Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

General use of ambulatory noninvasive 24-h blood pressure monitoring in many patients has shown that new criteria for arterial hypertension are useful. A classification of circadian blood pressure in "dippers" and "nondippers" (no physiologic drop of blood pressure) needs to be specified. An altered circadian blood pressure profile, like that in nondippers, was used as a diagnostic criterion for secondary hypertension. Recent epidemiologic studies in patients with essential hypertension have shown that nondippers are at higher risk for cardiovascular complications such as myocardial infarction and cerebrovascular insult. The studies also revealed that sleep-related breathing disorders (SRBD) are characterized by increased cardiovascular risk. Increases in blood pressure caused by SRBD could be documented, with the highest amount occurring during REM sleep. A study performed in a general practice showed a high incidence (40/112) of nondippers in a group of snoring middle-aged men with obesity and daytime fatigue. This indicates diagnostic and therapeutic consequences for the control of 24-h blood pressure, including nocturnal breathing pattern and daytime symptoms due to SRBD. The goal of antihypertensive drug therapy is to reduce blood pressure significantly during the day and during the night in different stages of wakefulness and sleep. A new protocol was designed to investigate blood pressure over 24 h under a standardized load, including nocturnal hypertension. The angiotensin-converting enzyme (ACE) inhibitor cilazapril was used in this test procedure and showed a significant and clinically relevant mean blood pressure reduction of 10.0 mm Hg (versus placebo 4.3 mm Hg) over 24 h.
 ...
PMID:Nocturnal hypertension and cardiovascular risk: consequences for diagnosis and treatment. 789 92

The effects of hypertension and REM sleep deprivation on spontaneous and postsigh apneas have been studied in normotensive Wistar-Kyoto (WKY) and spontaneously hypertensive (SHR) rats by simultaneously monitoring their respiration and sleep by the EEG. The amount of REM and non-REM sleep in SHR rats was identical to WKY rats under control as well as REM sleep-deprived recording conditions. Hypertension was associated with an increase in postsigh apneas, as was evident by the increased postsigh apnea index in non-REM and total sleep in SHR rats when compared to normotensive WKY rats. In contrast, REM sleep deprivation suppressed the postsigh apnea expression both in non-REM and total sleep in SHR rats. The incidence of spontaneous apneas was increased by a combination of hypertension and REM sleep deprivation, as was shown in REM-deprived SHR rats, while each of these conditions alone had no effect on spontaneous apneas. These results suggest a role for hypertension in the postsigh apnea genesis and the existence of partially distinct mechanisms for the two types of apneas.
 ...
PMID:Sleep apnea in normal and REM sleep-deprived normotensive Wistar-Kyoto and spontaneously hypertensive (SHR) rats. 877 73

To determine the mean blood pressure relative to sleep stages, two nocturnal cardiorespiratory polysomnographs were recorded in 60 male patients with hypertension and obstructive sleep apnea (OSA). The mean age was 50.2 years, the BMI 32.0 kg/m2, the respiratory disturbance index (RDI) 44, and the blood pressure by the WHO protocol 158/98 mm Hg. A new evaluation program was used to determine the invasively measured mean arterial pressure (mean +/- SEM) and heart rate (mean +/- SEM) during sleep (mean total sleep time 361 +/- 48 min) referred to sleep stages 1 (99.5 +/- 1.5 mm Hg/67.6 +/- 1.1 bpm), 2 (98.7 +/- 1.6 mm Hg/66.6 +/- 1.1 bpm), 3 (97.6 +/- 1.8 mm Hg/67.4 +/- 1.3 bpm), and 4 (97.6 +/- 2.2 mm Hg/66.3 +/- 1.6 bpm) and to REM sleep (103.3 +/- 1.7 mm Hg/68 +/- 1.2 bpm) as 1 s mean values and to compare them with the waking state (98.3 +/- 1.6 mm Hg/83.6 +/- 1.1 bpm). There was no physiological fall in blood pressure in patients with pronounced OSA. Sleep-stage-specific analysis of invasive continuous blood pressure signals is the gold standard. The sleep structure is disturbed less than with other methods.
 ...
PMID:Assessment of the nocturnal blood pressure relative to sleep stages in patients with obstructive sleep apnea. 889 11

