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      La cardioversión eléctrica en fibrilación auricular Translated title: Electrical cardioversion in atrial fibrillation

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          Abstract

          La cardioversión eléctrica para el tratamiento de la fibrilación auricular (FA) se introdujo en la década de los 60 y se mantiene actualmente como el tratamiento más efectivo y seguro para la conversión a ritmo sinusal. El método óptimo para la cardioversión eléctrica de la FA incluye tanto la selección del paciente adecuado como una técnica de cardioversión eléctrica apropiada. Los factores que han sido implicados en el éxito de la cardioversión eléctrica transtorácica incluyen aquéllos relacionados con: 1) la presencia de cardiopatía; 2) el habitus corporal del paciente; 3) la energía proporcionada; 4) la forma de onda eléctrica proporcionada, y 5) misceláneas. En vista de las consecuencias hemodinámicas y tromboembólicas, la conversión a ritmo sinusal puede esperarse que reduzca o suprima los síntomas y morbimortalidad asociadas con la FA. El éxito de la cardioversión eléctrica es alto de acuerdo al paciente seleccionado y la frecuencia de recurrencia inmediata o tardía postcardioversión puede ser alta y se requiere el uso de antiarrítmicos especialmente en presencia de comorbilidad como insuficiencia cardiaca o hipertensión descontrolada. El objetivo del tratamiento antiarrítmico concomitante es aumentar la posibilidad de éxito y prevenir las recurrencias, el cual debe considerarse de manera individual tomando en cuenta sobre todo el tiempo de evolución de la FA y la presencia y severidad de la cardiopatía. La posibilidad de cardioversión eléctrica exitosa en más probable en FA de corta duración y ausencia de cardiopatía.

          Translated abstract

          Electrical cardioversion for treatment of atrial fibrillation (AF) was introduced in the early 1960s and remains today as the most effective and safe treatment for conversion to sinus rhythm. The optimal method for electrical cardioversion of AF includes appropriate patient selection as well as an appropriate electrical cardioversion technique. Factors that have been implicated in the success of transthoracic electrical cardioversion include those associated with: 1) the presence of heart disease; 2) the patient body habitus; 3) the energy applied; 4) the electrical waveform supplied and 5) miscellaneous. In view of the hemodynamic and thromboembolic consequences, conversion to sinus rhythm can be expected to reduce or abolish symptoms and morbidity associated with AF. The success of electrical cardioversion is high according to selected patient and the frequency of immediate or delayed recurrence post-cardioversion may be high and require the use of antiarrhythmics, especially in the presence of co-morbidities like heart failure or uncontrolled hypertension. The objective of concomitant antiarrhythmic therapy is to increase the likelihood of success and prevent recurrences, which must be considered individually taking into account especially the duration of AF and the presence and severity of heart disease. The possibility of successful electrical cardioversion is more likely in AF of short duration and absence of heart disease.

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          Angiotensin II antagonist prevents electrical remodeling in atrial fibrillation.

          The blockade of angiotensin II (Ang II) formation has protective effects on cardiovascular tissue; however, the role of Ang II in atrial electrical remodeling is unknown. The purpose of this study was to investigate the effects of candesartan and captopril on atrial electrical remodeling. In 24 dogs, the atrial effective refractory period (AERP) was measured before, during, and after rapid atrial pacing. Rapid atrial pacing at 800 bpm was maintained for 180 minutes. The infusion of saline (n=8), candesartan (n=5), captopril (n=6), or Ang II (n=5) was initiated 30 minutes before rapid pacing and continued throughout the study. In the saline group, AERP was significantly shortened during rapid atrial pacing (from 149+/-11 to 132+/-16 ms, P<0.01). There was no significant difference in AERP shortening between the saline group and the Ang II group. However, in the candesartan and captopril groups, shortening of the AERP after rapid pacing was completely inhibited (from 142+/-9 to 147+/-12 ms with candesartan, from 153+/-15 to 153+/-14 ms with captopril, P=NS). Although rate adaptation of the AERP was lost in the saline group, this phenomenon was preserved in the candesartan and captopril groups. The inhibition of endogenous Ang II prevented AERP shortening during rapid atrial pacing. These results indicate for the first time that Ang II may be involved in the mechanism of atrial electrical remodeling and that the blockade of Ang II may lead to the better therapeutic management of human atrial fibrillation.
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            Role of prophylactic anticoagulation for direct current cardioversion in patients with atrial fibrillation or atrial flutter.

