Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0002962 (angina)
 21,142 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Twelve patients aged 33--70 years (mean 49.5) underwent nightly recordings in the ICU and subsequently on the ward following acute myocardial infarction. Sleep patterns were analyzed according to night after infarct and ICU versus ward environment. Significant differences in nocturnal sleep patterns from matched controls initially after infarction included greater wakefulness, low REM sleep per cent, long REM latency, fewer REM periods, more awakenings, more stage shifts and decreased sleep efficiency. The usual circadian variation in HR was absent, and there was an estimated 8--10 h of unrecorded daytime sleep, which together suggested a quite generalized disruption of biological rhythms. With time, there was loss of daytime sleep, lowered nocturnal wakefulness and increased REM sleep. Slow-wave sleep (sometimes with very long duration delta waves) increased above normal over post-infarction nights 3--9, and sleep was otherwise renormalized by post-infarction night 9. No sudden sleep changes occurred with transfer from ICU to ward. The altered sleep patterns appeared mainly attributable to infarction itself. Twelve nocturnal anginal attacks occurred. Ten began in NREM sleep and two in REM periods without particularly intense phasic activity. Post-infarction nocturnal angina therefore appears to differ in pathogenesis from angina outside this period, which usually occurs in REM sleep. ECG changes could occur during sleep before awakening with pain, and overall decrease in ECG amplitude sometimes accompanied angina. Most attacks (10 of 12) occurred on post-infarction nights 4 and 5, indicating that undetermined that undetermined factors produce a secondary period of heightened risk at that time.
 ...
PMID:Sleep patterns in the intensive care unit and on the ward after acute myocardial infarction. 7 74

Modern sleep research studies have provided the practicing physician with considerable new information concerning the basic psychophysiology of sleep, the effects of medical conditions on sleep and the role of maturational and emotional factors in producing certain sleep disorders. Medical and psychiatric disorders, sleep disorders and drug-induced sleep stage alterations are studied in the sleep laboratory using the same techniques developed to analyze sleep patterns in normal subjects. After initial sleep laboratory adaptation, a profile of the sleep characteristics of various clinical conditions is obtained. This profile can be compared to sleep profiles of normal subjects as well as to the effects on sleep of subsequent experimental or therapeutic procedures. Various studies have shown that coronary artery, duodenal ulcer and nocturnal headache patients experience angina, increased gastric acid secretion and migraine or cluster headaches, respectively during REM sleep. Adult nocturnal asthamtic episodes occur out of all sleep stages while attacks of dyspnea in asthmatic children occur in all stages except stage 4 sleep. Hypothyroid patients show decreases in stages 3 and 4 sleep, while in hyperthyroid patients the percentage of time spent in stages 3 and 4 sleep is markedly increased. Enuretic episodes occur predominantly in non-rapid eye movement (NREM) sleep. Sleepwalking and night terror episodes occur exclusively out of NREM sleep, particularly from stages 3 and 4 sleep. Most child somnambulists and children with night terrors "outgrow" this disorder, suggesting a delayed maturation of the central nervous system. Stimulant drugs are effective in the treatment of the sleep attacks of narcolepsy and in treating certain cases of hypersomnia, while imipramine is an effective treatment for the auxillary symptoms of narcolepsy. Psychological disturbances are frequent in adult somnambulism and night terrors as well as in hypersomnia and insomnia. Proper pharmacologic treatment to provide symptomatic relief for insomnia is recommended to enhance the psychotherapeutic process.
 ...
PMID:Nocturnal psychophysiological correlates of somatic conditions and sleep disorders. 77 62

Insomnia, a more or less chronic sleep disturbance, is a very common symptom in psychiatric patients but also relatively freguent in the general population to a lesser degree. Two broad types of insomnia may often be distinguished: (1) difficulty falling asleep and frequent wakening, characteristic of anxiety states or obsessive worrying; and (2) early morning wakening, sometimes in a panic, suggestive of endogenous depression. The first group of patients respond well to minor tranquilizers and psychotherapy, whereas the second do well with tricyclic anti-depressants. Many studies in sleep laboratories have declineated the stages and cycles of sleep physiology and pathology, especially the importance of REM or dreaming sleep. The clinician should be cautious in the use of hypnotics like barbiturates which suppress REM sleep and produce a rebound increase on withdrawal, as well as problems of dependence of habituation. Flurazepam and chloral hydrate are considerably safer in this respect. Understanding sleep neurophysiology and biochemistry permits appropriate individual clinical management for both psychiatric patients and medical patients with conditions like peptic ulcer and nocturnal angina pectoris.
 ...
PMID:Insomnia: often a therapeutic challenge. 114 59

A 56-year-old male was admitted because of respiration arrest during sleep, and precordial crushing sensation which repeatedly occurred early in the morning. He had been hypertensive and aware of daytime sleepiness for ten years. After admission, all night polysomnography was recorded a total of four times. Apnea index was 37.5 times/hour, and central type apnea was predominant. The diagnosis of sleep apnea syndrome was made. In the early morning of the fourteenth day after admission, the patient developed anterior chest pain associated with ST elevation in leads II, III, and aVF of the electrocardiogram. Thus, the case was thought to be complicated by variant angina. There were no anginal attacks during the all night polysomnography recordings. However, a causal relationship between the sleep apnea and variant anginal attacks was suspected. Since both the sleep apnea and the variant anginal attacks tended to occur during the stages of REM sleep, and they are both related to changes in activity of the autonomic nervous system. It was considered that hypoxemia following sleep apnea and/or the hyperventilation after the apneic episodes might be the cause of the variant anginal attacks.
 ...
PMID:[A case of sleep apnea syndrome with variant angina]. 180 88

Sleep-related disturbed breathing and parasomnia in very young children are in the focus of epidemiological interest. The cardinal symptom, i.e. snoring, in connection with nocturnal perspiration, mouth breathing, susceptibility to infection of the upper respiratory tract and tiredness during the day or hypermotility, can be an indication of obstructive sleep apnea (OSA). The common treatment is adenotomy unless there is indication of allergic swelling of the nasal mucous membrane. Other anatomic predispositions for OSA must be considered (tonsillar hypertrophy, midfacial hypoplasia, micro- and retrognathia, e.g. in patients with Down's syndrome or patients with preoperated cleft lip face palate). Inhalative nasal corticoids are a possible alternative to adenotomy in light to medium grade cases of OSA. Tonsillotomy is indicated only in serious OSA cases, tonsillectomy is only justified in cases of chronic tonsillitis or more than 4-6 cases of angina in the last 12 months. Treatment with nasal CPAP is tolerated well also in childhood. Patients with central hypoventilation syndromes, insufficiency of the respiratory musculature or obesitas hypoventilation syndrome can usually be ventilated by non-invasive approach using a nasal mask. Patients suffering from parasomnia should always be asked if they snore at night because if OSA is diagnosed and treated, there are very good prospects of curing somnambulism as well. Like with narcolepsy and REM sleep, a close HLA association has also been identified for family somnambulism. In cases of parasomnia which becomes manifest only after very young age frontal lobe epilepsy should be suspected and searched by polysomnographic and simultaneous continuous nocturnal video surveillance. If reversive development or unclear motoric and utterance phenomena are observed, sleep-bound convulsive disorder should be looked for. Syncopal events can require comprehensive cardiological diagnosis, including exclusion of nightly disorders of the cardiac rhythm.
 ...
PMID:[Sleep disorders in infancy--aspects of diagnosis and somatic background]. 1649 23