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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The phospholipid composition of 35 human lungs with pathological lesions was analysed by means of thin-layer chromatography and densitometric scanning. The pathological conditions studied were: bronchopneumonia, myocardial infarction, chronic heart failure, chronic obstructive airway disease and tuberculosis. The phospholipid composition was compared with that of a control group consisting of sudden death cases (due to unnatural causes), i.e. relatively normal lungs. The phospholipid composition of the lungs in a specific pathological group showed the same pattern. However, significant differences were observed between corresponding phospholipid fractions from lungs in the various pathological groups. Compared with the lipid fractions from relatively normal lungs, these differences were even more marked. From the results it would appear that the abnormal composition of the phospholipid fractions might possibly be a cause of lung pathology. The increase and/or decrease in individual fractions and abnormal ratios between fractions might indicate abnormalities in the biosynthesis and catabolism of the lung phospholipids. Further is necessary to elucidate the association of phospholipids with lung pathology. Phospholipid analysis of lung lavages and lung biopsies could be helpful in the diagnosis of lung diseases. Phospholipids in aerosol form could perhaps be used in treating certain lung disorders.
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PMID:[The clinical significance of phospholipids in lung pathology]. 725 61

Patients with chronic heart failure (CHF) have a resting restrictive ventilatory defect. Any type of exercise requires patients with CHF to markedly increase their minute ventilation. Patients with chronic obstructive pulmonary disease (COPD) have airflow obstruction that leads to dynamic lung hyperinflation and reduced ventilatory response to exercise. Because exercise is associated with abnormally high minute ventilation in patients with CHF and with a limited minute ventilation increase in patients with COPD, functional capacity is severely impaired in patients with coexistent CHF and COPD. Optimal treatment of both conditions is a prerequisite to maximally improve functional capacity in patients with CHF and COPD. Unfortunately, beta-adrenergic blockade, the current cornerstone of CHF therapy, is frequently omitted in patients with CHF and COPD for fear of inducing bronchoconstriction. Furthermore, when prescribed, beta-adrenergic blockade is often attempted with a moderate dose of metoprolol tartrate, a beta-1-blocker that results in lesser clinical benefits than combined non-selective beta-blockade with carvedilol at the maximally recommended dose. Recent experience indicates that combined non-selective beta- and alpha-blockade with carvedilol is well tolerated in patients with COPD who do not have reversible airway obstruction. Alpha-adrenergic blockade may promote mild bronchodilation that offsets non-selective beta blockade-induced bronchoconstriction in patients with obstructive airway disease.
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PMID:Therapeutic update: non-selective beta- and alpha-adrenergic blockade in patients with coexistent chronic obstructive pulmonary disease and chronic heart failure. 1535 10

The implementation of guidelines for medical therapy of heart failure may be problematic for the following reasons: 1. Elderly patients and women were underrepresented in large clinical trials which may limit their therapeutic impact in these patients. 2. Therapeutic decisions are influenced by co-morbidities like renal failure, obstructive airway disease (COLD, Asthma), stroke, and diabetes mellitus. We therefore discuss the differential therapy of heart failure in view of particular patient subgroups.
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PMID:[Differential therapy of heart failure. Which drug for which patient?]. 1552 78

30-50% of patients presenting with symptoms of congestive heart failure exhibit a near normal left ventricular systolic function at rest, and an impaired diastolic function of the heart may be causative. Despite a better prognosis than in systolic heart failure, frequency of hospitalizations due to diastolic heart failure is comparable with systolic heart failure. According to the criteria of Vasan and Levy diagnosis of diastolic heart failure is probable, if symptoms and signs of heart failure are accompanied in proximity (within 72 h) by objective evidence of normal left ventricular systolic function. Newer echocardiographic techniques (e. g., tissue Doppler) aid to confirm the diagnosis and to determine the severity of dysfunction and may substitute invasive demonstration of impaired left ventricular relaxation, filling, compliance or stiffness for standardized diagnosis. Incorporation of biochemical test (BNP [brain natriuretic peptide]) allows differential diagnosis and may increase the accuracy of diagnosis. Due to inconsistent diagnostic criteria, data from prospective randomized controlled trials for the treatment of diastolic heart failure are rare. Basic principles include treatment of the underlying disease, i. e., control of hypertension, diabetes, or obstructive airway disease. Angiotensin 1 antagonists (ARB) have proven effective in regression of left ventricular hypertrophy (LIFE) and may reduce morbidity, but not mortality (CHARM). Maintenance of sinus rhythm, heart rate control (beta-blockers, calcium channel blockers) and anti-ischemic therapy may be indicated in view of pathophysiological aspects. Diuretics should be administered with caution in patients with symptoms of congestion, digitalis is not useful in the treatment of isolated diastolic heart failure. The results of ongoing trials (e. g., I-Preserve) may offer new therapeutic options, and evidence-based guidelines for the so far often unsatisfactory treatment of diastolic dysfunction/heart failure are awaited.
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PMID:[Dyspnea and normal systolic function]. 1591 35

