Excessive Daytime Sleepiness Independently Predicts Increased Cardiovascular Risk After Myocardial Infarction.

BACKGROUND: Excessive daytime sleepiness (EDS), a common symptom among patients with sleep-disordered breathing, is closely associated with the development of cardiovascular diseases, but its long-term prognostic value is not completely understood. The aim of this study was to investigate whether EDS would be an independent prognostic factor after myocardial infarction. METHODS AND RESULTS: We prospectively recruited 112 post-myocardial infarction patients. The Epworth Sleepiness Scale was completed before polysomnography, and EDS was defined as a score ≥11. After exclusion of 8 patients who accepted treatment with continuous positive airway pressure, 104 patients were followed up for 48 months. The primary composite end point was major adverse cardiac events. Patients with EDS had higher rates of major adverse cardiac events (48.4% versus 27.4%, χ2=5.27, P=0.022) and reinfarction (29.0% versus 5.5%, χ2=13.51, P=0.0002) compared with those without EDS. In the Cox proportional hazards model, patients with EDS had 2.15 times (95% confidence interval, 1.08-4.18; P=0.030) higher crude risk of major adverse cardiac events, with prognostic significance persisting after adjusting for age, diabetes mellitus, depression, left ventricular ejection fraction, apnea-hypopnea index, and nocturnal nadir oxygen saturation (hazard ratio: 2.13, 95% confidence interval, 1.04-4.26, P=0.039). Furthermore, among participants with moderate to severe sleep-disordered breathing, the presence of EDS was associated with higher risk of major adverse cardiac events than those without EDS, after adjusting for age and nadir oxygen saturation (hazard ratio: 3.17, 95% confidence interval, 1.22-7.76, P=0.019). CONCLUSIONS: EDS may be an independent prognostic factor of adverse outcome in post-myocardial infarction patients with moderate to severe sleep-disordered breathing. Evaluation of EDS may shed new light on risk stratification and identify treatment responders for this patient population.

Nocturnal Hypoxemia Due to Obstructive Sleep Apnea Is an Independent Predictor of Poor Prognosis After Myocardial Infarction.

BACKGROUND: Obstructive sleep apnea (OSA) is an important risk factor for the development of cardiovascular diseases including myocardial infarction (MI). The aim of this study was to investigate the effects of OSA on prognosis after MI, and to determine which specific measures of OSA severity best predicted outcomes. METHODS AND RESULTS: We performed a prospective study, in which 112 patients without a prior diagnosis of sleep apnea underwent comprehensive polysomnography within a median of 7 days after MI. Patients were followed up at 6-monthly intervals (±2 weeks) for a total of 48 months. Patients classified with central apnea (n=6) or those using continuous positive airway pressure (n=8) after polysomnography were excluded from analyses. The primary end point was major adverse cardiac events, including death from any cause, recurrent MI, unstable angina, heart failure, stroke, and significant arrhythmic events. Forty of 98 patients (41%) had OSA (apnea-hypopnea index ≥15 events/h). OSA patients had higher major adverse cardiac event rates when compared to those without OSA (47.5% versus 24.1%; χ(2)=5.41, P=0.020). In a multivariate model that adjusted for clinically relevant variables including age, left ventricular ejection fraction, diabetes mellitus, oxygen desaturation index, and arousal index, significant hypoxemia, as defined by nocturnal nadir oxygen saturation ≤85%, was an independent risk factor for major adverse cardiac events (hazard ratio=6.05, P=0.004) in follow-up 15 months after baseline. CONCLUSIONS: Nocturnal hypoxemia in OSA is an important predictor of poor prognosis for patients after MI. These findings suggest that routine use of low-cost nocturnal oximetry may be an economical and practical approach to stratify risk in post-MI patients.

Obstructive sleep apnea and the risk of sudden cardiac death: a longitudinal study of 10,701 adults.

