[Thromboembolic risk factors in atrial flutter. Transesophageal echocardiographic study]. / Factores de riesgo tromboembólico en el flutter auricular. Estudio con ecocardiografía transesofágica.

BACKGROUND: The thromboembolic risk of atrial flutter (AFL) is not well defined. On the other hand, in atrial fibrillation (AF), the echocardiographic demonstration of thrombus or spontaneous echo contrast in the left atria or its appendage, a lower flow velocity in the left atrial appendage, and its reduced mobility, are well known risk factors of thromboembolism. AIM: To study the incidence of these echocardiographic risk factors in patients with AFL. MATERIAL AND METHODS: We prospectively studied 50 consecutive patients with AFL comparing them with two groups of patients with a well known increased risk of thromboembolism: 54 patients with AF and 24 patients with sinus rhythm and severe mitral stenosis (RSEMS). The group of patients with AFL was also compared with a control group of 27 patients with sinus rhythm and no increased risk of thromboembolism. In each group, we studied the presence of thrombi and spontaneous echo contrast in the left atria and left atrial appendage, emptying velocity (Vel A), filling flow (Vel B) and motility of the left atrial appendage and left atrial dimensions. RESULTS: When compared with control patients, AFL subjects had a higher incidence of spontaneous echo contrast in the left atria and left atrial appendage (11 and 42% respectively, p < 0.05); slower flow velocity in the left atrial appendage (Vel A 69.25 +/- 25 and 41 +/- 19 cm/s respectively, Vel B 55 +/- 16 and 46 +/- 20 cm/s respectively, p < 0.05); lower atrial appendage wall motility (4 and 84% respectively, p < 0.001) and a larger left atrium (40 +/- 10 and 45 +/- 0.6 mm respectively, p < 0.05). Patients with AFL had a lower incidence of echocardiographic abnormalities than subjects with AF or RSEMS. Thrombi were found in 2 patients with AFL, 12 patients with AF, 4 patients with RSEMS and in no control patient. CONCLUSIONS: In AFL, there are echocardiographic markers of increased thromboembolic risk in comparison with a control group. Nevertheless, the incidence of these factors is lower than in patients with AF or with RSEMS.

[When, why, and how to treat atrial fibrillation]. / Fibrilación auricular: por qué, cuándo y cómo tratarla.

Treatment of atrial fibrillation aims to convert it to sinus rhythm and maintain this rhythm after conversion, to reduce ventricular frequency when fibrillation is not converted and to prevent systemic embolies. Conversion to sinus rhythm is achieved with electrical cardioversion or with intravenous antiarrhythmic drugs (Lanatoside C, amiodarone or beta blockers). The most useful drugs to maintain sinus rhythm are amiodarone, quinidine alone or associated to verapamil, sotalol and propafenone. The best drug used to control cardiac frequency in a rapid atrial fibrillation is digitalis. However, when there is a decrease in vagal tone and an increase in sympathetic activity, digitalis losses its effectiveness and a betablocker or a calcium blocker must be added. Electrical cardioversion is the treatment of choice for atrial fibrillation of Wolff Parkinson White syndrome. When there is a rapid, symptomatic and uncontrollable atrial fibrillation, electrical ablation of atrio-ventricular junction and the implantation of a definitive pacemaker is the treatment of choice. Lately, a new procedure has been devised, called of the labyrinth, that can re-establish sinus rhythm, atrial contraction and atrio ventricular conduction. The embolic risk of atrial fibrillation depends on its etiology and the decision to anticoagulate must balance the risks and benefits of this treatment.

Role of endothelium-derived relaxing factor on coronary blood flow regulation in the dog.

The endothelium plays a key role in the regulation of vasoreactivity. To assess its importance on coronary flow regulation, we studied the participation of endothelium-derived relaxing factor-nitric oxide (EDRF-NO) on coronary reactive hyperemia and on the hyperemia that occurs secondary to an increase in myocardial oxygen consumption. In 15 dogs, the reactive hyperemic response decreased substantially after inhibition of EDRF-NO synthesis with N-omega-nitro-L-arginine (P < 0.01). In contrast, the hyperemia secondary to an increase in myocardial oxygen consumption, characterized by a linear correlation between myocardial oxygen consumption and coronary flow, did not change significantly after inhibition of EDRF-NO production (regression analysis, P > 0.1). Thus EDRF-NO synthesis by the endothelium is an important mechanism mediating the reactive hyperemic response but it does not seem to be essential for the metabolic regulation of coronary vascular resistance during hyperemia induced by an increased metabolic demand on the myocardium.

[Auricular fibrillation, systemic embolism and anticoagulant treatment]. / Fibrilación auricular, embolías sistémicas y tratamiento anticoagulante.

The risk of arterial embolism, specially cerebral, in patients with mitral stenosis associated atrial fibrillation is seventeen fold greater than that of the general population and five fold greater than that of non rheumatic atrial fibrillation. The usefulness of oral anticoagulant therapy in patients with atrial fibrillation and mitral stenosis is clear. In patients with non rheumatic atrial fibrillation, the controversy about its usefulness has been cleared with five recent reports showing a significant benefit or oral anticoagulation. We believe that these results may be applied to the routine management of these patients provided an adequate patient selection, consideration of contraindications and the use of a low anticoagulation range. Aspirin effectiveness in these patients is unsettled. One study showed benefits of 375 mg/day in patients younger than 75 years. The embolic risk in patients with atrial fibrillation must be stratified. High risk patients require the use of oral anticoagulation with an INR range between 3 and 4.5; those with medium risk require an INR between 2 and 3 and in some, aspirin use may be an alternative. When electrical cardioversion is indicated, oral anticoagulation must be used when atrial fibrillation has lasted for more than two days. In these cases, it is advisable to postpone cardioversion for three weeks after oral coagulation has started and to maintain this treatment for 3 or 4 additional weeks after cardioversion.