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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Obstructive sleep apnea syndrome (OSAS) is a common but still underrecognized disorder. It affects 2% to 4% of middle-aged adults, a significant proportion of whom are female. The spectrum of clinical presentations of OSAS and their severity is variable, ranging from neurocognitive complaints to cardiorespiratory failure. OSAS has a significant impact on quality of life, cardiovascular morbidity, and mortality. Its major sequelae include daytime somnolence and its consequences (motor vehicle accidents, poor work performance, disrupted social interactions), systemic and pulmonary hypertension, and ischemic heart disease. Treatment of OSAS results in improvement in symptoms, quality of life, and blood pressure control, and may improve mortality. An expansion of our understanding of this condition has resulted in increased awareness of its consequences, but the recognition of OSAS in clinical practice is still delayed. Identification of these patients in clinical practice requires attention to risk factors (history of snoring and witnessed apneas, obesity, increased neck circumference, hypertension, family history) and careful examination of the upper airway. Clinical impression alone, however, has poor (50% to 60%) sensitivity and specificity (63% to 70%) and the diagnosis is usually obtained on polysomnography. Physicians and other health care professionals need to be aware of the progress made in this area and recognize the necessity for prompt evaluation and treatment of these patients.
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PMID:Clinical presentations of obstructive sleep apnea syndrome. 1040 27

The association between snoring and myocardial infarction was studied in 1453 people of both sexes aged 20-70 years. The study was carried out in a population of 92,364 residents and the subjects were recruited using the Electoral Census. A questionnaire was sent to all participants, asking about snoring and cardiovascular risk factors. Hospital records were checked for the next 4 years to establish how many of them developed myocardial infarction. At the beginning of the follow-up study 39 patients were diagnosed with ischaemic heart disease. Of the other 1414 participants, 571 (40.4%) were snorers and 843 (59.6%) non-snorers. Twenty-one developed myocardial infarction in the snorer group and four in the non-snorer group. The snorer group presents an adjusted relative risk of myocardial infarction of 3.08 (95% CI 1.01-9.46) with respect to non-snorers. We conclude that snoring seems to be a potential risk factor for myocardial infarction.
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PMID:Snoring and myocardial infarction: a 4-year follow-up study. 1046 61

We studied the relationship between different ethnic groups, obstructive sleep apnoea (OSA) and ischaemic heart disease. Four hundred and thirty-two inpatients from the medical wards were interviewed. Limited overnight sleep studies were done in 129 of those who had habitual snoring, daytime sleepiness based on an Epworth sleepiness scale of 8 or more, or a large neck size of 40 cm or more. There were 315 Chinese (72.9%), 67 Malays (15.5%), 43 Indians (10%) and 3 from other races (1.4%). The prevalence of OSA was 19.7%, 30% and 12% among the Chinese, Malays and Indians, respectively. The prevalence ratio for OSA was 1.52 in Malays using Chinese patients as the baseline (P = 0.07). The median neck circumference was 37 cm in both racial groups. The median body mass index was 22.7 kg/m2 in Chinese compared to 23.6 kg/m2 in Malays. The median apnoea-hypopnoea index was 22.7, 19.0 and 26.9 events/hour among the Chinese, Malays and Indians, respectively. OSA was independently associated with the prevalence of IHD (adjusted prevalence ratio 1.68; 95% CI: 1.15, 2.46; P = 0.009). The prevalence of ischaemic heart disease (IHD) was 31%, 24% and 28% in Chinese, Malays and Indians, respectively. The prevalence ratio for IHD in Malays compared to Chinese was 0.77. After adjusting for OSA, there was an even greater reduction in the risk of IHD (adjusted prevalence ratio 0.70). This suggests that OSA is a confounder in the relationship between race and ischaemic heart disease.
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PMID:Ethnicity, obstructive sleep apnoea and ischaemic heart disease. 1049 69

Coronary heart disease (CHD) is a leading cause of death among middle-aged men. In the same age group the spectrum of upper airway obstruction from habitual snoring to obstructive sleep apnoea syndrome (OSAS) is frequent. In several studies snoring was found to be an important risk factor for ischaemic heart disease. The prevalence of OSAS in patients with CHD, profile of risk factors and ventricular arrhythmias was determined in a prospective manner in 78 patients with stenosis of one or more coronary arteries at coronary arterography. OSAS was found in 27 patients (34.6%). Mean respiratory disturbance index (RDI) was 23.9. RDI increased with higher age. No significant differences in both groups could be found in ventricular arrhythmias, left ventricular ejection fraction and risk factors, except hyperuricaemia and adiposity. OSAS is frequent in patients with CHD and may be an additional risk factor besides the known coronary risk factors. Patients with the combination of CHD and OSAS have to be regarded as a group at particular risk because of several interactions between OSAS and coronary haemodynamics. Furthermore the microstructure of sleep in patients with nocturnal myocardial ischaemia is disturbed.
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PMID:Coronary heart disease and upper airway obstruction. 1060 99

