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Biomedical subjects

O A Obel

Publications and source records attributed to O A Obel.

10 recordsLinked to original sources

Effects of ventricular rate and regularity on the velocity and magnitude of left atrial appendage flow in atrial fibrillation.

OBJECTIVE: To prospectively determine whether ventricular rate and regularity are significant determinants of the velocity and magnitude of left atrial appendage (LAA) flow. DESIGN AND PATIENTS: 12 patients with atrial fibrillation (AF), high degree atrioventricular block, and indwelling permanent pacemakers were studied. SETTING: Cardiology department of a tertiary referral centre. INTERVENTIONS: Pacing was triggered by an external programmable transcutaneous device. Patients were paced at 60, 120, and 150 beats/min in both regular and irregular rhythm. LAA flow velocity and magnitude were assessed with transoesophageal Doppler echocardiography. MAIN OUTCOME MEASURES: Peak and mean LAA inflow and outflow velocity, and time-velocity interval (TVI) of LAA flow. RESULTS: Increasing ventricular rate was associated with significantly lower peak inflow (p < 0.01), peak outflow (p < 0.05), mean inflow (p < 0.01), and mean outflow (p < 0.05) velocities and with a lower TVI of LAA filling and emptying velocities (p < 0.01). This effect was noted at rates of 60 beats/min compared with both 120 and 150 beats/min. At a pacing rate of 120 beats/min there was a significantly higher total TVI when pacing at a regular than at an irregular rhythm (40.16 (14.6) cm v 30.74 (10.9) cm, p < 0.05). CONCLUSIONS: In this study, LAA filling velocities in patients in AF were significantly influenced by paced ventricular rate and to a much lesser extent ventricular rhythm. These results suggest that rapid ventricular rates may predispose to stasis in the LAA in AF.

Adult↗

Arrhythmias in an athlete: the effect of de-training.

A 53 year old athlete with a history of severe palpitations and lightheadedness presented for a second opinion. He was found to exhibit very frequent atrial ectopy, frequent runs of symptomatic atrial tachyarrhythmia, and sinus bradycardia at rest. During exercise testing, his tachyarrhythmias increased in relation to the duration and intensity of exercise. A therapeutic trial of de-training was suggested. As a result, his symptoms completely resolved with a marked reduction in the frequency of atrial arrhythmia. Repeat exercise testing revealed an excellent exercise tolerance with no atrial ectopy. De-training should be considered when athletes present with arrhythmias.

Arrhythmias, Cardiac↗

Left atrial appendage: structure, function, and role in thromboembolism.

The left atrial appendage (LAA) is derived from the left wall of the primary atrium, which forms during the fourth week of embryonic development. It has developmental, ultrastructural, and physiological characteristics distinct from the left atrium proper. The LAA lies within the confines of the pericardium in close relation to the free wall of the left ventricle and thus its emptying and filling may be significantly affected by left ventricular function. The physiological properties and anatomical relations of the LAA render it ideally suited to function as a decompression chamber during left ventricular systole and during other periods when left atrial pressure is high. These properties include the position of the LAA high in the body of the left atrium; the increased distensibility of the LAA compared with the left atrium proper; the high concentration of atrial natriuretic factor (ANF) granules contained within the LAA; and the neuronal configuration of the LAA. Thrombus has a predilection to form in the LAA in patients with atrial fibrillation, mitral valve disease, and other conditions. The pathogenesis has not been fully elucidated; however, relative stasis which occurs in the appendage owing to its shape and the trabeculations within it is thought to play a major role. Obliteration or amputation of the LAA may help to reduce the risk of thromboembolism, but this may result in undesirable physiological sequelae such as reduced atrial compliance and a reduced capacity for ANF secretion in response to pressure and volume overload.

Atrial Appendage↗

The use of drugs for cardioversion of recent onset atrial fibrillation and flutter. Focus on ibutilide.

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.

Anti-Arrhythmia Agents↗

Accessory pathway reciprocating tachycardia.

