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.

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 pattern of sudden death in obstructive sleep apnea.

BACKGROUND: The risk of sudden death from cardiac causes in the general population peaks from 6 a.m. to noon and has a nadir from midnight to 6 a.m. Obstructive sleep apnea is highly prevalent and associated with neurohormonal and electrophysiological abnormalities that may increase the risk of sudden death from cardiac causes, especially during sleep. METHODS: We reviewed polysomnograms and the death certificates of 112 Minnesota residents who had undergone polysomnography and had died suddenly from cardiac causes between July 1987 and July 2003. For four intervals of the day, we compared the rates of sudden death from cardiac causes among people with obstructive sleep apnea and the following: the rates among people without obstructive sleep apnea, the rates in the general population, and the expectations according to chance. For each interval, we assessed the median apnea-hypopnea index and the relative risk of sudden death from cardiac causes. We similarly analyzed sudden death from cardiac causes during three time intervals that correlate with usual sleep-wake cycles. RESULTS: From midnight to 6 a.m., sudden death from cardiac causes occurred in 46 percent of people with obstructive sleep apnea, as compared with 21 percent of people without obstructive sleep apnea (P=0.01), 16 percent of the general population (P<0.001), and the 25 percent expected by chance (P<0.001). People with sudden death from cardiac causes from midnight to 6 a.m. had a significantly higher apnea-hypopnea index than those with sudden death from cardiac causes during other intervals, and the apnea-hypopnea index correlated directly with the relative risk of sudden death from cardiac causes from midnight to 6 a.m. For people with obstructive sleep apnea, the relative risk of sudden death from cardiac causes from midnight to 6 a.m. was 2.57 (95 percent confidence interval, 1.87 to 3.52). The analysis of usual sleep-wake cycles showed similar results. CONCLUSIONS: People with obstructive sleep apnea have a peak in sudden death from cardiac causes during the sleeping hours, which contrasts strikingly with the nadir of sudden death from cardiac causes during this period in people without obstructive sleep apnea and in the general population.

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.

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.

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

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.

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.

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.

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.

Familial premature coronary artery disease mortality and obstructive sleep apnea.

BACKGROUND: Obstructive sleep apnea (OSA) is linked to both coronary artery disease (CAD) and sudden death, but any causal role remains unclear. A family history of premature CAD and related mortality is an independent risk factor for the development of CAD. We hypothesized that OSA is associated with a family history of premature mortality from ischemic heart disease. METHODS: We prospectively studied 588 subjects who underwent polysomnography from May 2000 to June 2004. Demographics, comorbidities, family history of cardiovascular disease, and the ages and causes of death for 10 strata of family members were recorded for all subjects. We excluded those subjects with known causes of premature cardiac death, such as hypertrophic cardiomyopathy and long-QT syndrome. OSA was defined by American Academy of Sleep Medicine criteria (ie, apnea-hypopnea index >or= 5). Premature CAD mortality was defined as death due to ischemic heart disease or sudden cardiac death before 55 years of age (men) or 65 years of age (women). RESULTS: Polysomnography confirmed OSA in 316 subjects and excluded it in 202 subjects. The unadjusted odds ratio (OR) for OSA and a family history of premature CAD mortality was 2.11 (95% confidence interval [CI], 1.10 to 4.31; p = 0.031). After adjusting for each subject's sex, body mass index, and history of CAD, there was a significant and independent association between OSA and family history of premature CAD mortality (OR, 2.13; 95% CI, 1.04 to 4.66; p = 0.046). CONCLUSIONS: Regardless of their own CAD status, people with OSA are more likely than those without OSA to have a family history of premature CAD mortality.

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.

Association of atrial fibrillation and obstructive sleep apnea.

BACKGROUND: Obstructive sleep apnea (OSA) is associated with recurrent atrial fibrillation (AF) after electrocardioversion. OSA is highly prevalent in patients who are male, obese, and/or hypertensive, but its prevalence in patients with AF is unknown. METHODS AND RESULTS: We prospectively studied consecutive patients undergoing electrocardioversion for AF (n=151) and consecutive patients without past or current AF referred to a general cardiology practice (n=312). OSA was diagnosed with the Berlin questionnaire, which is validated to identify patients with OSA. We also assessed its accuracy compared with polysomnography in a sample of the study population. Groups were compared with the 2-tailed t, Wilcoxon, and chi2 tests. Logistic regression modeled the association of AF and OSA after adjustment for relevant covariates. Patients in each group had similar age, gender, body mass index, and rates of diabetes, hypertension, and congestive heart failure. The questionnaire performed with 0.86 sensitivity, 0.89 specificity, and 0.97 positive predictive value in our sample. The proportion of patients with OSA was significantly higher in the AF group than in the general cardiology group (49% versus 32%, P=0.0004). The adjusted odds ratio for the association between AF and OSA was 2.19 (95% CI 1.40 to 3.42, P=0.0006). CONCLUSIONS: The novel finding of this study is that a strong association exists between OSA and AF, such that OSA is strikingly more prevalent in patients with AF than in high-risk patients with multiple other cardiovascular diseases. The coinciding epidemics of obesity and AF underscore the clinical importance of these results.

Sleep and cardiovascular disease.

