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

Atrial fibrillation (AF) is the most common sustained arrhythmia in humans. The 3 basic tenets of therapy are (1) restoration and maintenance of sinus rhythm; (2) ventricular rate control; and (3) prevention of thromboembolism. Maintenance of sinus rhythm appears preferable to rate control alone in patients with significant symptoms caused by AF. Complete suppression of AF with drug therapy for >6 months is unusual, but it is not the sole criterion of success. As with other chronic cardiac disorders such as angina and heart failure, a marked reduction in frequency and duration of episodes of AF will likely translate into an excellent clinical outcome. The major risk of antiarrhythmic drug therapy is ventricular proarrhythmia, which is seen most frequently in patients with substantial left ventricular dysfunction. Torsade de pointes is the most frequent proarrhythmia that occurs with antiarrhythmic agents that prolong ventricular repolarization and the QT interval. To minimize the risk of proarrhythmia, antiarrhythmic drugs are started in-hospital in patients with significant heart disease, and agents are selected based on certain patient characteristics. For example, the drugs initially selected for patients with heart failure and coronary artery disease are amiodarone and sotalol, respectively. Two approaches may be used to decrease the thromboembolic risk associated with cardioversion of AF to sinus rhythm. In the conventional method, warfarin is given (INR 2.0-3.0) for 3 weeks before and at least 4 weeks after cardioversion. An alternative approach employs transesophageal echocardiography to rule out left atrial thrombi before cardioversion. Both methods appear reasonable and safe, and I prefer the conventional and transesophageal echocardiography-guided approaches for outpatients and in-hospital patients, respectively.
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PMID:Perspectives and controversies in atrial fibrillation. 973 48

It has been suggested that patients be admitted for the initiation of Class I and Class III antiarrhythmic drugs to avoid serious proarrhythmic consequences. The most clinically significant proarrhythmic response to Class IC agents is likely due to an interaction with acute ischemia, and hospitalization for initiation of drug therapy has little predictive or preventive value. Amiodarone has a low risk of proarrhythmia, and any proarrhythmic reactions are generally delayed. Class IA and Class III antiarrhythmic drugs cause acquired long QT syndrome arrhythmias, which can occur soon after initiation of therapy; however, only about half of the arrhythmic events occur within 3 days of initiation of therapy. It could be argued that all patients should be hospitalized to begin Class IA or Class III drugs; however, this approach has a low yield and is extremely expensive. An alternative is to use Class IA and Class III drugs for patients at low risk of torsades de pointes (e.g., males without heart failure, ventricular tachyarrhythmias, or active coronary disease), in whom hospitalization for drug initiation is not warranted. Higher risk patients are probably better treated with other agents, such as Class IC drugs or amiodarone for women without organic heart disease and amiodarone for patients with heart failure, a history of ventricular tachycardia, or active coronary disease. When a Class IA or Class III drug is required for patient with an increased risk of torsades de pointes, hospital admission for drug initiation may be indicated.
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PMID:Optimal management with Class I and Class III antiarrhythmic drugs should be done in the outpatient setting: protagonist. 1021 May 15

We present a case of early (within the first 24 hours) development of malignant torsades de pointes (TdP) associated with intravenous amiodarone therapy. After correction of predisposing factors (heart failure, hypokalemia, digoxin) amiodarone again resulted in torsades. This observation suggests that in patients who have experienced amiodarone-induced proarrhythmia, amiodarone administration under different, more stable clinical conditions may still be hazardous.
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PMID:Early proarrhythmia during intravenous amiodarone treatment. 1039