            The need for prophylactic anticoagulation to prevent embolism before direct current cardioversion is performed for atrial fibrillation or atrial flutter is controversial. To examine this issue further, a retrospective review was undertaken to assess the incidence of embolic complications after cardioversion. The review involved 454 elective direct current cardioversions performed for atrial fibrillation or atrial flutter over a 7 year period. The incidence rate of embolic complications was 1.32% (six patients); the complications ranged from minor visual disturbances to a fatal cerebrovascular event. All six patients had atrial fibrillation, and none had been on anticoagulant therapy (p = 0.026). The duration of atrial fibrillation was less than 1 week in five of the six patients who had embolic complications. Baseline characteristics of patients with a postcardioversion embolic event are compared with those of patients who did not have an embolic event. There was no difference in the prevalence of hypertension, diabetes mellitus or prior stroke between the two groups, and there was no difference in the number of patients who were postoperative or had poor left ventricular function. Left atrial size was similar between the two groups. No patient in the embolic group had valvular disease. No patient with atrial flutter had an embolic event regardless of anticoagulant status; therefore, anticoagulation is not recommended for patients with atrial flutter undergoing cardioversion. Prophylactic anticoagulation is pivotal in patients undergoing elective direct current cardioversion for atrial fibrillation, even those with atrial fibrillation of less than 1 week's duration.
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              Trandolapril reduces the incidence of atrial fibrillation after acute myocardial infarction in patients with left ventricular dysfunction.

              Studies have suggested that ACE inhibitors have an antiarrhythmic effect on ventricular arrhythmias. Whether they have an effect on atrial fibrillation is unknown. We investigated the effect of ACE inhibition with trandolapril on the incidence of atrial fibrillation in patients with reduced left ventricular function secondary to acute myocardial infarction. The patients in this study were those who qualified for inclusion into the TRAndolapril Cardiac Evaluation (TRACE) study, a randomized double-blind placebo-controlled study and who had sinus rhythm on the ECG obtained at randomization. Patients who fulfilled the criteria for inclusion were randomized to treatment with the ACE inhibitor trandolapril or placebo and were followed up for 2 to 4 years. Development and time to occurrence of atrial fibrillation in one 12-lead ECG recorded at the outpatient visits was the primary end point of this investigation. Of the 1749 patients included in the TRACE study, 1577 had sinus rhythm on the ECG recorded at randomization. Of these patients, 790 were randomized to trandolapril treatment and 787 to placebo treatment. The groups differed only slightly with respect to baseline characteristics. A total of 64 patients developed atrial fibrillation during the 2- to 4-year follow-up period. Significantly more patients developed atrial fibrillation in the placebo group than in the trandolapril group, 5.3% (n=42) versus 2.8% (n=22), respectively, P<0.05. Cox multivariable regression analysis, adjusting for important baseline characteristics, revealed that trandolapril treatment significantly reduced the risk of developing atrial fibrillation (RR, 0.45; 95% CI, 0.26 to 0.76; P<0.01). The results from the present study demonstrate that trandolapril treatment reduces the incidence of atrial fibrillation in patients with left ventricular dysfunction after acute myocardial infarction.
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                Author and article information

                Journal
                rmc
                Revista mexicana de cardiología
                Rev. Mex. Cardiol
                Asociación Nacional de Cardiólogos de México, Sociedad de Cardiología Intervencionista de México (México, DF, Mexico )
                0188-2198
                September 2012
                : 23
                : 3
                : 134-150
                Affiliations
                [01] orgnameInstituto Mexicano del Seguro Social orgdiv1UMAE Hospital de Cardiología, Centro Médico Nacional Siglo XXI orgdiv2Servicio de Electrofisiología
                Article
                S0188-21982012000300003 S0188-2198(12)02300300003
                4f6de98e-f1d2-4554-87e2-7914460d06c1

                This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License.

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                transthoracic impedance,atrial fibrillation,Electrical cardioversion,corriente directa,desfibrilación de onda bifásica,desfibrilación de onda monofásica,impedancia transtorácica,fibrilación auricular,Cardioversión eléctrica,biphasic defibrillation,monophasic defibrillation,direct current

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