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Query: UMLS:C0002962 (angina)
 21,142 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A number of studies have demonstrated an association between habitual snoring and ischemic heart disease like angina pectoris, myocardial infarction and ischemic changes on the electrocardiography (ECG). Control for the influence of potential confounders has been inadequate. To further elucidate the issue we examined the association between self-assessed snoring and the relation to atherosclerotic manifestations. 804 70-year-old males and females were classified according to snoring habits. Alcohol and tobacco consumption, blood pressure, body mass index, social group, plasma lipids (triglycerides, cholesterol, high density lipoprotein), fasting blood glucose, glucose tolerance test, plasma epinephrine and norepinephrine were determined. Presence of angina pectoris, claudication intermittens, use of nitroglycerine were questioned, a resting ECG and a distal arterial pressure by use of doppler technique in the lower limbs were determined. Distal atherosclerotic manifestations was defined as complaints of claudication intermittens, pulselessness in one or more foot arteries or a foot/arm systolic pressure ratio < 0.90. ECG changes were classified in accordance to standard criteria (Minnesota codes) into positive ECG signs (Q/OS waves, S-T depressions, T-wave inversion or flattering or left bundle branch block) and definitive myocardial infarction. Snoring showed a weak positive correlation to positive ECG signs and definitive myocardial infarction, but after adjustments for the above confounders, no association was found between snoring and atherosclerotic manifestations. We conclude that, in a 70-year-old population, self-reported snoring is not associated with atherosclerotic manifestations.
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PMID:Snoring and atherosclerotic manifestations in a 70-year-old population. 888 96

Many clinicians are familiar with the clinical symptoms and signs of obstructive sleep apnea (OSA). In its most blatant form, OSA is complete airway obstruction with repetitive, prolonged pauses in breathing, arterial oxyhemoglobin desaturation; followed by arousal with resumption of breathing. Daytime symptoms of this disorder include excessive daytime somnolence, intellectual dysfunction, and cardiovascular effects such as systemic hypertension, angina, myocardial infarction, and stroke. It has been recently recognized that increased pharyngeal resistance with incomplete obstruction can lead to a constellation of symptoms identical to OSA called "upper airway resistance syndrome" (UARS). The typical findings of UARS on sleep study are: (1) repetitive arousals from EEG sleep coinciding with a (2) waxing and waning of the respiratory airflow pattern and (3) increased respiratory effort as measured by esophageal pressure monitoring. There may be few, if any, obvious apneas or hypopneas with desaturation, but snoring may be a very prominent finding. Treatment with nasal positive airway pressure (NCPAP) eliminates the symptoms and confirms the diagnosis. Herein we describe two typical cases of UARS.
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PMID:Upper airway resistance syndrome. 967 67

Respiratory sleep disorders are a risk factor, sometimes independent, for acute cardiovascular diseases which are the most frequent cause of death among populations of industrialized countries. Snoring and obstructive sleep apnea (OSA) are generally involved, while the pathogenetic role of acute exacerbation of COPD seems less evident. The most important acute cardiovascular events related to sleep respiratory disorders are angina pectoris, acute myocardial infarction, cardiac arrhythmias (in some instances as paroxysmal attacks), systemic hypertension with hypertensive crisis, ischemic stroke. A respiratory sleep disorder should be suspected in all obese, cigarette smokers, alcoholics, hypertensives, who present symptoms of obstructive sleep apnea, where snoring may be a marker, and in patients with COPD. The diagnosis is readily established by performing polysomnography and, when needed, by 24-hour Holter monitoring and blood pressure ambulatory recording. Therapy aims at correcting risk factors with particular attention to weight reduction in obese patients. Furthermore, upper airway anatomic abnormalities should be eliminated. In obstructive sleep apnea, nasal continuous positive airway pressure during sleep is to be used, when necessary, while tracheostomy must be performed only in more severe cases.
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PMID:Acute cardiovascular diseases and respiratory sleep disorders. 1052 45

Obstructive sleep apnea (OSA) has been strongly associated with several cardiovascular disorders during the past decade, and studies suggested that there might be a causal relationship. Recent studies have described several pathophysiologic mechanisms that are active in OSA and may participate in the development of cardiovascular disorders. Primarily, the repetitive respiratory events that occur in OSA cause hypoxia, hypercapnea, arousals, or disrupted sleep singly or in combination. These abnormal physiologic events result in increased sympathetic outflow, alterations in blood pressure control mechanisms, dysfunctional ventilatory regulation, and vascular alterations. As a consequence of the relative impact and the genetic predisposition, these pathophysiologic alterations may lead to or complicate a wide variety of cardiovascular disorders. Frequently, patients who have OSA present with complaints of excessive daytime sleepiness, chronic fatigue, snoring, morning headache, and nocturnal arousals. Difficult-to-control hypertension, recurrent exacerbations of congestive heart failure, and nocturnal angina are common cardiovascular manifestations of undiagnosed OSA. This article reviews the major cardiovascular disorders associated with OSA and the pathophysiologic mechanisms associated with their development.
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PMID:Cardiovascular disease and obstructive sleep apnea: implications for physicians. 1090 7

