Nocturnal Pauses Research Articles

How Long is Too Long? Asymptomatic Nocturnal Pauses in Athletes: A Narrative Review

Athletes undergo mandatory or voluntary cardiac testing, which may include 24-h ambulatory electrocardiogram monitoring. This study can on occasion disclose nocturnal pauses in otherwise asymptomatic healthy individuals. In some athletes, particularly those engaging in endurance or mixed sports, the pauses can be longer than 2–3 s and/or be caused by sinus arrest high-degree atrioventricular block not typical for physiological adaptation to exercise. The manuscript discusses the physiology and potential pathologies behind long nocturnal pauses in athletes. Several management strategies are proposed including emerging treatment techniques such as cardioneuroablation.

C16 NONCOMPACTION OF VENTRICULAR MYOCARDIUM AND X–LINKED RECESSIVE ICHTYOSIS

Abstract Noncompact left ventricle is a rare congenital cardiomyopathy characterized by numerous ventricular trabeculae separated by deep intertrabecular recesses. It can occur in isolation or in association with neuromuscular disorders and congenital heart defects. The cause is not known but it is thought to be due to the arrest of the normal maturation process of the myocardium. Among the responsible mutations are taffazzine, ZASP and distrobrevin. It can manifest as left ventricular dilatation and dysfunction, arrhythmias, thromboembolic events, and sepsis. The echocardiogram is the investigation of first choice. Magnetic resonance allows you to more precisely distinguish compact and non–compact layers, thrombi and myocardial fibrosis. Clinical case A 19–year–old patient came for syncope. She presented with midfacial hypoplasia, cupped ears, synophrium, high palate, ichthyosis, small hands, and scarring from Achilles tendon lengthening. She denied a family history of cardiovascular disease and sudden cardiac death. Karyotype analysis showed karyotype 46Y, –X, + der t (X; Y) (p22.2; q11.1), with a chromosome derived from the X;Y translocation (a feature already known in the mother and in several maternal relatives ). Coronary angiography, electroencephalogram and brain MRI were within limits. Echocardiogram and MRI showed non–compact myocardium at the left ventricular apex and mild ventricular dysfunction with areas of anterior and posterior dyssynergia (Fig. 1). The ECG showed high QRS voltages. The Holter ECG showed numerous supraventricular extrasystoles even in pairs and runs, rare PVCs, and nocturnal pauses of up to 3 seconds. The patient underwent genetic screening by NGS for sarcomeric mutations which resulted negative. Subsequent genetic analysis showed deletion in two chromosomal regions that could be interpreted as pathogenic (chromosomal region Xp22.33 containing the SHOX gene and involving the deleted locus in Leri–Weill dyschondrosteosis and in the Xp22.33p22.31 region containing the STS gene involving the locus deleted in X–linked recessive ichthyosis) and a duplication in the chromosomal region Yq11.221q11.23 of uncertain significance. Conclusions After review of the scientific literature, the association of the illustrated complex deletion and translocation with non–compact myocardium represents a new finding, worthy of being explored in genetically affected patients.

Usefulness of Heart Rate Control in Atrial Fibrillation Patients With Obstructive Sleep Apnea

In patients without atrial fibrillation and flutter (AF), obstructive sleep apnea (OSA) is associated with cyclic and often marked changes in heart rate (HR). We aimed to assess whether presence of OSA impacts optimal HR control in patients in AF. We retrospectively correlated diurnal HR patterns (recorded by 24-hour Holter monitoring) in patients with AF who independently also underwent diagnostic polysomnography. Exclusion criteria were paced rhythm or inadequate recordings from polysomnography and Holter monitoring. The relationship between the presence and severity of OSA and the mean, minimum, maximum HR, as well as pauses (>2 seconds) and their diurnal variation were studied. Of the 494 studied patients (age 69 ± 10 years; 26% women) mild-moderate OSA (apnea hypoxia index ≥5 and <20) was present in 171 (34%) and severe OSA (apnea hypoxia index ≥20) in 254 (51%). Mean 24-hour HR in patients with severe OSA and mild-moderate OSA was similar to those without OSA (78 vs 80 vs 79 beats per minute; p = 0.39), and there was no significant difference observed in minimum and maximum HR of these groups. However, the frequency of short pauses was greater in OSA patients (p = 0.009), with a prominent nocturnal distribution. In conclusion, OSA was not associated with increased HR in patients with AF suggesting that adequate HR control was similarly achievable in patients with and without OSA. The increased frequency of nocturnal pauses in OSA patients may function as a clinical hallmark, and the timing of pauses (during sleep vs wakefulness) should be noted before making therapeutic decisions regarding HR control.

