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 51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A case of congenital, isolated tricuspid regurgitation is reported. A 48 year old woman has been admitted because of shortness of breath and progressive fatigue. Although the heart murmur had been heard in her childhood, the first symptoms appeared when she was 25. One year later she underwent a plastic surgery of tricuspid valve. During the following 20 years she remained asymptomatic, until dyspnea and fatigue developed again. On admission she was cyanotic and positive, systolic jugular venous pulse was seen. Atrial flutter was present and no systolic cardiac murmur was heart. The liver was enlarged without peripheral oedema. Echo-Doppler examination and cardiac catheterisation revealed huge right cardiac chambers and significant tricuspid regurgitation. During reoperation a valve consisting of only two cusps was found with extremely dilated valvular anulus. A Bex valvuloplasty was successfully performed. One month later a control echo-Doppler showed the diminution of right ventricle and right atrium with hardly visible regurgitant jet. The pathogenesis and the course of this extremely rare disease have been also discussed in the paper.
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PMID:[Isolated congenital tricuspid valve insufficiency--case report]. 147 73

This study describes six generations of a family with autosomal dominant cardiac conduction system and myocardial disease with recognizable clinical stages. A 20 year follow-up of nine family members, a medical questionnaire of 196, electrocardiographic screening of 91, noninvasive testing of 20, and catheterization with endomyocardial biopsy of six are the basis of this report. The clinical stages are as follows: Stage I occurs in the second and third decades of life and is characterized by an absence of symptoms, normal heart size, sinus bradycardia, and premature atrial contractions. Stage II is marked by first-degree atrioventricular block in the third and fourth decades. Stage III occurs in the fourth and fifth decades and is accompanied by chest pain, fatigue, lightheadedness, and advanced atrioventricular block followed by the development of atrial fibrillation or flutter. Stage IV, in the fifth and sixth decades of life, is characterized by congestive heart failure and recurrent ventricular arrhythmias. Light microscopy of right ventricular endomyocardial biopsy specimens from patients in stage II revealed very mild fibrosis; electron microscopy of the specimens demonstrated mild dilatation of tubules, mitochondrial swelling, and minimal myofibrillar loss. Biopsy specimens from patients with stage III disease were similar to those from patients with stage II disease except for an increase of myofibrillar loss. The stage IV specimens had diffuse fibrosis and more severe tubular dilatation, mitochondrial cristolysis, and myofibrillar loss. At autopsy in the proband, the atrial changes were more severe than the ventricular and were especially marked in the sinoatrial and atrial myocardium. Early recognition of the disease and use of pacemakers and antiarrhythmic agents have proved beneficial for affected family members. Thorough family studies of patients with conduction system disease and/or dilated cardiomyopathy are necessary to better understand the hereditary basis and natural course of this category of disease.
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PMID:Evolution of a hereditary cardiac conduction and muscle disorder: a study involving a family with six generations affected. 370 75

The pharmacokinetics, clinical efficacy, and adverse effects of three calcium-channel blocking agents--verapamil, nifedipine, and diltiazem--are reviewed. Verapamil, nifedipine, and diltiazem are absorbed well after oral dosing, but absolute bioavailability of each is reduced substantially by a first-pass effect. Each drug is metabolized extensively (verapamil and diltiazem to moderately active metabolites) by the liver. A substantial percentage of each drug is bound to plasma proteins, but the binding is of clinical importance only for nifedipine (92--98% protein bound). Intravenous verapamil has become the agent of first choice for treatment of acute paroxysmal supraventricular tachycardia (PSVT); use of chronic oral verapamil therapy for prophylaxis remains controversial. Verapamil and diltiazem have been evaluated with mixed results for atrial flutter and fibrillation. For treatment of myocardial ischemia, calcium-channel blockers may be of some value (possibly in combination with nitrates of B blockers). All three agents have been studied in patients with exertional angina with good results. Calcium-channel blockers appear to be equal with nitrates for treatment of variant angina. Patients with hypertropic cardiomyopathy have been treated with verapamil and nifedipine with promising results. Nifedipine has been effective for treatment of essential hypertension. Adverse effects of calcium-channel blockers have been relatively minor or infrequent. Diltiazem overall has the best side-effect profile, with adverse effects causing discontinuation of therapy in about 2--10% of patients; verapamil in intermediate (8--10%) and nifedipine the worst (17%) in this respect. The most common side effects generally are fatigue, headache, dizziness, skin rash, and peripheral edema. While they generally should be reserved for patients in whom more conventional therapy has failed (except those with PSVT), calcium-channel blockers appear to have a valid role as reserve agents for exertional and variant angina, cardiomyopathy, and hypertension.
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PMID:Update on calcium-channel blocking agents. 635 66

