Cardiac autonomic control in Brugada syndrome patients during sleep: the effects of sleep disordered breathing.

AIMS: Brugada syndrome is characterized by typical ECG features, ventricular arrhythmias and sudden cardiac death (SCD), more frequent during nighttime. Autonomic cardiovascular control has been implicated in triggering the ventricular arrhythmias. Sleep-disordered breathing (SDB) elicits marked autonomic changes during sleep and is also associated with an increased risk of nighttime SCD. Brugada patients may have a higher likelihood of SDB compared to controls. However, no data are available on cardiac autonomic control in Brugada patients, particularly with regard to the comorbidity of SDB. METHODS: We evaluated autonomic cardiovascular control in Brugada patients with SDB (BRU-SDB, n=9), without SDB (BRU, n=9), in controls (CON, n=8) and in non-Brugada patients with SDB (n=6), during wakefulness and sleep (N2, N3 and REM). Linear spectral and entropy-derived measures of heart rate variability (HRV) were performed during apnea-free stable breathing epochs. RESULTS: Total HRV was attenuated in BRU-SDB compared to CON and BRU. During N2 and REM, in BRU-SDB patients sympathetic modulation decreased compared to BRU and CON, while during REM, they showed an increased parasympathetic modulation, compared to the other two groups. BRU-SDB and SDB were similar in terms of spectral components. Entropy-derived indices showed preserved dynamic changes in Brugada patients compared to controls through the different sleep stages. CONCLUSION: Brugada syndrome per se does not appear associated with an altered autonomic cardiovascular control during wakefulness and sleep. The comorbidity with SDB may contribute to disrupted autonomic cardiovascular regulation during sleep, possibly predisposing to the increased likelihood of sleep-related ventricular tachyarrhythmias and SCD.

Effects of experimental sleep restriction on caloric intake and activity energy expenditure.

BACKGROUND: Epidemiologic studies link short sleep duration to obesity and weight gain. Insufficient sleep appears to alter circulating levels of the hormones leptin and ghrelin, which may promote appetite, although the effects of sleep restriction on caloric intake and energy expenditure are unclear. We sought to determine the effect of 8 days/8 nights of sleep restriction on caloric intake, activity energy expenditure, and circulating levels of leptin and ghrelin. METHODS: We conducted a randomized study of usual sleep vs a sleep restriction of two-thirds of normal sleep time for 8 days/8 nights in a hospital-based clinical research unit. The main outcomes were caloric intake, activity energy expenditure, and circulating levels of leptin and ghrelin. RESULTS: Caloric intake in the sleep-restricted group increased by +559 kcal/d (SD, 706 kcal/d, P=.006) and decreased in the control group by -118 kcal/d (SD, 386 kcal/d, P=.51) for a net change of +677 kcal/d (95% CI, 148-1,206 kcal/d; P=.014). Sleep restriction was not associated with changes in activity energy expenditure (P=.62). No change was seen in levels of leptin (P=.27) or ghrelin (P=.21). CONCLUSIONS: Sleep restriction was associated with an increase in caloric consumption with no change in activity energy expenditure or leptin and ghrelin concentrations. Increased caloric intake without any accompanying increase in energy expenditure may contribute to obesity in people who are exposed to long-term sleep restriction. TRIAL REGISTRATION: ClinicalTrials.gov; No.: NCT01334788; URL: www.clinicaltrials.gov.

Comparison of a shortened isosorbide dinitrate-potentiated head-up tilt testing with the conventional protocol: tolerance and diagnostic accuracy.

