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

A child in heart failure with homozygous sickle cell disease underwent corrective surgery on cardiopulmonary bypass. The use of early intra-operative exchange transfusion produced a rapid fall in the level of HbS. Postoperatively she developed falciparum malaria which responded to treatment. She was eventually discharged home to Nigeria 8 weeks after her operation.
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PMID:Open heart surgery in a patient with homozygous sickle cell disease. 709 7

There is controversy in the medical literature regarding the significance of "sickle cell cardiomyopathy." In an attempt to clarify this, we studied 14 patients with sickle cell anemia (age range 16 to 36 years) using simultaneous echocardiography and phonocardiography. The values of systolic time intervals and echocardiographic indices of left ventricular performance were similar to those reported for normal subjects and those with comparable degrees of anemia. We confirm a previous report of normal left ventricular function at rest in patients with sickle cell anemia and concur with the suggestion that a concomitant heart disease be considered in these patients when cardiac failure supervenes.
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PMID:Left ventricular function in sickle cell anemia: a noninvasive evaluation. 736 Nov 40

Sickle cell disease is transmitted as an autosomal recessive trait. Symptoms of pallor, fever, abdominal and joint pain, and swelling of the liver, spleen, hands and feet first appear near the latter part of the first year of life. Intravascular sickling affects all organs. For clinical and therapeutic purposes, exacerbations may be classified as vasoocclusive or pain, aplastic, hemolytic or sequestration crisis. In addition to infection, complications include severe pain, cerebrovascular accidents, cholelithiasis, bone infarction, heart failure, hypotension and priapism. The most common cause of early childhood death is septicemia or meningitis due to Streptococcus pneumoniae. Complications may be reduced or prevented by early diagnosis through newborn screening, patient education, routine immunizations, administration of folic acid, pneumococcal and influenza vaccinations, penicillin prophylaxis, and early diagnosis and aggressive treatment of complications.
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PMID:Common problems in sickle cell disease. 781 Apr 78

The frequency and severity of pneumococci infections, the isolation of invasive serotypes and the fact that certain serotypes develop cross-resistance to antibiotics constitute justifications for anti-pneumococci vaccination. A 23-valence vaccine (Pneumo 23) has been marketed since 1983. A meta-analysis of 9 randomized studies concluded that anti-pneumococci vaccination reduces the overall incidence of pneumococci pneumonia with bacteremia. The efficacy of the vaccine was demonstrated on 4 parameters: proven pneumococci pneumonia, proven pneumococci pneumonia and serotypes contained in the anti-pneumococci vaccine, presumed pneumococci pneumonia, presumed pneumococci pneumonia and serotypes contained in the anti-pneumococci vaccine. The efficacy of the vaccine was significant only for low-risk subjects. The protective effect was not demonstrated against pneumonia whatever the cause and against bronchitis. Other case-control or retrospective studies have also been reported. The results have been somewhat contradictory but there is a demonstration of the usefulness of vaccination in patients over 65 years of age with a moderate risk (living in institution, obstructive bronchopneumonary disease, heart failure). Vaccination is advocated not only after splenectomy and in subjects with sickle cell anemia, but also in frequently hospitalized subjects, particularly those with respiratory failure and smokers. Vaccination is also recommended in case of nephrotic syndrome or an osteomeningeal breach. In at-risk children under 2 years of age, antibiotic prophylaxis is recommended in association with vaccination. The data of revaccination is not clearly determined.
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PMID:[Anti-pneumococcal vaccine: justifications and results]. 929 13

Originally developed as an antianginal agent, amiodarone was soon found to have antiarrhythmic properties and to be a non-competitive inhibitor of alpha and beta-adrenergic receptors. Many trials studying the use of amiodarone in patients with heart failure have now been performed and are reviewed in this article. The trials appear to show that amiodarone possesses significant antiarrhythmic activity, even in heart failure patients. The drug appears to be well tolerated and proarrhythmia is uncommon. Based on the findings of a large Argentinian randomised trial (GESICA) and the Congestive Heart Failure Survival Trial of Antiarrhythmic Therapy (CHF STAT), it would appear there is a role for amiodarone in patients with non-ischaemic cardiomyopathy, but prospective studies are required to confirm this. The benefit of amiodarone in patients with non-ischaemic cardiomyopathy might be related to the beta-blocking effect that is seen with the use of conventional beta-blockers. Further studies, including the Sudden Cardiac Death Heart Trial (SCD HeFT), should help determine the role of amiodarone in heart failure patients.
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PMID:Amiodarone in congestive heart failure. 989 84