Patients who have an accessory pathway (AP) of atrioventricular (AV) conduction may develop circus movement tachycardia otherwise known as atrioventricular re-entrant tachycardia (AVRT). Orthodromic AVRT is the most common form. It occurs as a result of antegrade conduction through the normal AV conduction system and retrograde conduction to the atria via the AP. Less commonly, conduction occurs in the opposite direction resulting in antidromic AVRT. Tachycardia may also involve multiple APs which may provide both antegrade and retrograde conduction and may alternate antegradely or retrogradely. Tachycardia may occur in which the AP simply acts as a bystander, and does not participate in the tachycardia mechanism. When atrial fibrillation is conducted to the ventricles via and AP, the resultant ventricular rate may be extremely rapid, placing the patient at risk of developing ventricular fibrillation and cardiac arrest. This paper reviews the anatomical and physiological substrates involved in the pathogenesis of AVRT. The acute and long-term management of patients who suffer from these arrhythmias will then be discussed. The normal AV annulus is composed exclusively of electrically inert fibrous tissue. The AV node and His bundle normally act as the sole route of electrical conduction. Accessory pathways occur at all points along the AV ring, and usually occur as isolated abnormalities, although a proportion of patients have associated congenital abnormalities. This is particularly true of right-sided APs. Most APs exhibit non-decremental conduction properties, and conduct faster than normal AV conduction tissue. In many patients with APs the surface ECG reveals clear evidence of pre-excitation, and a good idea of pathway localization is possible using one or more of several algorithms which have been developed. Patients with latent pre-excitation, intermittent pre-excitation, and patients with concealed APs have not evidence of pre-excitation on a proportion or all of Their surface ECGs. Patients present with a history of paroxysmal palpitations, often with associated symptoms such as chest discomfort Syncope is a rare presenting symptom. Unless bundle branch block is present, patients with orthodromic AVRT exhibit a narrow complex tachycardia on the surface ECG. Patients with pre-excited tachycardia including antidromic AVRT, and other forms of SVT in which the AP conducts to the ventricles as a bystander but does not participate in the tachycardias mechanism, present as broad complex tachycardias on the surface ECG which may be difficult to distinguish from ventricular tachycardia. Adenosine is increasingly used for this purpose since it is highly efficacious and has an extremely short half-life. Adenosine is also very useful in the diagnosis of broad-complex tachycardia, and in unmasking latent pre-excitation during sinus rhythm. Electrophysiology study in these patients is frequently performed at the same time as an attempt at catheter ablation; it aims to diagnose, localize and determine the functional characteristics of an AP, and to characterize the role of the pathway in tachycardia. AVRT can be reliably terminated by effective AV nodal blockade. Drug therapy for the prevention of AVRT is useful for temporary control whilst awaiting more definitive measures and in certain cases as long-term management. No class of drug stands out as 'therapy of choice', and physician preference, pro-arrhythmic effects and associated conditions need to be taken into account such that an individual choice can be made in each patient. The management of patients with AVRT has been revolutionized in recent years with the advent of catheter-based techniques for their cure. Whilst this method of treatment is highly effective and has low complication rates, pathways in particular locations such as the septal region remain challenging.

Anti-Arrhythmia Agents↗

Supraventricular tachycardia. ECG diagnosis and anatomy.

This paper reviews the anatomical substrates responsible for the induction and maintenance of supraventricular tachycardia and discusses the ECG findings associated with these tachycardias. The normal anatomy of the supraventricular conducting system, particularly within the atria, is complex with conduction proceeding along preferential pathway, which are in turn determined in part by the anisotropic properties of the atrial myocardium. There appear to be at least dual inputs to the atrioventricular node, a posteriorly situated slow pathway and an anterior fast pathway. It is sometimes possible to relate ECG findings directly to anatomical substrates; for example, in some cases of atrial tachycardia the site of the atrial focus (left or right, superior or inferior) can be determined by the polarity of the P wave. The anatomical substrates responsible for intra-atrial re-entry, atrial flutter and atrial fibrillation relate to anatomical barriers to impulse propagation and areas of slow conduction. In atrial flutter the crista terminalis, Eustachian valve, inferior vena cava, coronary sinus os, and tricuspid annulus have been identified as anatomical barriers to conduction around which a macro re-entrant circuit within the right atrium may conduct, usually in a counter-clockwise direction. Clockwise direction of conduction, and other mechanisms of tachycardia, occur in some of the less typical forms of atrial fluter. Atrial fibrillation is caused by multiple wavelets which randomly conduct through the atrial myocardium and are responsible for the irregular 'fibrillation waves' on the ECG. Supraventricular tachycardia presents as a narrow complex tachycardia unless pre-existing or rate-related bundle branch block is present. Less common causes for a broad complex tachycardia occurring in supraventricular tachycardia include an accessory atrioventricular or atriofascicular pathway conducting antegradely during tachycardia, or accessory pathway participation as a bystander during supraventricular tachycardia. ECG features which can help to distinguish between atrioventricular nodal re-entrant tachycardia and atrioventricular re-entrant tachycardia include: (1) the presence of a delta wave during sinus rhythm which is highly suggestive of atrioventricular re-entrant tachycardia as the mechanism of supraventricular tachycardia; (2) the finding of a pseudo s (lead II) or pseudo r' (lead V1) during tachycardia in atrioventricular nodal re-entrant tachycardia; (3) lengthening of the tachycardia cycle length in cases of atrioventricular re-entrant tachycardia when bundle branch block occurs ipsilateral to the accessory pathway and (4) the finding of QRS alternans during tachycardia which is suggestive of atrioventricular re-entrant tachycardia. "Long RP' tachycardia may be caused by an atrial tachycardia due to an inferiorly situated area of abnormal automaticity, atypical atrioventricular nodal re-entrant tachycardia with slow retrograde conduction, or atrioventricular re-entrant tachycardia with an accessory pathway conducting slowly from ventricle to atrium during tachycardia.

Atrioventricular Node↗

Tachycardia-induced atrial myopathy: an important mechanism in the pathophysiology of atrial fibrillation?

The atrial myocardium of patients with chronic atrial fibrillation (AF) is often abnormal in its histologic features and in its electrophysiologic properties. These abnormalities have been interpreted in some cases as the cause of AF and in others as a consequence of AF. We believe that both are the case. We will review the features of this atrial myopathy and discuss the likely mechanisms and consequences of the process.

Animals↗