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)

For 13 years between 1980 and 1992, 23 patients needed pacemaker (PM) implantation because of bradyarrhythmia, 21 of atrial fibrillation and two of complete A-V block, after valve surgery. Five of 88 survivors (5.7%) after OMC, 11 of 227 (4.8%) after MVR, one of 169 (0.6%) after AVR, five of 67 (7.4%) after MVR + AVR and one of 15 (6.7%) after TVR underwent PM implantation in postoperative period. Two cases who had heart failure was implanted PM in early postoperative period. In late period, the mean duration between previous valve surgery and PM implantation was 6.4 years in 12 cases after initial valve surgery and 2.3 years in nine after second valve surgery. Postoperative course after PM implantation was almost good, but one case was died due to critical arrhythmia. And one case underwent re-MVR because of mitral bioprosthesis dysfunction and one, without anticoagulant after OMC, was complicated cerebral infarction.
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PMID:[A study of pacemaker implantation to cases performed valve surgery]. 942 29

Non-pharmacologic therapy has revolutionized the management of arrhythmias and prevention of sudden cardiac death (SCD). Of particular importance is the introduction of radiofrequent catheter ablation (RFCA) and implantable cardioverter-defibrillator (ICD). RFCA is effective and useful in the treatment and prevention of SCD, especially in supraventricular tachyarrhythmias related to dual or accessory atrioventricular pathways. There are some limitations in using this method in the prevention of SCD in ventricular tachyarrhythmias. RFCA is very successful, particularly in the treatment of bundle branch reentrant ventricular tachycardia and ventricular tachycardia in patients without structural heart disease. RFCA can be used as a palliative treatment of incessant or frequent VT before and after ICD implantation. Antibradycardia pacing decreases SCD not only by the removal of serious bradyarrhythmias but also by prevention of the occurrence of malignant ventricular tachyarrhythmias induced by bradyarrhythmia. Antitachycardia pacing is used in the prevention of SCD only as a part of ICD device. Implantation of an antitachycardia pacemaker as an isolated permanent treatment of tachycardias is currently almost not used. This method was replaced by RFCA in supraventricular tachyarrhythmias and by ICD in ventricular tachyarrhythmias. ICD is a very perspective non-pharmacologic approach to SCD prevention, particularly as transvenous leads were introduced and device construction was simplified. ICD is indicated especially in patients with spontaneous sustained hemodynamically significant ventricular tachycardia/ventricular fibrillation and when antiarrhythmic drug treatment, RFCA or antitachycardia surgery are ineffective, intolerated, contraindicated or cannot be performed. ICD as the treatment of first choice instead of antiarrhythmic drugs as well as prophylactic ICD implantation in asymptomatic patients at high risk is a subject of discussion. ICD decreases the incidence of SCD significantly. However, the decrease in overall mortality was not verified. Antitachycardia surgery is less frequently used after RFCA, and ICD have been introduced. At present, this therapy is reserved only for the cases of failure of RFCA or the impossibility to use RFCA and ICD. Surgical therapy can be combined also with concommitant surgical correction of associated structural heart disease. Sympathectomy is used in prevention of malignant ventricular tachyarrhythmias and SCD in patients with congenital long Q-T syndrome. Selective left cardiac sympathetic denervation significantly reduces the risk of SCD in these patients but does not remove it completely. Heart transplantation is the last alternative of non-pharmacologic prevention of SCD. It is indicated in cases when all pharmacologic and non-pharmacologic approaches have been exhausted. Heart transplantation is the only effective modality for the improvement of long-term prognosis in patients with malignant ventricular tachyarrhythmias and advanced chronic heart failure.
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PMID:[Non-pharmacologic prevention of sudden cardiac death]. 947 37

The challenge of preventing arrhythmic sudden death is one of the major issues in today's treatment of heart failure. To achieve this ambitious goal, an accurate selection of the candidates for sudden death is needed on the one hand, while on the other hand, the assessment of the real cost/benefit ratio of the implantable cardioverter-defibrillator in selected patients, as compared to ACE inhibitors, beta-blockers and antiarrhythmic drug therapy, should no longer be delayed. As is well known, the incidence of sudden death is higher in ischemic dilated cardiomyopathy than it is in non-ischemic dilated cardiomyopathy. Moreover, tachyarrhythmic sudden death is prevalent in NYHA classes I and II (80%), whereas its incidence is lower (50%) in NYHA classes III and IV, since bradyarrhythmia, electromechanical dissociation and thromboembolic events characterize the other 50% of sudden deaths in patients in the latter NYHA class. The stratification of arrhythmic risk in non-ischemic dilated cardiomyopathy is questionable from any point of view, considering the poor predictive power of invasive and non-invasive indexes. However, some subgroups of high-risk patients should be selected, such as patients waiting for heart transplant or those with a severe disease but without an extreme degree of ventricular dysfunction, in whom the prognosis in terms of pump failure events is better and life expectancy is longer if the risk of arrhythmia is properly assessed and sudden death prevented. Consequently, the ICD implant may be effective in order to pursue the aim of reducing the tachyarrhythmic and bradyarrhythmic mortality in patients with a more severe disease and of minimizing the tachyarrhythmic risk in those with a less severe disease. Further studies will be developed to identify the ideal candidates for ICD implants.
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PMID:[The stratification and prevention of the arrhythmia risk in nonischemic dilated cardiomyopathy]. 986 7