In normal subjects, the level and variability of blood pressure decrease during non-rapid eye movement (non-REM) sleep. In contrast, sleep apnea is associated with large swings in nocturnal pressure. In this study, we evaluated a computer-derived index of all-night blood pressure variability in normotensive snorers with or without sleep apnea. We also examined this index in snorers receiving medical treatment for coexistent ischemic heart disease. Beat-to-beat blood pressure was recorded with a photoplethysmographic device (Finapres) throughout polysomnography. Subjects were categorized into four groups: those without cardiovascular disease without or with sleep apnea (> or = 15 apnea plus hypopnea per hour of sleep), and those with ischemic heart disease without or with sleep apnea. A frequency distribution histogram of all increases and decreases of blood pressure according to their amplitudes was drawn and the SD of the distribution used as an estimation of variability. Mean systolic and diastolic pressures during the total sleep time were not different among the four groups. In contrast, the SD of the distribution of systolic and diastolic pressure variations that were higher in the apneic than in the nonapneic groups (P < .05) correlated with apnea plus hypopnea (P < .0001) and transient electroencephalographic arousal number per hour of sleep (P < .0001). In both apneic and nonapneic subjects, blood pressure variability as assessed by SD decreased during stages 3 and 4 of non-REM sleep compared with stages 1 and 2 and REM sleep (P < .001). Blood pressure variability was similarly increased in apneic subjects with or without ischemic heart disease. We speculate that in apneic individuals with coexistent ischemic heart disease, pressure variability that is increased despite treatment with beta-blockers or calcium antagonists may be a risk factor for acute coronary events.
Hypertension 1996 Dec
PMID:Short-term variability of blood pressure during sleep in snorers with or without apnea. 895 80

Previous investigations involving continuous blood pressure (BP) monitoring have shown an important alteration of the 24-hour BP profile in patients with obstructive sleep apnea syndrome (OSAS). We investigated the impact of REM sleep on the 24-hour BP cycle in 16 severe OSAS male patients (mean respiratory disturbance index = 66 +/- 16 events/hour of sleep), with hypertension (mean BP 162 +/- 21/105 +/- 11 mmHg World Health Organization (WHO) protocol). Two successive nights of polysomnography were performed, and arterial BP was monitored continuously during the second 24-hour period after brachial artery cannulation. During the daytime, subjects were kept awake and supine. At 3 p.m. BP was continuously monitored during quiet supine wakefulness for 20 minutes. Systolic, diastolic and mean BP and heart rate (HR) were analyzed and tabulated in mean values of 5 minute segments. Sleep/wake information were correlated with cardiovascular variables. Each uninterrupted REM sleep period was identified and comparison between the period of quiet supine wakefulness and REM sleep HR and BP values was performed. 8 OSAS patients presented a normal drop of the mean arterial BP during the nocturnal REM sleep periods compared to quiet supine wakefulness (mean value = -10.8 +/- 7.3 mmHg) ("dippers") while the other 8 subjects ("REM sleep non dippers"), revealed an elevated mean arterial BP during REM sleep (mean value = 18.9 +/- 10.9 mm Hg). The absence of the normal circadian BP dip seen during the nocturnal sleep period is considered as an indication of vascular risk. The REM sleep non dipping may play a role in this risk.
 ...
PMID:REM-sleep-hypertension in obstructive sleep apnea. 938 74

