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Biomedical subjects

L Grote

Publications and source records attributed to L Grote.

At least 19 recordsLinked to original sources
PubMed2006

Sleep apnoea and quality of life in growth hormone (GH)-deficient adults before and after 6 months of GH replacement therapy.

OBJECTIVE: To investigate the sleep architecture and breathing as well as quality of life (QoL) in adults with GH deficiency (GHD) before and 6 months after GH replacement therapy. DESIGN: A prospective observational study. PATIENTS: Nineteen consecutive adults with GHD (11 men, eight women; mean age 53, range 21-73 years) were studied. MEASUREMENTS: An overnight sleep study was performed and the Minor Symptom Evaluation Profile (MSEP), Functional Outcome of Sleep Questionnaire (FOSQ), Short Form 36 (SF-36) and Epworth Sleepiness Scale (ESS) questionnaires were applied at baseline and after the treatment period. RESULTS: For the whole group, there were no significant changes in mean total sleep time (TST; 370 min vs. 374 min), proportion of slow-wave sleep (SWS; 17.8%vs. 18.4%) and rapid eye movement (REM) sleep (12.1%vs. 13.9%) on GH replacement. Mean apnoea-hypopnoea index (AHI) was high and remained unchanged (28.2/h before vs. 28.0/h following GH replacement). Twelve patients (63%) were found to have obstructive sleep apnoea (OSA; AHI >or= 10/h) at baseline. Compared with GH-deficient patients without OSA (AHI 3.9/h), the OSA patients (AHI 42.4/h) had less SWS (11.4%vs. 28.6%, P = 0.010) and REM sleep (10.1%vs. 15.5%, P = 0.036). A marginal increase was observed in REM sleep time (10.1% before vs. 12.7% after GH; P = 0.048) while SWS was unchanged in this group. Moreover, MSEP for General Well-being and Responsiveness, FOSQ scores for General Productivity, Activity Level and Vigilance as well as SF-36 domains for Vitality and Mental Health were improved. CONCLUSIONS: Contrary to some previous observations in a smaller group of patients, our data suggest that GH therapy does not induce or aggravate OSA in GH-deficient adults. Moreover, GH therapy may improve some of the QoL dimensions in these patients.

Adult↗
PubMed2006

Hypertension prevalence in obstructive sleep apnoea and sex: a population-based case-control study.

Obstructive sleep apnoea (OSA) is a recognised risk factor for hypertension (HT). The current authors investigated confounders of this association in a sex-balanced community-based sample of patients with HT (n=161) from the Skaraborg Hypertension and Diabetes Project (n=1,149) and normotensive controls (n=183) from an age and sex stratified community-based population sample (n=1,109). All participants underwent ambulatory home polysomnography. Severe OSA (apnoea-plus-hypopnoea index (AHI)>or=30 events.h-1) was found in 47 and 25% of hypertensive and normotensive males, respectively. The corresponding numbers in females were 26 and 24%, respectively. The odds ratio (OR) for HT increased across AHI tertiles from 1.0 to 2.1 (95% confidence interval: 0.9-4.5) and 1.0 to 3.7 (95% CI: 1.7-8.2) in males, but not in females where the OR increased from 1.0 to 1.8 (95% CI: 0.8-3.9) and 1.0 to 1.6 (95% CI: 0.7-3.5). Regression analysis correcting for age, body mass index (or waist-hip ratio) and smoking did not eliminate the association between OSA and HT in males. The present data suggest that obstructive sleep apnoea is highly prevalent in both the general population and in patients with known hypertension. The contribution of obstructive sleep apnoea to hypertension risk may be sex dependent and higher in males than in females.

Case-Control Studies↗
PubMed2004

[Influence of circadian rhythms on cardiovascular function].

The clinical importance of circadian biological rhythms has been strengthened by a number of studies showing a circadian distribution of cardiovascular events like myocardial infarction, stroke, complex arrhythmia, or sudden cardiac death. Incidence of diseases showed a maximum during the early morning hours after awakening from sleep. In addition, a number of pathophysiological mechanisms has been identified to coincide with this peak including blood pressure and heart rate surges, decreased endothelial dilatory capacity of peripheral and coronary arteries, enhanced sympathetic activity, decreased cardiac electrical stability, and increased platelet aggregation. This time window of high risk for the incidence of cardiovascular events has been identified as a target for new treatment and prevention strategies including new release forms of antihypertensive and coronary-dilatory drugs. The use of melatonin as an antihypertensive drug has been successfully explored and opens new opportunities for the management of cardiovascular dysfunction and disease from a circadian perspective.

