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

The incidence and the nature of medium-term complications of automatic implantable cardiac defibrillators (AICD) were studied. Seventy-nine AICD were implanted in 50 consecutive patients (42 men, aged 54.5 +/- 13.7 years). Forty-six patients had spontaneous ventricular arrhythmia. These arrhythmias were resistant to treatment (N = 9), reproducible with treatment (N = 28). In 4 patients, the indication was prophylactic, in 2 a Brugada syndrome, in 2 syncope with reinducible ventricular tachycardia and in 1 patient, torsades with a short coupling interval. Forty-six patients had underlying cardiac disease (ischaemic, N = 28, primary dilated cardiomyopathy, N = 10, others, N = 8). The ejection fraction was > 40% in 32 patients. The average follow-up was 41.3 +/- 34.9 months. Eight patients died, 2 from cardiac failure. Twenty-one patients (42%) had 1 or more complications related to their AICD. These occurred: in the operative period (N = 3): 1 post-shock atrioventricular block, 1 ruptured electrode and 1 increased threshold with amiodarone; in the postoperative period (N = 6): infection in 3 cases, cerebrovascular accident in 1 case, deep venous thrombosis of the left arm in 1 case, pneumothorax in 1 case. In the medium-term, the complications were mainly inappropriate electrical shocks observed in 14 patients related to atrial arrhythmias in 7 cases, sinus tachycardia in 1 case, over-detection of myopotentials in 2 cases and electrode dysfunction in 4 cases. In addition, the authors observed complications related to the material: AICD failure in 1 case, electrode displacement in 1 case, and electrode rupture in 3 cases. The authors conclude that AICD are effective for the treatment of malignant ventricular arrhythmias which justify strict specialist follow-up given the incidence and diversity of their complications.
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PMID:[Mid-term complications of automatic implantable cardiac defibrillators]. 1119 Apr 54

Myocarditis has in several case reports been associated with use of clozapine. Eight cases of myocarditis during treatment with clozapine that were submitted to the Swedish Adverse Drug Reaction Advisory Committee and 18 cases that were reported in the literature are summarized. As part of the routine signal detection process on the World Health Organization (WHO) Program on International Drug Monitoring database, which contains more than two million case reports of spontaneously reported suspected adverse drug reactions, a Bayesian confidence propagation neural network (BCPNN) is used. This article also shows the retrospective output of the BCPNN over time for clozapine and myocarditis and discusses its implications. In 19 (79%; duration of treatment not stated for 2 patients) of 24 patients with myocarditis, the symptoms occurred within the first 6 weeks of clozapine treatment. Many patients shared a similar clinical course, with symptoms such as an influenza-like illness, fever, sinus tachycardia, hypotension, chest discomfort, and heart failure. The reaction was fatal in 12 (46%) of these patients. The other patients generally had a prompt recovery. By using the BCPNN technique, a quantitative association between clozapine and myocarditis was demonstrated, and the association might have been high-lighted for clinical review in 1994 had this BCPNN method been in use at the WHO center at the time. Myocarditis seems to be a rare and potentially lethal adverse effect of clozapine. Admittance for observation, interruption of the clozapine treatment, and treatment with corticosteroids should be considered for patients in whom this reaction is suspected.
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PMID:Myocarditis related to clozapine treatment. 1147 22

Dilated cardiomyopathy may be primary or secondary. Although some causes are well known, such as toxic substances (alcohol, chemotherapy...) or viral infections, biochemical abnormalities are much less common. The authors report the case of a 58 year old woman with no previous history admitted to hospital for an inaugural episode of cardiac failure. The ECG showed sinus tachycardia with a long QT interval (560 mm) and a dilated hypokinetic cardiomyopathy with a left ventricular ejection fraction of 20%. The aetiological investigation showed severe hypocalcaemia (0.66 mmol/L) related to primary hypoparathyroidism. This is an important cause to remember because its treatment leads to correction of the cardiac disease, usually within weeks.
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PMID:[Reversible hypokinetic cardiomyopathy revealing severe hypocalcemia]. 1149 34

We report a 49-year-old man with primary hyperthyroidism who presented with pancytopenia. The patient presented with leg edema, sinus tachycardia, cardiomegaly, and pleural effusions, all from congestive heart failure. Laboratory data showed pancytopenia and primary hyperthyroidism; echocardiogram showed diffuse hyperkinesis of the left ventricular wall and right ventricular overloading. The bone marrow was moderately hypercellular and compatible with arrested hematopoiesis. Pancytopenia and heart failure improved after administration of methimazole and diuretics. However, high levels of thyroid hormone recurred with pancytopenia 4 months after admission. Therefore, subtotal thyroidectomy was performed, and the levels of thyroid hormones and peripheral blood cell counts have remained normal. Pancytopenia may be caused by hyperthyroidism.
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PMID:A case of thyrotoxicosis with pancytopenia. 1152 11