The purpose of this review is to examine the potential contribution of arrhythmia to the occurrence of sudden death in dilated cardiomyopathy (DCM) and to discuss current treatment options. We performed a search of the MEDLINE database from 1985 to the present and the reference citations of selected articles pertaining to the prognostic significance, management, and pathophysiology of arrhythmias in DCM. A large proportion of patients with DCM die suddenly, most secondary to ventricular arrhythmia and a smaller proportion due to bradyarrhythmia. The presence and severity of ventricular ectopy may predict risk for sudden death, but the role of electrophysiologic study and signal-averaged electrocardiography in further risk stratifying patients remains uncertain. Abnormalities of the autonomic nervous system and renin-angiotensin-aldosterone axis appear to promote the occurrence of ventricular arrhythmias. Angiotensin-converting enzyme inhibitors improve overall mortality in congestive heart failure, and the use of direct angiotensin-receptor antagonists is currently being studied. In addition, beta-receptor antagonists appear to improve morbidity and may prove to improve mortality in heart failure as well. Other interventions still under investigation include amiodarone and the implantable cardioverter-defibrillator. The underlying pathophysiology of sudden death in DCM involves primarily ventricular tachyarrhythmia. Angiotensin-converting enzyme inhibitors remain a mainstay of improving overall mortality, while further study on the roles for newer drugs and devices is ongoing.
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PMID:Sudden death in dilated cardiomyopathy. 1019 36

Clearly, sudden cardiac death syndrome in heart failure is linked to severely perturbed neurohumoral, hemodynamic, and mechanical systems. Routine antiarrhythmic drug therapy has not proven beneficial and, therefore, there is no justification for using these agents in unselected heart failure patients who are without significant symptomatic ventricular arrhythmia. Aggressive treatment of the failure syndrome seems most important. Because many of the problematic arrhythmias arise from triggering automaticity, which is known to occur in excessive ventricular stretch and wall stress, systemic vascular "unloading" with vasodilators and angiotensin-converting enzyme inhibitors is likely helpful. The most recent American College of Cardiology/American Heart Association Guidelines regarding therapeutic management of heart failure suggest that aggressive pharmacologic treatment of asymptomatic ventricular arrhythmias is best avoided. To be considered strongly for pharmacologic prescription or for implantation of a tachyarrhythmia termination device, a patient should have symptomatic ventricular tachycardia with an episode of syncope or sudden cardiac death syndrome rather than simply having palpitations of asymptomatic, unsustained ventricular tachycardia. Indeed, aggressively treating congestive heart failure with medication often eliminates potentially life-threatening arrhythmias. Appropriate use of vasodilators and, particularly, angiotensin-converting enzyme inhibitors is important. Correction of fluid balance and electrolyte disorders may be helpful to address symptoms and certainly is likely to decrease the potential for morbidity and mortality. On occasion it may be necessary to consider bradyarrhythmia pacemaker insertion or the use of atrioventricular nodal-ablation techniques with subsequent ventricular or atrioventricular pacer insertion. Obviously, sudden cardiac death due to sudden heart block or asystole might be attenuated with this strategy.
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PMID:Sudden cardiac death syndrome and pump dysfunction: the link. 1101 84

Pacing for patients with severe heart failure without bradyarrhythmia has been proposed as an addition to medical therapy over the past decade. Alteration of the normal electrical activation sequence of the heart modifies its mechanical action, especially when ventricular function is poor. Both the site of ventricular-lead placement and timing with the atria have been manipulated in attempts to alleviate the symptoms of heart failure. Most recently, in addition to the conventional two leads used for pacing, a third lead to pace the left ventricle has been advocated in some patients with heart failure. We review the evidence for pacing in heart failure.
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PMID:Pacing for heart failure. 1141 72

