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Nocturnal Hypoxemia Predicts Incident Cardiovascular Complications in Dialysis Patients

CNR, Centre of Clinical Physiology and Division of Nephrology, Ospedali Riuniti, Reggio Calabria, Italy.

Correspondence to: Professor Carmine Zoccali, CNR Centro Fisiologia Clinica, Divisione di Nefrologia, Via Sbarre Inferiori 39, 89100, Reggio Calabria, Italy. Phone: 0039-965-397010; Fax: 0039-965-593341; E-Mail: carmine.zoccali{at}tin.it

	Abstract

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ABSTRACT. Nocturnal hypoxemia secondary to sleep apnea has long been implicated as a cardiovascular risk factor in renal failure, but to date there is no study that links nocturnal hypoxemia to cardiovascular outcomes in end-stage renal disease. Fifty uremic patients on regular dialysis treatment without primary sleep apnea, pulmonary diseases, or other illnesses that may cause sleep apnea underwent pulse oximetry studies during night and were followed up for 32 mo. Average nocturnal SaO₂, minimal SaO₂, and the number of episodes of hypoxemia were similar in patients who died during the follow-up and in patients who survived, and none of these parameters predicted all-cause mortality. Average nocturnal SaO₂ was significantly lower (P = 0.006) in patients who had cardiovascular events during the follow-up (94.7 ± 2.9%) than in event-free patients (97.1 ± 1.3%). In a Cox model, average nocturnal SaO₂ was the second factor in rank explaining these outcomes. In this model a 1% decrease in average nocturnal SaO₂ was associated with a 33% increase in the incident risk of fatal and nonfatal cardiovascular events. Furthermore the risk of cardiovascular events was 5.05 times higher in patients with average nocturnal SaO₂ <95% (95% CI 1.61 to 15.86) than in those above this threshold (P = 0.005). This study adds weight to the hypothesis that nocturnal hypoxemia in dialysis patients represents an important cardiovascular risk factor.

	Introduction

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The sleep apnea syndrome (SAS) is a frequent complication of chronic renal failure. Snoring, restless sleep, frequent waking, morning headaches, daytime sleepiness, and even personality and mood changes are all considered typical symptoms of this syndrome. In uremic patients who complain of at least one of these symptoms, sleep apnea has a 73% frequency (1). Although the true prevalence of the syndrome in the uremic population is still unknown, it was estimated that it probably ranges from 21% to 47% (2), which is at least 12 times higher than the figure reported in the general population (2% to 4%) (3).

Episodes of nocturnal hypoxemia that develop during the apneic phases of sleep probably represent the most serious consequence of SAS, because they trigger an increase in sympathetic tone and cause nocturnal hypertension. Sleep apnea and nocturnal hypoxemia in the general population are well recognized risk factors for cardiovascular events (4). Recent studies in patients with end-stage renal disease (ESRD) have shown that nocturnal hypoxemia is associated with left ventricular hypertrophy (5,6) as well as with altered sympathovagal balance (i.e., blunted parasympathetic and enhanced sympathetic activity) (7). However, to date there has been no evidence that nocturnal hypoxemia in these patients predicts cardiovascular outcomes.

We have followed up a cohort of 50 patients who underwent nocturnal pulse oxymetry studies. These patients were carefully selected to ensure that nocturnal hypoxemia was truly associated with ESRD rather than with concomitant diseases and comorbidities (5–7). This selection produced a cohort that enabled us to detect the independent effects of nocturnal hypoxemia on cardiovascular outcomes, and herein we report the follow-up of these patients.

	Materials and Methods

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The protocol was in conformity with the local ethical guidelines of our institution, and informed consent was obtained from each participant.