OBJECTIVES: This study sought to identify the risk of sudden cardiac death (SCD) associated with obstructive sleep apnea (OSA). BACKGROUND: Risk stratification for SCD, a major cause of mortality, is difficult. OSA is linked to cardiovascular disease and arrhythmias and has been shown to increase the risk of nocturnal SCD. It is unknown if OSA independently increases the risk of SCD. METHODS: We included 10,701 consecutive adults undergoing their first diagnostic polysomnogram between July 1987 and July 2003. During follow-up up to 15 years, we assessed incident resuscitated or fatal SCD in relation to the presence of OSA, physiological data including the apnea-hypopnea index (AHI), and nocturnal oxygen saturation (O2sat) parameters, and relevant comorbidities. RESULTS: During an average follow-up of 5.3 years, 142 patients had resuscitated or fatal SCD (annual rate 0.27%). In multivariate analysis, independent risk factors for SCD were age, hypertension, coronary artery disease, cardiomyopathy or heart failure, ventricular ectopy or nonsustained ventricular tachycardia, and lowest nocturnal O2sat (per 10% decrease, hazard ratio [HR]: 1.14; p = 0.029). SCD was best predicted by age >60 years (HR: 5.53), apnea-hypopnea index >20 (HR: 1.60), mean nocturnal O2sat <93% (HR: 2.93), and lowest nocturnal O2sat <78% (HR: 2.60; all p < 0.0001). CONCLUSIONS: In a population of 10,701 adults referred for polysomnography, OSA predicted incident SCD, and the magnitude of risk was predicted by multiple parameters characterizing OSA severity. Nocturnal hypoxemia, an important pathophysiological feature of OSA, strongly predicted SCD independently of well-established risk factors. These findings implicate OSA, a prevalent condition, as a novel risk factor for SCD.

Anatomy of the coronary sinus and epicardial coronary venous system in 620 hearts: an electrophysiology perspective.

INTRODUCTION: Cannulation of the coronary sinus (CS) is a prerequisite for left ventricular (LV) pacing and certain ablation procedures. The detailed regional anatomy for the coronary veins and potential anatomic causes for difficulty with these procedures has not been established. METHODS AND RESULTS: Therefore, we performed macroscopic measurements in 620 autopsied hearts (mean age 60 ± 23 years, 44% female). The CS was preserved for analysis in 96%. Sixty-three percent had a Thebesian valve that covered the posterior aspect of the CS ostium with extension to the superior (50%) and inferior aspects (18%) and was obstructive with fenestrations in 3 specimens. Partial or near occlusive valves were present occasionally at the ostium of the great cardiac vein (Vieussens; 8%) and middle cardiac vein (5%). Ninety-three percent had left atrial branches, and 41% had at least one branch with lumen > 3 French. For CRT lead placement, the mid-lateral LV was accessible from the middle cardiac vein (20%), the left posterior vein (92%) or the anterior interventricular vein (86%). Among specimens where the left phrenic nerve was preserved it crossed the LV mid-lateral wall in 45%. CONCLUSIONS: Epicardial coronary vein anatomy is variable, and the mid-lateral LV wall can potentially be accessed through various tributaries of the epicardial veins. The orientation of the Thebesian valve favors cannulation of the CS from an anterior (ventricular) and inferior approach. Anterobasal, mid-lateral, and inferior apical LV coronary veins lie in proximity to the course of the phrenic nerve.

Myocardium of the superior vena cava, coronary sinus, vein of Marshall, and the pulmonary vein ostia: gross anatomic studies in 620 hearts.

INTRODUCTION: Radiofrequency ablation for atrial fibrillation (AF) frequently involves energy delivery at the ostia of the thoracic veins. Detailed evaluation of the myocardium extending into the caval veins, vein of Marshall, as well as at the pulmonary vein ostia has not been completely evaluated. METHODS AND RESULTS: Post-mortem assessment of 620 formalin-fixed hearts (mean age 60 ± 23 years, 44% female) was performed. The hearts were examined for integrity of venous structures and their atrial connections. Systematic gross anatomic evaluation including measurements on myocardial extensions in these veins was performed. Macroscopic myocardial extensions into pulmonary veins were noted in 99% of specimens evaluated and were circumferentially symmetric (99.6%). Myocardial extensions into the superior vena cava (SVC) occurred in 78% with the majority being circumferentially asymmetric (61%). Occasionally, myocardium extended into the azygos vein (6%). There were no myocardial extensions in the inferior vena cava (IVC). In some cases, the right atrial pectinate muscle extended into the coronary sinus (7%). The vein of Marshall was consistently located anterior to the left-sided pulmonary veins and posterior to the left atrial appendage, overlying the left atrial endocardial ridge. CONCLUSIONS: Myocardial extensions into the pulmonary veins are usually circumferential at the ostia validating the necessity for wide area rather than segmental ablation to isolate these veins during AF ablation. Myocardial extensions into the SVC are common and less likely to be circumferential, whereas extensions into the IVC are not present. The left atrial ridge is a reliable endocardial target for radiofrequency ablation of the vein of Marshall.