Dystrophinopathies are due to mutations in the dystrophin gene on chromosome Xp21.1 and comprise the allelic entities Duchenne muscular dystrophy (DMD), Becker muscular dystrophy (BMD) and X-linked dilative cardiomyopathy (XLDCM). In all three entities, the heart is affected to various degrees, depending on the stage of the disease and the type of the mutation (cardiac involvement, CI). The pathoanatomic evidence of CI in dystrophinopathies is the replacement of myocardium by connective tissue or fat. In DMD/BMD, the left ventricular posterobasal and lateral walls are most extensively affected, sparing the right ventricle and the atrium. Degree and dynamics of CI vary among the three entities. In DMD/BMD, CI usually remains subclinical in the early stages of the disease. Typical initial manifestations of CI in DMD/BMD are sinus tachycardia, tall R1 in V1, prominent Q in I, aVL, V6 or in II, III, and aVF, increased QT dispersion and possibly autonomic dysfunction. Initially, echocardiography is normal or shows regional wall motion abnormalities in areas of fibrosis. With spreading of fibrosis, left ventricular dysfunction and ventricular arrhythmias additionally occur. In the final stages of the disease, systolic function may lead to heart failure and sudden death. Subclinical or clinical CI is present in about 90% of the DMD/BMD patients but is the cause of death in only 20% of the DMD and 50% of the BMD patients. XLDCM is a rapidly progressive, almost exclusively myocardial disorder, starting in teenage males as heart failure due to dilative cardiomyopathy (CMP), leading to death from intractable heart failure within 1-2 years after diagnosis. Therapy of arrhythmias and CMP in all three disorders follows the established cardiological recommendations. Due to its protective effect, ACE inhibitors are recommended already at the early stages of the disease. Beta-blockers may be an additional option if indicated.
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PMID:The heart in human dystrophinopathies. 1258 17

Biventricular pacing has emerged as a modality for treatment of patients with heart failure. Combined biventricular pacers and implantable cardioverter defibrillators offer treatment of heart failure as well as protection from sudden cardiac death. However, inappropriate ICD shocks as a result of double sensing due to widely spaced ventricular bipoles may pose a significant problem in these patients. We examined the ICD records of twenty-three patients with biventricular ICDs, and evaluated all episodes of double sensing that resulted in aborted or delivered therapy. In follow-up of 3.7 +/- 2.6 months, thirty-three shocks in fifteen episodes occurred in five patients (21.7%) due to double sensing. Four patients (17.4%) had aborted shocks due to double sensing. All episodes resulting in shock occurred because of sinus tachycardia or supraventricular tachycardia above the upper programmed pacing rate of the device with resultant AV conduction and double sensing of the nonpaced ventricular depolarization. In conclusion, double sensing of the R-wave is a common and clinically important cause of inappropriate ICD detection and shock in patients with biventricular ICDs. Appropriate programming of the ICD can prevent episodes of inappropriate shocks.
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PMID:Frequent ICD shocks due to double sensing in patients with bi-ventricular implantable cardioverter defibrillators. 1461 60

A 21-year-old male patient underwent aortic and mitral valve replacement for progressive cardiac failure due to acute bacterial endocarditis. Ischemic myocardial contracture developed during attempts to restore cardiac activity following hypothermic, ischemic, cardioplegic arrest. An abdominal left ventricular assist device (ALVAD) was implanted and supported the circulation for nearly six days prior to cardiac transplantation. The preoperative EKG showed sinus tachycardia with left anterior hemiblock. Postoperatively, there was complete electromechanical dissociation. The postoperative EKG showed a superior and leftward shift of the axis. There was a marked loss of QRS voltage and variable degrees of atrioventricular block. At times, only P waves were present. On the fourth postoperative day, there was an axis shift to the extreme right. Prior to transplantation, sinus rhythm returned, and the axis shifted leftward once again. The common denominator of all the abnormal postoperative electrocardiograms was the conspicuous low voltage that probably signified early and extensive myocardial damage. To our knowledge, this is the first instance wherein a sequential electrocardiographic analysis of stone heart syndrome has been undertaken.
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PMID:SEQUENTIAL ELECTROCARDIOGRAPHIC ANALYSIS OF STONE HEART SYNDROME IN A PATIENT SUPPORTED SIX DAYS WITH AN ABDOMINAL LEFT VENTRICULAR ASSIST DEVICE (ALVAD). 1521 21