Patients
Fifty patients (31 men and 19 women) selected from the dialysis population of the urban area of Reggio Calabria (approximately 200,000 residents) participated in the study. This dialysis population consisted of 224 patients who were being treated at our institution and at an affiliated dialysis center during the period of February 1995 through April 1998. The protocol of the study involved the exclusion of patients with primary sleep apnea or patients affected by pulmonary diseases or other illnesses that may cause sleep apnea independently of chronic renal failure (see below) and of those unable to cooperate. Thus, in a dialysis population of 224 patients, 29 were excluded because of preexisting pulmonary disease (defined on the basis of medical history, physical examination, chest radiography, and respiratory functional tests when indicated), 33 because of diabetes mellitus, 9 because of symptomatic heart failure, 5 because of very severe hypertension, 1 because of AL amyloidosis, 1 because of severe obesity, and 28 because of advanced neoplasia, liver disease, or dementia. The remaining 68 patients couldn’t participate due to technical or logistic reasons. Thus, the 50 patients who took part in the study represented 48% (50 of 105) of all eligible cases. Their mean age was 50.1 ± 16.0 yr, and the median duration of dialysis treatment was 32 mo (interquartile range, 11 to 82 mo).

The causes of chronic renal disease were chronic glomerulonephritis in 17 cases, polycistic kidney in 7 cases, pyelonephritis and interstitial nephritis in 6 cases, Alport disease in 2 cases, nephroangiosclerosis and vascular renal disease in 3 cases, Lawrence-Moon syndrome in 1 case, and undefined in 14 cases. No patient had had myocardial infarction or cerebrovascular events. Nineteen patients were habitual smokers (cigarettes/d: median, 10 [interquartile range, 3 to 20]), and none were heavy drinkers or frequent users of sedative drugs. Forty patients were on hemodialysis (HD) and ten on continuous ambulatory peritoneal dialysis (CAPD). Hemodialysis patients were being treated thrice weekly with standard bicarbonate HD (n = 37) or high-flux HD (n = 3) and 1.1 to 1.7 m² hollow-fiber or flat plat dialysers (either cuprophan or semisynthetic membranes). Dry weight was targeted in each case to achieve a normotensive, edema-free state. The average Kt/V in these patients was 1.33 ± 0.30. Patients on CAPD were all on 4 exchanges/d schedule with standard dialysis bags. The average weekly Kt/V in these patients was 1.80 ± 0.23. Twenty-one patients were on a treatment of erythropoietin, and twenty-three were taking antihypertensive drugs (beta-blockers in two, calcium channel blockers in nine [in 1 case associated with angiotensin-converting enzyme (ACE) inhibitors], ACE inhibitors or angiotensin type 1 antagonists in four, beta-blockers associated with calcium channel blockers or vasodilators in five, triple therapy in three].

Protocol
For HD patients, all studies were performed during a midweek nondialysis day. All patients were admitted to the nephrology ward of our unit between 7 a.m. and 7.30 a.m..

Echocardiography
All echocardiographic measurements were carried out according to the recommendations of the American Society of Echocardiography by an observer, who was unaware of the biochemical results. Left ventricular mass (LVM) was calculated according to the Devereux formula and indexed to height^2.7 (LVMI) (8). The height-based indexing of LVM was specifically chosen to minimize any potential distortion attributable to extracellular volume expansion (surface area indexing being weight-sensitive).

Nocturnal Pulse Oximetry
Pulse oximetry was measured by means of the Ohmeda-Biox 3700 Digital Pulse Oximeter (Ohmeda, Milan, Italy) by placing the sensor on the patient’s index finger. The recordings were carried out between 11 p.m. and 7 a.m while the patients were sleeping in a quiet single bedroom. Minimal and average nocturnal oxygen saturation (SaO₂) were obtained by using the standard software provided with the Ohmeda Biox Pulse Oximeter.

Follow-Up Study
After the initial assessment, patients were followed up for 30 ± 17 mo. During the follow-up, cardiovascular events (ECG-documented anginal episodes and myocardial infarction, heart failure, symptomatic arrhythmia requiring hospitalization, transient ischemic attacks and stroke, peripheral vascular disease, and major arterial and venous thrombotic episodes except for arterio-venous fistula thrombosis) were accurately recorded. Each death was reviewed and assigned an underlying cause by a panel of three physicians unaware of the pulse oximetry studies. As part of the review process, all available medical information concerning each death was collected. This information always included study and hospitalization records. In the case of an out-of-hospital death, family members were interviewed by telephone to better ascertain the circumstances surrounding death.