Diagnostic accuracy of the Berlin Questionnaire in detecting sleep-disordered breathing in patients with a recent myocardial infarction.

BACKGROUND: The Berlin Questionnaire (BQ) has been used to identify patients at high risk for sleep-disordered breathing (SDB) in a variety of populations. However, there are no data regarding the validity of the BQ in detecting the presence of SDB in patients after myocardial infarction (MI). The aim of this study was to determine the performance of the BQ in patients after MI. METHODS: We conducted a cross-sectional study of 99 patients who had an MI 1 to 3 months previously. The BQ was administered, scored using the published methods, and followed by completed overnight polysomnography as the "gold standard." SDB was defined as an apnea-hypopnea index of ≥ 5 events/h. The sensitivity, specificity, and positive and negative predictive values of the BQ were calculated. RESULTS: Of the 99 patients, the BQ identified 64 (65%) as being at high-risk for having SDB. Overnight polysomnography showed that 73 (73%) had SDB. The BQ sensitivity and specificity was 0.68 and 0.34, respectively, with a positive predictive value of 0.68 and a negative predictive value of 0.50. Positive and negative likelihood ratios were 1.27 and 0.68, respectively, and the BQ overall diagnostic accuracy was 63%. Using different apnea-hypopnea index cutoff values did not meaningfully alter these results. CONCLUSION: The BQ performed with modest sensitivity, but the specificity was poor, suggesting that the BQ is not ideal in identifying SDB in patients with a recent MI.

Patients with obstructive sleep apnea exhibit impaired endothelial function after myocardial infarction.

BACKGROUND: Impaired brachial flow-mediated dilation (FMD) is associated with risk for subsequent cardiovascular events in patients after myocardial infarction (MI). These patients often have obstructive sleep apnea (OSA). We tested the hypothesis that patients with OSA post MI will exhibit more severe impairment in FMD. METHODS: We studied 64 patients with MI admitted to our hospital. OSA was determined using polysomnography. FMD was measured using high-resolution ultrasonography, with researchers blind to the OSA diagnosis. RESULTS: The mean age was 60 ± 11 years, and the mean BMI was 29 (26, 32 kg/m(2)), 84% of patients were men, 39% had moderate to severe OSA (apnea-hypopnea index [AHI] > 15), and 31% of the patients had mild OSA (5 ≤ AHI < 15). FMD was severely impaired in patients with moderate to severe OSA (0.8% ± 0.7%) as compared with patients without OSA (4.7% ± 0.8%, P = .001) and with mild OSA (3.9% ± 0.8%, P = .015). Linear regression showed that FMD was associated with log nocturnal nadir oxygen saturation (minSaO(2)) (ß = 31.17, P = .0001), age (ß = -0.11, P = .006). MinSaO(2) was an independent predictor of FMD after adjustment for possible confounders (ß = 26.15, P = .001). CONCLUSIONS: FMD is severely impaired in patients with moderate to severe OSA post MI, which may be partially related to nocturnal hypoxemia. Patients with OSA may, therefore, be at higher risk for subsequent cardiovascular events after an MI. Identifying and treating OSA may have important implications in the long-term prognosis of patients post MI. Further studies are necessary to determine if the presence of OSA would affect the long-term occurrence of cardiovascular events after an MI.

Anatomical correlates relevant to ablation above the semilunar valves for the cardiac electrophysiologist: a study of 603 hearts.

