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Query: UMLS:C0038454 (stroke)
147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The initiation of cardiac impulse is located in the sinus node, in the upper anterior part of the right atrium. The importance of the atrium is not only linked to the regulation of heart rate, but also to its haemodynamic function. Indeed, atrial depolarization leads to atrial contraction which can be responsible for up to 30% of cardiac output by way of ventricular filling. Supraventricular arrhythmias are related to one of the following mechanisms: abnormal automaticity, triggered activity, and reentry. Most of supraventricular tachycardias are due to a reentrant phenomenon (intranodal reentrant tachycardia, orthodromic circusmovement tachycardia, atrial flutter and atrial fibrillation). At the onset of a supraventricular tachycardia, the loss of efficacious atrial contraction as well as the increased heart rate may abruptly decrease ventricular filling. As a consequence, stroke volume is reduced, leading to a decrease in cardiac output and in arterial blood pressure, explaining that the patient may experience syncope. Usually, blood pressure reduction resumes within 30 seconds after activation of the autonomic adrenergic nervous system. In case of an underlying heart disease, the supraventricular tachycardia may lead to acute cardiac failure. When reentry is concerned, the tachycardia is going around a specific circuit. The existence of such a circuit in most of supraventricular tachycardias has led to the development of ablation therapy, the goal of which is to destroy a critical portion of the circuit hence making the recurrence of reentrant tachycardia impossible.
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PMID:[Atrial activity and its effects]. 823 2

Two cases of fetal tachyarrhythmias were treated in utero. One case showed supraventricular tachycardia which was successfully treated with procainamide. The other case was an atrial flutter with 2:1 atrioventricular conduction (AVC) which was treated with digoxin and verapamil. In both cases, the blood flow in the descending aorta was observed using pulsed Doppler ultrasound during therapy. In the first case, the interval of blood flow peaks was suddenly prolonged to normal heart rate, and in the second case, the blood flow peaks appeared irregularly which indicated that (AVC) was intermittently blocked. The blood flow pattern represented the mode of cardioversion. The blood flow velocity was also measured in both cases; it decreased transiently during therapy representing a depression in cardiac function. The cause of this was thought to be the negative inotropic effects of procainamide and verapamil. In spite of these negative inotropic effects, a greater R-R interval means a greater stroke volume. This relationship has a favorable effect on the fetal circulation as a result of therapy for fetal tachyarrhythmias.
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PMID:Hemodynamic changes during cardioversion in utero: a case report of supraventricular tachycardia and atrial flutter. 845 47

A retrospective review was done to determine the efficacy and hemodynamic effects of slow intravenous amiodarone administration on invasively monitored patients with acute onset of atrial fibrillation or atrial flutter and left ventricular ejection fractions < 15%. Eight patients met predefined inclusion criteria. All received 300 mg amiodarone intravenously over 1 hour. Seven reverted to sinus rhythm within 1 hour, with return of most hemodynamic variables to baseline. Before reversion, each patient experienced a beneficial slowing of heart rate (mean, 28%) resulting in significant improvement of stroke volume index (mean, 49%) and left ventricular stroke work index (mean, 61%). No patient had hemodynamic deterioration attributable to amiodarone infusion. Slow intravenous infusion of amiodarone appears to be an effective and hemodynamically well-tolerated therapy for atrial fibrillation and atrial flutter in critically ill patients with marked depression of left ventricular systolic function.
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PMID:Intravenous amiodarone for therapy of atrial fibrillation and flutter in critically ill patients with severely depressed left ventricular function. 870 76