Statistical Analyses
Data are presented as mean ± SD or as median and interquartile range and analyzed by parametric and nonparametric tests as appropriate.

The risk of death and cardiovascular events was analyzed using the Cox proportional hazards model. As a first step, we tested the univariate relationships of all-cause mortality and of cardiovascular outcomes with a series of traditional and nontraditional risk factors (age, gender, duration of regular dialysis therapy, smoking, systolic pressure, LVMI, serum cholesterol, serum albumin, calcium phosphate product, hematocrit, serum parathyroid hormone (PTH), average and minimal nocturnal SaO₂, number of episodes of O₂ desaturation during nighttime, and treatment modality). Variables that could significantly predict death or cardiovascular events on univariate analysis were used to construct the multivariate Cox models. Hazard ratios (HR) and their 95% confidence intervals (CI) were calculated by the use of the estimated regression coefficients and their SE in the Cox regression analysis. All calculations were performed by using a standard statistical package (SPSS for Windows Version 9.0.1; SPSS, Chicago, IL).

	Results

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Demographic, somatometric, clinical, and biochemical data are reported in Table 1. Average nocturnal SaO₂ (96.40 ± 2.19%) was significantly lower (P < 0.01) in comparison to the average SaO₂ recorded in awake conditions in the morning hours (97.50 ± 1.25%). Nine patients (18%) displayed average nocturnal SaO₂ 95%. The average nocturnal SaO₂ was strongly and inversely related to the number of episodes of nocturnal hypoxemia (r = -0.69; P < 0.001) as well as to the minimal SaO₂ (r = -0.70; P < 0.001) during the nighttime. No significant difference was observed in pulse oximetry parameters between HD and CAPD patients (all P > 0.20), and no relationship was found between average nocturnal SaO₂ and hematocrit (P = NS).

Cardiovascular Events
Nineteen patients had incident nonfatal cardiovascular events (Table 2). Overall, 13 patients died, 7 (54%) of them for cardiovascular causes. Average nocturnal SaO₂ was significantly lower (P = 0.006) in patients who had fatal or nonfatal cardiovascular events during the follow-up (94.7 ± 2.9%) than in event-free patients (97.1 ± 1.3%). At univariate analysis, average nocturnal SaO₂ as well as age and serum cholesterol predicted incident cardiovascular events (Table 3), but male gender, systolic pressure, smoking, duration of regular dialysis treatment, LVMI, calcium phosphate product, hematocrit, PTH, treatment modality, minimal nocturnal SaO₂, and the number of episodes of nocturnal hypoxemia failed to significantly predict cardiovascular events. When univariate predictors of cardiovascular outcomes were concurrently introduced in a Cox model, average nocturnal SaO₂ ranked as the second factor explaining these outcomes (Table 4). Furthermore, the risk of fatal and nonfatal cardiovascular events (adjusted for the other independent risk factors, see Table 4) was 5.05 times higher in patients with average nocturnal SaO₂ <95% (95% CI, 1.61 to 15.86) than in those above this threshold (P = 0.005) (Figure 1). In accordance with this combined analysis, separate analysis of these outcomes also showed that the risk of fatal (HR, 1.91; 95% CI 0.42 to 8.60; P = NS) and nonfatal (HR, 6.05; 95% CI, 1.50 to 24.44; P = 0.01) cardiovascular events was higher in patients with SaO₂ <95% than in the remaining patients.

View larger version (16K): [in this window] [in a new window] [as a PowerPoint slide]   Figure 1. Cox proportional hazard survival curves for fatal and nonfatal cardiovascular events in the study cohort. Patients were divided in two groups according to the individual average nocturnal SaO2 (see Materials and Methods). Data were adjusted for the other independent predictors of cardiovascular events (see Table 4). The SaO2 = 95% coincides with the average SaO2 (97.5%) in awake conditions minus 2 SD (2 x 1.25).

