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

The high incidence, great import, and long duration of cardiovascular diseases are reflected in high demands placed on the health services. Experience shows that utilization of the results of research in general practice is lagging behind. The application of any improvement in the diagnosis, therapy, and prevention in health care waits several years for its accomplishment. In order to improve this situation, the Ministry of Health of the CSR constituted, in line with WHO recommendations, a Department for Cardiovascular Diseases Control. The Department has worked out a programme of prevention and control of the major cardiovascular diseases, in particular, ischaemic heart disease, systemic hypertension and its complications, rheumatic heart disease, congenital cardiac and vascular defects, and cor pulmonale. New diagnostic, therapeutic, and preventive procedures are first tried out in so-called model areas and are only after this introduced into the national health care of people suffering from or endangered by cardiovascular diseases. In parallel, organizational measures necessary for comprehensive care are implemented. The authors report on the experience gained so far with the realization of the programme of care of people suffering from IHD and acute myocardial infarction. They emphasize the importance of continual schooling of medical personnel and of health education of the entire population. They describe the implementation on a national scale of postgraduate cardiological courses intended especially for first-line doctors.
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PMID:Present state of cardiovascular community control programme in the Czech Socialist Republic. 94 76

Cardiac adaptation due to sport activity are usually interpreted as physiological process induced by cardiac overload during vigorous and continued muscle activity. The aim of this work was to evaluate long term cardiac effects of competitive sport activity performed in youth, after retirement. In particular we investigated: 1) whether cardiac adaptations to exercise are reversible and 2) whether or not previous competitive activity affects the cardiac ageing process or modifies ventricular function. We studied 23 professional retired athletes (PRA): 16 football players and 7 boxers, aged 40-60, who had been active in their sports for 16 years mean and who completely interrupted training and competition for at least 10 years. Our evaluation consisted of a questionnaire, a clinical assessment, an electro- and echocardiographic examination at rest. Data obtained in PRA were compared with those of twenty subjects matched for sex, age and weight who had never been athletes (control group = C) (Tab. I). We found: left ventricular hypertrophy in 5 cases (according to the "Point Score System" electrocardiographic evaluation): tall T waves in the precordial leads in 4 and conduction defects in other 4 cases. One subject had evidence of ischemic heart disease. Eleven cases were normal (Tab. II). Echocardiographic data demonstrated concentric heart hypertrophy and depressed ventricular function in PRA. Cardiac mass calculations were significantly higher in PRA with respect to C, more so for wall thickening than for cavitary enlargement. We concluded that: 1) cardiac adaptation due to physical exercise are not completely reversible and 2) systolic ventricular work, evaluated by means echocardiographic indices (EF, CSF and CSR) is depressed in PRA.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Long-term effects of competitive sport activity on the heart of professional ex-athletes]. 295 85

Obstructive and central sleep apnea are common in patients with congestive heart failure (CHF). These sleep-related breathing disorders are characterized by two pathophysiologic features that could have important implications for disease progression in CHF: sympathetic nervous system activation, and adverse changes in cardiac loading conditions. In patients with obstructive sleep apnea, blood pressure is frequently elevated as a result of excessive sympathetic nervous system activity elicited by the combination of apnea, hypoxia, and arousals from sleep. The generation of exaggerated negative intrathoracic pressure during obstructive apneas further increases left ventricular afterload, reduces cardiac output, and may promote the progression of pump failure. Increased afterload and hypoxia can also predispose such patients to myocardial ischemia and arrhythmias. In patients with CHF, abolition of coexisting obstructive sleep apnea by nasal continuous positive airway pressure improves left ventricular function. Central sleep apnea (i.e., Cheyne-Stokes respiration) is also characterized by apnea, hypoxia, and increased sympathetic nervous system activity and, when present in CHF, is associated with increased risk of death. Recent medium-term trials involving small numbers of patients have demonstrated that nocturnally applied continuous positive airway pressure in patients with CHF and central sleep apnea alleviates central sleep apnea, improves left ventricular function, reduces sympathetic nervous system activity and improves symptoms of CHF. These studies emphasize the importance of considering obstructive and central sleep apnea in the differential diagnosis of conditions that could contribute to the development or progression of CHF. They also suggest that continuous positive airway pressure is a promising nonpharmacologic adjunctive therapy for patients with CHF and coexisting sleep-related breathing disturbances that warrants further investigation.
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PMID:Pathophysiologic and therapeutic implications of sleep apnea in congestive heart failure. 889 61

Death from heart disease is sometimes observed at night. Life threatening arrhythmias or ischemic heart disease are suspected to be the cause of sudden death during night. Cheyne-Stokes respiration (CSR) is frequently observed in patients with chronic cardiac failure. CSR augments sympathetic nervous activity and reduces the quality of sleep. Sleep apnea or snoring is another stressful condition during sleep. During hyperventilatory phase of sleep apnea, the blood pressure, heart rate, end-systolic ventricular volume and vosomotor tone increases, and the periodic EEG arousal patterns are observed. Sleep apnea is suspected to be one of the risk factors of hypertension. The detection and early treatment of sleep apnea or Cheyne-Stokes respiration are required to reduce the mortality due to cardiac events during sleep.
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PMID:[Cardiovascular diseases]. 950 52

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

Cardiovascular and cerebrovascular diseases are the most common diseases in industrialized societies. The main objectives of this article were to summarize the physiological effects of sleep apnea on the circulatory system and to review how treatment of this condition influences cardiovascular disease. Acute sleep apnea has a number of hemodynamic consequences, such as pulmonary and systemic hypertension, increased ventricular afterload and reduced cardiac output, all of which result from sympathetic stimulation, arousal, alterations in intrathoracic pressure, hypoxia and hypercapnia. When chronic, sleep apnea-hypopnea syndrome is associated with systemic hypertension, ischemic heart disease, congestive heart failure, and Cheyne-Stokes respiration in patients with congestive heart failure. Nocturnal treatment with continuous positive airway pressure decreases both the number of central apneic episodes and blood pressure in patients with sleep apnea-hypopnea syndrome and arterial hypertension.
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PMID:[Sleep apnea-hypopnea syndrome and the heart]. 1693 14

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

Sleep-disordered breathing (SDB) causes hypoxemia, negative intrathoracic pressure, and frequent arousal, contributing to increased cardiovascular disease mortality and morbidity. Obstructive sleep apnea syndrome (OSAS) is linked to hypertension, ischemic heart disease, and cardiac arrhythmias. Successful continuous positive airway pressure (CPAP) treatment has a beneficial effect on hypertension and improves the survival rate of patients with cardiovascular disease. Thus, long-term compliance with CPAP treatment may result in substantial blood pressure reduction in patients with resistant hypertension suffering from OSAS. Central sleep apnea and Cheyne-Stokes respiration occur in 30-50% of patients with heart failure (HF). Intermittent hypoxemia, nocturnal surges in sympathetic activity, and increased left ventricular preload and afterload due to negative intrathoracic pressure all lead to impaired cardiac function and poor life prognosis. SDB-related HF has been considered the potential therapeutic target. CPAP, nocturnal O2 therapy, and adaptive servoventilation minimize the effects of sleep apnea, thereby improving cardiac function, prognosis, and quality of life. Early diagnosis and treatment of SDB will yield better therapeutic outcomes for hypertension and HF.
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PMID:Therapeutic strategies for sleep apnea in hypertension and heart failure. 2350 23