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

Arrhythmic death can be reduced by antiarrhythmic drugs to a range of 24%. Electrophysiologic study by testing noninducibility of ventricular arrhythmia represents the classic method for evaluating the effectiveness of drug therapy. Several clinical studies have shown thaat sotalol suppresses VT induction and prevents arrhythmias recurrences at long term follow-up in 23% to 67% of patients. The efficacy of sotalol EP guided therapy in preventing VT/VF is not necessarily related to prevention of sudden death. In the ESVEM study the superiority of d,l-sotalol to other antiarrhythmic drugs was confirmed. The response to programmed ventricular stimulation was found to be strongly predictive for arrhythmia free state while the failure of sotalol therapy to suppress VT at the EP study was associated with an high recurrence rate (40%). However, EP study failes to predict freedom from sudden death. The beta-blocking activity of racemic sotalol may account for some of the observed survival benefit.Beta-blockers therapy reduces mortality in patients after myocardial infarction primarily by a reduction of sudden death. A reduction of death, worsening heart failure and life threatening ventricular arrhythmias was shown in a recent study on carvedilol. In the prospective study of Steinbeck the EP guided-therapy did not improve the overall outcome when compared to metoprolol. Suppression of inducible arrhythmias by antiarrhythmic drugs was associated with a better outcome. The effectiveness of defibrillator therapy in reducing overall mortality, has been uncertain since great clinical trials have been concluded. MADIT, AVID and CASH trials confirmed the superiority of ICD therapy over antiarrhythmic drugs therapy: ICD should be considered the first choice therapy in post-cardiac arrest patients. The ongoing BEST Trial will give us further responses about the interaction between EP study and metoprolol effect compared to ICD in patients post myocardial infarction also focusing on tolerability and compliance of the beta-blocking therapy in patients with low ejection fraction. In this study will be useful to optimize therapy in patients at high risk of sudden death.
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PMID:The role of EP-guided therapy in ventricular arrhythmias: beta-blockers, sotalol, and ICD's. 1059 Apr 90

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

This paper aims at studying the development and the risk factors for stroke prospectively during a 6-year follow-up in the Turku Elderly Study, Turku, Finland. The study cohort consisted of 1032 people aged 70 years at baseline. The stroke events (ICD-9 codes 430-434) were identified by computer linkage from the hospital discharge and death registers, and from a follow-up questionnaire. During the 6 years of follow-up, 71 patients (6.9%) suffered a stroke. Previous stroke (RR 5.82), history of transient ischemic attack (RR 4.14), diabetes mellitus (RR 2.50), poorly controlled hypertension (RR 2.42), smoking (RR 1.94) and male sex (RR 1.65) were independent risk factors for stroke. Atrial fibrillation, cardiac failure and previous myocardial infarction did not appear to be significant independent predictors of stroke in the elderly. The risk of stroke in the elderly population appears to be strongly related to the concomitant clinical disease, and this should be remembered when identifying persons at increased risk of stroke. Poorly controlled hypertension was associated with an increased risk of stroke. Thus, achieving a good control of blood pressure in elderly hypertensives receiving treatment has the potential to prevent strokes.
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PMID:Long-term predictors of stroke in a cohort of people aged 70 years. 1098 63

The Ventak CHF/CONTAK CD Biventricular Pacing Study is a prospective randomized trial to examine the safety and efficacy of biventricular (BV) pacing in patients with standard indications for an ICD, symptomatic heart failure, a LVEF < or = 0.35, and a QRS > or = 120 ms. Patients underwent implantation of a BV pacing and sensing system with backup defibrillation capability, which includes a steroid-eluting coronary venous lead that is advanced into the coronary venous vasculature by over-the-wire techniques. LV pacing threshold, BV impedance, and BV R wave amplitude were measured in 58 consecutive patients. Using a percutaneous over-the-wire insertion technique, steroid-eluting coronary venous leads were associated with satisfactory mean LV pacing threshold, BV impedance, and BV R wave amplitude acutely up to 4 months after implantation. Pacing threshold stabilized 2 weeks after lead implantation and sensing threshold remained stable from the time of implant.
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PMID:Performance of a new steroid-eluting coronary sinus lead designed for left ventricular pacing. 1113 14

While much is known concerning the hemodynamic effects of biventricular (BV) pacing, little has been reported concerning the efficacy of BV sensing and pacing in the detection and treatment of ventricular tachyarrhythmias. Two hundred nineteen heart failure (HF) patients with VT or VF and a QRS > or = 120 ms during sinus rhythm received an ICD capable of BV pacing and sensing. Detection times of induced VF and success rates for terminating induced VT were measured. The ICD system used a left ventricular epicardial lead implanted via thoracotomy (52 patients) or a specially designed percutaneous, over-the-wire lead inserted in the coronary venous system. VF detection times and VT termination rates by antitachycardia pacing (ATP) were compared with those measured in a population of recipients of ICD using a RV lead alone. Median induced VF detection times were comparable (2.0-s BV vs 1.8-s RV). Termination of induced VT on the first attempt was comparable with BV pacing (87.4%) versus RV pacing (89.6%). The time to detect induced VF was not different with ICDs using BV sensing versus conventional ICDs using RV sensing alone. Similarly, the rates of successful termination of induced VT by ATP with BV or RV pacing were comparable.
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PMID:Efficacy of biventricular sensing and treatment of ventricular arrhythmias. 1113 74