	Discussion

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Sleep apnea has long been implicated as a cardiovascular risk factor in renal failure (13,14). Severe hypertension (15), obesity, atherosclerosis (16), diabetes mellitus (17), heart failure (18), bronchopulmonary diseases (19), autonomic failure (20), and other diseases that trigger cardiovascular and renal damage are frequently associated with sleep apnea. Thus sleep apnea in dialysis patients may depend on cardiovascular diseases that are conducive to terminal renal failure, or it may constitute a consequence of chronic renal failure on respiratory control (21). We have previously reported that nocturnal hypoxemia is linked to a nocturnal rise in arterial pressure (5) and that it is associated with left ventricular concentric hypertrophy (6,7), an alteration that is also very frequent in patients with primary sleep apnea (22).

The hypothesis that sleep apnea is a risk factor for mortality in dialysis patients has been tested only in a series of 29 patients with disrupted sleep or daytime sleepiness (23). This study showed that periodic limb movements during sleep, rather than nocturnal hypoxemia, is an independent predictor of survival. The cohort enrolled in the present study was composed of a series of patients without preexisting pulmonary diseases, diabetes mellitus, obesity, or autonomic failure and without previous cardiovascular complications or severe hypertension and heart failure. From an epidemiologic point of view, studying a population in whom the presence of confounding factors is excluded represents an ideal situation for the identification and the analysis of putative risk factors (24). In keeping with the study by Benz et al. (25), we found that SaO₂ was unrelated to all-cause mortality in dialysis patients. Furthermore, in keeping with the SLEEPO study (25), we found no relationship between nocturnal SaO₂ and hematocrit. However, nocturnal hypoxemia was a strong and independent predictor of cardiovascular events, and the prediction power of this parameter remained strong and substantially unmodified after statistical adjustment for established cardiovascular risk factors in the dialysis population. Nocturnal hypoxemia in dialysis patients is associated with LVH and concentric geometry, and this link is independent of arterial pressure (6). Raised sympathetic activity is the main neurohumoral response to nocturnal hypoxemia (26,27). We found that nocturnal hypoxemia alters the sympathovagal balance (7), and it is well demonstrated that blunted vagal control of the heart may precipitate fatal arrhythmias in a high-risk situation like myocardial infarction (28). Several mechanisms may thus concur to explain the high rate of incident cardiovascular events associated with nocturnal hypoxemia in dialysis patients. The observation that nocturnal continuous ambulatory positive pressure in dialysis patients has a favorable influence on obstructive and central sleep apnea is important because it indicates that sleep apnea is a potentially modifiable risk factor in this population (2).

Two points deserve comment. First, it has to be noted that our data were obtained in a selected population. Although it seems plausible that the risk of adverse cardiovascular outcomes may be even greater in patients with nocturnal hypoxemia and high cardiovascular risk (diabetic-uremic patients and dialysis patients with cardiopulmonary diseases and heart failure) this possibility must still be demonstrated. Second, the fact that patients were not submitted to detailed polysomnographic recordings to document sleep apnea is an objective limitation of our study. Polysomnography represents the gold standard for documenting sleep apnea, and this technique provides very useful diagnostic and prognostic information. However, because hypoxemia represents the actual stimulus that triggers the adverse effects of sleep apnea on the heart and on the vascular system (29,30), nocturnal oxygen saturation appears a sound predictor of the cardiovascular sequelae of this disease. Furthermore, pulse oximetry reliably identifies patients with sleep apnea (31), and the use of this technique is of proven value in HD patients (32).

In conclusion, this study adds further weight to the hypothesis that, independently of comorbid conditions, nocturnal hypoxemia in dialysis patients represents not only a marker of altered cardiac geometry and nocturnal hypertension but also an important cardiovascular risk factor. Further studies extended to patients in the predialysis phase and including patients at high cardiovascular risk will allow a more detailed appreciation of the cardiovascular risk associated with nocturnal hypoxemia in patients with chronic renal failure.

	References

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