Atrial fibrillation is a frequent arrhythmia which has a high prevalence after 65 years of age, thus the typical patient's age is about 75. There are two atrial fibrillation predictors: traditional factors of cardiovascular risk (age, male sex, high blood pressure, diabetes), and structural heart disorders (heart failure, valvular heart disease). All preventive measures to reduce atrial fibrillation incidence, must be directed towards these factors. Additionally, left atrial size, ejection fraction and ventricular hypertrophy are echocardiographic predictors. Atrial fibrillation doubles the mortality rate and is related to an annual stroke rate of 4.5%. The stroke risk factors are: age, hypertension, diabetes, previous stroke, congestive heart failure, coronary heart disease, mitral stenosis, prosthetic heart valves and thyrotoxicosis. Left atrial size and ventricular disfunction are echocardiographic stroke risk factors. Each patient's risk can be stratified on the basis of these factors. All of this information is essential to handle the arrhythmia appropriately; this arrhythmia may be more important than has been thought. Atrial flutter is not very frequent and so it is less studied; however it is an arrhythmia with a similar clinical context to atrial fibrillation, although, probably, with a smaller embolic risk.
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PMID:[Epidemiology, risk factors, and pathogeny of atrial fibrillation and atrial flutter]. 875 90

Atrial fibrillation is associated with three major risk of complications: thromboembolism, hemodynamic compromise, and arrhythmogenesis. In patients with chronic atrial fibrillation the incidence of embolization is about 5% per year. The risk of embolism and in particular of stroke can be reduced by warfarin anticoagulation. Aspirin is generally less effective than warfarin, although it is probably more effective than placebo. The hemodynamic complications which may occur during atrial fibrillation are mainly due to the loss of effective atrial contraction, the irregular ventricular rhythm, and the possible excessively rapid ventricular rate. Sudden death is a recognized manifestation of Wolff-Parkinson-White syndrome and is considered to be precipitated by atrial fibrillation in the majority of patients. Torsades de pointes is perhaps the most widely recognized proarrhythmia associated with treatment of atrial fibrillation, especially with 1A antiarrhythmic drugs and sotalol. The chronic treatment with type 1C drugs in 3.5%-5% of patients may induce atrial flutter with 1:1 conduction with significant hemodynamic compromise.
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PMID:Risk of complications of atrial fibrillation. 935 15

The aim of this work was to investigate the cardiologic risk factors for stroke. 232 patients were studied. All of them had a stroke. There were 133 males and 99 females. The most often observed cardiologic risk factor for stroke was ischaemic heart disease, which was present in 48.2% of all the cases. Usually ischaemic heart disease was observed as stable angina pectoris (34.4%) and past cardiac infarction (9.9%). Dysrrhythmia and conduction abnormalities were present in 46.1% of cases, mostly as premature ventricular beats (13.4%) and atrial fibrillation and atrial flutter (12.5%). Congenital and acquired heart diseases (11.6%) and chronic circulatory failure (15.9%) were recognized in lower per cent of the cases. The assessments of other authors and our observations evidence the relevance of cardiologic risk factors in stroke.
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PMID:[Cardiologic risk factors for stroke]. 963 76

Atrial fibrillation (AF) is the most common sustained arrhythmia, particularly in the elderly population. It is well recognised that AF is a major cause of stroke, even in the absence of underlying heart disease. Although AF and atrial flutter share many causes and may be seen in the same patient, there are differences between these arrhythmias: atrial flutter is less common, and the risk of stroke associated with it is less than that with AF. In addition to stroke, both AF and atrial flutter may cause cardiomyopathy, which may be fully reversible with effective treatment of the arrhythmia. Both AF and atrial flutter can result in severe symptoms and may precipitate heart failure, ischaemia and syncope. Recent research indicates that AF is a self-perpetuating arrhythmia, and that the longer it is left untreated the less likely it is that effective cardioversion will be possible. Drugs are an attractive option for the cardioversion of AF and atrial flutter because their use does not require anaesthesia. Antiarrhythmic drugs in class III of the Vaughan-Williams classification are effective in the treatment of AF, but they have adverse effects; several new 'pure' class III agents are under development. The first of these to be made available is ibutilide, a methanesulphonamide derivative. Initial results are encouraging, particularly for atrial flutter. However, the drug has the potential for proarrhythmic effects and physicians who use it will need to be aware of these.
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PMID:The use of drugs for cardioversion of recent onset atrial fibrillation and flutter. Focus on ibutilide. 963 94