Optimal pacing in patients with paroxysmal atrial fibrillation/flutter following AV node ablation remains to be determined because VVIR pacing cannot restore AV synchronization and conventional DDD(R) pacing cannot properly cope with atrial tachyarrhythmias. The objective of the present investigation was to study the clinical outcome of 16 of these patients who received a new DDDR pacemaker with an automatic mode switch (Thera DR; Medtronic) immediately after AV node ablation. Arrhythmia-related symptoms before ablation were palpitations in 12, dizziness in 10, exercise intolerance in 8, and syncope in 6 patients. Pacing modes at hospital discharge were DDDR (n = 14) and DDD (n = 2) with an activated mode switch in all patients. After 1 month 12 patients were symptom free. Clinical events occurred in 4 patients (palpitations in 2, dizziness in 1, chest pain in 1, and fatigue in 1), which could be relieved in 3 patients. At discharge as well as at the 1-month follow-up, Holter ECG recorded a total of 12 episodes of atrial fibrillation in 5 patients, which were correctly detected by the pacemaker and followed by mode switching. At the 3-month follow-up (n = 14), 12 patients were symptom free and 2 continued to report symptoms which could not be resolved. All patients remained on an automatic mode switch in either the DDDR (n = 12) or DDD (n = 2) mode. There were no hints of inappropriate mode switching or reports of pacemaker syndrome, and there were no new symptoms related to automatic mode switching. The patients studied were highly symptomatic before implantation due to paroxysmal atrial fibrillation/flutter. After the first follow-up, 81% of the patients reported no symptoms. Paroxysmal atrial fibrillation/flutter combined with a high-degree AV-block seems no longer to be a contraindication for AV-synchronous pacing.
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PMID:DDD(R) pacing with automatic mode switch in patients with paroxysmal atrial fibrillation following AV nodal ablation. 919 25

Atrial tachycardias, in particular atrial flutter after surgery for congenital heart disease, is associated with a high mortality. Treatment with various antiarrhythmic drugs and/or antitachycardia pacemakers is not very successful. Sotalol, a Class III drug, has shown to be a promising drug in adults with atrial tachycardias. However, the experience with sotalol in children after surgery for congenital heart disease is limited. Therefore, we describe our results here. Between December 1990 and February 1997, 26 children with atrial tachycardias, most of them with atrial flutter or fibrillation (n = 20), after surgery for congenital heart disease were treated with sotalol orally. The age of the children at the start of treatment was 7.5 +/- 5.8 years (mean +/- SD). The time interval between surgery and the start of atrial tachycardia ranged from 1 day to 14.3 years (3.8 +/- 3.8 years). Conversion to sinus rhythm was achieved in 16 out of 22 hemodynamically stable children with a dosage of 4.0 +/- 1.6 mg/kg per day. The six children without sinus rhythm on sotalol and four hemodynamically unstable patients were treated prophylactically with sotalol after DC cardioversion for their tachycardias. Two children complained of mild transient fatigue. Heart rate decreased during therapy (95 +/- 33 vs 81 +/- 21 beats/min; P = 0.01). QTc-intervals did not change. Proarrhythmias such as torsades de pointes were not encountered. Two children with a preexistent sick sinus syndrome showed aggravation of bradycardia and needed pacemaker implantation. The percentage of children with a recurrence-free interval of 1 and 2 years was 96% and 81%, respectively, for all atrial tachycardias, and 92% and 66% for atrial flutter. The recurrences of atrial tachycardias during the follow-up period, which ranged from 0.1-6.1 years (2.5 +/- 1.8 years) could be treated with only an increase of the dosage of sotalol in all but one patient. We conclude that sotalol is an effective drug for the treatment and prevention of atrial tachycardia in children after surgery for congenital heart disease.
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PMID:Sotalol for atrial tachycardias after surgery for congenital heart disease. 927 23

