Left Ventricular Dysfunction, Pulmonary Hypertension, Obesity, and Sleep Apnea

The purpose of this study was to determine the frequency of central and obstructive sleep apnea in adult patients who have echocardiographic evidence of left ventricular dysfunction and pulmonary hypertension. Subjects with left ventricular dysfunction, pulmonary hypertension (pulmonary artery systolic pressure >30 mm Hg) and no lung disease were evaluated for risk factors associated with pulmonary hypertension. Of eight eligible adults, six completed the study. Subjects were from suburban and inner city family practices. Spirometric assessment, pulse oximetry on room air, rheumatologic evaluation, polysomnography, and additional history were taken. All six subjects had sleep apnea (apnea-plus-hypopnea index, or AHI, 20): obstructive, central, or mixed. All were obese, and almost all the subjects had a restrictive pattern on spirometry, which is consistent with obesity. All had a pulmonary artery systolic blood pressure of 35 mm Hg or greater. None had daytime hypoxemia or collagen vascular disease, and none had ever used appetite suppressants. This study found a strong association between pulmonary hypertension and obstructive or central sleep apnea in obese patients with congestive heart failure (CHF). We propose that a pulmonary artery systolic pressure of 35 mm Hg or greater in ambulatory patients with CHF may signify an increased risk of sleep apnea.     

An update on obstructive sleep apnea and the metabolic syndrome

PURPOSE OF REVIEW: Patients with obstructive sleep apnea are often overweight or obese, and they frequently exhibit metabolic aberrations, collectively known as the metabolic syndrome, an established cardiovascular risk factor. We review recent data on the relationship between obstructive sleep apnea and metabolic syndrome or its components, including abdominal obesity, insulin resistance, hypertension, and dyslipidemia. RECENT FINDINGS: There is accumulating evidence for an independent association between obstructive sleep apnea and metabolic syndrome or its components. Recent epidemiologic and clinical data suggest a causal role of severe obstructive sleep apnea in development of hypertension, but findings for insulin resistance and dyslipidemia are controversial. Visceral obesity remains a confounding issue in analyses. Animal models and translational studies indicate that obstructive sleep apnea may promote metabolic dysfunction through cycles of intermittent hypoxia; proposed underlying pathophysiologic mechanisms include oxidative stress, sympathetic activation, and inflammation. SUMMARY: There is suggestive evidence, but independent associations between obstructive sleep apnea and metabolic syndrome or its components are not fully established because of the confounding effect of obesity. Large randomized interventional trials are needed to identify any cause-effect relationship. Long-term follow-up studies would help to clarify the role of treatment of sleep apnea in reducing cardio-metabolic morbidity.     

Alveolar hypoventilation in the obese: the obesity-hypoventilation syndrome

The obesity-hypoventilation syndrome (or alveolar hypoventilation in the obese) is a new name for an old syndrome, Pickwickian syndrome. It is defined as chronic alveolar hypoventilation (PaO(2)<70 mmHg, PaCO(2) > 45 mmHg) in obese patient with a body mass index > 30 kg/m(2) who have no other respiratory disease explaining the gas anomalies. The large majority of obese subjects are not hypercapnic, even in case of severe obesity. There are three principal causes explaining alveolar hypoventilation in obese subjects: high cost of the work of respiration, dysfunction of the respiratory centers, repeated episodes of nocturnal obstructive apnea. The obesity-hypoventilation syndrome is generally found in males aged over 50 years. Exercise-induced breathlessness is a constant finding. Diagnosis is often made after an episode of severe respiratory failure. Associated diseases favored by obesity are frequent: diabetes, high blood pressure, heart disease. By definition, there is a hypoxemia-hypercapnia syndrome persisting after an acute episode. Spirography usually demonstrates moderate volume restriction. Pulmonary hypertension is frequent but not constant. Obesity-hypoventilation syndrome must be distinguished from obstructive sleep apnea, although the two conditions are often associated. Obstructive sleep apnea may be absent in certain patients with obesity-hypoventilation syndrome (we have had several cases) and inversely, obesity is not observed in certain patients with obstructive apnea. It should be recalled that the term Pickwickian syndrome designates obesity-hypoventilation syndrome (with or without obstructive apnea) and not obstructive sleep apnea syndrome.     