An ECG recording time of 24 hours has a low yield to detect atrial arrhythmias in patients after an acute ischemic stroke. The present study investigated whether a recording time of 72 instead of 24 hours detects paroxysmal atrial fibrillation in more patients. The study prospectively included 82 consecutive patients 2-3 weeks after an acute ischemic stroke. All patients had sinus rhythm in the resting ECGs and no history of atrial fibrillation or flutter. The frequency of atrial fibrillation was assessed after 24, 48, and 72 hours of ambulatory ECG monitoring. An ECG monitoring time of 72 hours documented paroxysmal atrial fibrillation in five (6%) patients. The episode of paroxysmal atrial fibrillation occurred in only one patient within 24 hours. The other patients had their first episode of atrial fibrillation between 24 and 48 hours (n = 2) and between 48 and 72 hours (n = 2). These five patients were older (age = 70 +/- 5 years), whereas the mean age of the remaining patients was 59 +/- 13 years. All five patients had cardiovascular disease in comparison to 36 of 77 patients and reported palpitations in comparison to 6 of 77 of the remaining patients. In conclusion, ambulatory ECG monitoring over 72 hours detected after the first recording day four of five patients in whom paroxysmal atrial fibrillation could be documented for the first time. The 72-hour recording time improved, compared to the 24-hour period, the detection of paroxysmal atrial fibrillation in patients after an ischemic stroke. It seems to be more efficient to perform prolonged ECG recording mainly in older patients with a cardiovascular disease and/or a history of palpitations.
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PMID:Impact of long-term ECG recording on the detection of paroxysmal atrial fibrillation in patients after an acute ischemic stroke. 1045 38

Atrial fibrillation (AF) is the most common sustained cardiac dysrhythmia, predominating in the elderly, with stroke as a potentially devastating complication. Prevention of the thromboembolic sequelae from AF remains a central focus of practicing clinicians. Although the risk of thromboembolism in chronic AF is well recognized, less is known about the potential risk of systemic embolism in acute AF. In addition, recent data support the notion of a group at considerable risk of embolism from atrial flutter, an arrhythmia typically believed to bestow little increased risk of thromboembolism. The mechanism of thrombus formation, embolization, and resolution in atrial arrhythmias is not well defined, particularly in that of acute AF or atrial flutter. The traditional concept proposes that atrial thrombus forms only after > 2 days of AF and embolizes by being dislodged from increases in shear forces. This widely accepted concept further holds that newly formed atrial thrombus, in the setting of AF, organizes over a span of 14 days. The results of studies based on observations from transesophageal echocardiography examinations have provided provocative insight into the temporal sequence of atrial thrombus formation, embolization, and resolution in AF or atrial flutter and have expanded the traditional concept of thromboembolism in these atrial dysrhythmias. Namely, left atrial thrombus may form before the onset of AF in the face of sinus rhythm. Conversion to sinus rhythm may increase the thrombogenic milieu of the left atrium. Importantly, atrial thrombus may form in the acute phase of AF. Last, thrombi may require > 14 days to become immobile or to resolve. Findings similar to those of acute AF have been reported in patients with atrial flutter and coexisting cardiac pathology. On the basis of these emerging insights fostered by the use of transesophageal echocardiography, it appears appropriate to consider anticoagulation in patients presenting with acute AF or atrial flutter with coexisting cardiac pathology predisposing to left atrial thrombus.
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PMID:Risk of thromboembolism in acute atrial fibrillation or atrial flutter. 1097 12

Using a Medicare-based retrospective cohort study, the stroke risk in patients with atrial flutter (RR = 1.41) was determined to be greater than that in a control group (RR = 1.00) but less than that in an atrial fibrillation group (RR = 1.64). Furthermore, patients with atrial flutter who subsequently had an episode of atrial fibrillation had a higher risk of stroke (RR = 1.56) than patients with atrial flutter who never had a subsequent episode of atrial fibrillation (RR = 1.11).
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PMID:Risk of stroke in patients with atrial flutter. 1116 76


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