Multisite pacing for the treatment of heart failure has added a new dimension to the electrocardiographic evaluation of device function. During left ventricular (LV) pacing from the appropriate site in the coronary venous system, a correctly positioned lead V1 registers a right bundle branch block pattern with few exceptions. During biventricular stimulation associated with right ventricular (RV) apical pacing, the QRS is often positive in lead V1. The frontal plane QRS axis is usually in the right superior quadrant and occasionally in the left superior quadrant. Barring incorrect placement of lead V1 (too high on the chest), lack of LV capture, LV lead displacement or marked latency (exit block or delay from the stimulation site), ventricular fusion with the spontaneous QRS complex, a negative QRS complex in lead V1 during biventricular pacing involving the RV apex probably reflects different activation of an heterogeneous biventricular substrate (ischemia, scar, His-Purkinje participation in view of the varying patterns of LV activation in spontaneous left bundle branch block) and does not necessarily indicate a poor (electrical or mechanical) contribution from LV stimulation. In this situation, it is imperative to rule out the presence of coronary venous pacing via the middle cardiac vein or even unintended placement of two leads in the RV. During biventricular pacing with the RV lead in the outflow tract, the paced QRS in lead V1 is often negative and the frontal plane paced QRS axis is often directed to the right inferior quadrant (right axis deviation). In patients with sinus rhythm and a relatively short PR interval, ventricular fusion with competing native conduction during biventricular pacing may cause misinterpretation of the ECG because narrowing of the paced QRS complex simulates appropriate biventricular capture. This represents a common pitfall in device follow-up. Elimination of ventricular fusion by shortening the AV delay, is often associated with clinical improvement. Anodal stimulation may complicate threshold testing and should not be misinterpreted as pacemaker malfunction. One must be cognizant of the various disturbances that can disrupt 1:1 atrial tracking and cause loss of ventricular resynchronization. (1) Upper rate response. The upper rate response of biventricular pacemakers differs from the traditional Wenckebach upper rate response of conventional antibradycardia pacemakers because heart failure patients generally do not have sinus bradycardia or AV junctional conduction delay. The programmed upper rate should be sufficiently fast to avoid loss of resynchronization in situations associated with sinus tachycardia. (2) Below the programmed upper rate. This may be caused by a variety of events (especially ventricular premature complexes and favored by the presence of first-degree AV block) that alter the timing of sensed and paced events. In such cases, atrial events become trapped into the postventricular atrial refractory period at atrial rates below the programmed upper rate in the presence of spontaneous AV conduction. Algorithms are available to restore resynchronization by automatic temporary abbreviation of the postventricular atrial refractory period.
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PMID:Electrocardiographic follow-up of biventricular pacemakers. 1584 37

Thyrotoxicosis is associated with increased cardiovascular morbidity and mortality, primarily due to heart failure and thromboembolism. Palpitations, caused by sinus tachycardia and occasionally by atrial fibrillation, are the most frequent cardiovascular symptom. As atrial fibrillation may be the only manifestation of thyrotoxicosis, thyroid hormone excess should routinely be excluded in patients with this rhythm disturbance. Heart failure occurs mostly in the presence of underlying heart disease or tachycardia-induced cardiomyopathy in patients with long-standing atrial fibrillation. On occasion, long-standing hyperthyroidism may lead to heart failure even in the absence of concomitant cardiac conditions. Beta-blockers offer symptomatic relief and at the same time slow the ventricular response in patients with atrial fibrillation. Amiodarone, and occasionally iodinated contrast agents, may cause iodine-induced thyrotoxicosis. Clinical suspicion is essential in the diagnosis of amiodarone-induced thyrotoxicosis (AIT), because the antiadrenergic effect of the drug may conceal symptoms. AIT should be considered in any patient on amiodarone in the presence of new-onset or recurrent atrial arrhythmias or unexplained weight loss. Beyond discontinuation of amiodarone, treatment options include propylthiouracil or methimazole, potassium perchlorate, steroids, lithium and, if pharmacological treatment fails, surgery. Amiodarone may potentially be used less frequently in the future since recent studies have shown that this drug is inferior to implantable cardioverter defibrillators in prevention of sudden cardiac death in patients with severe heart failure. In addition, non-iodinated amiodarone analogues are currently in advanced phase of clinical testing.
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PMID:Thyrotoxicosis and the cardiovascular system. 1598 1

20-30% of ICD patients suffer from inappropriate ICD therapy due to misclassification of supraventricular tachycardia (SVT) as ventricular tachycardia. Inappropriate ICD therapies are not only painful for patients, but also proarrhythmogenic and can reduce device longevity due to battery depletion. Therapy of inappropriate ICD episodes is a puzzle of optimized ICD programming, antiarrhythmic therapy and radiofrequency (RF) ablation. Single-chamber ICD detection algorithms are effective in reducing inappropriate ICD therapy particularly due to sinus tachycardia or atrial fibrillation. Dual-chamber ICD detection algorithms were developed to improve specificity of SVT discrimination. However, large prospective, controlled trials showing superiority of dualchamber over single-chamber devices are lacking. It appears that patients with slow ventricular tachycardias, being at high risk for inappropriate ICD therapy, might benefit from dual-chamber ICD therapy. Concerning pharmacological therapy of inappropriate ICD episodes, the OPTIC study recently showed superiority of class III antiarrhythmics (sotalol and amiodarone) over beta-blockers. RF ablation of cavotricuspid isthmus is of proven benefit in ICD patients with inappropriate episodes due to typical flutter and should also be considered in atrial tachycardia. If patients with paroxysmal atrial fibrillation despite optimized antiarrhythmic medication will benefit from trigger elimination or substrate modification by RF ablation has still to be proven. In patients with inappropriate ICD episodes and drug-refractory chronic permanent atrial fibrillation, AV node ablation can effectively eliminate inappropriate ICD therapy, however, at the price of potential ventricular asynchrony and progression of heart failure due to right ventricular pacing. Thus, upgrading to biventricular ICD therapy should be considered in these patients.
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PMID:[Therapeutic strategies in inappropriate ICD therapy]. 1633 88


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