Four basic control mechanisms of breathing (brainstem respiratory centre, peripheral and central chemoreceptors, intero- and exteroceptive reflexes and suprapontine influences), as well as their sleep-related disorders are analysed. A decrease in central chemoreceptor sensitivity to CO2 and an increase in upper airway resistance during sleep result in hypoventilation and mild hypoxaemia already in physiological conditions. Compensatory increase in ventilatory effort with synchronous inhibition of pharyngeal dilators during sleep reduces the upper airway lumen manifesting with snoring, upper airway resistance syndrome, and OSA. The resulting hypoxaemia may cause marked cardiovascular, neuro-psychic, endocrine-metabolic and behavioural disorders. The augmented ventilatory effort and hypoxaemia evoke reflex dilation of airways and arousal from sleep, stimulating the sympatho-adrenal system, which provokes autoresuscitation by gasping preventing fatal asphyxia. Failure of this autoresuscitation mechanism seems to cause SIDS. Elimination of voluntary breathing by sleep either in Ondine's curse induced by lesions of respiratory centre, or in congenital central hypoventilation syndrome caused by insufficient central chemoreceptors result in respiratory failure and death. Nocturnal attacks of bronchial and cardiac asthma, lung oedema and other consequences of pulmonary congestion are also discussed. The pathomechanism of extreme daytime sleepiness, chronic fatigue, and disorders of memory, cognitive and other brain functions, are also analysed. Severe cardiovascular consequences of SAS may manifest acutely as angina pectoris, myocardial infarction. dysrhythmias, transient ischaemic attacks and even stroke or sudden cardiac death. OSAS may result also in development of hypertension, central obesity, diabetes mellitus, erectile dysfunction, depression, and various behavioural disorders.
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PMID:[Regulation of respiration and its sleep-related disorders]. 1244 39

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.
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PMID:[Sleep disorders in infancy--aspects of diagnosis and somatic background]. 1649 23

One of the most common yet unidentified conditions in heart disease is sleep-disordered breathing (SDB). Although it is most prevalent in patients with heart failure, it has been epidemiologically and pathophysiologically linked to ischemic heart disease, hypertension, sudden cardiac death, atrial fibrillation, and stroke. There are two primary SDB syndromes: obstructive sleep apnea (OSA) and central sleep apnea (CSA; also known as Cheyne-Stokes respiration). The pathophysiologic mechanisms that underlie these disorders appear to be distinct but both involve recurrent cycles of excessive sympathetic activation, hypoxemias and hypercapnias, and increases in ventricular wall stress. Signs and symptoms may include daytime somnolence, snoring, difficult-to-control hypertension, and refractory arrhythmias or angina. In heart failure, half of patients will have SDB and most patients will exhibit evidence of both OSA and CSA, although one or the other may predominate. The current standard diagnostic method is overnight laboratory polysomnography. Primary therapies for OSA include lifestyle changes, various facial and oral appliances, head and neck surgery, and continuous positive airway pressure (CPAP). CPAP is the most effective form of therapy for OSA, with few side effects, but is limited by compliance because of comfort-related issues. In patients with cardiovascular disease who predominantly suffer from OSA, treatment recommendations should be based on current guidelines for OSA. For patients with heart failure with predominant CSA, the current cornerstone of therapy is the optimization of medical therapy and resynchronization therapy when indicated. When SDB persists despite optimal medical management, referral to a sleep medicine consultant should be considered.
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PMID:Diagnosis and treatment of sleep apnea in heart disease. 1822 2