Obstructive sleep apnoea (OSA) is a common disorder with numerous potential sequelae. Although the majority of these consequences can be reduced with appropriate treatment, only limited data exist regarding the natural progression ofthis disorder in untreated individuals. We hereby report a long-term follow-up of all untreated patients (n = 40) followed-up in the Technion Sleep Clinic, using both subjective and objective measurements. In addition, we report a long-term follow-up of 11 patients who attempted dietary weight loss. The average time interval between the first and second polysomnographies for the untreated group was 5.0 +/- 2.8 yrs, and 2.5 +/- 2.3 yrs for the weight reduction group. There was no significant change in Body Mass Index (BMI) or Respiratory Disturbance Index (RDI) between the two Polysomnographic (PSG) evaluations in the untreated patients. However, eight patients developed hypertension (n=5) or ischaemic heart disease (IHD) (n=3) between the two evaluations. RDI, age and BMI at the time ofthe initial evaluation were not predictive of changes in RDI, snoring intensity or minimal oxygen saturation. However, the patients who developed hypertension/IHD had significantly higher RDI than the patients who did not (46 +/- 27 vs. 23 +/- 17 h(-1), P < 0.005). In the weight-loss group, BMI decreased by a mean of 3.1 kg m(-2), and RDI decreased by 20events h(-1), P<0.05 for both. There was a significant correlation between the weight loss and improvement in RDI (R = 0.75, P = 0.005). We conclude that in untreated obstructive sleep apnoea patients RDI does not necessarily increase over time, but associated hypertension or ischaemic heart disease may develop. When weight loss is successfully achieved, sleep apnoea significantly improves with a high correlation between the extent of weight loss and the improvement in apnoea status.
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PMID:Long-term follow-up of untreated patients with sleep apnoea syndrome. 1211 84

The obstructive sleep apnea syndrome (OSAS) is caused by an intermittent and repetitive obstruction of the upper respiratory tract during sleep, which leads to a complete (apnea) or partial (hypopnea) block of air flow. It is quite prevalent, being seen in 4-6% of males and 2% of females. Structural abnormalities present in the upper respiratory tract and obesity are the fundamental etiological factors. Clinical manifestations are due to sleep fragmentation and oxygen desaturation which cause the apnea. Day hypersomnia, snoring and episodes of apnea described by the spouse are the three basic symptoms. The diagnosis is based on polysomnography, which can be substituted for a night cardiorespiratory polygraphy. It has an important morbimortality rate, mainly due to traffic and labor accidents, ischemic heart disease and chronic respiratory failure. The treatment is multifactorial. First, eliminating alcohol and hypnotic drugs. Obesity, which is almost always present, must also be corrected. Structural abnormalities of the upper respiratory tract may require a surgical solution. The treatment preferred nowadays is the application of a nasal continuous positive airway pressure (CPAP) while the patient is asleep. It should be considered for those symptomatic patients with an apnea-hypopnea index over 30, or if the index is below 30, than when a respiratory insufficiency or cardiovascular risk factors are present. In some cases surgical procedures may be considered, such as uvulopalatopharyngoplasty.
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PMID:[Obstructive sleep apnea syndrome]. 1219 5

Obstructive sleep apnea (OSA) is a newly recognized risk factor for the development of systemic hypertension, ischemic heart disease and congestive heart failure. Mechanisms responsible for these links include OSA-related hypoxemia and arousal from sleep-induced increased sympathetic activity, large negative intrathoracic pressure-induced increased left ventricular transmural pressure gradient, and impaired vagal activity plus oxygen radial formation. Secondary phenomena include increased platelet aggregability, insulin resistance, and endothelial dysfunction with reduced endogenous nitric oxide production. Safe nonpharmacologic, nonsurgical therapy, namely continuous positive airway pressure, can attenuate OSA, and improve cardiac function and quality of life. Searching for signs or symptoms of OSA from the patient (or bed partner), namely loud habitual snoring, apneas, nocturnal choking, orthopnea, paroxysmal nocturnal dyspnea, excessive daytime sleepiness, or cardiovascular disease, which is difficult to control, may reward the curious physician with another treatment avenue.
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PMID:The link between obstructive sleep apnea and heart failure: underappreciated opportunity for treatment. 1586 63