Sleep is an important modulator of cardiovascular function, both in physiological conditions and in disease states. In individuals without a primary sleep disorder, sleep may exert significant effects on the autonomic nervous system, systemic hemodynamics, cardiac function, endothelial function, and coagulation. Some of these influences can be directly linked to specific modulatory effects of sleep stages per se; others result from the natural circadian rhythm of various physiological processes. There is a temporal association between physiological sleep and occurrence of vascular events, cardiac arrhythmias, and sudden death. Epidemiological and pathophysiological studies also indicate that there may be a causal link between primary sleep abnormalities (sleep curtailment, shift work, and sleep-disordered breathing) and cardiovascular and metabolic disease, such as hypertension, atherosclerosis, stroke, heart failure, cardiac arrhythmias, sudden death, obesity, and the metabolic syndrome. Finally, sleep disturbances may occur as a result of several medical conditions (including obesity, chronic heart failure, and menopause) and may therefore contribute to cardiovascular morbidity associated with these conditions. Further understanding of specific pathophysiological pathways linking sleep disorders to cardiovascular disease is important for developing therapeutic strategies and may have important implications for cardiovascular chronotherapeutics.

Therapy Insight: interactions between atrial fibrillation and obstructive sleep apnea.

Atrial fibrillation (AF) and obesity are coinciding epidemics. Obstructive sleep apnea (OSA) correlates directly with obesity and is highly prevalent among middle-aged adults. Emerging evidence supports a strong association between AF and OSA. The rate of AF among patients with OSA is low but is nevertheless higher than that in the general population. The prevalence of OSA among patients with AF is strikingly high-at least 32% and possibly as high as 49%-although differences in the AF populations studied and the criteria used to diagnose OSA have prevented more accurate measurement of this rate. Data in focused populations at risk of AF show that OSA increases the frequency and recurrence of AF. These findings cannot, however, be reliably generalized to the larger OSA population. Although the available information is limited, treatment of OSA, particularly with continuous positive airway pressure, seems to substantially reduce the frequency of AF. If true, this approach would provide a safe and noninvasive therapy for some patients with AF. Randomized controlled trials are necessary to rigorously answer this question. Many data have been obtained from studies with focuses other than the direct relationship between OSA and AF. Studies carefully designed to investigate the relevant issues are now needed.

Electrocardiographic poor R-wave progression: analysis of multiple criteria reveals little usefulness.

BACKGROUND: Poor or reverse R-wave progression (PRWP) is a common statement on electrocardiogram (ECG) interpretations, but its value in diagnosing anterior myocardial infarction (MI) is disputed. We assessed the accuracy of PRWP criteria in diagnosing anterior MI. METHODS: We searched MEDLINE (1960-1998) and found 3 criteria for PRWP. We included a modified version of the Marquette Muse system's criteria and multiple novel criteria. We interpreted resting ECGs of consecutive patients undergoing pharmacologic stress tests with dual isotope gated single photon emission computed tomography. Subjects with Q-wave anterior MI, bundle branch block, or Wolf-Parkinson-White syndrome were excluded. We established whether patients met the PRWP criteria. A nuclear cardiologist blinded to PRWP classifications reviewed the scintigrams. Chi2 methods were used for statistical analysis. RESULTS: Inclusion criteria were met by 122 subjects. The standard PRWP criteria were met in 15% to 42% of ECGs. Of subjects meeting PRWP criteria, 2% to 9% had anterior MI and 27% to 33% had anterior MI or ischemia. These proportions were similar to those expected by chance. The performance of PRWP criteria did not improve when subjects with electrocardiographic left ventricular hypertrophy were excluded or when more stringent criteria for right precordial R-wave amplitude were tested. CONCLUSIONS: In our study of patients undergoing cardiac stress tests, only a small percentage of patients who met various criteria for PRWP (a proportion no different than would be expected by chance) had anterior MI. Conclusions about the presence of anterior MI solely on the basis of PRWP have little usefulness.

Obesity and obstructive sleep apnea.

There is a very high prevalence of OSA in obese individuals and a high prevalence of obesity in patients with OSA. The pathophysiology of OSA is intimately linked to obesity. Anatomic and functional considerations of the pharyngeal airway, the CNS, central obesity, and leptin likely interact in the development of OSA in obese individuals. OSA may itself predispose individuals to worsening obesity because of sleep deprivation, daytime somnolence, and disrupted metabolism. The diagnosis of OSA requires the clinician's awareness of its potential to cause a spectrum of acute and chronic neurocognitive, psychiatric, and nonspecific symptoms in patients who may be unaware that their sleep is disturbed. Symptoms and examination findings help predict which obese individuals have OSA, and polysomnography is the gold standard by which to make the diagnosis and assess the effects of treatment. Numerous disease states are associated with both OSA and obesity, and it is becoming clear that the relationships are mediated by complex interrelated mechanisms. Common diseases and disease mechanisms in OSA and obesity suggest that conditions related to obesity may be better managed if patients, particularly those who are morbidly obese, are evaluated and treated for previously undiagnosed OSA. OSA is cured in only specific cases with craniofacial or upper airway surgery, and the general application of UVP is not efficacious. OSA also can be cured with sufficient lifestyle-mediated or surgical weight loss; however, in the absence of long-term weight maintenance, OSA returns with weight gain. Although not curative, nasal CPAP is the initial treatment of choice for most patients because of its noninvasive approach and technical efficacy. It is limited, however, by patient acceptance and long-term compliance. Advances in mask comfort and use of humidified air should increase its acceptance. Future management strategies include newer generations of positive airway devices that automatically titrate pressures (which are not yet recommended by expert organizations) and multidisciplinary approaches to managing the care of patients with OSA.

Contrast nephropathy after coronary angiography.

Contrast nephropathy after coronary angiography is associated with considerable morbidity and mortality. We discuss the incidence, definition, and pathologic mechanisms of contrast nephropathy; provide an overview of risk factors; highlight proven preventive interventions; clarify which interventions have shown no benefit; and discuss future possibilities. The prevention of contrast nephropathy is crucial for the care of patients undergoing coronary angiography and should be possible with an understanding of risk factors and proven management strategies.