INTRODUCTION: Certain outflow tract tachyarrhythmias require ablation above the semilunar valves. Understanding of the regional anatomy of these arrhythmogenic sites is required to avoid complications. METHODS AND RESULTS: We examined 603 formalin-fixed autopsy hearts from October 1998 to July 2003. Three hundred forty-two of 603 (57%) had myocardial extensions above the aortic valve, and 446 of 602 (74%) had extensions above the pulmonary valve. Extensions were noted above the aortic right coronary cusp (RCC) in 332 of 603 (55%; 2.8 ± 1.2 mm), left coronary cusp (LCC) in 145 of 603 (24%; 1.5 ± 0.5 mm), and non-coronary/posterior cusp in four of 603 (0.66%; 1.3 ± 0.5 mm; p < 0.0001), intercuspally in 295 of 603 (49%; 2.2 ± 1.1 mm) and into the cusps in 13 of 603 (2.2%). Extensions were noted above the pulmonary right cusp in 360 of 602 (60%; 4.0 ± 2.5 mm), posterior/left cusp in 313 of 602 (52%; 3.6 ± 2.1 mm), and anterior cusp in 268 of 602 (45%; 3.7 ± 2.2 mm; p < 0.0001), intercuspally in 438 of 602 (73%; 3.4 ± 1.8 mm) and into the cusps in ten of 602 (1.7%). The left main coronary artery was closer to the myocardial extensions above the nearest pulmonary valve cusp (posterior) than those above the nearest aortic valve cusp (LCC; 4.8 ± 1.7 vs. 16.3 ± 3.3 mm, p = 0.0005). CONCLUSION: Myocardial extensions are common into the great arteries above the semilunar cusps and intercuspally, and rarely into the cusps themselves. The extensions are larger and more symmetric above the pulmonary cusps as compared to the aortic cusps, the most prominent aortic extensions being above the RCC. The left main coronary artery courses close to the extensions above the posterior pulmonary cusp.

Electrophysiological anatomy of typical atrial flutter: the posterior boundary and causes for difficulty with ablation.

BACKGROUND: The electrophysiological anatomy of cavotricuspid isthmus-dependent atrial flutter (CVTI-AFL) has not been fully elucidated. METHODS: We studied 602 autopsied human hearts from individuals aged 0 to 103 years. We measured morphological features of the right atrium, including the crista terminalis (CT), pectinate muscles, sub-Eustachian pouch, Thebesian valve (TV), and the coronary sinus (CS) ostium. RESULTS: In adults, the mean right atrium dimensions were 4.7 cm x 4.5 cm x 4.4 cm. Pectinate muscles extended medial to the CT in 54% of hearts. In 19% of hearts, these ended in another ridge termed the second CT. Pectinate muscles extended into the CVTI in 70% of hearts. A sub-Eustachian pouch was present in 16% of hearts, was always located on the septal CVTI, and was more likely when a prominent TV was also present. A TV, present in 62% of all hearts, covered the inferior quadrant of the CS ostium in 9% of these hearts. CONCLUSION: The posterior boundary of the reentrant circuit of CVTI-AFL comprises the Eustachian ridge and CT, but in some patients may also include a second CT. Sub-Eustachian pouches on the septal CVTI are strongly associated with a prominent TV. The lateral CVTI can have prominent pectinate muscles. This comprehensive characterization of the electrophysiological anatomy of the reentrant circuit of CVTI-AFL may provide guidance and improve success during difficult ablations.

Day-night variation of acute myocardial infarction in obstructive sleep apnea.

