Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Considerable progress has been made in the medical treatment of chronic heart failure. A large number of patients with NYHA class II and III heart disease can be improved to class I and II. Treatment is maintained on an outpatient basis in order to prevent episodes of acute failure, while avoiding the adverse effects of drugs at high doses or in combination. Diuretics are still the drug class most frequently prescribed, especially loop diuretics (furosemide) which have the advantage of being able to be used in patients with renal failure. Aldosterone antagonists have the pathophysiological value of reducing the development of myocardial fibrosis. Digitalis alkaloids have a positive inotropic effect, which is even observed in the presence of sinus rhythm and which is associated with slowing of the heart rate in tachyarrhythmias. Angiotensin converting enzyme inhibitors are among the most recently used drugs. They decrease the left ventricular post-load and prevent activation of the renin-angiotensin-aldosterone system. Phosphodiesterase inhibitors cannot be administered orally in the long-term and are therefore not suitable for outpatient treatment. However, they are very effective by intravenous injection during the acute phase of heart failure and cardiogenic shock in hospital.
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PMID:[Ambulatory treatment of chronic cardiac insufficiency]. 866

Myocardial infarction represents a crossroads in the natural history of coronary artery disease. The prognosis is determined by the severity of coronary artery disease, infarct size (and hence ejection fraction), and age of the patient. After infarction, patients may remain symptomless, or suffer angina, silent ischemia, reinfarction, heart failure or sudden death. Hence patient management after infarction includes (1) estimation of risk, (2) the use of stress tests to detect ischemia and rhythm disorders, (3) PTCA or bypass if required and (4) medical therapy. Cardiac catheterization is indicated in patients with angina or silent ischemia, non-Q wave infarction or large infarctus; its use is less well established in patients without ischemia and left ventricular dysfunction, but this indication is nevertheless increasingly accepted. PTCA is primarily utilized in patients with single or two vessel disease, while coronary bypass surgery is indicated in patients with left main or three vessel disease. All these measures are designed to improve symptoms and prognosis. For secondary prevention medical therapy should be used to treat cardiovascular risk factors (antihypertensive drugs, lipid-lowering drugs etc.), to inhibit platelets (aspirin, ticlopidine) or coagulation (coumarins), to block neurohumoral activation (betablocker, ACE-inhibitors), for vasoconstriction (calcium channel blockers, nitrates) and to suppress arrhythmias. The large number of drugs requires reasoned use depending on the risk profile of the individual patient. Cardiovascular risk factors should be treated appropriately. Platelet inhibitors should be given to all patients except those with atrial fibrillation or large ventricles (coumarins). Betablockers reduce mortality, reinfarction and sudden death after infarction and hence should be used if no contraindications exist. ACE-inhibitors are particularly effective in improving symptoms and prognosis in patients with impaired left ventricular function. Calcium antagonists should be used with caution and only in patients with normal left ventricular function. Nitrates are primarily effective in improving symptoms in patients with angina or heart failure. Antiarrhythmic drugs (amiodarone) are only useful in patients with complex arrhythmias. Digitalis has been shown to improve symptoms in patients with heart failure, while other inotropic drugs are virtually no longer used. These guidelines allow reasoned differential therapy after myocardial infarction to the maximum benefit of the patient and at minimum cost.
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PMID:[Therapeutic measures following acute myocardial infarct: differential use of PTCA, surgery and drugs]. 868 87

This article provides a detailed overview of the rationale for key aspects of the protocol of the Digitalis Investigation Group (DIG) trial. It also highlights unusual aspects of the study implementation and the baseline characteristics. The DIG trial is a large, simple, international placebo-controlled trial whose primary objective is to determine the effect of digoxin on all cause mortality in patients with clinical heart failure who are in sinus rhythm and whose ejection fraction is < or = 0.45. An ancillary study examines the effect in those with an ejection fraction > 0.45. Key aspects of the trial include the simplicity of the design, broad eligibility criteria, essential data collection, and inclusion of various types of centers. A total of 302 centers in the United States and Canada enrolled 7788 patients between February 1991 and September 1993. Follow-up continued until December 1995 with the results available in Spring 1996.
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PMID:Rationale, design, implementation, and baseline characteristics of patients in the DIG trial: a large, simple, long-term trial to evaluate the effect of digitalis on mortality in heart failure. 872 4