Obesity cardiomyopathy: pathophysiology and evolution of the clinical syndrome

Obesity produces an increase in total blood volume and cardiac output because of the high metabolic activity of excessive fat. In moderate to severe cases of obesity, this may lead to left ventricular dilation, increased left ventricular wall stress, compensatory (eccentric) left ventricular hypertrophy, and left ventricular diastolic dysfunction. Left ventricular systolic dysfunction may occur if wall stress remains high because of inadequate hypertrophy. Right ventricular structure and function may be similarly affected by the aforementioned morphologic and hemodynamic alterations and by pulmonary hypertension related to the sleep apnea/ obesity hypoventilation syndrome. The term obesity cardiomyopathy is applied when these cardiac structural and hemodynamic changes result in congestive heart failure. Obesity cardiomyopathy typically occurs in persons with severe and long-standing obesity. The predominant causes of death in those with obesity cardiomyopathy are progressive congestive heart failure and sudden cardiac death.     

肥胖型支气管哮喘患者合并阻塞性睡眠呼吸暂停综合征临床分析

目的本研究初步探讨了肥胖型支气管哮喘患者合并阻塞性睡眠呼吸暂停低通气综合征(OSAHS)的临床特点。方法评价95例诊断为肥胖型支气管哮喘患者的年龄、性别、睡眠打鼾史、高血压史、吸烟史、饮酒史、动脉血压。使用多导睡眠监测系统记录睡眠过程中的多次生理事件,评价AHI和最低血氧饱和度(SaO_2),使用哮喘控制测试问卷(ACT)评估哮喘控制情况。结果肥胖型支气管哮喘患者48.4%合并有阻塞性睡眠呼吸暂停,肥胖型支气管哮喘合并阻塞性睡眠呼吸暂停组与单纯哮喘组对比,肺通气功能更差、哮喘控制率更低。结论肥胖型支气管哮喘患者易合并阻塞性睡眠呼吸暂停,导致哮喘不易控制。     

老年重叠综合征患者肺动脉高压临床分析

目的探讨阻塞性睡眠呼吸暂停低通气综合征（OSAHS）合并慢性阻塞性肺病（COPD）,即重叠综合征（OS）与肺动脉高压的关系。方法回顾性分析2000年1月至2009年1月北京世纪坛医院老年医学科门诊及住院,经过完整的肺功能、动脉血气分析、超声心动图及夜间多导睡眠监测的60岁以上患者89例。结果 OSAHS组与OS组之间性别比例、年龄及体质量指数（BMI）均无显著差异（P〉0.05）。超声心动图检查结果提示：5例（5/53,9%）OSAHS患者、23例（23/36,67%）OS患者存在肺动脉高压;多导睡眠监测结果提示,OSAHS组与OS组患者夜间均存在明显低氧血症,表现为夜间最低血氧饱和度的降低及氧减指数的增加,但以OS组患者更为显著;日问的动脉血气分析结果提示,与OSAHS患者比较,OS组患者日间氧饱和度（SaO_2）、动脉氧分压（PaO_2）降低、二氧化碳分压（PaCO_2）增高。结论相对于OSAHS患者,OS患者发展为肺动脉高压和Ⅱ型呼吸衰竭的风险更高。     

阻塞性睡眠呼吸暂停综合征对右心结构和功能的影响

目的 探讨阻塞性睡眠呼吸暂停综合征（OSAS）对右心结构和功能的影响。方法 用二维及多普勒超声心动图测定30例OSAS患者右心结构和功能。结果 中、重度的OSAS患者右室舒张末期容积（RVEDV）、右室搏出量（SV）、右肺动脉内径（RPAD）均较正常组增大,而右室E峰速和A峰速比值（E/A）较正常组减小。结论 OSAS不仅使右心结构发生明显异常,而且使右心舒张功能及收缩功能也受损,成为右心功能不全的重要原因之一。     

