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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A nationwide survey of institutions in the United States that perform congenital heart disease surgery was conducted to obtain an overview of the current use of myocardial protection in pediatric patients (aged 0-16 years). One hundred and one (55%) of 183 institutions responded, completing a 4-page questionnaire about pediatric cases in 1989. A total of 12,072 cases were represented. Caseloads ranged from 7 to 498 at these institutions (mean 124, median 30). Cardioplegia was used by 100 institutions (44 blood, 45 crystalloid, 11 both). Administration was guided by formulas alone in 69 and by clinical criteria alone in 32. A wide variety of compositions of cardioplegic solutions was found with no preference for any particular type. No correlation between caseloads and cardioplegic solutions was found. Hypothermia was used by all institutions, with a mean of 25.8 +/- 3.5 degrees C for a simple ventricular septal defect closure. Deep hypothermia and circulatory arrest were used in 3048 cases (25.2%). A clear trend indicated that circulatory arrest was used more frequently in larger institutions (p less than 0.0001). Fibrillation as a strategy was used in 45 institutions. Twenty-five institutions changed cardioplegia technique during 1989. The findings suggest that, even though no consensus exists about its ideal composition, cardioplegia in conjunction with hypothermia is currently the strategy most often used for pediatric myocardial protection.
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PMID:Pediatric myocardial protection in the United States: a survey of current clinical practice. 141 97

To minimize drug problems in the treatment of supraventricular tachycardias, it is important to understand the spectrum of adverse events and to identify patients at high risk for these problems. Adverse cardiac and non-cardiac effects are associated, to varying degrees, with currently available antiarrhythmics. Cardiac adverse events include the development of rhythm disturbances, such as ventricular tachycardia or torsades des pointes, may result in syncope or death. In a meta-analysis of six randomized trials of quinidine vs placebo for atrial fibrillation, 1.8% of quinidine-treated patients died as opposed to 0.3% of placebo-treated patients. This increase in mortality was also noted in patients enrolled in the Stroke Prevention in Atrial Fibrillation Trial who were treated with type I antiarrhythmics. This increase in mortality was confined primarily to patients with a history of congestive heart failure. In a randomized trial of propafenone and sotalol for the treatment of atrial fibrillation, two out of 50 patients receiving sotalol died suddenly, one of whom had hypokalaemia-associated torsades des pointes. No patient receiving propafenone died during this trial. In a meta-analysis of propafenone's effect in treating supraventricular tachyarrhythmias in over 3100 adult patients, overall mortality was extremely low at 0.3%. Structural heart disease may increase the risk of antiarrhythmic agents. During inpatient drug trials in patients treated for atrial fibrillation at Brigham and Women's Hospital, adverse cardiac events, primarily bradyarrhythmias, occurred in up to 15% of the patients. Older age and prior myocardial infarction were associated with an increased risk of adverse events. Adverse drug problems may be minimized by careful attention to electrolytes, medications, concomitant medical illnesses, and underlying conduction disease. Careful monitoring of patients during initiation of therapy, especially those patients with ischaemic heart disease, congestive heart failure, and who are older, may minimize drug-related problems.
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PMID:Avoiding drug problems. The safety of drugs for supraventricular tachycardia. 915 74

Measured in 119 patients with chronic heart disease (exercise-induced angina in 62, cardiosclerosis in 57 cases) presenting with arrhythmias (extrasystolic arrhythmia, permanent form cardiac fibrillation, association of cardiac fibrillation with ventricular arrhythmia, with n = 58, 38, 23 respectively) were blood levels of thyroid-stimulating hormone (TSH), triiodothyronine (T3) and thyroxin (T4) using immunoradiometric assay. In extrasystolic arrhythmia, permanent form cardiac fibrillation, there were no deviations from the norm in the basal TSH blood levels, reduction in (T3) as well as augmentation of (T4) in cardiac fibrillation. With permanent form cardiac fibrillation associated with ventricular arrhythmia the TSH blood level got decreased, the (T3) and (T4) content undergoing no changes The posttreatment blood content of (T3) tended to augment in extrasystolic arrhythmia.
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PMID:[The function of the thyroid and thyrotropic function in patients with chronic ischemic heart disease and rhythm disorders]. 962 22