OBJECTIVES: This study sought to evaluate the day-night variation of acute myocardial infarction (MI) in patients with obstructive sleep apnea (OSA). BACKGROUND: Obstructive sleep apnea has a high prevalence and is characterized by acute nocturnal hemodynamic and neurohormonal abnormalities that may increase the risk of MI during the night. METHODS: We prospectively studied 92 patients with MI for which the time of onset of chest pain was clearly identified. The presence of OSA was determined by overnight polysomnography. RESULTS: For patients with and without OSA, we compared the frequency of MI during different intervals of the day based on the onset time of chest pain. The groups had similar prevalence of comorbidities. Myocardial infarction occurred between 12 am and 6 am in 32% of OSA patients and 7% of non-OSA patients (p = 0.01). The odds of having OSA in those patients whose MI occurred between 12 am and 6 am was 6-fold higher than in the remaining 18 h of the day (95% confidence interval: 1.3 to 27.3, p = 0.01). Of all patients having an MI between 12 am and 6 am, 91% had OSA. CONCLUSIONS: The diurnal variation in the onset of MI in OSA patients is strikingly different from the diurnal variation in non-OSA patients. Patients with nocturnal onset of MI have a high likelihood of having OSA. These findings suggest that OSA may be a trigger for MI. Patients having nocturnal onset of MI should be evaluated for OSA, and future research should address the effects of OSA therapy for prevention of nocturnal cardiac events.

Implications of obstructive sleep apnea for atrial fibrillation and sudden cardiac death.

Obstructive sleep apnea (OSA) is a sleep-related breathing disorder with important cardiovascular consequences, including arrhythmogenesis. The unique pathophysiology of OSA results in multiple intermediate mechanisms that may promote atrial fibrillation, ventricular arrhythmias, and sudden cardiac death. These mechanisms may act acutely to trigger nocturnal dysrhythmias, or chronically by affecting the electrical and myocardial substrates. Burgeoning epidemiological data have identified an increased risk for atrial fibrillation and sudden cardiac death related to OSA. Currently, few data exist to support the efficacy of OSA therapy, namely continuous positive airway pressure, as an adjunct for arrhythmia prevention or management.

Successful ablation of atrial tachycardia in the right coronary cusp of the aortic valve in a patient with atrial fibrillation: what is the substrate?

Atrial tachycardias have been successfully ablated from the noncoronary cusp of the aortic valve. The anatomical substrate responsible for the arrhythmia in these patients is unknown. We report a case of intracardiac ultrasound confirmed ablation in the right coronary cusp of the aortic valve. Pacing maneuvers performed in this case, along with the regional anatomy of the right coronary cusp, strongly suggest that the ablated substrate is muscular extensions above the aortic valve. Ablation in the right coronary cusp eliminated tachycardia without valve damage or AV conduction abnormality.

Independent association between obstructive sleep apnea and subclinical coronary artery disease.

BACKGROUND: Obstructive sleep apnea (OSA) is associated with coronary risk factors, but it is unknown if OSA is associated with development of coronary disease. We evaluated the association between OSA and the presence of subclinical coronary disease assessed by coronary artery calcification (CAC). METHODS: Consecutive patients with no history of coronary disease who underwent electron-beam CT within 3 years of polysomnography between March 1991 and December 2003 were included. OSA was defined by an apnea-hypopnea index (AHI) > or = 5 events per hour, and patients were grouped by quartiles of AHI severity. Logistic regression modeled the association between OSA severity and presence of CAC. RESULTS: There were 202 patients (70% male; median age, 50 years; mean body mass index, 32 kg/m(2); 8% diabetic; 9% current smokers; 60% hypercholesterolemic; and 47% hypertensive). OSA was present in 76%. CAC was present in 67% of OSA patients and 31% of non-OSA patients (p < 0.001). Median CAC scores (Agatston units) were 9 in OSA patients and 0 in non-OSA patients (p < 0.001). Median CAC score was higher as OSA severity increased (p for trend by AHI quartile < 0.001). With multivariate adjustment, the odds ratio for CAC increased with OSA severity. Using the first AHI quartile as reference, the adjusted odds ratios for the second, third, and fourth quartiles were 2.1 (p = 0.12), 2.4 (p = 0.06), and 3.3 (p = 0.03), respectively. CONCLUSIONS: In patients without clinical coronary disease, the presence and severity of OSA is independently associated with the presence and extent of CAC. OSA identifies patients at risk for coronary disease and may represent a highly prevalent modifiable risk factor.

Atrial fibrillation and obesity--results of a meta-analysis.