Effective treatment of heart failure depends on a correct functional and aetiological diagnosis. In asymptomatic patients with cardiac dysfunction following myocardial infarction, treatment is directed to prevent recurrent infarction by aggressive lipid lowering with statins and antiplatelet drugs. Beta blockers are important to reduce sudden death. In symptomatic heart failure, clinical improvement is obtained by inhibition of the renin-angiotensin and sympathetic system. Angiotensin-converting-enzyme inhibitors in combination with diuretics reduce morbidity and mortality caused by progression of the myocardial dysfunction and recurrent myocardial infarction. Drugs that activate the neurohormonal systems are clearly counteractive. Digitalis has a definite favourable effect on systems, and in patients with atrial fibrillation, but its effect on mortality is still unsettled. Beta blockers in routine treatment of symptomatic heart failure still remains controversial, but may benefit selected patients.
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PMID:Treatment of heart failure. 877 88

Atrial fibrillation is a very common arrhythmia in patients with structural heart disease, but it also occurs in patients without underlying heart disease. Acute therapy for paroxysmal atrial fibrillation is very dependent on the clinical condition of the patient. Direct current cardioversion is usually the first choice whenever the arrhythmia precipitates heart failure or severe angina, while more stable patients are normally treated with drugs. Most episodes of atrial fibrillation eventually convert to sinus rhythm even in the absence of treatment. Antiarrhythmic drugs can be used to control the ventricular response or to restore sinus rhythm, and several have been tested to assess their ability to convert recent onset atrial fibrillation. The success rate has varied, but generally flecainide and propafenone appear the most effective. Digitalis and calcium channel blockers do not increase the likelihood of reversion but they reduce ventricular rate. Amiodarone has been tested as a possible alternative to flecainide and propafenone. The pros and the cons of these and other drugs in the setting of paroxysmal atrial fibrillation will be discussed. In particular, special emphasis will be given to the differences in the design and in patient selection of the trials that tested antiarrhythmic drugs in paroxysmal atrial fibrillation.
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PMID:Clinical challenge. II. Management of recent onset atrial fibrillation. PAFIT-2 Investigators. 880 38

Digoxin has been a controversial drug since its introduction >200 years ago. Although its efficacy in patients with heart failure and atrial fibrillation is clear, its value in patients with heart failure and sinus rhythm has often been questioned. In the 1980s, reports of some large-scale trials indicated that digoxin, with or without vasodilators or angiotensin-converting enzyme inhibitors, reduced signs and symptoms of congestive heart failure and improved exercise tolerance. This beneficial influence was mainly found in patients with more advanced heart failure and dilated ventricles, whereas the effect in those with mild disease appeared to be less pronounced. In the last few years, new data have shown that digoxin may also have clinical value in mild heart failure, either when used in combination with other drugs or when administered alone. As neurohumoral activation has increasingly been recognized to be a contributing factor in the disease progression of chronic heart failure, the modulating effects of digoxin on neurohumoral and autonomic status have received more attention. Also, there is evidence that relatively low doses of digoxin may be at least as effective as higher doses and have a lower incidence of side effects. Further, the recognition that the use of digoxin too early after myocardial infarction may be harmful and the development of other drugs, in particular angiotensin-converting enzyme inhibitors, have obviously changed the place of digoxin in the treatment of chronic heart failure. The large-scale survival trial by the Digitalis Investigators Group (DIG), whose preliminary results have recently been presented, has shown that although digoxin has a neutral effect on total mortality during long-term treatment, it reduces the number of hospital admissions and deaths due to worsening heart failure. The potentially new features of the old drug digoxin are discussed in this review.
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PMID:Value of digoxin in heart failure and sinus rhythm: new features of an old drug? 883 53

Treatment of heart failure attempts to reduce symptoms, increase functional capacity and prolong survival. Optimal therapy usually requires a combination of several drugs. At present, ACE inhibitors are the drugs of first choice, but must be combined with diuretics in symptomatic patients. Digitalis glycosides are still an important supplement to diuretics and ACE inhibitors. Specific angiotensin receptor antagonists such as losartan have an effect comparable with that of ACE inhibitors and may possess certain advantages because of their direct effect at the receptor level. Extensive research has been conducted in the treatment of heart failure. Newer direct acting vasodilators such as flosequinan and epoprostenol have demonstrated improved exercise tolerance but have an adverse effect on mortality. Positive inotropic agents consisting of a heterogeneous group of drugs have been evaluated. Although novel agents such as xamoterol, milrinone, pimobendan and vesnarinone have demonstrated improved haemodynamics and improved symptoms, they are not advisable at present due to increased mortality related to treatment or a high incidence of adverse events. beta-Blockers, used judiciously, may improve functional capacity as well as mortality and may be an important supplement to current conventional treatment. The new generation of beta-blockers with vasodilating properties such as carvedilol and bucindolol appear promising.
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PMID:Novel drugs and current therapeutic approaches in the treatment of heart failure. 888 74