Nonvalvular atrial fibrillation (AF) is the most common cardiac disorder causing stroke and systemic emboli. Recent clinical trials have clearly demonstrated the effects of antithrombotic treatment in preventing these devastating complications of AF. This review summarizes the salient findings of the first 5 published studies the Atrial Fibrillation, Aspirin, Anticoagulation Study (AFASAK) from Copenhagen, Denmark; the Boston Area Anticoagulation Trial for Atrial Fibrillation (BATAFF); the Canadian Atrial Fibrillation Anticoagulation study (CAFA); the Stroke Prevention in Non-rheumatic Atrial Fibrillation (SPINAF) study; and the Stroke Prevention in Atrial Fibrillation study (SPAF I) from the United States. These trials emphasize the unequivocal benefits of warfarin therapy compared with no treatment. SPAF II showed that aspirin is quite effective in younger patients (<75 years) who have no risk factors. The European Atrial Fibrillation Trial (EAFT) and SPAF III demonstrated that in older patients (>75 years) who had associated risk factors, warfarin therapy at the target international normalized ratio (INR) of 2-3, is the best treatment; however, a combination of low intensity fixed-dose warfarin and aspirin is ineffective. Thus, the guidelines recommended by the American College of Chest Physicians should be followed in treating patients with AF.
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PMID:Long-term antithrombotic treatment for atrial fibrillation. 980 99

Despite recent advances in our understanding of the mechanisms and consequences of atrial fibrillation, appropriate management of this common condition presents something of a dilemma. Control of ventricular rate alone is a common strategy, considered by many physicians to be the safest treatment option and a relatively simple approach to preserving left ventricular function. Rhythm control using antiarrhythmic agents, however, offers a number of important advantages, with the potential to correct abnormal physiology, increase exercise tolerance, reduce thromboembolic risk, prevent atrial remodelling and eliminate the risk of tachycardia-induced cardiomyopathy. Selection of an appropriate antiarrhythmic agent for such long-term prophylaxis is however problematic. Class I agents are associated with an unacceptable proarrhythmic risk especially in patients with structural heart disease and long-term therapy with the class III agent amiodarone can result in serious non-cardiac adverse effects. It is apparent, therefore, that there is little consensus on appropriate management strategies for atrial fibrillation and less still on the antiarrhythmic agent to be used. A number of studies are, however, ongoing which attempt to determine the benefits of rhythm versus rate control. These include the PIAF (Pharmacological Intervention in Atrial Fibrillation), AFFIRM (Atrial Fibrillation Follow-up Investigation of Rhythm Management) and RACE (Rate Control versus Electrical Cardioversion) studies, which should provide valuable answers which will help to guide physicians in their therapy choices.
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PMID:Maintenance of sinus rhythm as a therapy goal. 1122 May 18