BACKGROUND: Obesity has been shown to be associated with atrial enlargement and ventricular diastolic dysfunction, both of which are risk factors for atrial fibrillation (AF). However, the role of obesity as a risk factor for the development of AF is unknown. The study aims to evaluate the role of obesity as a risk factor for the development of AF. METHODS: The MEDLINE/ PUBMED and Cochrane databases were searched for studies in human subjects published in English language between 1966 and May 2007. Studies were included in our analyses if they were population-based cohort or postcardiac surgery cohort and investigated the incidence of AF in relation to the body mass index (BMI) categories. RESULTS: Of the 468 articles identified, 16 studies that enrolled a total of 123,249 individuals met the inclusion criteria. These 16 articles included 5 population-based cohort studies that enrolled 78,602 adult individuals from the United States and 3 European countries and 11 postcardiac surgery studies that enrolled 44,647 patients. Based on the population-based cohort studies, obese individuals have an associated 49% increased risk of developing AF compared to nonobese individuals (relative risk 1.49, 95% CI 1.36-1.64). The risk of AF increased in parallel with greater BMI in this cohort. In contrast, in the postcardiac surgery studies, obese individuals do not have an associated increased risk of developing AF compared to nonobese individuals (relative risk 1.02, 95% CI 0.99-1.06). CONCLUSIONS: Our findings demonstrate that obesity increased the risk of developing AF by 49% in the general population, and the risk escalated in parallel with increased BMI. Thus, AF evolves as yet another pathogenetic factor by which obesity may increase cardiovascular and cerebrovascular events.

Differentiating atrioventricular nodal reentrant tachycardia from junctional tachycardia: novel application of the delta H-A interval.

INTRODUCTION: Junctional tachycardia (JT) and atrioventricular nodal reentrant tachycardia (AVNRT) can be difficult to differentiate. Yet, the two arrhythmias require distinct diagnostic and therapeutic approaches. We explored the utility of the delta H-A interval as a novel technique to differentiate these two tachycardias. METHODS: We included 35 patients undergoing electrophysiology study who had typical AVNRT, 31 of whom also had JT during slow pathway ablation, and four of whom had spontaneous JT during isoproterenol administration. We measured the H-A interval during tachycardia (H-A(T)) and during ventricular pacing (H-A(P)) from the basal right ventricle. Interobserver and intraobserver reliability of measurements was assessed. Ventricular pacing was performed at approximately the same rate as tachycardia. The delta H-A interval was calculated as the H-A(P) minus the H-A(T). RESULTS: There was excellent interobserver and intraobserver agreement for measurement of the H-A interval. The average delta H-A interval was -10 ms during AVNRT and 9 ms during JT (P < 0.00001). For the diagnosis of JT, a delta H-A interval >or= 0 ms had the sensitivity of 89%, specificity of 83%, positive predictive value of 84%, and negative predictive value of 88%. The delta H-A interval was longer in men than in women with JT, but no gender-based differences were seen with AVNRT. There was no difference in the H-A interval based on age

The incidence of ischemic stroke in chronic heart failure: a meta-analysis.

BACKGROUND: There is marked variability in the reported stroke rates among persons with heart failure (HF). We performed a meta-analysis to provide summary estimates of the stroke rate in HF and to explain heterogeneity in the existing literature. We will summarize the ischemic stroke rate at various time points during follow-up among adults with chronic heart failure. METHODS AND RESULTS: A systematic review of the electronic literature in Medline and PubMed as well as hand searching of the reference lists of identified articles and of the meeting abstracts for the 1995-2004 American College of Cardiology and American Heart Association scientific sessions was performed to identify qualifying studies. Articles were included if they included a population with chronic HF and reported the number (or percent) of persons with HF who experienced an ischemic stroke during follow-up. Studies were excluded if the study population included > or = 50% of persons with acute (postmyocardial infarction) HF, or if > or = 50% of the study population required artificial support with a ventricular assist device or parenteral inotropic medications. Case reports, case series, and nonoriginal research articles were not included. Determination of study eligibility and data extraction were conducted by 2 independent reviewers using standardized forms. Results are reported as stroke rate per 1000 cases of HF, with 95% Poisson confidence intervals. Pooled estimates of the stroke rate were calculated with fixed and random effects models. Heterogeneity was explored according to a priori specified subgroup analyses. Overall, 26 studies met inclusion criteria. Eighteen of every 1000 persons suffered a stroke during the first year after the diagnosis of HF. The stroke rate increased to a maximum of 47.4 per 1000 at 5 years. Studies with fewer women, those conducted in 1990 or earlier, and cohort studies reported higher stroke rates than studies with more women, those conducted after 1990, and clinical trials. CONCLUSIONS: Stroke is an important complication among persons with HF. Variability among reported stroke rates can be explained in part by differences in study design, patient population, and HF standards of care at the time of the study. Despite the heterogeneity in reported stroke rates, this meta-analysis shows that stroke prevention in HF represents an opportunity to prevent morbidity and save many lives in this highly fatal disease.