Sleep-disordered breathing is very common and is associated with an increased risk of cardiovascular disease, cardiac arrhythmia and stroke. There are two types of sleep apnea: obstructive and central. The objective of this review is to provide a broad perspective of the pathophysiological and clinical aspects of the two types of apnea and to discuss their cardiovascular adverse effects. The diagnosis of sleep apnea syndrome is based on polysomnography, and severity is measured with an apnea-hypopnea index that counts the total number of apneas per hour of sleep. Recent large epidemiologic studies have shown that sleep apnea affects about 16% of men and 5% of women between 30 and 65 years of age. Obstructive sleep apnea is characterized by abnormal collapse of the pharyngeal airway during sleep, snoring, vigorous inspiratory efforts causing frequent arousal, and excessive daytime drowsiness. Central sleep apnea with Cheyne-Stokes respiration is a form of periodic breathing with frequent periods of hyperventilation, and carries a poor prognosis in patients with heart failure. Obstructive apnea can also have substantial health consequences. Although the exact mechanism linking sleep apnea with cardiovascular disease is unknown, there is evidence that obstructive apnea is associated with a group of proinflammatory and prothrombic factors that are also important in the development of atherosclerosis. Nocturnal and daytime sympathetic activity is elevated after sleep apnea. Autonomic abnormalities include an increased resting heart rate, decreased cardiac rhythm activity, and increased blood pressure variability. Obstructive apnea is associated with endothelial dysfunction, increased C-reactive protein and cytokine expression, elevated fibrinogen levels and decreased fibrinolytic activity. Enhanced platelet activity and aggregation, leukocyte adhesion and accumulation of endothelial cells are common in both obstructive apnea and atherosclerosis. Surges in sympathetic activity, blood pressure, ventricular wall tension and afterload adversely affect ventricular function. Many studies have shown that patients with obstructive apnea have an increased incidence of daytime hypertension, and this syndrome is recognized as an independent risk factor for hypertension. Obstructive apnea is associated with myocardial ischemia (silent or symptomatic), acute coronary events, stroke and transient ischemic attacks, cardiac arrhythmia, pulmonary hypertension and heart failure. Central sleep apnea is frequent in severe heart failure. Most heart failure patients with pulmonary congestion chronically hyperventilate because of stimulation of vagal irritant receptors and central and peripheral chemosensitivity. When PaCO2 falls below the threshold required to stimulate breathing, the central drive to respiratory muscles and air inflow ceases and central apnea ensues. Apnea, hypoxia, CO2 retention and arousals provoke elevated sympathetic activity, increased afterload and elevated left ventricular transmural pressure, and promote the progression of heart failure. Tentative relationships have been identified between central apnea and markers of inflammation, oxidative stress and endothelial dysfunction. Recent mid-terms trials showed that nocturnal use of positive airway pressure in patients with the two types of apnea alleviates symptoms, reduces sympathetic activity, improves ventricular function and quality of life, and reduces daytime drowsiness. More studies are needed to understand the mechanisms underlying the relationship between sleep apnea and cardiovascular disease, but clinicians should be aware of this link and should attempt to identify patients with these syndromes.
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PMID:[Sleep apnea syndromes and cardiovascular disease]. 1614 10

Obstructive sleep apnea (OSA) is a newly recognized risk factor for the development of systemic hypertension, ischemic heart disease, and congestive heart failure. Mechanisms responsible for these links include OSA-related hypoxemia and arousal from sleep-induced increased sympathetic activity, large negative intrathoracic pressure-induced increased left ventricular transmural pressure gradient and impaired vagal activity, plus formation of oxygen radicals. Secondary phenomena include increased platelet aggregability, insulin resistance, and endothelial dysfunction with reduced endogenous nitric oxide production. Safe, nonpharmacologic, nonsurgical therapy, namely continuous positive airway pressure, can attenuate OSA and improve cardiac function and quality of life. Searching for signs or symptoms of OSA from the patient (or bed partner), namely loud habitual snoring, apneas, nocturnal choking, orthopnea, paroxysmal nocturnal dyspnea, excessive daytime sleepiness, or cardiovascular disease which is difficult to control, may reward the curious physician with another treatment avenue.
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PMID:The link between obstructive sleep apnea and heart failure: underappreciated opportunity for treatment. 1712 12

The aim of the study was to compare the incidence of obstructive sleep apnoea syndrome (OSAS) symptoms in relatives of subjects with OSAS and in relatives without OSAS but with clinical symptoms of this disease. The study group consisted of 186 relatives of patients with OSAS and 117 relatives of patients with symptoms of OSAS in whom the disease was not confirmed by polysomnography. They were all mailed a questionnaire with questions concerning anthropometric data, the presence of symptoms typical for OSAS and the presence of concomitant diseases. Analysis of the obtained data revealed an increased frequency of snoring, sleep apnea and nycturia in the relatives of patients with OSAS when compared to relatives of patients without OSAS, but the difference was not statistically significant. The incidence of daytime OSAS symptoms was significantly higher in the group of relatives of patients with OSAS. No differences in the incidence of arterial hypertension, ischaemic heart disease and diabetes mellitus were found.
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PMID:[Familial clustering of symptoms typical for OSAS]. 1717 78


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