Biological Clocks↗
PubMed2004

Sympathetic activity is reduced by nCPAP in hypertensive obstructive sleep apnoea patients.

There is increasing evidence that nasal continuous positive airway pressure (nCPAP) lowers blood pressure in obstructive sleep apnoea (OSA) patients, not only during sleep but also in the daytime. However, both the mechanisms of blood pressure reduction and the considerable differences in the magnitude of the effect in the studies presented to date are not fully understood. Therefore, the authors prospectively studied the effect of nCPAP on noradrenaline plasma levels (NApl), blood pressure and heart rate (HR) in 10 normotensive and eight hypertensive OSA patients before and after 41.6 +/- 16.9 days of nCPAP therapy. Polysomnography and invasive blood pressure were continuously monitored over 24 h in the supine position before and with nCPAP. NApl were analysed every 15 min. In hypertensives, nCPAP reduced NApl by 36 +/- 25%, lowered mean arterial blood pressure substantially (night-time: -8.89 +/- 14.09 mmHg; daytime: -7.94 +/- 10.47 mmHg) and decreased HR by 6.6 +/- 5.4 beats x min(-1), whereas in normotensives there were only minor changes. The decrease in heart rate was associated with a decrease in mean arterial blood pressure and noradrenaline plasma levels, suggesting a causal effect of nasal continuous positive airway pressure therapy. This nasal continuous positive airway pressure effect occurs mainly in hypertensive obstructive sleep apnoea patients, whereas the effect is small in normotensives. This may explain, at least in part, some of the discrepant results in previous treatment studies.

Adult↗
PubMed2001

Mean blood pressure, pulse pressure and grade of hypertension in untreated hypertensive patients with sleep-related breathing disorder.

OBJECTIVE: To test the hypothesis that sleep-related breathing disorder (SRBD) is associated with increasing severity of cardiovascular risk markers. DESIGN: A cross-sectional study of sleep laboratory patients. SETTING: University Hospital Sleep Disorders Centre. PATIENTS: We studied 591 patients referred for a sleep study, all of them without a history of systemic hypertension. INTERVENTIONS: Clinical interview, two unattended sleep studies, and assessment of office blood pressure, cholesterol concentration, alcohol and nicotine consumption and daytime blood gases. MAIN OUTCOME MEASURE: Post-hoc analysis of different cardiovascular risk markers: mean blood pressure, pulse pressure, and the type and grade of systemic hypertension. RESULTS: Patients were classified as normotensive (blood pressure < 140/90 mmHg, n = 228) or hypertensive (blood pressure > or = 140/90 mmHg, n = 363) according to office blood pressure measurements. Mixed (systolic and diastolic) hypertension was the most common type of hypertension (n = 182), followed by isolated diastolic hypertension (n = 101), borderline isolated systolic hypertension (n = 70), and isolated systolic hypertension (n = 10). The frequency of mixed hypertension increased with SRBD activity (P < 0.05) and respiratory disturbance index (RDI; the number of breathing disorders per hour of estimated sleep time) was increased in those with mixed hypertension compared with those with normotension (24.8 compared with 15.7; t test: P < 0.01). In hypertensive patients classified as having grades 1 -3 of hypertension (n = 265, 80 and 18, respectively), there was a progressive increase in RDI (18.9, 27.2 and 30.3, respectively, P < 0.01). Mean blood pressure increased significantly with RDI. Pulse pressure increased significantly with age (P < 0.001), but was unrelated to the degree of SRBD. CONCLUSION: We conclude that mean blood pressure and the severity of hypertension, but not pulse pressure, increase with the severity of the SRBD.

Adult↗
PubMed2001

Treatment options for sleep apnoea.

Sleep apnoea (SA) is a common sleep disorder affecting 4 to 25% of the adult population. The most common form, obstructive SA, is characterised by recurrent upper airway obstruction during sleep associated with sleep disruption and hypoxaemia. There is increasing evidence that SA leads to impaired vigilance, quality of life, driving accidents and probably represents a vascular disease risk factor. Currently, the most effective treatments are aimed at increasing upper airway space by either air pressure [(continuous positive airway pressure (CPAP)], upper airway surgery or oral appliances. CPAP is the main treatment modality for moderate to severe SA but noncompliance approaches 50% in clinic populations. A number of pharmacological agents have been used in SA but at this stage, none are indicated in moderate to severe SA.