In managing atrial fibrillation (AF), the main therapeutic strategies include rate control, termination of the arrhythmia, and the prevention of recurrences and thromboembolic events. Safety and efficacy considerations are important in optimizing the choice of an antiarrhythmic drug for the treatment of AF. Recently approved antiarrhythmics, such as dofetilide, and promising investigational drugs, such as azimilide and dronedarone, may change the treatment landscape for AF. For medical conversion of recent-onset AF, class IC antiarrhythmic drugs, administered as an oral bolus, have been demonstrated to be the most efficacious pharmacologic conversion agents. Intravenous ibutilide and oral dofetilide both have efficacies superior to placebo in controlled trials for converting persistent AF. Comparative trials in paroxysmal AF have demonstrated that flecainide, propafenone, quinidine, and sotalol are equally effective in preventing recurrences of AF. Amiodarone has been demonstrated to be more efficacious than propafenone or sotalol in the Canadian Trial of Atrial Fibrillation. In persistent AF, twice-daily dofetilide has been shown to be as or more effective than low-dose sotalol given twice daily for the maintenance of sinus rhythm in patients with AF. Trials have demonstrated that subjective adverse effects are less frequent with class IC drugs, sotalol, and dofetilide compared with such drugs as quinidine. In patients without structural heart disease, flecainide, propafenone, and D,L-sotalol are the initial drugs of choice, given their reasonable efficacy, low incidence of subjective side effects, and lack of significant end-organ toxicity. Treating AF in patients with left ventricular dysfunction can be difficult because of associated electrophysiologic derangements, potential proarrhythmic concerns, and negative inotropic effects of antiarrhythmics. Some data exist suggesting that angiotensin-converting enzyme inhibitors and angiotensin receptor blockers can prevent AF either by preventing atrial dilation and stretch-induced arrhythmias or by blocking the renin-angiotensin system. In post-myocardial infarction patients, D,L-sotalol, dofetilide, and amiodarone-and in congestive heart failure patients, amiodarone and dofetilide-have demonstrated neutral effects on survival in controlled trials. In the Congestive Heart Failure Survival Trial of Antiarrhythmic Therapy (CHF-STAT), amiodarone lowered the frequency of AF development and improved left ventricular ejection fraction over time. In CHF-STAT, there was lower mortality in patients who converted from AF to sinus rhythm. Dofetilide decreased rehospitalization for congestive heart failure in the Danish Investigations of Arrhythmia and Mortality on Dofetilide (DIAMOND) trials. Neutral effects on survival and favorable hemodynamics have positioned amiodarone and dofetilide as the antiarrhythmics of choice in patients with left ventricular dysfunction. In post-myocardial infarction patients, sotalol is an additional agent to consider for treatment of AF in this setting.
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PMID:Old and new antiarrhythmic drugs for converting and maintaining sinus rhythm in atrial fibrillation: comparative efficacy and results of trials. 1267 Jun 38

The clinical relevance and high social costs of atrial fibrillation have boosted interest in rate control as a cost-effective alternative to long-term maintenance of sinus rhythm (i.e. rhythm control). Prospective studies show that rate control (coupled with thromboembolic prophylaxis) is a valuable treatment option for all forms of atrial fibrillation. The rationale for rate control is that high ventricular rates, frequently found in atrial fibrillation, lead to haemodynamic impairment, consisting of a variable combination of loss of atrial kick, irregularity in ventricular response and inappropriately rapid ventricular rate, depending on the type of underlying heart disease. Long-term persistence of tachycardia at a high ventricular rate can lead to various degrees of ventricular dysfunction and even to tachycardiomyopathy-related heart failure. Identification of this reversible and often concealed form of left ventricular dysfunction can permit effective management by rate (or rhythm) control. Although acute rate control (to reduce ventricular rate within hours) is still often based on digoxin administration, for patients without left ventricular dysfunction, calcium channel antagonists or beta-adrenoceptor antagonists (beta-blockers) are generally more appropriate and effective. In chronic atrial fibrillation, long-term rate control (to reduce morbidity/mortality and improve quality of life) must be adapted to patients' individual characteristics to grant control during daily activities, including exercise. According to current guidelines, the clinical target of rate control should be a ventricular rate below 80-90 bpm at rest. However, in many patients, assessment of the appropriateness of different drugs should include exercise testing and 24h-Holter monitoring, for which specific guidelines are needed. In practice, rate control is considered a valid alternative to rhythm control. Recent prospective trials (e.g. the Pharmacological Intervention in Atrial Fibrillation [PIAF] and the Atrial Fibrillation Follow-up Investigation of Rhythm Management [AFFIRM] trials) have shown that in selected patients, rate control provides similar benefits, more economically, in terms of quality of life and long-term mortality. The choice of a rate control medication (digoxin, beta-blockers, calcium channel antagonists or possibly amiodarone) or a non-pharmacological approach (mainly atrioventricular node ablation coupled with pacing) must currently be based on clinical assessment, which includes assessing the presence of underlying heart disease and haemodynamic impairment. Definite guidelines are required for each different subset of patients. Rate control is particularly tricky in patients with heart failure, for whom non-pharmacological options can also be considered. The preferred pharmacological options are beta-blockers for stabilised heart failure and digoxin for unstabilised forms.
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PMID:Rate control in atrial fibrillation: choice of treatment and assessment of efficacy. 1283 66