Bilateral leg edema, obesity, pulmonary hypertension, and obstructive sleep apnea

BACKGROUND: Pulmonary hypertension is usually due to an underlying cardiac or pulmonary condition. An association between unexplained pulmonary hypertension and bilateral leg edema in primary care patients was found previously. We undertook this study to identify the frequency of obstructive sleep apnea (OSA) in ambulatory, adult patients with pulmonary hypertension who initially presented with bilateral leg edema. METHODS: Twenty ambulatory adults with bilateral leg edema, echocardiocardiographic evidence of pulmonary hypertension (estimated pulmonary artery systolic pressure >30 mm Hg) without left ventricular dysfunction, and no clinically apparent pulmonary disease [corrected] were enrolled from a suburban family practice and an inner-city family practice during a 3-year period. Spirometric assessment, pulse oximetry, rheumatologic evaluation, polysomnography, and questionnaire information regarding risk factors for pulmonary hypertension were obtained for each subject. RESULTS: Fifteen patients (75%) completed the study. Almost all of the subjects were obese. Nine (60%) of the 15 had OSA. None of the subjects demonstrated an obstructive pattern on spirometric evaluation results, but 9 (60%) had a restrictive spirometry pattern, consistent with their obesity. None of the subjects had daytime hypoxemia. Systemic hypertension was present in two-thirds of the subjects with OSA, and was absent in all of the subjects who lacked OSA. CONCLUSIONS: Bilateral leg edema in obese primary care patients is associated with both OSA and modest pulmonary hypertension. If these findings are generalizable, then bilateral leg edema may be an important clinical marker for underlying OSA.     

Funktionelle Dynamik des rechten Ventrikels und des Lungenkreislaufes bei obstruktiver Schlafapnoe

Obstructive sleep apnea (OSA) is common with an incidence of at least 500,000 patients in the German population. Typical symptoms are daytime sleepiness, headache in the morning, and snoring. Presumably obstructive sleep apnea via various mechanisms increases cardiovascular morbidity. Hypoxemia causes nocturnal hypertension in most of the patients. Nevertheless, about 20% of the patients develop daytime pulmonary hypertension and right heart dysfunction. Clinical and animal studies demonstrated right ventricular hypertrophy as a consequence of intermittent hypoxemia and pulmonary hypertension. Right ventricular hemodynamics differ essentially from left ventricular hemodynamics. Right ventricular function is substantially influenced by right ventricular afterload, which is mainly determined by pulmonary vascular resistance, and slightly influenced by preload. Application of continuous positive airway pressure (CPAP) via a nose mask normalizes nocturnal breathing disorders and reduces pre- and afterload, especially in patients with cardiomegaly. Therefore, CPAP generates positive effects on the myocardium.     

Rechtsherzinsuffizienz und Cor pulmonale

Whereas the right ventricle tolerates volume loads without any substantial increase of the pressure in the pulmonary circulation by recruiting capacitance vessels and capillaries, it possesses only small contractile reserves and reacts unadapted with right ventricular dysfunction. Its size and pressure load are relevant factors for prognosis of all forms of pulmonary hypertension, in particular if linked to left-sided heart failure. Differentiation of pulmonary hypertension according to the Venice classification is highly important. Right-sided ventricular heart failure worsens left ventricular hemodynamics due to reduced ejection fraction and in addition due to direct diastolic ventricular interaction in which left ventricular diastolic dysfunction increases even though the left ventricular systolic function is still intact. Right ventricular ejection fraction <40% is an important predictor of prognosis after myocardial infarction or chronic stages of left ventricular heart failure. The most important noninvasive diagnostic method is transthoracic echocardiography with determination of the Tei index and Doppler echocardiographic estimation of pulmonary artery pressure. Chronic obstructive pulmonary disease is the most frequent cause of cor pulmonale. While long-term oxygen therapy in patients with COPD and cor pulmonale and for example the administration of endothelin receptor antagonists in patients with idiopathic pulmonary hypertension is beneficial, the therapeutic use of drugs effective for left-sided heart failure is very limited in patients with right ventricular dysfunction.     