Acetazolamide↗
PubMed2000

Association between blood pressure reduction with antihypertensive treatment and sleep apnea activity.

This study investigated whether a drug therapy-induced reduction in nocturnal blood pressure (BP) was associated with decreased sleep apnea activity. Two polysomnographies from 54 hospitalized male hypertensive, obstructive sleep apnea patients were analyzed in a double-blind, randomized, parallel-group trial of the angiotensin-converting enzyme inhibitor cilazapril (C), 2.5 mg once daily, or placebo (P). Blood pressure was measured by means of an intra-arterial catheter. Compared with P, C lowered mean arterial BP during non-rapid eye movement (NREM) (-8.3 +/- 10.7 mm Hg, P = .05) and REM sleep (-8.6 +/- 10.1 mm Hg, P = .02). Respiratory disturbance index (-8.6 +/- 3.2 events/h of sleep (n/h), P = .01) and apnea index (AI) (-6.6 +/- 3.0 n/h, P = .04) during NREM sleep were lowered by C and, to a lesser extent, by P (-5.9 +/- 3.2 n/h, P = .07 and -5.0 +/- 3.6 n/h, P = .18, respectively). The effect on AI and hypopnea index (HI) during REM sleep was not significant for C (-5.9 +/- 3.4 and 0.1 +/- 2.0, NS, respectively) and P (-2.6 +/- 3.9 and 1.6 +/- 2.0, NS, respectively). There was a significant linear correlation between the change in REM systolic BP and the change in REM AI (r = 0.28, P = .04); the mean BP change correlated negatively with the change in HI (-0.28, P = .04). During NREM sleep there was no significant correlation between changes in BP and the treatment effects on sleep apnea activity. Blood pressure reduction after short-term antihypertensive treatment did not affect sleep disordered breathing during NREM sleep. Reduced BP was associated with a weak reduction of AI and a slight increase of HI during REM sleep. It appears that elevated BP contributes only marginally to sleep apnea severity in hypertensive patients with obstructive sleep apnea.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2000

Sleep-related breathing disorder is an independent risk factor for uncontrolled hypertension.

OBJECTIVE: To test the hypothesis that sleep-related breathing disorder (SRBD) is associated with poor blood pressure control in hypertensive patients independent from confounding factors such as age, body mass index, alcohol, smoking and daytime blood gases. DESIGN AND METHODS: This cross-sectional study of a sleep laboratory cohort was carried out at the University Hospital Sleep Disorders Centre, Marburg. The study comprised 599 patients referred for a sleep study, all of them with a documented history of systemic hypertension and/or previously initiated antihypertensive therapy. Data were obtained from a clinical interview, two unattended sleep studies and assessment of clinic blood pressure, cholesterol level, alcohol and nicotine consumption and daytime blood gases. The main outcome measure was a post hoc analysis of predictors for poor blood pressure control. RESULTS: Respiratory disturbance index (RDI) was significantly higher in patients with uncontrolled hypertension (blood pressure > or = 160 and/or 95 mmHg, n = 463) than in those with controlled hypertension (n = 136) (34.0 +/- 26.8 versus 27.0 +/- 23.5, P < 0.01). The relative proportion of patients with uncontrolled hypertension increased significantly as SRBD activity increased (chi2, P< 0.05). Body mass index was the only independent predictor (P = 0.006) of uncontrolled hypertension in the whole study sample. However, in the subset of patients aged < or = 50 years, RDI (P= 0.006) and age (P = 0.016) were the only independent predictors. The probability of uncontrolled hypertension increased by approximately 2% (B = 0.019, P= 0.006) for each RDI unit. CONCLUSION: SRBD should be considered, in addition to traditional confounders, as a risk factor for poor blood pressure control in younger hypertensive patients (< or = 50 years of age).

Adult↗
PubMed2000

Comparison of atenolol, amlodipine, enalapril, hydrochlorothiazide, and losartan for antihypertensive treatment in patients with obstructive sleep apnea.