Chronic migraine (CM) is the most disabling of the 4 types of primary chronic daily headache (CDH) of long duration, a syndrome defined by primary headaches 15 or more days per month for at least 3 months with attacks that last 4 hours or more per day on average. CDH of long duration includes CM, chronic tension-type headache, new daily persistent headache, and hemicrania continua. CM affects approximately 2% of the adult population in Western countries, imposing substantial burdens on individual sufferers and their families and, more broadly, upon society. Although this disorder is highly disabling and prevalent, it remains largely underdiagnosed and undertreated. Diagnosing CM requires a systematic approach that includes these steps: (1) exclude a secondary headache disorder, and (2) diagnose a specific primary headache syndrome based on frequency and duration, for example, short-duration episodic, long-duration episodic, or long-duration chronic. CM usually develops as a complication of episodic migraine after a period of increasing headache frequency. This migraine transformation is associated with a number of risk factors, some of which cannot be modified, including age and race. Other risk factors for CM are modifiable, such as obesity, snoring, head injury, stressful life events, and overuse of opioids and barbiturates. However, risk factor modification has not yet been shown to decrease the likelihood of CM onset. According to a cross-sectional analysis of data from the American Migraine Prevalence and Prevention study published this year in Journal of Neurology, Neurosurgery, and Psychiatry, when compared to patients with episodic migraine, patients with CM were significantly less likely to be employed full-time and almost twice as likely to be occupationally disabled. In addition, patients with CM were nearly twice as likely to have anxiety, chronic pain, or depression. Furthermore, patients with CM had higher cardiovascular and respiratory risk, were 40% more likely to have heart disease and angina, and were 70% more likely to have a history of stroke. These findings highlight the paramount importance of clinical vigilance, accurate diagnosis, and appropriate, effective management - including treatment or referrals - to improve patient outcomes.
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PMID:Chronic migraine, classification, differential diagnosis, and epidemiology. 2177 Sep 29

Habitual snoring may be associated with cardiovascular disease (CVD); however, limited evidence exists among women. We investigated whether frequent snoring is a predictor of coronary heart disease (CHD) and stroke among 42,244 postmenopausal women participating in the Women's Health Initiative Observational Study. Participants provided self-reported information regarding snoring habits at baseline (1993 to 1998) and were followed up for outcomes through August 2009. Physician adjudicators confirmed CHD (defined as myocardial infarction, CHD death, revascularization procedures, or hospitalized angina) and ischemic stroke. Cox proportional hazards models were used to evaluate whether snoring frequency is a significant predictor of the adjudicated outcomes. We observed 2,401 incident cases of CHD during 437,899 person-years of follow-up. After adjusting for age and race, frequent snoring was associated with incident CHD (hazard ratio [HR] 1.54, 95% confidence interval [CI] 1.39 to 1.70) and stroke (HR 1.41, 95% CI 1.19 to 1.66), and all CVD (HR 1.46, 95% CI 1.34 to 1.60). In fully adjusted models that included CVD risk factors such as obesity, hypertension, and diabetes, frequent snoring was associated with a more modest increase in incident CHD (HR 1.14, 95% CI 1.01 to 1.28), stroke (HR 1.19, 95% CI 1.02 to 1.40), and CVD (HR 1.12, 95% CI 1.01 to 1.24). In conclusion, snoring is associated with a modest increased risk of incident CHD, stroke, and CVD after adjustment for CVD risk factors. Additional studies are needed to elucidate the mechanisms by which snoring might be associated with CVD risk factors and outcomes.
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PMID:Self-reported snoring and risk of cardiovascular disease among postmenopausal women (from the Women's Health Initiative). 2321 75

Obstructive sleep apnea (OSA), which is characterized by recurrent upper airway obstruction during sleep with resultant hypoxia-reoxygenation and sleep fragmentation, is prevalent among patients with cardiovascular disease. Refractory hypertension, nocturnal angina or arrhythmias, and stroke in particular should prompt consideration of OSA. The symptoms of OSA include snoring and excessive daytime sleepiness; risk factors include obesity and reduced upper airway dimensions. Up to 50% of patients with congestive heart failure (CHF) may manifest OSA, central sleep apnea-Cheyne-Stokes respiration (CSA-CSR), or both. Patients with CSA-CSR may present with fatigue, disrupted sleep, and paroxysmal nocturnal dyspnea. Objective sleep recording is required to document the nature and severity of sleep apnea. The gold standard is in-laboratory overnight polysomnography (PSG), including monitoring of electroencephalography and other signals to determine sleep-wake state, and recording of body position, airflow, respiratory effort, and pulse oximetry. Portable cardiorespiratory recorders are now approved for diagnosis in patients without comorbidities. Full PSG is recommended for diagnosis in all other cases, although OSA and CSA-CSR can be identified from portable recorders in some patients with CHF and other conditions. The objectives of treatment are to improve symptoms, quality of life, and cardiovascular outcomes. The mainstay of treatment for moderate-to-severe OSA is positive airway pressure (PAP). Automated PAP devices may be used in uncomplicated OSA, whereas continuous fixed PAP is the treatment of choice for other patients with OSA, and may also treat a proportion of patients with CSA-CSR. A form of bi-level PAP known as adaptive servoventilation is effective in treating a majority of patients with CSA-CSR.
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PMID:When to Suspect Sleep Apnea and What to Do About It. 2611 5


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