Apoor S. Gami

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 &khgr;2 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.

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 clinicians 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.

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.

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.

Obstructive sleep apnea: Implications for cardiac and vascular disease

ALONG WITH THE EPIDEMIC OF obesity, there is a growing awareness of sleep-disordered breathing as a potential and treatable risk factor for cardiovascular disease. The repetitive nocturnal hypoxemia experienced by patients with obstructive sleep apnea (OSA) is associated with activation of a number of neural, humoral, thrombotic, metabolic, and inflammatory disease mechanisms, all of which have also been implicated in the pathophysiology of cardiac and vascular disease. Activation of these mechanisms is often evident even in patients with OSA who are free of overt cardiovascular disease, suggesting that OSA may conceivably contribute to the initiation and progression of cardiovascular disease (FIGURE 1). SleepapneacanbecategorizedasOSA, in which there is preserved and increased respiratory effort despite partial or complete occlusion of the upper airway; or as central sleep apnea (CSA), in which there is absence of both respiratory efforts and airflow. The apneahypopnea index (ie, the number of apneic and hypopneic events per hour) is used as one index of the presence and severity of sleep apnea. For OSA, an apnea-hypopnea index of 5 to 15 indicates mild apnea; of 15 to 30, moderate apnea; and of greater than 30, severe apnea. Approximately 1 in 5 adults has at least mild OSA (apnea-hypopnea index, 5-15), and 1 in 15 adults has at least moderate OSA (apnea-hypopnea index, 15-30). Other measures of the severity of sleep apnea include the severity of oxygen desaturation and the level of daytime sleepiness. Obstructive sleep apnea is commonly associated with obesity and also is often present in patients with

Under-diagnosis of Sleep Apnea in Patients after Acute Myocardial Infarction

TO THE EDITOR: Obstructive sleep apnea (OSA) is highly prevalent in the general population and has been associated with arrhythmias, hypertension, stroke, and heart failure (1). Identification of OSA in cardiovascular patients is especially important as untreated OSA may be accompanied by increased cardiovascular events, and this risk may be attenuated by treatment with continuous positive airway pressure (CPAP)(2). We sought to investigate how the rates of recognition and diagnosis of obstructive sleep apnea compare to the actual prevalence of OSA in patients after myocardial infarction (MI). This study comprised two parts: a chart review of consecutive patients presenting with acute MI, and a prospective evaluation of MI patients who were recruited to undergo polysomnography. These studies were approved by the Institutional Review Board. First, we reviewed the medical records of 798 consecutive patients who were hospitalized with a diagnosis of acute MI between January and September 2007. Electronic records, including admission and dismissal notes were searched for diagnosed or suspected sleep disordered breathing, and especially for mention of OSA during the MI hospitalization. In the event of several hospital admissions for the same patient, only the first admission was used in our analysis. We further prospectively studied 74 patients who were hospitalized with acute myocardial infarction between 2004 and 2008, and were recruited to undergo attended overnight polysomnography, which is the gold standard in the diagnosis of OSA (Compumedics Siesta Wireless Sleep Recorder, Oxford Instruments, UK). All polysomnographies were performed within 6 weeks of the MI hospitalization, and scored by standard criteria (1). OSA was defined as present when the apnea hypopnea index (AHI) was >5. The diagnosis of MI was based on standard guidelines, and was made by the attending physicians who were blinded to this study. Patients were approached during their MI hospitalization, and their participation was based on their consent and availability of the study personnel and equipment. There was no systematic selection for specific demographic or patient characteristics. A review of electronic and paper records of these patients was also performed in similar fashion to that of the first part of our study. Between January and September 2007 there were 798 patients admitted to our institution with the diagnosis of acute MI. The mean age of this cohort was 69±14 years, and 512 (64%) were male. Diagnosed and suspected OSA was recorded in 97 (12%) patient records. The prospective cohort of 74 patients had a mean age of 62±13 years, and 46 (78%) were male. On review of their hospital records, 10 (14%) had documentation of diagnosed or suspected OSA. All of these patients underwent overnight polysomnography (PSG). For this group the mean AHI was 17±18 events/hour. OSA was present in 51 (69%), and severe OSA (AHI >15) in 30 (41%) patients. The main finding of this study was the low rate of documented or suspected OSA in patients hospitalized for acute MI, contrasting with the high prevalence of OSA in those in whom we conducted prospective PSG studies. This suggests a lack of awareness and recognition of OSA during treatment of acute MI. A high prevalence of OSA in the unselected general population has been well documented (1). Our results suggest that only 12 percent of patients hospitalized with acute MI had documentation of diagnosed or suspected OSA. When prospectively evaluated by overnight PSG a subgroup of patients had a much higher actual prevalence of OSA (over two thirds had at least mild OSA) but even in these patients with proven sleep apnea the possibility of OSA was documented in only 14 percent of patients. There are several limitations to our study. First, documentation in the medical record does not necessarily reflect the entire scope of medical evaluation; it is possible that in some patients OSA was suspected and they were verbally recommended to have an OSA evaluation which was not documented in the records, or this was left for a follow-up visit. Even so, it would be advantageous to arrange for screening for OSA during the hospitalization, just as we routinely initiate aspirin, beta-blocker, statin, and ACE inhibitor therapy before patient discharge. Cardiovascular disease patients with untreated severe OSA are thought to have worse cardiovascular outcomes (2,3), which may be improved with CPAP. Randomized controlled trials testing this assumption are lacking. Demonstrated beneficial effects of CPAP could lead to significant practice and guidelines changes. An absence of such clinical trials may help explain the relatively low awareness of OSA as an important consideration in the patient with MI.