We compared the effects of atenolol (50 mg), amlodipine (5 mg), enalapril (20 mg), hydrochlorothiazide (25 mg), and losartan (50 mg) given in once-daily oral doses on office and ambulatory blood pressures (BPs) in patients with hypertension and obstructive sleep apnea (OSA). Each of 40 randomized patients was treated in sequence with two of the five agents (balanced incomplete block design). Treatment periods lasted 6 wk and were separated by a 3-wk washout period. Changes in BP from baseline with the study substances were compared through analysis of variance. Office diastolic BP, our primary outcome variable, was most effectively lowered by atenolol, with all four post hoc differences between atenolol and the remaining substances being statistically significant. Reductions in office systolic and daytime ambulatory BP were not significantly different among the five compounds. However, atenolol reduced mean nighttime ambulatory diastolic and systolic BP more effectively than did amlodipine, enalapril, or losartan (but not hydrochlorothiazide). Severity of sleep-disordered breathing and well-being during the day were not significantly influenced by any of the study compounds. Our findings are in accordance with the hypothesis that an overactivity of the sympathetic nervous system is an important mechanism behind the development or maintenance of hypertension in patients with OSA.

Adrenergic beta-Antagonists↗
PubMed2000

Reduced alpha- and beta(2)-adrenergic vascular response in patients with obstructive sleep apnea.

Obstructive sleep apnea (OSA) has been associated with increased sympathetic activity. This study tested the hypothesis that the alpha- and beta(2)-receptor-mediated vascular response is altered in patients with OSA. Forearm vascular resistance was evaluated by venous occlusion plethysmography in 10 normotensive OSA patients and 10 normotensive controls (apnea/hypopnea index [mean +/- SD] 29.4 +/- 2.3 and 1.6 +/- 0.3 per hour, respectively) roughly matched for body mass index (BMI) and age. Forearm vascular resistance was measured after intraarterial infusion of norepinephrine (NE) (7.4, 31, 120, 472 and 1421 pmol/100 ml forearm volume [FAV]/min), before and after phentolamine infusion (2 microgram/100 ml FAV/min), and isoproterenol (ISO) (1, 2, 6, and 15 ng/100 ml FAV/min). NE-induced vasoconstriction was significantly attenuated in OSA patients compared with controls (65.0 +/- 36.6% versus 129.4 +/- 81.8%, p = 0.049). The reduction of vascular resistance after phentolamine was similar in patients and control subjects (-50.8 +/- 16.7% versus -43.4 +/- 20.0%, p = 0.38). During ongoing phentolamine infusion NE increased resistance to a similar extent in both groups (0.5 +/- 4.9% versus -0.9 +/- 10.1%, p = 0.96). Vasodilation following ISO was significantly attenuated in OSA patients compared with control subjects (-53.3 +/- 9.0% versus -64.7 +/- 10.3%, p = 0.049). Moreover, the vascular response to NE in OSA patients was negatively correlated with plasma NE concentration (r = -0.76, p < 0.05). The reduced vascular response to alpha- and beta-receptor stimulation suggests a functional downregulation of vascular sympathoadrenergic receptors in patients with sleep apnea.

Adult↗
PubMed2000

Therapy with nCPAP: incomplete elimination of Sleep Related Breathing Disorder.

Correct assessment of the overall treatment effectiveness requires knowledge about therapy compliance and efficacy. This study aimed to determine overall long-term apnoea alleviation after continuous positive airway pressure (CPAP) in a complete sleep laboratory cohort. Out of 209 consecutive CPAP candidates (mean age 57+/-12 yrs, body mass index (BMI) 30.0+/-5.1 kg x m2, respiratory disturbance index (RDI) 32.9+/-29 h), follow-up treatment was performed in 149 of them at 9, 18 and 30 months after CPAP prescription. Compliance with CPAP (machine run time/days CPAP available) was adjusted for the individual subjective sleep-time. Apnoea alleviation was defined as adjusted compliance multiplied by the CPAP effect (RDI with CPAP applied), remaining RDI was calculated. The baseline RDI, age or BMI in 75 patients, who did not tolerate nasal continuous positive airway pressure (nCPAP), did not differ from those accepting CPAP (acceptors, n=74). In acceptors at 9 months follow-up RDI with CPAP applied was 1.4+/-2.6 (CPAP effect, n=66), mean CPAP use was 3.6+/-2.5 x 24 h(-1) (n=68), mean apnoea alleviation was 52.4+/-32.0% (range 1-100%, n=47), the average remaining whole-night RDI was 17.8+/-26. At 9, 18 and 30 months (n=47), the mean daily CPAP use increased from 3.6+/-2.5 h to 4.1+/-2.5 h and 4.4+/-2.4 h (p<0.01). Effectiveness of continuous positive airway pressure is potentially high but acceptance was low. When accounting for sleep-time, its actual effect and use, only 50% adjusted continuous positive airway pressure effectiveness was observed.

