Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Primary sleep disorders include narcolepsy, the Pickwickian syndrome, sleep apnea in infants and other rare conditions. Secondary sleep disorders occur in depression, alcoholism, endocrinopathies, heart failure and pregnancy. Medical symptomatology often increases during rapid-eye-movement (REM) sleep, when physiologic activity is high. Insomnia, the most common sleep disorder, requires careful work-up, attempts at environmental manipulation and judicious short-term pharmacotherapy. Pharmacologic manipulation of sleep is beset with complications. A basic understanding of properties and side effects of the sleep-inducing drugs is needed in order to select the optimal agent.
 ...
PMID:Sleep disorders and insomnia. 62 43

The Pickwickian Syndrome stimulated new pathophysiological concepts in regard to control of ventilation. With the advent of sleep laboratories, the peculiar sleep apnea occurring in some of these patients has been explained on the basis of intermittent upper airway obstruction. Two patients with different manifestations of the Pickwickian Syndrome are presented. The suggestion is made that these two subsyndromes should have unique designations. The Auchincloss Syndrome is manifested by right heart failure and respiratory acidosis in obese patients who are alert and have no major abnormality of breathing pattern. The fundamental cause of this abnormality is the increased work of breathing caused by the obesity. The cost of breathing is so high that the ventilatory regulation is compromised and respiratory acidosis results. The Gastaut Syndrome is characterized principally by hypersomnia and sleep apnea. The fundamental defect is upper airway obstruction during sleep, resulting in increased work of breathing, which together with the increased work caused by obesity leads to respiratory acidosis and right ventricular failure. Hypersomnia, rather than heart failure or respiratory acidosis, is the major manifestation of this syndrome, and is the result of sleep loss.
 ...
PMID:Pickwickian syndrome, 20 years later. 117 87

The patient was a 74-year-old woman who had been obese since age 18. Her obesity was refractory to dietary manipulation. She had been suffering from increasing dyspnea for several months and eventually could not even move. She was admitted to a hospital and diagnosed as having heart failure. Although her cardiac function recovered with medical treatment, her symptoms did not improve. The patient was then sent to our hospital. On admission, her height and weight were 149 cm and 81.9 kg, respectively, yielding a body mass index (BMI) of 36.6 kg/m2. Arterial blood gas analysis in room air revealed hypoxemia and an apnea index of 27 per hour. She was given a daily 500-1000 kcal diet. After four months of treatment, her weight decreased to 65 kg with a BMI of 29.3 kg/m2. Weight reduction together with the usage of progesterone-derivatives resulted in marked improvement of sleep apnea. The apnea index decreased to 3/h and arterial blood gas values normalized. This patient seemed to have suffered from both obesity hypoventilation syndrome and sleep apnea syndrome. Improvement of respiratory function was achieved through relief of airway obstruction and weight reduction, with activation of the respiratory center due to progesterone treatment.
 ...
PMID:[Improvement of respiratory function with weight reduction in obese elderly]. 149 51

Voluntary end-expiratory apnoea in a 23-year-old asymptomatic mild hypertensive patient consistently elicited bradyarrhythmias (complete heart block and sinus pause) and sympathetic activation to muscle blood vessels, indicating simultaneous sympathetic and parasympathetic activation during apnoea. The sympathetic bradyarrhythmic response to apnoea was potentiated by hypoxia and eliminated by atropine. Baroreflex activation also attenuated the bradycardic response to apnoea. A 43-year-old hypertensive patient with sleep apnoea also exhibited bradyarrhythmias (sinus arrest for up to 10 s) and a fall in perfusion pressure to less than 50 mmHg during episodes of sleep apnoea. These cardiovascular changes were associated with a reduction in oxygen saturation to levels as low as 35%. Neither patient was on any medication. Simultaneous sympathetic and parasympathetic activation during episodes of apnoea may predispose to cardiovascular catastrophe. These chemoreflex mediated autonomic changes are inhibited by baroreflex activation. We propose that patients with impaired baroreflexes (patients with hypertension or heart failure and premature infants) may be especially susceptible to excessive autonomic responses to chemoreflex stimulation during periods of apnoea. In these patient groups, bradyarrhythmias, hypoxia, hypoperfusion and sympathetic activation during apnoea may predispose to sudden death.
 ...
PMID:Parasympathetic hyperresponsiveness and bradyarrhythmias during apnoea in hypertension. 149 63

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.
 ...
PMID:Right and left ventricular functional impairment and sleep apnea. 152 13