The authors summarize the up-to-date knowledge relating to the pharmacological treatment of atrial fibrillation. They emphasize that drug treatment continues to be in the forefront of the therapy of the arrhythmia, which can now be considered to constitute a cardiovascular epidemic. In the era following the Atrial Fibrillation Follow-up Investigation of Rhythm Management (AF-FIRM) trial, the strategy of pharmacological treatment will certainly change: in place of "rhythm control", which in recent decades has been overforced in patients identical with the elderly, cardiac patients with an impaired left ventricular function who were enrolled into AFFIRM, there will be a more frequent use of ventricular "rate control". Naturally, this does not mean that, in certain patient groups, an effort should not be made to restore and maintain the sinus rhythm. In cases involving congestive heart failure and structural heart disease complicated by a depressed left ventricular systolic function, atrial fibrillation is currently treated with antiarrhythmic drugs possessing low proarrhythmic activity that prolong refractory period (Class 3), and with the even safer mortality-reducing beta-receptor blockers. The classical antiarrhythmic drugs (quinidine, procainamide, disopyramide) are being increasingly forced into the background, and the areas of indication of the novel Na(+)-channel blocker antiarrhythmics (propafenone, flecainide) have also narrowed: they are administered only in the event of atrial fibrillation in patients with a structurally intact heart or left ventricular hypertrophy. After a brief survey of the more important aspects of ventricular rate control, and of the drugs available, the research trends aimed at the progression of the pharmacological treatment of atrial fibrillation are outlined. The clinical introduction of procedures based on myocardial gene therapy is now a realistic therapeutic approach as concerns atrial fibrillation too.
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PMID:[Drug therapy of atrial fibrillation]. 1286 49

In the post-AFFIRM era, treatment of AF has become the treatment of symptoms. In some patients, this will be simple rate control, but there remain a significant cohort of patients in whom rate control alone does not give acceptable symptom relief. In this group, antiarrhythmic therapy still has a role, and the AFFIRM trial indicates that this therapeutic strategy is without significant deleterious effect on mortality. The choice of antiarrhythmic agent must be individualized according to underlying cardiac pathologies and comorbidities, however. Most recently, the introduction of dofetilide has widened the therapeutic options in patients with severe heart disease, and the Canadian Trial of Atrial Fibrillation indicated the superior efficacy of amiodarone at low doses. The release/ development of newer Class III antiarrhythmic agents may offer hope for the benefits of amiodarone without the serious adverse effects with long-term therapy.
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PMID:Antiarrhythmic drug therapy of atrial fibrillation. 1499 45

Atrial fibrillation (AF) is an important risk factor for stroke. According to a pooled analysis of controlled clinical trials with warfarin, anticoagulation therapy reduces stroke risk by 62%. However, clinicians must decide whether the benefit of long-term anticoagulation therapy with available agents outweighs the risk of bleeding for individual patients. Guidelines issued by the American College of Chest Physicians and by the joint American College of Cardiology, American Heart Association, and the European Society of Cardiology task force recommend antithrombotic therapy to protect AF patients from stroke based on risk-stratification algorithms. Risk factors for stroke AF patients include age > or =75 years; hypertension; thyrotoxicosis; diabetes; cardiovascular disease; congestive heart failure; and history of stroke, transient ischemic attack, or thromboembolism. Patients at high risk for stroke experience greater absolute benefit from anticoagulation therapy than patients at low risk. The guidelines are consistent in recommendations for high-risk patients (warfarin therapy, international normalized ratio 2.0 to 3.0) and low-risk patients (aspirin 325 mg), but differ for intermediate-risk patients with diabetes or heart disease. The guidelines continue to evolve, and future guidelines are likely to incorporate new clinical data, including the CHADS(2) algorithm for determining risk and the results of the Atrial Fibrillation Follow-up Investigation of Rhythm Management trial, the Rate Control versus Electrical Cardioversion for Persistent Atrial Fibrillation study, and the Stroke Prevention Using an Oral Thrombin Inhibitor in Atrial Fibrillation II to V trials.
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PMID:Comparing the guidelines: anticoagulation therapy to optimize stroke prevention in patients with atrial fibrillation. 1502 46


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