The authors developed a canine model of pacing induced cardiomyopathy to study the possible mechanisms of ibutilide induced torsades de pointes (TP) in heart failure. Thirteen dogs received intravenous ibutilide after acute AV block for 60 minutes, and after implantation of a VVI pacemaker, with a rate of 270 beats/min for 2-3 weeks. Twelve-lead ECG and right and left ventricle monophasic action potentials were recorded at different right ventricle pacing cycle lengths from 600 ms to 1200 ms during the study. The results showed ibutilide could significantly prolong ventricular repolarization and increase the dispersion in a dose dependent and reverse use dependent manner. Furthermore, after ibutilide administration, cardiomyopathic dogs had a greater dispersion of ventricular repolarization, and also had higher incidences of early afterdepolarizations and spontaneous or pacing induced TP than acute AV block dogs.
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PMID:Proarrhythmic effects of ibutilide in a canine model of pacing induced cardiomyopathy. 1070 22

A noteworthy shift from class I to class III antiarrhythmic agents for suppression of atrial fibrillation has occurred. Sotalol, amiodarone, and dofetilide have been evaluated for their ability to maintain sinus rhythm in patients with chronic atrial fibrillation. All of these agents are moderately effective; however, amiodarone appears to be most efficacious. Aside from their common class III actions, these agents have profoundly different pharmacologic, pharmacokinetic, safety, and drug interaction profiles that help guide drug selection. Amiodarone and dofetilide are safe in patients who have had a myocardial infarction and those with heart failure. The safety of commercially available d,l-sotalol in these patients is poorly understood. Torsades de pointes is the most serious adverse effect of sotalol and dofetilide, and risk increases with renal dysfunction. Amiodarone has minimal proarrhythmic risk but has numerous noncardiac toxicities that require frequent monitoring. Overall, an ideal antiarrhythmic agent does not exist, and drug selection should be highly individualized.
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PMID:A review of class III antiarrhythmic agents for atrial fibrillation: maintenance of normal sinus rhythm. 1176 3

Although men have a higher risk of atrial fibrillation compared with women, the absolute number of women with atrial fibrillation is greater. Congestive heart failure increases the risk of developing atrial fibrillation in women more than in men, and the prognosis for women with atrial fibrillation is worse than for men. The longer baseline corrected QT interval in women is well known. The mechanism is likely the result of increased circulating androgens, causing the QT interval to shorten in men after puberty. Female sex is associated with an increased risk of torsades de pointes in the setting of potassium antagonists. Class III antiarrhythmic drugs are frequently used for the treatment of atrial fibrillation in heart failure patients because of their neutral effect on mortality and their tolerance by patients with low ejection fractions. Although amiodarone and azimilide carry a low potential for producing torsades de pointes compared with sotalol and dofetilide, the prevalence of torsades de pointes in women is at least twice that in men for all these drugs. Careful monitoring of the QT interval and potassium level, as well as control of congestive heart failure, can help reduce the risk of proarrhythmia. Avoidance of polypharmacy with other potassium antagonists and unmonitored drug formulation changes are important in the management of all patients taking class III agents, but they are particularly crucial in women with additional risk factors for torsades de pointes.
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PMID:Risk of proarrhythmia with class III antiarrhythmic agents: sex-based differences and other issues. 1267 Jun 41

Levosimendan is a novel calcium sensitizing agent in development for the treatment of acute and chronic heart failure. The agent increases myocardial force without increasing myocyte calcium concentrations, thus reducing the possibility for myocardial necrosis. In addition, the agent also causes vasodilation of coronary and peripheral vessels to improve coronary blood flow and reduce afterload. The short half-life is a benefit for intravenous administration but could be problematic for the drug's use in chronic heart failure. The risk of the development of arrhythmias from levosimendan appears small secondary to an increase in the QTc interval of 15 msec but needs to be evaluated in light of the ability of levosimendan to open adenosine triphosphate (ATP)-sensitive potassium channels. In addition, the agent has not been studied in patients with additional risks for torsades de pointes. Levosimendan has been shown to have beneficial survival effects in several populations; its use improves patient outcomes relative to the standard of care and has the potential to reduce hospital costs associated with heart failure.
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PMID:Levosimendan: implications for clinicians. 1451 89