Aortic elastic properties and left ventricular diastolic dysfunction in patients with obstructive sleep apnea

Although the responsible mechanisms are not yet fully known, obstructive sleep apnea is associated with an increased risk for cardiovascular disease and events. The aorta is not only a conduit delivering blood to the tissues but is also an important modulator of the entire cardiovascular system, its elastic properties also affecting left ventricular function and coronary blood flow. The aim of this study was to determine left ventricular diastolic function and aortic elastic properties in patients with obstructive sleep apnea syndrome. Fourteen male patients with obstructive sleep apnea and 14 age- and body mass index-matched healthy male controls took part in the study as a control group. All subjects underwent echocardiographic examination; left ventricular cavity dimension, standard and tissue Doppler parameters, and aortic diameter (3 cm above aortic valve) at systole and diastole were measured. While the aortic stiffness index in patients with obstructive sleep apnea was significantly higher than that of the control group (4.5 ± 0.3 vs 2.1 ± 0.1, P = 0.001), the aortic distensibility index was found to be lower in this group compared with controls (2.4 ± 1.2 vs 3.9 ± 1.5 cm² dynes⁻¹ 10⁻⁶, P = 0.009). Furthermore, peak velocity of myocardial systolic wave and peak velocities of myocardial diastolic waves in sleep apnea patients were lower than in controls. There was an association between aortic stiffness and the apnea hypopnea index (coefficient = 0.49, P = 0.002). We also found an inverse correlation between peak velocity of myocardial diastolic wave and aortic stiffness (coefficient = −0.43, P = 0.003), using multiple linear regression. Increased aortic stiffness that is associated with the severity of disease in patients with obstructive sleep apnea may lead to diastolic dysfunction of the left ventricle.     

Autonomic function in sleep apnea patients: increased heart rate variability except during REM sleep in obese patients

The objective of this study was to examine heart rate variability (HRV) among sleep stages in obstructive sleep apnea (OSA) patients. The study was retrospective within subjects and examined the sleep stages and HRV in relation to OSA, age, body mass index (BMI), and sex. Data collected during diagnostic polysomnograms were used in this study. There were 105 clinical patients undergoing polysomnography for suspected OSA. We sampled the electrocardiogram (ECG) from wakefulness, stage 2, and REM sleep and analyzed for frequency domain HRV. Sampled epochs were free of apnea and arousals. Heart rate variability decreased with age. Total frequency variability (TF) and low frequency variability (LF) in wakefulness and REM sleep increased as apnea severity increased. Measures of TF, LF, and the LF/HF ratio were greatest in REM sleep. There was less LF and TF in Stage REM sleep in patients with higher BMI. In conclusion, the decrease in HRV with aging is a robust finding that occurs even in a clinical sleep apnea population. However, apnea does not mimic aging effects on the heart because HRV increased as apnea severity increased. The decrease in HRV during REM sleep in the obese apnea patients suggests the possibility of an autonomic dysfunction in this subgroup. Educational objective: To review and expand the knowledge of heart rate variability in sleep apnea patients.     