The objective of this study was to determine whether abnormal microstructure of sleep in non-dipper hypertensive patients was present in their offspring. Subjects included 11 normotensive offspring of non-dipper hypertensive parents (FH + ND), 6 of dipper hypertensive parents (FH + D) and 5 of normotensive parents (Controls). We measured blood pressure beat-to-beat by Finapres and all stages of sleep by polysomnographically recording simultaneously during spontaneous nocturnal sleep. We analysed blood pressure pattern for 4-min long random periods while the subjects were awake and during all stages of sleep; sleep efficiency (SE), sleep latency (SL), delta-sleep latency (delta-SL), REM sleep latency (REM-SL), Stage 1, Stage 2, Stage 3, Stage 4 and REM duration and percentage values, and microstructural aspects of sleep (arousal and microarousal temporization and features). FH + D and controls showed a fall in blood pressure greater than 10% in all stages of NREM sleep and in the FH + ND blood pressure fall in less than 10% of waking values in all NREM stages. REM sleep and heart rate were similar in the three groups during all stages of sleep. FH + ND showed the same number of arousals but more microarousals than FH + D and controls (p < 0.0001). Microarousals induced several stage shifts through lighter sleep. For this reason, FH + ND spent more time in stage 2 than FH + D and controls. In conclusion, offspring of non-dipper hypertension parents showed a greater number of microarousals than the other two groups.
 ...
PMID:Normotensive offspring with non-dipper hypertensive parents have abnormal sleep pattern. 965 33

Male patients with arterial hypertension and obstructive sleep-related breathing disorders (mean age 50 y, Body Mass Index (BMI) 32.4 kg m-2, Respiratory Disturbance Index (RDI) 47.2 and systolic/diastolic blood pressure (SBD/DBD) 162/103 mmHg) were examined before and after 8 days of treatment with the long-acting angiotensin-converting-enzyme (ACE) inhibitor cilazapril 2.5 mg vs. placebo in a double-blind design with parallel groups. Cardiorespiratory polysomnography was carried out at night; during daytime wakefulness patients submitted to examinations of physical and mental exertion. Cilazapril reduced the mean pressure during the entire examination period (day and night) by 9.55 (SD +/- 7.13) mmHg, compared to 4.57 (SD +/- 7.20) mmHg for placebo (P < 0.006), independently from systematic changes of heart rate (x = -3.3 and -3.5 bpm, respectively). During REM sleep, mean arterial pressure was significantly reduced by 8.63 (SD +/- 10.1) mmHg, compared to a reduction on placebo of 3.17 (SD 9.6) mmHg (P = 0.023). Under psychometric strain, the mean arterial pressure was reduced by 15.31 (SD +/- 8.7) mmHg with cilazapril; under placebo medication by 6.19 (SD +/- 7.3) mmHg (P < 0.0001). Heart rate was not significantly changed.
 ...
PMID:Arterial hypertension and sleep apnoea: effect of the angiotensin-converting enzyme (ACE) inhibitor cilazapril on continuously measured blood pressure during sleep and wakefulness. 1060 86

Sleep-disordered breathing (SDB) in the form of obstructive sleep apnea is a possible risk factor for stroke. We carried out a cross-sectional survey out in a rehabilitation center among patients with first-ever stroke to further determine the incidence and types of SDB and its relationship to known risk factors for stroke. Full polysomnography was performed in 147 consecutive patients (95 men, 52 women, age 61+/-10 years) admitted to our neurological Rehabilitation Department 46+/-20 days after first-ever stroke. Subjective sleepiness (Epworth Sleepiness Scale), vascular risk factors, anthropometric data, and polysomnographic findings were compared between stroke patients with varying degrees of SDB. With a cutoff point for the respiratory disturbance index (RDI) of 5, 10, 15, or 20 the respective prevalence of SDB was 61%, 44%, 32%, and 22%. The type of SDB was generally obstructive, with dominant central apneas in only 6% of patients. Patients with an RDI of 20 or higher had less REM sleep, thicker necks, and a more central type of obesity. Even in patients with an RDI of 20 or higher subjective sleepiness, although higher than in those without SDB, was not a predominant symptom. Snoring and anthropometric data suggest that obstructive SDB may have existed prior to stroke. The prevalence of hypertension and coronary heart disease were higher among stroke patients with an RDI of 20 or higher than in those without SDB. We conclude that the prevalence of SDB among patients with stroke is high. Examination of stroke should include screening for SDB.
 ...
PMID:Sleep-disordered breathing among patients with first-ever stroke. 1070 96