A 71-year-old man was noted to habitually snore loudly at night and have a predisposition to somnolence during the daytime. While dozing during the day, he developed cardiac arrest at the time when snoring stopped, and was resuscitated. By means of a respiration monitor, he was diagnosed as having sleep apnea syndrome (SAS) with a combination of obstructive, central, and mixed type. However, neither respiratory insufficiency nor cardiac insufficiency was observed, and there were no abnormal findings on laboratory tests and bronchoscopy. SAS complicated by cardiac arrest is usually seen in cases with concomitant symptoms such as excessive obesity, hypertension, arrhythmia, right heart insufficiency, secondary polycythemia, or mental disorder. The present case abruptly developed cardiac arrest in the absence of such symptoms. This case therefore suggests the importance of screening tests using a respiration monitor during sleep in subjects who have a loud snore or a predisposition to somnolence during the daytime. Although treatment with UPPP alone had no noticeable effect, UPPP treatment combined with sleeping in the lateral position was effective in the present case. The efficacy rate of UPPP has been reported to be 50 to 60%. The early establishment of a method for precise evaluation of the site of obstruction as well as criteria for appropriate application of UPPP are urgently required.
 ...
PMID:[A resuscitated case of sleep apnea syndrome with cardiac arrest]. 160 64

It is assumed, that patients with coronary heart disease (CHD) more often suffer from sleep related disorders of breathing than healthy subjects. A relation to an impaired left ventricular performance is discussed. In 40 CHD-patients and 30 cardio-respiratory healthy controls we therefore measured arterial oxygenation during sleep by means of pulse-oximetry. Our results show a marked increase in the frequency of nocturnal oxygen-desaturations along with the degree of impaired left ventricular function independent of a special sleep apnea risk. In case of cardiac insufficiency at rest cyclical oxygen-desaturations were observed ten times as often as in the healthy controls. A central disturbance of the respiratory control, which leads to periodic breathing (type Cheyne-Stokes) has to be discussed. Because of the general high risk of CHD-patients concerning the development of nocturnal complications of their disease, sleep-related disturbances of ventilation have to be detected early by means of routinely applied screening-methods.
 ...
PMID:[Nocturnal oxygen saturation in patients with coronary heart disease--dependent on degree of left ventricular functional impairment]. 186 4

The benzodiazepines are sedative hypnotic drugs, i.e., central nervous system depressant drugs, that may adversely affect the control of ventilation during sleep. Prescription of these drugs may worsen sleep-related breathing disorders, especially in patients with chronic obstructive pulmonary disease or cardiac failure. The most frequent users of sedative hypnotics are the polymorbid elderly with a secondary complaint of insomnia. Although the benzodiazepines may reduce sleep fragmentation, their long-term use may also cause health problems, such as complete obstructive sleep apnea in heavy snorers or short repetitive central sleep apnea in patients with recent myocardial infarction. Since drugs of this class vary in their effects, it is crucial to note the action of a given benzodiazepine on the control of vital functions during sleep.
 ...
PMID:Benzodiazepines, breathing, and sleep. 196 16

Continuous registration of breath, ECG, O2 tension was carried out in sleeping chronic obstructive bronchitis (COB) patients (n-46). Sleep apnea was detected in 19 of them. It was found that signs of pulmonary insufficiency in association of COB and sleep apnea occur significantly earlier. No correlation was observed between the severity of bronchial obstruction and pathological sleep apnea. The discussion covers mechanisms of pulmonary and cardiac insufficiency onset in COB patients with sleep apnea, therapeutic responses to long-term oxygen treatment and introduction of artificial respiratory control.
 ...
PMID:[The role of sleep apnea in the pathogenesis of cardio-pulmonary insufficiency in patients with chronic obstructive bronchitis]. 202 4

Epidemiologic studies revealed that up to 10 percent of middle-aged men show more than 10 cessations of breathing of more than 10 seconds' duration. In these patients, increased morbidity and mortality rates have been proved. More than 50 percent of apnea patients exhibit arterial hypertension, and up to 50 percent of hypertensive patients experience sleep apnea. Patients with sleep apnea and essential hypertension need special attention paid to their antihypertensive therapy because the following side effects of drugs have to be avoided: increases of cardiac insufficiency, hyperviscosity of the blood, intensification of the hypersomnia by central sedation, intensification of a pre-existing tendency towards arrhythmias, and deprivation of deep and rapid eye movement sleep. In this study, the effects of angiotensin-converting enzyme inhibitors in patients with sleep apnea and hypertension are examined. An interim evaluation of six patients (aged 50 to 57) yielded the following results: Average Broca index, 124; average blood pressure before therapy, 159/102 mm Hg; average blood pressure after therapy, 132/78; a decrease of the apnea and hypopnea index from x = 31 (range, 12 to 77) to x = 20 (range, two to 54). Therapy did not influence sleep structure: before therapy, an average of 19 percent of sleep episodes were of the rapid eye movement type (range, 11 to 32 percent); after therapy, 23 percent were of this type on average (range, 21 to 25 percent). A final evaluation will be carried out after the second study phase for 12 patients who have been treated in a double-blind scheme with metropolol versus cilazapril.
 ...
PMID:Effects of cilazapril on hypertension, sleep, and apnea. 253 65


1 2 3 4 5 6 7 8 9 10 Next >>