Sudden cardiac death due to ventricular arrhythmias remains a significant problem. In most studies about 50% of all death related to coronary artery disease and heart failure are sudden and unexpected and are caused by acute fatal ventricular tachycardia and fibrillation. Most of the patients suffering sudden cardiac death have some kind of structural heart disease but 80% of SCD events are associated with coronary artery disease, 10-15% with dilated and hypertrophic cardiomyopathy, and only small fraction with the less common disorders as valvular heart disease, ventricular dysplasia and cardiac involvement in sarcoidosis or amyloidosis. In some patients the anomaly responsible for sudden cardiac death is not structural but mainly electrical as in patients with the long QT syndrome, WPW syndrome or in patients with a proarrhythmic effect from antiarrhythmic drugs. In this review, data from clinical trials and other studies on on antiarrhythmic therapies have been evaluated in order to determine effective strategies for the prevention sudden cardiac death in high risk patients. Taken together with the mortality data routine prophylactic use of class I antiarrhythmic drugs in the patients survivors of acute myocardial infarction and patients with heart failure is associated with increased risk of death. Conversely beta-blockers are associated with significant reduction in nonfatal cardiac arrest in the short term trials and sudden cardiac death in long term trials. These benefits are likely due to relief ischemia, reduction of heart rate and maintenance favourable autonomic nervous system balance. Overall trial data on amiodarone suggests that this agent is effective in reducing the risk of death in survivors of cardiac arrest, post infarction patients, and patients with heart failure but the routine prophylactic use of amiodarone remains of uncertain efficacy. The physician who considers the use of antiarrhythmic medications in patients with ventricular arrhythmias must be aware of which arrhythmias are malignant or potentially malignant and which are benign and the decision to initiate antiarrhythmic therapy should be based on consideration of the patients absolute mortality risk.
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PMID:[Antiarrhythmic agents in the prevention of sudden cardiac death]. 1036 92

SCD continues to be an important cause of death and morbidity. Despite expanding insight into the mechanisms causing SCD, the population at high risk is not being effectively identified. Although there is still much to do in the management phase of SCD (predicting the efficacy of various therapies), recent clinical trials have helped define the relative risks and benefits of therapies in preventing SCD. Trials are underway to determine whether treating other patient populations, including asymptomatic patients after MI, will improve survival rate. The approach to reducing mortality rate will always be multifaceted; primary prevention of coronary artery disease and prompt salvage of jeopardized myocardium are 2 important aspects of this approach. In addition to interventions for MI, such as myocardial revascularization when indicated, simple and easily administered therapies that are likely to remain the most effective prophylactic interventions are aspirin, ACE inhibitors, beta-blockers, and cholesterol-lowering agents. However, the MADIT and AVID data clearly demonstrate a role for ICD therapy in a subgroup of patients who have VT/VF and are at risk of cardiac arrest. Even though the absolute magnitude of benefit associated with ICDs is still to be determined, the AVID study and other recent reports provide convincing evidence that patients who have VT/VF fare better with ICDs than with antiarrhythmic drug therapy. For the high-risk population described in this article, in addition to aggressive anti-ischemic and heart failure therapy, ICDs are now a mainstay of life-saving treatment. Still to be surmounted is the challenge of identifying patients who have nonischemic substrates and of providing them with the appropriate therapy. Guided by genetic studies and new insight into the mechanisms of such problems as congenital long QT syndrome, life-saving and life-enhancing therapies may soon be available for the management of SCD.
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PMID:Sudden cardiac death. 1045 74

Patients with congestive heart failure frequently have ventricular arrhythmias on ambulatory electrocardiographic recordings and sudden cardiac death is seen in almost 50% of such patients. Many antiarrhythmic agents have been approved to suppress the arrhythmia in an effort to improve survival. Some sodium-channel blockers not only failed to improve survival but have been shown to be harmful. This led to the development of potassium-channel blockers, such as d-sotalol, amiodarone, dofetilide, and azimilide. d-Sotalol was associated with excess mortality in patients with left ventricular dysfunction; amiodarone seems to be potentially beneficial; and dofetilide has a neutral effect on mortality. The Sudden Cardiac Death Heart Failure Trial (SCD HEFT) is testing the implantable cardioverter defibrillator (ICD) against amiodarone and placebo. The ICDs appear to be superior to antiarrhythmic drugs in certain high-risk patients, although not proved in unstratified patients with heart failure.
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PMID:Class III drugs and congestive heart failure: focus on the congestive heart failure-survival trial of antiarrhythmic therapy. 1056 68