Based on a case report, we offer brief guidelines on the perioperative management of patients with Sleep-Apnea-Syndrome (SAS) who present with a high incidence of a difficult airway and a high risk of respiratory depression during the perioperative period. A 39 year old male patient with a body mass index of 34.22 kg/m2 and receiving continuous-positive-airway-pressure-(CPAP) therapy for known SAS was scheduled for elective plastic surgery. After induction of anaesthesia and direct laryngoscopy no adequate airway could be established and the patient became hypoxic, hypercapnic and developed hypotension and bradycardia. With the use of a laryngeal mask airway the patient was stabilized and did not show neurologic sequale after immediate awakening. The following fiberoptic intubation of the awake patient, still showing tendency of upper airway obstruction, confirmed the difficult anatomical structures. The subsequent general anesthesia was uneventful. The patient received CPAP therapy and was monitored during the first postoperative night in the Intensive Care Unit. He made an uneventful recovery. He was advised to have regional anaesthesia or planned fiberoptic intubation, where possible, in the case of further anesthetic intervention. SAS has major implications for the anaesthesiologist and whenever patients exhibiting the high risk factors (obesity, male sex, history of intense snoring, impaired daytime performance, nonrefreshing daytime naps) are presented for surgery this condition should be considered. Elective surgery should be postponed until after adequate examination and treatment when necessary. Patients with SAS should always be suspected of having cardiopulmonary dysfunctions such as hypertension, cardiac dysrhythmia or cor pulmonale. It is most important to avoid sedative premedication, to initiate CPAP therapy preoperatively, to encourage regional anaesthesia if possible and to ensure close monitoring over the complete perioperative period. Planned fiberoptic intubation, preferably with surgical personnel available for an emergency airway, is a safe method for the induction of anaesthesia. Postoperatively, patients are at high risk from respiratory depression, even in the awake state. Postoperative opioid analgesia, no matter what route, should only be given under close monitoring. Independently of regional or general anaesthesia there is an increased risk of respiratory depression in the middle of the first postoperative week, suspected to be caused by the catching up on lost REM-sleep, due to shifts in the normal sleep pattern during the first postoperative days.
 ...
PMID:[Induction of anesthesia for a patient with sleep apnea syndrome]. 1084 May 41

Increased prevalence of sleep-related breathing disorders has been reported in patients with essential hypertension and we have described disordered breathing in spontaneously hypertensive rats, an animal model of genetic hypertension. The mechanisms coupling hypertension to respiratory dysfunction during sleep remain, however, largely unknown. To determine if sleep-related respiratory disorder reflects cardiovascular derangement or, alternatively, represents an independent phenotype in hypertensive rats, we polygraphically recorded groups (n = 10) of genetically hypertensive, genetically normotensive, and phenotypically normotensive rats carrying a genetic background for hypertension. Apnea index was elevated more than 15-fold during NREM sleep in both animal groups carrying hypertension-related genes (p < 0.0001 for each) versus normotensive Wistar Kyoto rats. During REM sleep, a genetic background for hypertension was associated with an increased apnea index of at least 500% versus normotensive Wistar Kyoto rats (p < 0.0001 for each comparison). Still, overall mean respiratory rate, minute ventilation, and sleep architecture were equivalent among all animal groups. As expected, blood pressure and heart period were similar in both normotensive groups but elevated in the hypertensive animals. Persistent sleep-related breathing disorder despite effective cardiovascular normalization in the phenotypically normotensive but genetically hypertensive rats suggests that disordered breathing represents a genetically determined phenotype in these animals that is not secondary to the cardiovascular derangements. The model system described here may provide a powerful tool for investigation of the determinants of sleep-related breathing disorder.
 ...
PMID:Sleep-disordered respiration in phenotypically normotensive, genetically hypertensive rats. 1102 64


<< Previous 1 2 3 4 5 Next >>