Emerging evidence has suggested that with minimal prerequisite training, slow deep breathing around 0.10 Hz can acutely enhance cardiovagal baroreflex sensitivity (BRS) in humans. Such reports have led to the speculation that behavioral interventions designed to reduce breathing frequency may serve a therapeutic role in ameliorating depressed baroreflex function in conditions such as chronic heart failure, essential hypertension, and obstructive airway disease. This study sought to test the hypothesis that slow controlled breathing acutely enhances cardiovagal baroreflex function in young healthy volunteers. Distinct from earlier studies, however, baroreflex function was examined (n = 30) using the classical pharmacological modified Oxford method, which enabled the assessment of cardiovagal BRS through experimentally driven baroreceptor stimulation across a wide range of blood pressures. For a comparison against existing evidence, spontaneous cardiovagal BRS was also assessed using the alpha-index and sequence method. Compared with fast breathing (0.25 Hz), slow breathing (0.10 Hz) was associated with an increase in the alpha-index (8.1 +/- 14 ms/mmHg, P < 0.01) and spontaneous up-sequence BRS (10 +/- 11 ms/mmHg, P < 0.01). In contrast, BRS derived from spontaneous down sequences and the modified Oxford method were unaltered by slow breathing. The lack of change in BRS derived from the modified Oxford method challenges the concept that slow breathing acutely augments arterial baroreflex function in otherwise healthy humans. Our results also provide further evidence that spontaneous BRS may not reflect the BRS determined by experimentally driven baroreceptor stimulation.
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PMID:Respiratory modulation of cardiovagal baroreflex sensitivity. 1960 28

Mortality and other long-term outcomes of COPD from epidemiological studies of cohorts based on the general population are still rare. In contrast, data from follow-ups of patients from hospitals and general practices are more common and demonstrate often a 5-year mortality of about 50% and even higher. The aim was to study 20-year outcomes, mainly mortality, in a COPD cohort derived from a population study. The Obstructive Lung Disease in Northern Sweden (OLIN) Study's first postal survey was performed in 1985, and 5698 subjects (86%) responded. A stratified sample of symptomatic subjects and controls was invited to clinical examinations including lung function tests in 1986, 1506 (91%) of the invited participated and 266 subjects fulfilled the GOLD criteria of COPD. All alive and possible to trace had participated at least at two follow-up examinations. Of the 266 subjects with COPD 46% were still alive after 20 years. The proportion of survived among subjects with severe and very severe COPD at entry was 19%. Death was significantly related to age, male sex, disease severity and concomitant ischemic heart disease or cardiac failure at entry. Socioeconomic status (manual workers) was significant in the univariate analysis, but failed to reach statistical significance in the multivariate model. The annual decline in FEV(1) among survivors was low to normal. Long-term follow-ups of subjects with COPD derived from population studies provide data reflecting the course of COPD in society better than follow-ups of hospital recruited patients, who represent the top of the iceberg. Surprisingly many with severe COPD were still alive after 20 years.
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PMID:A 20-year follow-up of a population study-based COPD cohort-report from the obstructive lung disease in Northern Sweden studies. 1981 85

Ivabradine, an I(f) inhibitor, acts primarily on the sinoatrial node and is used to reduce the heart rate with minimal effect on myocardial contractility, blood pressure, and intracardiac conduction. Heart rate reduction is an important aspect of care in patients with chronic stable angina and heart failure. Many patients with coronary artery disease have coexisting asthma or chronic obstructive airway disease, and most of them are unable to tolerate beta blockers. Ivabradine may thus be a useful medicine in therapeutic heart rate management especially in patients who are intolerant of beta-blockers.
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PMID:Heart rate and cardiovascular disease: an alternative to Beta blockers. 1993 14