BACKGROUND: The head-up tilt test (HUT) is widely used to investigate unexplained syncope; however, in clinical practice, it is long and sometimes not well tolerated. OBJECTIVES: To compare the sensitivity, specificity, accuracy, and patients' tolerance of a conventional and shortened HUT. METHODS: Patients with a history of vasovagal syndrome (VVS) were randomized to a conventional HUT (group I) consisting of 20-minute passive tilt followed by 25 minutes after administration of sublingual isosorbide dinitrate (ISDN), or a shortened HUT (group II) where ISDN was given immediately after tilt and observed for 25 minutes. The control group consisted of age- and gender-matched subjects without VVS symptoms. A specific questionnaire to evaluate tolerance was applied. RESULTS: Sixty patients (29 ± 10 years, 82% female) were included. In group I, 22/30 patients had a positive HUT compared to 21/30 in group II (73% vs 70%, P = 0.77). There was also no difference in the accuracy between the two protocols (63% vs 73%, P = 0.24). The time to positivity was shorter in group II (13.2 minutes vs 30 minutes, P < 0.001). Within the control group (n = 60), the frequency of false-positives was 47% and 23% for the conventional and shortened HUT, respectively (P = 0.058). After conventional HUT, 65.2% subjects reported that the test was too long compared to 25% subjects after the shortened HUT (P = 0.002). CONCLUSION: In this study, the HUT without passive phase was not inferior to the conventional HUT regarding sensitivity, specificity, and accuracy. Furthermore, the shortened ISDN-potentiated protocol allowed faster diagnosis and was better tolerated.

Sleep-disordered breathing in patients with the Brugada syndrome.

We investigated breathing patterns and the occurrence of arrhythmias and ST-segment changes during sleep in patients with Brugada syndrome. Patients with Brugada syndrome are more likely to die from ventricular arrhythmias during sleep. ST-segment changes have been correlated with risk of sudden cardiac death. Whether sleep disturbances may contribute to arrhythmogenesis is unknown. Patients with Brugada syndrome underwent overnight polysomnography with simultaneous 12-lead electrocardiographic recording. A control group matched by age, gender, and body mass index (BMI) also underwent polysomnography. Twenty patients were included (50 ± 15 years old, 75% men). Despite their normal BMI (24.7 ± 2.7 kg/m(2)), 45% had sleep-disordered breathing (SDB), with a mean apnea-hypopnea index of 17.2 ± 14 events/hour. In patients with a high risk of arrhythmias, 5 (63%) had SDB. In the control group, 27% had SDB. Atrial or ventricular arrhythmias were not observed. Spontaneous ST-segment changes occurred in 2 patients over 45 different time points. Most ST-segment changes were observed during rapid eye movement sleep (31%) or within 1 minute of arousals (44%). Regarding respiratory events, 25 (56%) of ST-segment changes were related to occurrence of apnea or hypopnea. In conclusion, patients with Brugada syndrome have a high prevalence of SDB even in the setting of normal BMI. The higher incidence of nocturnal death in patients with Brugada syndrome may be conceivably related to co-morbid SDB. Moreover, autonomic instability encountered in rapid eye movement sleep and arousals could potentiate the risk of arrhythmias.

Apneia do sono e arritmias cardíacas / Sleep apnea and cardiac arrhythmias

A apneia obstrutiva do sono é muito comum na população em geral, sendo ainda mais comum entre os pacientes com doença cardiovascular estabelecida. A apneia obstrutiva do sono é considerada fator de risco para o desenvolvimento de hipertensão arterial sistêmica, insuficiência cardíaca, infarto do miocárdio, acidente vascular encefálico e arritmias cardíacas. Dentre as arritmias mais comuns e associadas com apneia obstrutiva do sono destacamos a fibrilação atrial, as bradiarritmias e as arritmias ventriculares. Diversos mecanismos fisiopatológicos, incluindo as vias neural, humoral hemodinâmica e metabólica, são responsáveis pelos efeitos negativos da apneia obstrutiva do sono nas doenças cardiovasculares. Evidências científicas atuais sugerem que os cardiologistas identifiquem os subgrupos de pacientes portadores de alto risco para apneia obstrutiva do sono, sua referência para a polissonografia e a indicação do tratamento com pressão positiva contínua em vias aéreas (CPAP). A identificação e o tratamento da apneia obstrutiva do sono melhoram a qualidade de vida dos pacientes e podem prevenir os efeitos negativos da apneia obstrutiva do sono nas arritmias cardíacas.

Septal accessory pathway: anatomy, causes for difficulty, and an approach to ablation.

