalent diseases, from both the epidemiologic and pathophysiologic viewpoints. On the other hand, IAB is a known predictor of AF. Furthermore, a study also reported an association of OSA severity with P-wave delay depolarization and that older age and OSA severity are independent predictors of IAB (defined as P-wave duration ≥120 ms).[3] Two previous studies also indicated that OSA severity is significantly and independently correlated with P-wave duration and that treatment of OSA with continuous positive airway pressure can shorten the P-wave duration.[1011]

Accordingly, Dimitri et al. also found an association of OSA severity with wave duration.[12] In the present case, IAB was present, but with the MVP, the predictive AF score was of intermediate severity (equal to 4). It is very useful to estimate (in similar cases) also the P-wave morphology in lead V1 and especially the terminal force (Ptf). In this direction, Spodick et al.[8] Also suggest that P-wave alterations should be evaluated simultaneously (P-wave duration and morphology in the inferior leads, as well as P-wave terminal force in lead V1) because both are well correlated and should be expected, in most cases, when one is detected. Although the reasons for this association are still not clear, atrial remodeling due to delayed and abnormal left atrium activation, especially in the case of advanced IAB, is probably the key factor in the chain of events that lead to atrial fibrosis.

Furthermore, Martín García et al. reported that abnormal Ptf is suggested as an indicator of atrial structural remodeling shown to be predictive of AF relapse following electrical cardioversion.[13] Furthermore, Yagmur et al. applied tissue Doppler imaging to patients with moderate-to-severe OSA, and found prolonged interatrial and intraatrial electromechanical delay, as well as P-wave dispersion.

Another potential mechanism is the marked autonomic imbalance that occurs in OSA.[14] The marked vagal predominance at the end of apneas, which is associated with bradyarrhythmias, may change the conduction properties of the atria to promote AF. Furthermore, in other previous studies, P-wave durations have been reported to be influenced by the autonomic tone.[1516] The initiation of anticoagulation therapy is another important factor in the treatment of these patients. IAB patients without previous episodes of documented AF have an increased risk of stroke, especially if a high CHA2DS2VASc score is present. However, at this time, we do not have clinical trials that support the use of anticoagulants in the absence of documented AF. Therefore, it is important to carry out monitoring to look for AF episodes that can support anticoagulation in these patients.

In our case, after monitoring for a long time, we found short repetitive runs of AF (<30 s) that does not support anticoagulation therapy also because of the low CHA2DS2-VASc score.

CONCLUSION

IAB seems to be well associated with OSA. Both conditions are important to induce AF and its relapse after electrical cardioversion. IAB and the presence of Ptf in lead V1 may predict future AF events. In this case, the presence of IAB and Ptf in OSA may increase the pathophysiological arrhythmic substrate that easily promotes AF events. Regarding anticoagulation therapy decision, it is essential to assess future studies which help to elucidate whether anticoagulation is needed in these patients.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient (s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.