Diagnosis of Obstructive Sleep Apnoea in Patients Presenting with Nocturnal Pauses May Prevent the Unnecessary Insertion of Permanent Pacemakers

Introduction: Obstructive sleep apnoea (OSA) is a common medical condition with an estimated prevalence of around 7% worldwide. Patients with OSA have an increased risk of cardiovascular morbidity and mortality. Previous studies have shown a higher incidence of cardiac arrhythmias in OSA. Case Report: We report a 37-year-old male who presented with a significant syncope episode while driving a motor vehicle. His cardiac risk factors include obesity (BMI = 54.1 kg/m2), diabetes and tobacco consumption. He reported two similar syncopal episodes over the last twenty years. Transthoracic echocardiogram and baseline ECG were unremarkable for structural heart disease and conduction disorder. Twenty-four hour Holter monitor however, revealed significant nocturnal pauses lasting up to 7.56 seconds. He had a loop recorder (Medtronic Reveal LINQ LNQ 11) confirming episodes of significant nocturnal pauses which diminished after commencing CPAP for the co-diagnosis of severe sleep apnoea as part of the investigation of his symptoms. Conclusion: The use of a loop recorder has gained extensive role for discovering high degree AV block as primary cause of syncope by providing real time ECG monitoring up to 3-4 years. In this particular case, by discovering reversible organic cause of nocturnal pause, we avoid longitudinal potential side effects or complications related to PPM implant including infections, limitation in certain work activities like arc welding and the need for future surgeries related to generator replacement in an otherwise young patient.

Nocturnal Pauses in a Patient With Incompletely Treated OSA After Liver Trasplantation

Nocturnal Pauses in a Patient With Incompletely Treated OSA After Liver Trasplantation

Relationship among the severity of sleep apnea syndrome, cardiac arrhythmias, and autonomic imbalance.

The relationship between obstructive sleep apnea syndrome (OSAS), cardiac arrhythmias, and conduction disturbances in adults remains controversial. Early studies showed a higher prevalence than more recent and designed epidemiological studies. To clarify the actual prevalence of cardiac arrhythmias and conduction disturbances in patients referred for assessment of OSAS, a prospective cohort study was conducted: 147 consecutive patients (103 men; mean age of 54.5 +/- 10.7 years) underwent time-synchronized polysomnography and ECG Holter monitoring. OSAS was diagnosed in 66 (44.9%) of them based on an apnea hypopnea index (AHI) > or = 10. Prevalence of heart failure, of prior myocardial infarction, of hypertension, and of ventricular arrhythmias were similar in patients with or without OSAS. Nocturnal paroxysmal asystole was significantly more prevalent in OSAS patients (10.6 vs 1.2%; P < 0.02) and the number of episodes of bradycardia and pauses increased with the severity of the syndrome. Almost all bradycardic events occurred in patients with severe OSAS (AHI > 30), prolonged periods of arterial oxyhemoglobin desaturation, and low diurnal awake PaO2. Moreover, using heart rate variability analysis, nocturnal sinusal dysfunction contrasted with a blunted diurnal parasympathetic modulation of the sinus node. Frequent nocturnal nonsustained supraventricular tachycardias were predominantly found in patients with severe sleep related breathing disorders; however, an increased risk of ventricular arrhythmias was not found. Under continuous positive airway pressure treatment, the 1-year follow-up of OSAS patients with nocturnal pauses did not reveal any arrhythmic event justifying a specific intervention.