Adult↗
PubMed2000

Heart rate variability during sleep stages in normals and in patients with sleep apnea.

Heart rate and heart rate variability are under the control of the autonomous nervous system. It can be assumed that during sleep internal influences dominate the autonomous nervous system. During the different sleep stages heart rate regulation differs in normal subjects. Obstructive sleep apnea is a disorder which has its origin in sleep and has strong modulating effects on the autonomous nervous system with prominent heart rate variations in consequence. In order to separate the influences of sleep stages and sleep apnea on heart rate variability we applied detrended fluctuation analysis in 12 healthy subjects and 20 patients with sleep apnea. We could show that the differences between sleep stages observed in healthy subjects were still present in subjects with sleep apnea despite their cyclical variation in heart rate. We conclude, that detrended fluctuation analysis is able to separate the influences of sleep stages and sleep apnea on heart rate variability.

Autonomic Nervous System↗
PubMed1999

Does short-term treatment with modafinil affect blood pressure in patients with obstructive sleep apnea?

OBJECTIVE: To investigate the effects of modafinil, a central nonamphetamine awakening substance, on blood pressure and heart rate in hypersomnolent patients with obstructive sleep apnea. DESIGN: This double-blind, randomized, placebo-controlled crossover trial was performed over 2 days and 3 nights in a single-center study of hospitalized patients from a referred care center. Twenty-six otherwise healthy men (age range, 30 to 60 years) with mild to moderate obstructive sleep apnea were recruited by the outpatient department of the Marburg University Sleep Laboratory. Patients were given 200 mg oral modafinil in the morning and 100 mg at midday. Placebo was given in the same manner in a crossover design. Mean arterial (radial) blood pressure was monitored continuously during nocturnal sleep and during a series of standardized daytime physical and psychologic performance tests. RESULTS: The difference in the main end point between the treatment with modafinil and placebo was 1.17+/-0.83 (mean +/- SE) mm Hg (95% confidence interval: -0.56 to 2.91 mm Hg). The maximal differences in blood pressure values occurred under loaded conditions (systolic blood pressure, ergometry: 5.62+/-1.13 mm Hg; mental stress test: 6.19+/-1.33 mm Hg). CONCLUSION: Short-term administration of modafinil did not elicit a significant response with regard to the main end point. However, cardiovascular effects during mental and physical load were observed. Longterm studies that include subjects with hypertension are necessary to investigate the clinical relevance of the cardiovascular effects of modafinil.

Adult↗
PubMed1999

Sleep-related breathing disorder is an independent risk factor for systemic hypertension.

The exact influence of sleep-related breathing disorder (SRBD) on blood pressure control remains unknown. We investigated the influence of different degrees of SRBD on daytime blood pressure and its association to documented hypertension by examining 1,190 consecutive patients referred for diagnosis of SRBD. The protocol includes clinical interview, physical examination, office blood pressure measurement, cholesterol, and blood gas analysis. Unattended home monitoring of nocturnal breathing was performed for assessment of SRBD activity (respiratory disturbance index [RDI]). RDI was independently and linearly associated with systolic blood pressure (unstandardized coefficient [B] = 0.07 +/- 0.03, p = 0.03), diastolic blood pressure (B = 0.07 +/- 0.02, p = 0 < 0.001), and heart rate (B = 0.10 +/- 0.02, p < 0.001) at rest. The relative risk for hypertension (blood pressure >/= 160/95 mm Hg) increased with SRBD severity (odds ratio [OR], 4.15 for RDI >/= 40 versus < 5 [95% CI, 2.7 to 6.5]). This relative risk was also elevated in younger (</= 50 yr) compared with older patients (> 50 yr) (OR, 7.15 versus 2.70 for RDI >/= 40 versus < 5). These cross-sectional clinical data suggest a relationship between SRBD severity and systolic blood pressure, diastolic blood pressure, and heart rate after control for confounders such as body mass index (BMI), age, alcohol/nicotine consumption, cholesterol level, and daytime PO(2) and PCO(2). SRBD is an independent risk factor for systemic hypertension with an increased likelihood in subjects </= 50 yr of age.

Age Factors↗