Mucopolysaccharidosis (MPS) type II (Hunter syndrome, OMIM 309900) is an X-linked lysosomal storage disorder caused by a deficiency of the lysosomal enzyme iduronate-2-sulfatase (IDS). Major clinical manifestations include joint contractures, obstructive and restrictive airway disease, cardiac disease, skeletal deformities and often mental retardation. As with all the MPS disorders, mucopolysaccharidosis type II is a clinically heterogeneous disease in terms of the extent and rate of progression of organ impairment in affected individuals. Common causes of death, which usually occurs within the second decade of life, are obstructive airway disease and cardiac failure due to valvular dysfunction, pulmonary hypertension and myocardial disease. Patients with the more attenuated (so-called adult) form usually have a normal intelligence, but often have many complaints such as progressive loss of vision due to retinal dysfunction, spastic paresis due to myelon compression at the cranio-cerevical region, severe hip disease and cardiac complications. Clinical investigations that have been performed in the last years in a great number of patients have shown that many of these complications are still underdiagnosed and untreated. Until recently, no specific treatment was available for the affected patients; management mainly consisted of supportive care and treatment of complications. Enzyme replacement therapy with recombinant iduronate-2-sulphatase (idursulfase), however, has now been introduced. And it could be demonstrated that weekly intravenous infusions of idursulfase is able to improve many of the symptoms and signs of Hunter syndrome. This review will present the efficacy and safety data of the enzyme preparation and discuss benefits and limitations of this new therapeutic option.
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PMID:Mucopolysaccharidosis Type II (Hunter Syndrome): clinical picture and treatment. 2123 46

The clycoxygenase (COX) enzyme forms locally active prostaglandins responsible for producing inflammation and pain. Classical non-steroidal anti-inflammatory drugs (NSAID) inhibit the COX-2 enzyme that produces inflammatory prostaglandins as well as the COX-1 enzyme that produces gastric mucosa protecting prostaglandins. By specifically inhibiting only the COX-2 enzyme, coxibs thus reduce pain but do not damage the gastric mucosa. However, COX-2 at the vascular endothelium produces antithrombotic prostaglandins, and so by inhibiting COX-2 enzyme, the coxibs promote thrombosis. Rofecoxib and valdecoxib have been withdrawn because of the adverse cardiovascular events they induce. Amongst presently available coxibs cardiovascular risk is highest with enterocoxib and lowest with celecoxib. NSAIDS also increase cardiovascular events, the risk is highest with diclofenac and lowest with naproxen. Paracetamol and corticosteroids induce hypertension, while steroids also adversely affect the heart from metabolic change as well as fluid retention. Aspirin is an anti-thrombotic agent because of its ability to inhibit the COX-1 enzyme that produces the pro-aggregatory thromboxane. However, it increases gastrointestinal bleeding, can promote fluid retention and is nephrotoxic, all of which may lead to adverse cardiovascular outcomes. Patients at especially high risk of cardiovascular events from analgesic use include the elderly, and those with heart failure, hypertension, rheumatoid arthritis, chronic renal disease, chronic obstructive airway disease and previous myocardial infarction, cerebrovascular disease or peripheral vascular disease. Adverse cardiovascular events can occur within a week of initiation of analgesic treatment.
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PMID:Cardiovascular effects of common analgesics. 2362 78

Mucopolysaccharidosis type II (MPS II), also known as Hunter syndrome, is a rare, X-linked disease caused by a deficiency of the lysosomal enzyme iduronate-2-sulfatase, which catalyses a step in the catabolism of glycosaminoglycans resulting in accumulation of heparan and dermatan sulfate in many organs and tissues. This accumulation favors the appearance of neurologic involvement, severe airway obstruction, skeletal deformities, and cardiomyopathy, especially mitral and aortic valve regurgitation. In severe cases, obstructive airway disease and cardiac failure due to valvular dysfunction are the most common causes of death within the second decade of life. However, in mild cases, intelligence remains normal, stature is almost normal and death usually occurs due to cardiac failure in the fourth decade of life. We report the presentation, diagnosis, management, and outcome of 2 siblings with MPS II and the G374sp mutation at the nucleotide c.1246 of the gene encoding for the iduronate-2-sulfatase.
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PMID:Mucopolysaccharidosis Type II and the G374sp Mutation. 2380 37


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