Severe obstructive sleep apnea is associated with left ventricular diastolic dysfunction

INTRODUCTION: Hypertension is common in patients with obstructive sleep apnea (OSA). However, the effect of OSA on ventricular function, especially diastolic function, is not clear. Therefore, we have assessed the prevalence of diastolic dysfunction in patients with OSA and the relationship between diastolic parameters and severity of OSA. METHODS: Sixty-eight consecutive patients with OSA confirmed by polysomnography underwent echocardiography. Diastolic function of the left ventricle was determined by transmitral valve pulse-wave Doppler echocardiography. Various baseline characteristics, severity of OSA, and echocardiographic parameters were compared between patients with and without diastolic dysfunction. RESULTS: There were 61 male and 7 female patients with a mean age of 48.1 +/- 11.1 years, body mass index of 28.5 +/- 4.3 kg/m(2), and apnea/hypopnea index (AHI) of 44.3 +/- 23.2/h (mean +/- SD). An abnormal relaxation pattern (ARP) in diastole was noted in 25 patients (36.8%). Older age (52.7 +/- 8.9 years vs 45.1 +/- 11.3 years, p = 0.005), hypertension (56% vs 20%, p = 0.002), and a lower minimum pulse oximetric saturation (SpO(2)) during sleep (70.5 +/- 17.9% vs 78.8 +/- 12.9%, respectively; p = 0.049) were more common in patients with ARP. By multivariate analysis, minimum SpO(2) < 70% was an independent predictor of ARP (odds ratio, 4.34; 95% confidence interval, 1.23 to 15.25; p = 0.02) irrespective of age and hypertension. Patients with AHI > or = 40/h had significantly longer isovolumic relaxation times than those with AHI < 40/h (106 +/- 19 ms vs 93 +/- 17 ms, respectively; p = 0.005). CONCLUSION: Diastolic dysfunction with ARP was common in patients with OSA. More severe sleep apnea was associated with a higher degree of left ventricular diastolic dysfunction in this study.     

Cardiac diastolic function and hypercapnic ventilatory responses in central sleep apnoea.

Hyperventilation is the key factor contributing to the development of idiopathic nonhypercapnic central sleep apnoea (ICSA), where left ventricular systolic function is normal. ICSA is reported to occur in 20% of patients with left ventricular diastolic dysfunction, in whom elevated pulmonary vascular pressures and resultant increased pulmonary vagal afferent traffic may contribute to hyperventilation. The contribution of the two potential mechanisms responsible for the hyperventilation seen in the following ICSA was measured: 1) left ventricular diastolic dysfunction-induced pulmonary hypertension; and 2) increased peripheral and central hypercapnic ventilatory responses (HCVR). The pulmonary artery pressure, left ventricular diastolic function and chemosensitivity to hypercapnia were measured during wakefulness in 16 subjects with ICSA. All subjects had systolic pulmonary artery pressures <3.99 kPa (<30 mmHg) and only four had diastolic dysfunction. All subjects had elevated peripheral and central HCVR compared with historical normal control subjects. Diastolic dysfunction correlated with increasing age but not with HCVR or markers of central sleep apnoea severity. Idiopathic nonhypercapnic central sleep apnoea is likely to be dependent upon raised hypercapnic ventilatory responses, and not pulmonary hypertension due to left ventricular diastolic dysfunction.     

Role of Mineralocorticoid Receptors in Obstructive Sleep Apnea and Metabolic Syndrome

Purpose of Review

This review will summarize recent developments in the research on the mineralocorticoid receptor and its impact on obstructive sleep apnea and metabolic syndrome.

Recent Findings

Aldosterone excess plays an important role in the association between resistant hypertension and obstructive sleep apnea. The prevalence of obesity is increasing rapidly worldwide and is especially common among patients with obstructive sleep apnea, resistant hypertension, and metabolic syndrome, suggesting probable mechanistic links between these three conditions. Mineralocorticoid receptor expression is increased in obese individuals, which may contribute to the common association between obesity and hyperaldosteronism. Mineralocorticoid receptor blockers reduce the severity of obstructive sleep apnea among resistant hypertension patients.

Summary

A large body of literature demonstrates a strong association between obesity, hyperaldosteronism, resistant hypertension, and sleep apnea, including specific benefit of treatment with mineralocorticoid receptor blockers for these separate disorders.