The mortality of heart failure remains high despite recent therapeutic progress. The objectives of treatment are to relieve symptoms, but also to improve survival. The secondary objectives are extension of the duration of effort, improvement of the ejection fraction, reduction of arrhythmias and neuroendocrine disturbances, although these criteria are not strictly related to the primary objectives. Diuretics should be used from the first symptoms, but their effect on survival has not been evaluated. Digitalis alkaloids, with no effect on survival, also improve functional signs, even in patients in sinus rhythm. All other positive inotropic agents increase mortality. Nitrates improve symptoms and, when associated with hydralazine, prolong survival. Amiodarone should be reserved to patients with dangerous arrhythmias. Angiotensin converting enzyme inhibitors have the best demonstrated effect on survival and must be used as first-line treatment. Their preventive effect on mortality is limited, except in post-infarction ventricular dysfunction. Beta-blockers, which appear very promising for the improvement of survival, functional signs and ejection fraction, are currently under evaluation. Their mechanisms of action and the choice of the most active drugs have yet to be determined.
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PMID:[Drug therapy of heart failure. What choice in 1996?]. 895 37

In dogs, it has been reported that acute ischemia or severe and terminal heart failure results in a selective reduction of myocardial alpha 3 isoform of Na, K-ATPase activity. The aim of this study was to evaluate if a similar change in the two canine digitalis receptor isoforms occurs following 4 weeks of rapid ventricular pacing-induced heart failure without profound necrosis. Heart failure was induced in dogs by rapid ventricular pacing (240 beats x min-1). Digitalis receptors were quantitated by [3H]-ouabain binding with isolated microsomal membranes from sham-operated (n = 3) and heart failure dogs (n = 4) and by Western blot analysis using specific alpha 1 and alpha 3 polyclonal antibodies. In kinetic studies, similar dissociation rates of 19 to 22 x 10(-4) s-1 and 1.3 to 2.4 x 10(-4) s-1 corresponding to high and low affinity sites respectively, were found in sham-operated and CHF dogs. Immunoblotting showed similar abundance of alpha 1 isoform in the two groups; however, levels of alpha 3 were increased by at least 50% in pacing-induced heart failure animals. In conclusion, heart failure selectively modulates the expression of cardiac alpha 3 isoform in dogs.
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PMID:Canine cardiac digitalis receptors are preserved in congestive heart failure induced by rapid ventricular pacing. 902 7

Congestive heart failure is a lethal condition that affects an increasing number of patients. In recent years a great amount of data have accumulated on the pathophysiology and medical and surgical therapy of this condition. In spite of the advances in its management and the great number of patients affected, common errors are still made by internists and cardiologists in the use of drugs and therapeutic strategies. Digitalis has only recently been shown to affect hemodynamics, exercise capacity, and clinical symptoms, but the effects on survival still have to be demonstrated. Loop diuretics, eventually combined with thiazides and antialdosterone drugs in patients with clinical signs and symptoms of fluid retention, are the mainstays of therapy of congestive heart failure. In order to make diuretic therapy efficacious, moderate salt and water intake restriction is mandatory. Angiotensin-converting enzyme (ACE) inhibitors are now considered unavoidable drugs in the management of heart failure, and an attempt to reach the doses that have been shown to be efficacious for survival in the large trials has to be made in every patient with this condition. Other vasodilators, such as hydralazine and nitrates, which show a less pronounced effect on survival but more effective hemodynamic actions than ACE inhibitors, may be used to control mitral insufficiency or to improve hemodynamics in very sick patients. Hemodynamic instability refractory to increasing doses of vasodilators and diuretics is a severe condition that requires hospital admission to administer drugs parenterally. These patients are usually treated with the combination of catecholamines and phosphodiesterase inhibitors associated with intravenous diuretics until clinical stability is again achieved and oral therapy is resumed and restructured. The use of aggressive pharmacological therapy and phosphodiesterase inhibitors has reduced the need for assisted circulatory support in these patients. Beta-blockers have shown promising results when administered to patients with heart failure, although a definitive demonstration of their effects on survival is still lacking. Other additional measures that need to be considered in patients with end-stage congestive heart failure are the use of antiarrhythmic drugs and anticoagulation.
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PMID:Medical treatment of end-stage heart failure. 911 55


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