In patients with severe chronic heart failure, many deaths are sudden due to life-threatening ventricular arrhythmias. Supraventricular arrhythmias such as paroxysmal or chronic atrial fibrillation may also cause serious complications in those patients due to acute loss of atrial contraction, pump failure during rapid ventricular response and embolic events. Two therapeutic strategies are currently available for therapy and prevention of malignant ventricular arrhythmias and subsequent sudden arrhythmic death: antiarrhythmic drug therapy and implantable defibrillators. However, selection of the most beneficial strategy for the individual patient to reduce the risk of sudden death remains a major challenge in cardiology. Betablockers exert a favorable antiarrhythmic action without increasing proarrhythmia, thus betablockers may serve as a basic medication in patients at risk for sudden death. However, the general use of antiarrhythmic drug therapy for symptomatic ventricular arrhythmias is not recommended, as these drugs have been shown to increase mortality in patients with severe congestive heart failure due to proarrhythmic or negative inotropic effects (e.g. class Ia antiarrhythmics). Even class III antiarrhythmic drugs such as amiodarone, which has been studied sufficiently in patients with left ventricular dysfunction, is not effective enough for significant reduction of cardiac mortality in patients with symptomatic ventricular arrhythmias and depressed ventricular function (e.g. EMIAT, CAMIAT). But as a positive result of available studies, amiodarone does not increase mortality in those patients. Dofetilide has also not been shown to prolong life significantly by suppressing malignant ventricular arrhythmias (DIAMOND-Study). In patients with symptomatic ventricular arrhythmias or aborted sudden death, ICD therapy has been proven to be superior to antiarrhythmic drug therapy in cardiac mortality reduction as a secondary prevention strategy (e.g. AVID, CASH, CIDS). For primary prevention of sudden arrhythmic death in high risk patients, 2 studies (MADIT, MUSST) have already demonstrated favorable results, decreasing mortality by ICD therapy in selected patient populations with partly-reduced ventricular function and unsustained but inducible ventricular tachycardias. This topic is, however, undergoing further evaluation by ongoing trials (e.g. MADIT II, SCD-HeFT). From available data, antiarrhythmic drug therapy in high risk patients is not justified on a routine basis, whereas ICD therapy as a secondary and perhaps primary prevention strategy will significantly reduce cardiac mortality in patients with severe heart failure. Sotalol, a class III antiarrhythmic agent, has recently been shown to reduce ICD-shock delivery which indicates that concomitant drug therapy in patients with an ICD device already implanted may be beneficial in terms of reducing ICD discharges due to ventricular and supraventricular tachycardias. In patients with paroxysmal atrial fibrillation and congestive heart failure, restitution of sinus rhythm is the primary therapeutic goal which can be safely achieved by amiodarone and dofetilide (DIAMOND). In the latter, continuous monitoring of the patient is mandatory because of increased risk of torsade de pointes arrhythmias during the first days of drug administration. In patients with chronic atrial fibrillation rate control and anticoagulation with warfarin is the primary therapeutic option, which can be achieved with either drug treatment (Digoxin, betablockers, amiodarone) or by His bundle ablation with subsequent pacemaker insertion.
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PMID:[Antiarrhythmic therapy in patients with heart failure]. 1085 93

Prenatal administration of iron and folate can prevent nutritional anemia and boost the hemoglobin of those who are already anemic, strengthening women for delivery and building their resistance against infection. Regular screening is needed, since women with more than mild anemia need additional treatment. Ideally a woman should have a hemoglobin level of at least 110 g/l by the time of delivery. Many lack the iron stores they need for pregnancy, delivery, and lactation. Yet prenatal administration of oral iron supplements could give them higher hemoglobin levels and adequate stores. Folate deficiency is less important as a cause of anemia than lack of iron, but folate needs are increased by malaria, thalassemia, and sickle cell disease. Malaria causes severe complications in pregnancy, and studies from sub-Saharan Africa report malaria parasite rates 30-40% higher in primigravidae than in nonpregnant women. Persistent infection increases the level of anemia. Where intestinal parasites are common, anthelmintic drugs should be routinely given to all pregnant women. The transmission of HIV by blood transfusion makes it more urgent to prevent anemia and avoid the need for blood transfusions. According to a WHO document in southern Asia, 75% of pregnant women are anemic compared with 17% in Europe and North America. In Africa, 50% of pregnant women are anemic, as are 39% in Latin America and 71% Oceania (excluding Australia and New Zealand). Moderate anemia (70-109 g/l) is estimated to be present in 25-33% of pregnant women, with the highest prevalence in Southern Asia, Oceania, and Sub-Saharan Africa. Surveys show that from 3-7% of women suffer from severe anemia 70 g/l), which carries a high risk of death from heart failure. In pregnant women, even the relatively small blood loss associated with a normal delivery can result in death.
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PMID:Anaemia -- the weak get weaker. 1228 38


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