     

Nocturnal oxyhemoglobin desaturation following tracheostomy for obstructive sleep apnea

Eleven obese men with coexistent obstructive sleep apnea and chronic obstructive pulmonary disease underwent tracheostomy. Nocturnal polysomnography prior to tracheostomy revealed oxyhemoglobin desaturation associated with obstructive apnea. Following surgery, repeated polysomnography was performed to assess the effect of tracheostomy on nocturnal oxygen saturation. Non-apneic desaturation characteristic of that previously described in patients with "type B" chronic obstructive pulmonary disease was noted in six subjects. Oxyhemoglobin saturation in these six fell more than 8 percent below baseline waking and non-rapid-eye-movement (REM) sleep levels. These episodes usually lasted five minutes or longer, occurred almost uniformly during REM sleep, and were acutely ameliorated by low-flow (4 liters per minute) supplemental oxygen. The subjects with REM-associated desaturation did not differ from the subjects without desaturation by preoperative anthropomorphic, blood gas, or pulmonary function criteria. However, subjects with REM-associated desaturation tended to have lower right and left ventricular ejection fractions by pooled gated wall studies. It is concluded that patients with obstructive sleep apnea and chronic obstructive pulmonary disease should be re-evaluated after tracheostomy, since they may be at risk for continued oxyhemoglobin desaturation and progressive right ventricular deterioration despite adequate treatment of their apneic condition.     

Right and left ventricular functional impairment and sleep apnea.

Obstructive sleep apnea may contribute to the development of pulmonary hypertension and RVF primarily through pulmonary vasoconstriction secondary to hypoxia. Several recent studies indicate, however, that intermittent apnea-related hypoxia is not sufficient to cause sustained pulmonary hypertension. These studies have been consistent in showing that pulmonary hypertension and RVF are almost invariably seen in the presence of diurnal hypoxia. Sustained pulmonary hypertension, therefore, appears to be associated with sustained hypoxia as is the case in COPD. Patients with OSA who have hypoxia while awake are, as a rule, obese and have mild-to-moderate diffuse obstructive airways disease. Thus, most cases of pulmonary hypertension in association with OSA result from a combination of OSA, obesity, and diffuse obstructive airways disease, a so-called overlap syndrome. However, from the therapeutic viewpoint, it is apparent that treatment of OSA by NCPAP or tracheostomy, in such cases, is usually sufficient to reverse pulmonary hypertension and RVF. More recent work has provided strong evidence that OSA can play a role in the pathogenesis of LV heart failure in patients with CHF of otherwise unknown etiology. It is likely that this occurs through a combination of increased LV afterload related to exaggerated negative Pit swings during obstructive apneas, to intermittent hypoxia, and to chronically elevated sympathoadrenal activity. Reversal of OSA by NCPAP in these patients may relieve LV heart failure. These findings add a new dimension to our understanding of the pathophysiologic effects of OSA on the cardiovascular system by demonstrating that the LV is a structure that may suffer functional impairment secondary to the stresses imposed by OSA. Finally, it has now become apparent that CSR in patients with CHF can cause symptoms of a sleep apnea syndrome when associated with intermittent hypoxia and arousals from sleep. Reversal of CSR during sleep by NCPAP can lead to alleviation of these symptoms and possibly to reduced cardiac dyspnea and LV systolic function as well. Taken together, this suggests that much more extensive use of polysomnography may be warranted in the investigation of cardiovascular disease. The reasons are compelling: sleep apnea disorders are common and eminently treatable conditions whose reversal can result in improved right and left heart function and symptomatic improvement in patients with impaired myocardial function.     

Association of subclinical right ventricular dysfunction with obesity.

