Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An awakening has taken place over the last 25 years to the science of sleep disorders. Foremost amongst these, both in the medical world and the public eye, has been Sleep Apnoea Syndrome (SAS). The prevalence is thought to be the order of 1-2%. Males are eight times more commonly affected than females, although after the menopause the gap narrows considerably. Sleep apnoea occurs in children, usually in relation to large tonsils and adenoids, but in adult life patients usually present between the age of 40 and 60 and the prevalence increases with age. Numerous apnoeas or hypopnoeas during the night's sleep result in disordered sleep architecture and unrefreshing sleep. This is usually accompanied by night-long snoring which may lead to marital discord and even complaints from neighbours. Symptoms on waking may be a headache and a feeling of not being refreshed by sleep. Sleepiness during the day can interfere with work and social activities and may produce risks to the patient and others if it occurs while operating dangerous machinery or driving. Over a longer time scale SAS results in intellectual and memory deterioration, a higher incidence of ischaemic heart disease, hypertension, polycythemia and pulmonary hypertension. Right heart failure is particularly likely if there is chronic airflow obstruction contributing to a low arterial oxygen level. Asystolic periods and tachyarrhythmias may occur during apnoeic periods. The increased mortality of SAS relates to coronary and cerebrovascular disease and arrhythmias. Sudden death occurs with greater frequency in patients with SAS, mainly at night.
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PMID:Sleep apnoea: causes, consequences and treatment. 141 52

The possible methods of preventing myocardial infarction have been discussed. The desirability of prevention in the total problem of myocardial infarction is stressed. The methods consist of the prevention of the underlying coronary atherosclerosis, and the secondary prevention of myocardial ischemia contributed by other factors than those presumed to relate to atherosclerosis. In the primary prevention of coronary atherosclerosis the two major risk factors are elevation of serum lipids and of blood pressure. The benefits to be achieved by reduction of elevation of both of these abnormalities are discussed. Both require a long-term approach starting as early in life as possible. The major methods of prevention or retardation of coronary ischemia irrespective of coronary artery disease involve discontinuance of cigarette-smoking and a program of increased physical activity. In addition, prevention or correction of polycythemia, anemia or hypercoagulability should be included. The use of oxygen, in higher percentage or at higher pressure than in the atmosphere, surgical intervention to improve the myocardial blood supply and pharmacologic agents to improve myocardial metabolism are also considered. Quantitation of the benefit of preventive programs is still impossible. Benefit from lowering blood lipids and blood pressure requires long-term therapy begun early in life. Discontinuance of cigarette smoking and increasing the amount of physical activity offer reasonable assurance of immediate benefit. So also does correction of hematologic abnormalities. Pharmacologic agents and surgery to improve coronary blood flow still require further evaluation.
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PMID:Prevention of myocardial infarction. 521 90

Altitude exposure is associated with major changes in cardiovascular function. The initial cardiovascular response to altitude is characterized by an increase in cardiac output with tachycardia, no change in stroke volume, whereas blood pressure may temporarily be slightly increased. After a few days of acclimatization, cardiac output returns to normal, but heart rate remains increased, so that stroke volume is decreased. Pulmonary artery pressure increases without change in pulmonary artery wedge pressure. This pattern is essentially unchanged with prolonged or lifelong altitude sojourns. Ventricular function is maintained, with initially increased, then preserved or slightly depressed indices of systolic function, and an altered diastolic filling pattern. Filling pressures of the heart remain unchanged. Exercise in acute as well as in chronic high-altitude exposure is associated with a brisk increase in pulmonary artery pressure. The relationships between workload, cardiac output, and oxygen uptake are preserved in all circumstances, but there is a decrease in maximal oxygen consumption, which is accompanied by a decrease in maximal cardiac output. The decrease in maximal cardiac output is minimal in acute hypoxia but becomes more pronounced with acclimatization. This is not explained by hypovolemia, acid-bases status, increased viscosity on polycythemia, autonomic nervous system changes, or depressed systolic function. Maximal oxygen uptake at high altitudes has been modeled to be determined by the matching of convective and diffusional oxygen transport systems at a lower maximal cardiac output. However, there has been recent suggestion that 10% to 25% of the loss in aerobic exercise capacity at high altitudes can be restored by specific pulmonary vasodilating interventions. Whether this is explained by an improved maximum flow output by an unloaded right ventricle remains to be confirmed. Altitude exposure carries no identified risk of myocardial ischemia in healthy subjects but has to be considered as a potential stress in patients with previous cardiovascular conditions.
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PMID:Physiological adaptation of the cardiovascular system to high altitude. 2041 39