The clinical manifestations of ventricular arrhythmias encompass a broad spectrum, from complete absence of symptoms to sudden death. Although our understanding of the pathophysiology and natural history of these arrhythmias has advanced significantly over the past decade, large gaps in our knowledge remain, especially in patients with heart failure not due to coronary artery disease. We have learned much about the appropriate roles of antiarrhythmic drugs and implantable defibrillators in the prevention of sudden death. Studies performed over the past decade have made clear that the primary treatment for patients at high risk for life-threatening ventricular arrhythmias should be the implantable defibrillator. However, specific syndromes causing ventricular tachyarrhythmias are being recognized, and care must be individualized. Although hospital mortality from acute myocardial infarction has decreased as a result of newer therapies, sudden death after hospital discharge remains an important problem, causing at least 30% of post-infarction deaths, even in patients who have received thrombolytic therapy. Two independent studies have confirmed that patients with asymptomatic non-sustained ventricular tachycardia in the presence of left ventricular ejection fraction < .40 after myocardial infarction who have sustained ventricular tachycardia inducible by electrophysiologic study are at significant risk for sudden death. This risk is significantly reduced by ICD, but not pharmacologic, antiarrhythmic therapy. Our major challenge at this time is not how best to treat high risk patients, but how best to identify them prior to events. Finally, physicians should be aware that many symptomatic ventricular tachycardias are now curable at low risk, using catheters to deliver radiofrequency energy.
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PMID:Current approaches to evaluation and management of patients with ventricular arrhythmias. 1127 62

The energy needed by cardiac muscle to maintain proper function is supplied by adenosine Ariphosphate primarily (ATP) production through breakdown of fatty acids. Metabolic cardiomyopathies can be caused by disturbances in metabolism, for example diabetes mellitus, hypertrophy and heart failure or alcoholic cardiomyopathy. Deficiency in enzymes of the mitochondrial beta-oxidation show a varying degree of cardiac manifestation. Aberrations of mitochondrial DNA lead to a wide variety of cardiac disorders, without any obvious correlation between genotype and phenotype. A completely different pathogenetic model comprises cardiac manifestation of systemic metabolic diseases caused by deficiencies of various enzymes in a variety of metabolic pathways. Examples of these disorders are glycogen storage diseases (e.g. glycogenosis type II and III), lysosomal storage diseases (e.g. Niemann-Pick disease, Gaucher disease, I-cell disease, various types of mucopolysaccharidoses, GM1 gangliosidosis, galactosialidosis, carbohydrate-deficient glycoprotein syndromes and Sandhoff's disease). There are some systemic diseases which can also affect the heart, for example triosephosphate isomerase deficiency, hereditary haemochromatosis, CD 36 defect or propionic acidaemia.
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PMID:Metabolic cardiomyopathies. 1129 85

In a time series study, air pollution was associated with specific cardiovascular causes of death. Deaths due to heart failure (ICD-9 428), arrhythmia (ICD-9 427), cerebrovascular causes (ICD-9 430-436), and thrombocytic causes (ICD-9 415.1, 433-4, 444, 452-3) were more strongly associated with air pollution than cardiovascular deaths (ICD-9 390-448) in general. Excess relative risks were 2.5 to 4 times larger for these categories than for total cardiovascular disease mortality. Heart failure deaths, which made up 10% of all cardiovascular deaths, were found to be responsible for about 30% of the cardiovascular deaths related to particulate matter, SO2, CO, and NO2.
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PMID:The association between air pollution and heart failure, arrhythmia, embolism, thrombosis, and other cardiovascular causes of death in a time series study. 1209 9

A patient with congestive heart failure and an ICD had undergone atrioventricular nodal ablation and optimization of heart failure medical therapy. Intracardiac T wave sensing by the ICD drew attention to the new development of asymptomatic hyperkalemia. Surface ECG features of hyperkalemia were not readily identified due to pacemaker dependence.
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PMID:Hyperkalemia diagnosed by implantable cardioverter defibrillator T wave sensing. 1138 16

This report describes a patient with advanced heart failure, pronounced intraventricular conduction delay, and ventricular tachycardias who underwent implantation of a multisite pacing ICD. Pacing leads were placed in the right atrium, right ventricular apex, and to the left ventricular posterior wall via a coronary sinus vein. The system proved to have correct sensing and pacing function in an atrial synchronized biventricular pacing mode and an appropriate detection of ventricular fibrillation. However, 1 month after implantation the patient received an inappropriate shock delivery due to double detection of ventricular premature beats. The inherent detection problem of dual ventricular sensing is discussed.
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PMID:Inappropriate shock delivery due to ventricular double detection with a biventricular pacing implantable cardioverter defibrillator. 1147 33


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