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.

Author self-citation in the diabetes literature

Background: Author self-citation is the practice of citing ones previous publications in a new publication. Its extent is unknown. We studied author self-citation, choosing the major clinical field of diabetes mellitus to represent the general medical literature. Methods: We identified every article about diabetes mellitus in 170 hand-searched clinical journals published in 2000. For every article, we recorded the bibliographic citation and publication type (original or review article) and assessed the methodologic rigour. Citation information was obtained from the ISI Web of Knowledge in April 2003. Results: Of 49 028 articles, 289 were about diabetes mellitus and had citation information. Citation counts ranged from 0 to 347 (median 6, interquartile range [IQR] 2–12). Author self-citation counts ranged from 0 to 16 (median 1, IQR 0–2). Author self-citations accounted for an average of 18% (95% confidence interval [CI] 15%–21%) and a median of 7% (95% CI 5%– 11%) of all citations of each publication that was cited at least once (n = 266). Original articles had double the mean proportion of author self-citations compared with review articles (19% v. 9%; median 7% v. 0%, difference 7%, 95% CI 0– 10%). Methodologic rigour and review type were not significantly associated with subsequent author self-citation. Interpretation: Nearly one-fifth of all citations to articles about diabetes mellitus in clinical journals in the year 2000 were author self-citations. The frequency of self-citation was not associated with the quality of publications. These findings are likely applicable to the general clinical medicine literature and may have important implications for the assessment of journal or publication importance and the process of scientific discovery.

Modest Visceral Fat Gain Causes Endothelial Dysfunction in Healthy Humans

OBJECTIVES The aim of this study was to determine the impact of fat gain and its distribution on endothelial function in lean healthy humans. BACKGROUND Endothelial dysfunction has been identified as an independent predictor of cardiovascular events. Whether fat gain impairs endothelial function is unknown. METHODS A randomized controlled study was conducted to assess the effects of fat gain on endothelial function. Forty-three normal-weight healthy volunteers were recruited (mean age 29 years; 18 women). Subjects were assigned to gain weight (approximately 4 kg) (n=35) or to maintain weight (n=8). Endothelial function (brachial artery flow-mediated dilation [FMD]) was measured at baseline, after fat gain (8 weeks), and after weight loss (16 weeks) for fat gainers and at baseline and follow-up (8 weeks) for weight maintainers. Body composition was measured by dual-energy X-ray absorptiometry and abdominal computed tomographic scans. RESULTS After an average weight gain of 4.1 kg, fat gainers significantly increased their total, visceral, and subcutaneous fat. Blood pressure and overnight polysomnography did not change after fat gain or loss. FMD remained unchanged in weight maintainers. FMD decreased in fat gainers (9.1+/-3% vs. 7.8+/-3.2%, p=0.003) but recovered to baseline when subjects shed the gained weight. There was a significant correlation between the decrease in FMD and the increase in visceral fat gain (rho=-0.42, p=0.004), but not with subcutaneous fat gain (rho=-0.22, p=0.15). CONCLUSIONS In normal-weight healthy young subjects, modest fat gain results in impaired endothelial function, even in the absence of changes in blood pressure. Endothelial function recovers after weight loss. Increased visceral rather than subcutaneous fat predicts endothelial dysfunction. (Fat Gain and Cardiovascular Disease Mechanisms; NCT00589498).

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.