Atrial fibrillation is the most common cardiac rhythm disorder associated with hospitalization. Two therapeutic options have been available: antiarrhythmic drug therapy, and external or internal electrical cardioversion. Electrical cardioversion of atrial fibrillation remains one of the most widely used and effective treatments for the restoration of normal sinus rhythm. However, many patients continue to receive an antiarrhythmic drug before and after cardioversion in an attempt either to cardiovert the arrhythmia chemically or to maintain sinus rhythm after successful cardioversion. Because some pharmacological agents can affect the cardioversion procedure for atrial fibrillation or flutter, and because many patients with such arrhythmias may require electrical cardioversion when they are taking antiarrhythmic drugs, the question of a possible effect of drug therapy on the efficacy and safety of electrical cardioversion of atrial fibrillation arises. Early reports of direct current cardioversion provoking potentially lethal ventricular arrhythmias raised suspicions of an arrhythmogenic role for digoxin antiarrhythmic therapy, and it is customary to withhold these drugs for 24 to 48 h before cardioversion is attempted. However, this complication is likely to arise only in patients who are close to, or actually manifesting, signs of drug toxicity. On the other hand, treatment with therapeutic concentrations of antiarrhythmic drugs before cardioversion may in some cases be associated with a significant reduction in the number of shocks and decreased energy required to restore sinus rhythm, a lower incidence of postshock arrhythmias and a reduced risk of early recurrence of atrial fibrillation.
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PMID:Atrial fibrillation: what are the effects of drug therapy on the effectiveness and complications of electrical cardioversion? 985 40

Between 1992. 2 and 1997. 12, the maze procedure for lone fibrillation or flutter (lone af) was performed in 8 patients including 2 patients with a sustained atrial fibrillation, 5 patients with a paroxysmal atrial fibrillation and 1 patient with a sustained atrial flutter. All patients had suffered from a drug resistance lone af which induced sever symptom that is the dyspnea, palpitation and fatigue. Therefore patients requested to receive the maze procedure, and they agreed with the informed concent. After the maze operation, the normal sinus rhythm was recovered in 7 of 8 patients (87.5%). In only 1 patient, a paroxysmal atrial fibrillation remained but his symptoms improved after surgery. So this operation is a good choice of a treatment for a drug resistance lone af.
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PMID:[Maze procedure for a lone atrial fibrillation]. 1047 38

A patient with congenital complete heart block underwent implantation of a dual-chamber pacemaker. He presented to the emergency room with fatigue and was found to be in atrial flutter. Device interrogation revealed undersensing of 5 mV flutter waves at a programmed sensitivity of 0.5 mV. Due to undersensing, mode switch did not occur. This case illustrates apparently paradoxical undersensing of atrial flutter waves by a dual-chamber pacemaker and can be explained by a phenomenon known as "quiet timer blanking."
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PMID:Paradoxical undersensing during atrial flutter: what is the mechanism? 1687 30

An 85-year-old man with persistent atrial flutter (AFL) with slow ventricular rate of 44/min, causing fatigue and presyncope, was referred for urgent treatment. In spite of thromboembolic risk scale value 4, he had not been treated with anticoagulants because of high risk of bleeding. The decision was made to perform urgent catheter ablation to interrupt and cure AFL. Intracardiac echocardiography probe was placed in the pulmonary artery and visualized left atrial appendage free from thrombus with its proper function. Heparin was administered and AFL stopped during energy application. Intracardiac echocardiography showed immediate thrombus formation in left atrial appendage owing to complete atrial standstill and no retrograde conduction during hemodynamically effective escape nodal rhythm. This case report shows that in patients with sinus node disease effective ablation of AFL with escape rhythm without retrograde conduction to the atria may result in complete 'electrically induced' atrial standstill and immediate thrombus formation.
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PMID:Intracardiac echocardiography for immediate detection of intracardiac thrombus formation. 2619 13

In this paper, we propose an algorithm that classifies whether a generated cardiac arrhythmia alarm is true or false. The large number of false alarms in intensive care is a severe issue. The noise peaks caused by alarms can be high and in a noisy environment nurses can experience stress and fatigue. In addition, patient safety is compromised because reaction time of the caregivers to true alarms is reduced. The data for the algorithm development consisted of records of electrocardiogram (ECG), arterial blood pressure, and photoplethysmogram signals in which an alarm for either asystole, extreme bradycardia, extreme tachycardia, ventricular fibrillation or flutter, or ventricular tachycardia occurs. First, heart beats are extracted from every signal. Next, the algorithm selects the most reliable signal pair from the available signals by comparing how well the detected beats match between different signals based on [Formula: see text]-score and selecting the best match. From the selected signal pair, arrhythmia specific features, such as heart rate features and signal purity index are computed for the alarm classification. The classification is performed with five separate Random Forest models. In addition, information on the local noise level of the selected ECG lead is added to the classification. The algorithm was trained and evaluated with the PhysioNet/Computing in Cardiology Challenge 2015 data set. In the test set the overall true positive rates were 93 and 95% and true negative rates 80 and 83%, respectively for events with no information and events with information after the alarm. The overall challenge scores were 77.39 and 81.58.
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PMID:Reduction of false arrhythmia alarms using signal selection and machine learning. 2745 28


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