The scoring of cardiac events during sleep.

Standardized guidelines for polysomnography (PSG) have not specified methods for acquiring or interpreting electrocardiographic (ECG) data. The practice of single lead ECG monitoring during PSG may allow identification of simple measures of cardiac rhythm but reduces the ability to detect myocardial ischemia and to define cardiac intervals. Although simple measures of cardiac rhythm such as heart rate and cardiac pauses are inherently reliable, there is limited data regarding outcome measures relative to sleep related heart rates and cardiac events during sleep. Several observational and cross-sectional studies demonstrate that average heart rate drops nearly 50% from infancy through young adulthood and that the average heart rate slows during sleep compared with wakefulness; the definitions of sinus bradycardia and sinus tachycardia should therefore be lower during sleep than wakefulness. Asystoles of up to 2 seconds are seen in normal populations during sleep. Although there may be an increased risk of certain arrhythmias at night, particularly in sleep disordered breathing, there is no evidence that supports different definitions for these arrhythmias during sleep compared with wakefulness. When the quality of tracings permits, the standard definitions of narrow- and wide-complex tachycardias and atrial fibrillation may be employed. In the future, expansion to multiple ECG leads and the use of alternative tools may provide better definition of heart rates and cardiac events during sleep.

Comparison of cardiac structural and functional changes in obese otherwise healthy adults with versus without obstructive sleep apnea.

Obstructive sleep apnea (OSA) and obesity have been linked to systolic and diastolic dysfunction of the left ventricle. Right ventricular function is poorly understood in the 2 clinical conditions. Data from this study show that otherwise healthy obese patients with OSA had increased an left atrial volume index compared with similarly obese patients without OSA (16.3 +/- 1.2 ml/m in obese patients without OSA vs 20.2 +/- 1.0 ml/m in those with OSA, p = 0.02) and altered diastolic function reflected by changes in mitral annular late diastolic velocity (-5.7 +/- 0.7 cm/s in obese patients without OSA vs -7.3 +/- 0.7 cm/s in those with OSA, p = 0.007), mitral annular early diastolic velocity (-7.9 +/- 0.6 cm/s in obese patients without OSA vs -6.4 +/- 0.3 cm/s in those with OSA, p = 0.05), and early to late diastolic annular ratio >1 (82% of obese patients without OSA vs 26% of those with OSA, p = 0.001), which may be signs of early subclinical impairment of cardiac function. Importantly, healthy obese subjects had similarly increased left ventricular mass compared with obese patients with OSA but normal diastolic function and left atrial size. There was a trend toward abnormal right ventricular filling in patients with OSA, measured by altered superior vena cava diastolic velocity during expiration (-15 +/- 2 cm/s in obese patients without OSA vs -10 +/- 3 cm/s in those with OSA, p = 0.2) and a tendency toward diastolic dysfunction reflected by decreased lateral tricuspid annular early diastolic velocity (-7.2 +/- 0.5 cm/s in obese patients without OSA vs -6.1 +/- 0.5 cm/s in those with OSA, p = 0.1) beyond that seen in obesity alone. In conclusion, OSA independent of obesity may induce cardiac changes that could predispose to atrial fibrillation and heart failure.