We describe an elderly case of idiopathic dilatation of the right atrium in which right-sided heart failure was exacerbated by drug-induced bradyarrhythmia. An 84-year-old man, who had a 10-year history of episodic edema, was treated with proscillaridin and verapamil hydrochloride at another hospital. He had experienced a poor appetite and general malaise 2 months previously, and exertional dyspnea 10 days previously. On admission, he had jugular venous dilatation, systemic edema, and hepatomegaly. On auscultation, a third heart sound originating from the right ventricle and systolic murmur of tricuspid regurgitation were heard. An admission electrocardiogram showed an atrial standstill and junctional escape rhythm with a QRS rate of 31 beats/minute. Chest roentgenogram revealed a bilateral pleural effusion and cardiomegaly with a cardiothoracic ratio of 76%, but no pulmonary congestion. Echocardiogram disclosed idiopathic dilatation of the right atrium and secondary tricuspid regurgitation. He was given a diagnosis of right-sided heart failure due to idiopathic dilatation of the right atrium exacerbated by bradyarrhythmia, which was suspected to derive from the side effects of proscillaridin and verapamil hydrochloride. Thus, these agents were withheld. In addition, the patient reduced sodium intake and was treated with diuretics and beta-adrenergic agonist. Thereafter, right-sided heart failure markedly improved. At the time of the last follow-up 16 months after discharge, he felt well.
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PMID:[An elderly case of idiopathic dilatation of the right atrium in which right-sided heart failure was exacerbated by drug-induced bradyarrhythmia]. 1152 70

The selective beta blockers metoprolol, bisoprolol and atenolol, but also the non-selective beta blocker carvedilol, are drugs with individually specific properties that are widely prescribed for a wide range of indications. Modern beta blockers are safe drugs with a low profile of side effects, which, applied with proper consideration being given to contraindications, rarely produce serious side effects such as bradyarrhythmia, bronchial obstruction, or aggravation of heart failure. Their prognostic benefit, for example, in the treatment of post-myocardial infarction patients, or in cardiac insufficiency, has been demonstrated in large randomized clinical trials.
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PMID:[Differential therapy with beta blockers. What is their value, what are the risks?]. 1168 Sep 26

In patients with heart failure, sudden death is very common, particularly in subjects in NYHA functional class II and III (respectively 50-80% and 30-50% of all deaths). The mechanisms at the root of sudden death depend on whether heart failure is secondary to an ischemic or non-ischemic heart disease. In ischemic heart disease, sudden death is mainly arrhythmic (ventricular tachycardia/ventricular fibrillation caused by the reentry circuits in the infarct area or by acute ischemic episodes or bradyarrhythmia). In non-ischemic heart disease, the percentage of arrhythmic sudden deaths seems to be lower. Furthermore, a percentage of sudden death cases with heart failure can be linked to electromechanical dissociation and to pulmonary or systemic embolism. Moreover the risk stratification level differs depending on whether heart failure is caused by an ischemic or a non-ischemic heart disease. The various non-invasive studies mainly employed in patients with ischemic heart disease cannot be reliably used to study patients with non-ischemic heart disease. Even the programmed ventricular stimulation demonstrated prognostic reliability only in cases involving ischemic heart disease. The therapeutic approach may also be conditioned by the heart disease responsible for heart failure. To date, for example, all the studies published on primary prevention of sudden death with an implantable defibrillator have been carried out in patients with ischemic heart disease.
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PMID:[Arrhythmia risk stratification based on etiological and anatomo-structural factors]. 1183 46

Increased inducible nitric oxide synthase (iNOS) expression is a component of the immune response and has been demonstrated in cardiomyocytes in septic shock, myocarditis, transplant rejection, ischemia, and dilated cardiomyopathy. To explore whether the consequences of such expression are adaptive or pathogenic, we have generated a transgenic mouse model conditionally targeting the expression of a human iNOS cDNA to myocardium. Chronic cardiac-specific upregulation of iNOS in transgenic mice led to increased production of peroxynitrite. This was associated with a mild inflammatory cell infiltrate, cardiac fibrosis, hypertrophy, and dilatation. While iNOS-overexpressing mice infrequently developed overt heart failure, they displayed a high incidence of sudden cardiac death due to bradyarrhythmia. This dramatic cardiac phenotype was rescued by specific attenuation of transgene activity. These data implicate cardiomyocyte iNOS overexpression as sufficient to cause cardiomyopathy, bradyarrhythmia, and sudden cardiac death.
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PMID:Cardiomyocyte overexpression of iNOS in mice results in peroxynitrite generation, heart block, and sudden death. 1190 Nov 82


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