OBJECTIVES: The purpose of this research was to identify the determinants of right ventricular (RV) dysfunction in overweight and obese subjects. BACKGROUND: Right ventricular dysfunction in obese subjects is usually ascribed to comorbid diseases, especially obstructive sleep apnea. We used tissue Doppler imaging to identify the determinants of RV dysfunction in overweight and obese subjects. METHODS: Standard and tissue Doppler echocardiography was performed in 112 overweight (body mass index [BMI] 25 to 29.9 kg/m2) or obese (BMI >30 kg/m2) subjects and 36 referents (BMI <25 kg/m2), including 22 with obstructive sleep apnea but no obesity. Tissue Doppler was used to measure RV systolic (s(m)) and diastolic (e(m)) velocities and strain indexes. RESULTS: Obese subjects with BMI >35 kg/m2 had reduced RV function compared with referent subjects, evidenced by reduced s(m) (6.5 +/- 2.4 cm/s vs. 10.2 +/- 1.5 cm/s, p < 0.001), peak strain (-21 +/- 4% vs. -28 +/- 4%, p < 0.001), peak strain rate (-1.4 +/- 0.4 s(-1) vs. -2.0 +/- 0.5 s(-1), p < 0.001), and e(m) (-6.8 +/- 2.4 cm/s vs. -10.3 +/- 2.5 cm/s, p < 0.001), irrespective of the presence of sleep apnea. Similar but lesser degrees of reduced systolic function (p < 0.05) were present in overweight (BMI 25 to 29.9 kg/m2) and mildly obese (BMI 30 to 35 kg/m2) groups. Differences in RV e(m), s(m), and strain indexes were demonstrated between the severely versus overweight and mildly obese groups (p < 0.05). Body mass index remained independently related to RV changes after adjusting for age, log insulin, and mean arterial pressures. In obese patients, these changes were associated with reduced exercise capacity but not the duration of obesity and presence of sleep apnea or its severity. CONCLUSIONS: Increasing BMI is associated with increasing severity of RV dysfunction in overweight and obese subjects without overt heart disease, independent of sleep apnea.     

Ventricular function in snorers and patients with obstructive sleep apnea.

We hypothesized that intermittent hypoxemia and increased ventricular afterload due to obstructive apnea during sleep (OSA) would cause chronic left ventricular dysfunction. Overnight polysomnography, M-mode and two-dimensional echo-Doppler studies while awake were performed on 51 consecutive snorers, 30 with OSA and 21 without apnea. Patients with previous myocardial infarction, awake hypoxemia or hypercapnia, or other causes of nocturnal hypoxemia were excluded. Echo-Doppler measurements included end-diastolic right and left ventricular dimensions and wall thickness, indices of left ventricular systolic performance (fractional shortening, ejection fraction and ejection time and diastolic performance, (isovolumic relaxation time, ratio of peak early [E] to late [A] diastolic transmitral flow and mitral pressure half-time). Both OSA patients and nonapneic snorers were of similar age. Although OSA patients were heavier, had a greater apnea-hypopnea index, and significant nocturnal hypoxemia, their echo-Doppler measurements were within normal limits and were not significantly different from nonapneic snorers. It is concluded that isolated obstructive sleep apnea does not cause chronic left ventricular dysfunction.     

Joint interaction effect of metabolic syndrome and obstructive sleep apnea on hypertension

Numerous studies have observed a relationship between obstructive sleep apnea and hypertension, but the effects of metabolic syndrome on hypertension, and their interaction with obstructive sleep apnea, remain unclear. For this study, a total of 2972 patients were recruited from the Shanghai Sleep Health Study. Data from overnight polysomnography parameters, serum lipids, fasting blood glucose, blood pressure, and anthropometric measurements were collected. The authors then explored the independent associations and multiplicative and additive interactions of predictors of metabolic syndrome with hypertension. A positive dose–response relationship was observed between systolic blood pressure and diastolic blood pressure and quartiles of fasting glucose, triglyceride, low‐density lipoprotein cholesterol, body mass index, and apnea–hypopnea index. Furthermore, logistic regression analysis showed that, in men, a high triglyceride level, hyperglycemia, and overweight status (and their interaction effect on obstructive sleep apnea) were associated with hypertension. Being overweight and hyperglycemic may markedly augment the adverse effect of obstructive sleep apnea on hypertension in men. Therefore, hypertension therapy should be individualized based on the specific comorbidities of each patient.