Hypomagnesemia is common in hospitalized patients, especially in elderly patients with coronary artery disease (CAD) and/or those with chronic heart failure. Hypomagnesemia is associated with increased all cause mortality and mortality from CAD. Magnesium supplementation improves myocardial metabolism, inhibits calcium accumulation and myocardial cell death; it improves vascular tone, peripheral vascular resistance, afterload and cardiac output, reduces cardiac arrhythmias and improves lipid metabolism. Magnesium also reduces vulnerability to oxygen-derived free radicals, improves endothelial function and inhibits platelet function, including platelet aggregation and adhesion, which potentially confers upon magnesium physiologic and natural effects similar to adenosine-diphosphate inhibitors such as clopidogrel. However, data regarding the use of magnesium in patients with acute myocardial infarction (AMI) are conflicting. Although some previous relatively small randomized clinical trials demonstrated a remarkable reduction in mortality when intravenous magnesium was administered to relatively high risk AMI patients, two recently published large-scale randomized clinical trials (the Fourth International Study of Infarct Survival [ISIS 4] and Magnesium in Coronaries [MAGIC]) were unable to demonstrate any advantage of intravenous magnesium over placebo. Nevertheless, the theoretical benefits of magnesium supplementation as a cardio-protective agent in CAD patients, promising results from animal and human studies, its relatively low-cost and ease of handling requiring no special expertise, together with its excellent tolerability, gives magnesium a place in treating CAD patients, especially in those at high risk, such as CAD patients with heart failure, the elderly and hospitalized patients with hypomagnesemia. Furthermore, magnesium therapy is indicated in life-threatening ventricular arrhythmias such as torsades de pointes and intractable ventricular tachycardia.
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PMID:Does magnesium have a role in the treatment of patients with coronary artery disease? 1472 75

Nutritional and herbal supplements may have harmful or beneficial effects on arrhythmias. Potential supplements that may have antiarrhythmic activity include omega-3 polyunsaturated fatty acids (N-3 PUFA), coenzyme Q10, and carnitine. Clinical studies show that N-3 PUFA or fish oil supplementation appears to reduce mortality and sudden death. Coenzyme Q10, used in treatment of heart failure, and carnitine and its derivatives may have beneficial effects on arrhythmias, although clinical studies have been limited. Antioxidant supplements may be beneficial, but large studies with vitamin E have been disappointing in that it does not reduce mortality. Correction of electrolyte disturbances has been long advised and magnesium supplementation has been beneficial in the treatment of torsades de pointes and in some studies after cardiac surgery. However, routine electrolyte supplementation with empiric potassium or magnesium in non-deficient patients has not been convincingly beneficial. Several herbal supplements have also been promoted to have antiarrhythmic activity. However, clinical studies are lacking to support routine use of these herbal medications. In addition, some herbal supplements may cause serious proarrhythmia, and many supplements significantly interact with warfarin and digoxin.
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PMID:Vitamins, supplements, herbal medicines, and arrhythmias. 1476 22

Many cases have been successfully treated by us with experimented nifekalant hydrocholoride to prevent ventricular tachycardia (VT) during cardiac surgery. The 13 patients who underwent cardiac surgery at our hospital from 1999 to 2002 were retroactively given nifekalant hydrocholoride against VT. Lidocaine hydrochloride was not effective for VT, and it was difficult for 3 patients to be weaned for cardio-pulmonary bypass, while 6 patients needed aortic balloon pumping or percutaneous cardio-pulmonary support. Nifekalant hydrochloride suppressed VT induction in 9 patients (69.2%). Blood pressure and heart rate did not change, but QTc intervals were significantly increased with nifekalant hydrochloride (p < 0.005). Proarrhythmic events (Torsades de pointes) occurred in 2 patients, but none of the cases showed drug-induced worsening of cardiac function. Nifekalant hydrochloride is a class III antiarrhythmic drug that has been found to be effective against VT and ventricular fibrillation. While class I antiarrhythmic drugs are usually ineffective and induce severe heart failure, nifekalant hydrochloride can be effective.
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PMID:[The efficiency of nifekalant hydrochloride for the prevention of ventricular tachycardia during cardiac surgery]. 1503 72


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