Accessory pathway (AP) ablation is one of the most satisfying invasive electrophysiology procedures associated with high success rates and relatively few complications. Nevertheless, when APs are found on the cardiac septum, ablative procedures become complex, and unique pitfalls need to be avoided.These difficulties with septal ablation are magnified in the pediatric population. The relatively small heart, rapid nodal conduction, and proximity of the arterial system specifically complicate septal ablation in children. The electrophysiologist must use every tool in his or her armamentarium, including exact delineation of pathway location, identification of pathway potentials, detection of the presence of pathway slant, etc. In addition, an exact knowledge of the complex anatomy of the cardiac septum, including the posteroseptal space, the aortic cusp region, and the proximity of the AV conduction system and coronary vessels, becomes mandatory.In this review, we describe the developmental anatomy and regional anatomy of septal accessory pathways. We then discuss approaches to map specific to pathways in particularly problematic regions at or near the septum, including venous and aortic cusp related accessory pathways.

Correlative anatomy for the electrophysiologist: ablation for atrial fibrillation. Part II: regional anatomy of the atria and relevance to damage of adjacent structures during AF ablation.

Ablation procedures for atrial fibrillation have become an established and increasingly used option for managing patients with symptomatic arrhythmia. The anatomic structures relevant to the pathogenesis of atrial fibrillation and ablation procedures are varied and include the pulmonary veins, other thoracic veins, the left atrial myocardium, and autonomic ganglia. Exact regional anatomic knowledge of these structures is essential to allow correlation with fluoroscopy and electrograms and, importantly, to avoid complications from damage of adjacent structures within the chest. We present this information as a series of 2 articles. In a prior issue, we have discussed the thoracic vein anatomy relevant to paroxysmal atrial fibrillation. In the present article, we focus on the atria themselves, the autonomic ganglia, and anatomic issues relevant for minimizing complications during atrial fibrillation ablation.

Correlative anatomy for the electrophysiologist: ablation for atrial fibrillation. Part I: pulmonary vein ostia, superior vena cava, vein of Marshall.

Ablation procedures for atrial fibrillation (AF) have become an established and increasingly used option for managing patients with symptomatic arrhythmia. The anatomic structures relevant to the pathogenesis of AF and ablation procedures are varied and include the pulmonary veins (PVs), other thoracic veins, the left atrial myocardium, and autonomic ganglia. Exact regional anatomic knowledge of these structures is essential to allow correlation with fluoroscopy and electrograms, and, importantly, to avoid complications from damage of adjacent structures within the chest. We have presented this information in a 2-part series. In the present article, we examine the general anatomic characteristics of the PVs, superior vena cava, and vein of Marshall. Features of particular relevance for the invasive electrophysiologist are pointed out. In a subsequent article, we discuss the regional anatomy of the left and right atria and anatomic considerations in preventing complications during AF ablation.

Life-threatening cardiac manifestations of pheochromocytoma.

Pheochromocytoma is a catecholamine-secreting tumor of the adrenal glands, usually with benign manifestations, whose typical clinical presentation includes the triad of headache, palpitations and diaphoresis. However, a wide range of signs and symptoms may be present. In the cardiovascular system, the most common signs are labile hypertension and sinus tachycardia. Systolic heart failure and ST-segment deviations mimicking myocardial infarction have also been reported, as well as QT interval prolongation and, rarely, ventricular tachycardia. We describe a challenging diagnosis of pheochromocytoma with many cardiovascular manifestations, which could have been missed due to the absence of typical symptoms.

Catecholaminergic polymorphic ventricular tachycardia: a current overview.

Catecholaminergic polymorphic ventricular tachycardia occurs in healthy children and young adults causing syncope and sudden cardiac death. This is a familial disease, which affect de novo mutation in 50% of the cases. At least two causative genes have been described to be localized in the chromosome 1; mutation of the ryanodine receptor gene and calsequestrin gene. The classical clinical presentation is syncope triggered by exercise and emotion in children and adolescents with no structural heart disease. Polymorphic ventricular tachycardia during treadmill testing, or after isoproterenol infusion, is the most common feature. Therapeutic options include, beta-blockers, calcium-channel blockers and, an implantable cardioverter defibrillator is indicated in high-risk patients. Risk stratification of this disease is very challenging, since some risk factors proved to be useful in some series but not in others. However, family history of sudden cardiac death and symptoms initiated in very young children are important predictors.