Restoring sinus rhythm in atrial fibrillation: a Pyrrhic victory?
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Publications and source records attributed to Iqwal Mangat.
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The purpose of this study was to show that multipolar electrographic recordings along the subeustachian isthmus (SI) can better differentiate slow conduction from complete isthmus block after atrial flutter ablation, leading to a lower incidence of recurrent atrial flutter (Afl). Despite the presence of various techniques to identify bidirectional conduction block (BDB) after isthmus ablation for typical Afl, several studies, including a report from a national registry, suggest that radiofrequency ablation is still associated with a 15% recurrence rate. Thus, techniques that can distinguish slow conduction from complete isthmus block have the potential for reducing long-term recurrences. We evaluated patients who underwent radiofrequency ablation for typical isthmus-dependent Afl. Patients were separated into 2 groups. Group A underwent assessment of BDB with conventional methods. In group B, BDB was assessed by placing a multipolar catheter along the floor of the SI, pacing adjacent to the line of radiofrequency application, and assessing electrographic activation on either side. One hundred thirty-one cases of Afl ablation were analyzed (86 in group A, 45 in group B). Over a mean follow-up period of 17 months, recurrence rates of Afl were 16.5% in group A and 4.3% in group B (p = 0.043). Thus, assessment of BDB by placement of a multipolar catheter across the SI after ablation of typical Afl is associated with a significant reduction in long-term recurrence of Afl.
The purpose of this study was to explore the mechanisms of conversion from atypical atrial flutter (AFL) to atrial fibrillation (AF), and the long-term results of cavotricuspid isthmus ablation in these patients. We retrospectively reviewed the records of 221 patients with typical AFL referred to our hospital for ablation. A total of 25 patients had atypical AFL, and cavotricuspid isthmus ablation was performed in 23 with isthmus-dependent atypical AFL, as well as in 180 patients with typical counterclockwise and/or clockwise AFL. In all, 13 spontaneous transitions from atypical AFL to AF were documented in 11 of 17 patients. Before AF, a pattern of lower loop reentry was observed in 11 of 13 patients (85%) and upper loop reentry in 3 (1 had both). Multiple early breaks along the tricuspid annulus during AFL were noted in 6 of 13 patients (46%). Among the 13 transitions, discrete atrial premature complexes before AF were found in 5 patients with lower loop reentry and in 1 with upper loop reentry (46%). In the remaining patients, a more rapid atrial rhythm was involved in the development of AF with a pulmonary venous focus in 2. In some cases, additional "breaks" in the functional line of block occurred before the development of AF. There was a significant increased incidence of AF (68%) in those with atypical AFL compared with those with typical AFL (38%) (p = 0.004). After a mean follow-up of 28 +/- 9 months for the atypical group and 18 +/- 11 months for the typical group, the AF recurrence rate was similar (57% vs 48%, p = 0.4). Discrete atrial premature complexes or atrial tachycardia may initiate AF either directly or by producing further breaks in lines of functional block. Bidirectional cavotricuspid isthmus block is associated with cure or control of AF in approximately 50% of patients with AFL.
Many patients with atrial fibrillation develop symptoms attributable to the cardiac arrhythmia itself. These symptoms may be improved either by restoring sinus rhythm or by controlling the rapid and irregular ventricular response that often accompanies this arrhythmia. One of the principal goals of therapy of atrial fibrillation management is improvement of patient symptoms; it is important to quantify these symptoms by some form of quality of life analysis. The Canadian Trial of Atrial Fibrillation (CTAF) was a multi-centre randomized clinical trial of amiodarone compared with either propafenone or sotalol in patients with recent atrial fibrillation. The quality of life (QOL) substudy of CTAF was a prospective, comprehensive assessment of quality of life of patients enrolled in CTAF. Summary measures of physical and mental health on the generic QOL scale (SF-36) improved significantly with treatment from baseline to 3 months (41.9 +/- 9.6 to 43.7 +/- 9.2, p = 0.001 for the physical component and 47.5 +/- 10.4 to 49.0 +/- 9.8, p = 0.023 for the mental component). On an arrhythmia specific scale (SCL), a significant and larger improvement was noted from baseline to 3 months in both arrhythmia symptom frequency and severity (symptom frequency from 20.4 +/- 9.4 to 16.2 +/- 9.5, symptom severity from 16.7 +/- 8.2 to 12.9 +/- 7.6, both p < 0.001). The quality of life improvements were similar in the amiodarone group compared to the sotalol or propafenone groups, both for the SF-36 and the disease-specific symptom checklist (SCL) measures. In contrast, an atrial fibrillation severity scale (AFSS) did show differences between the assigned drug therapies, which were associated with different rates of arrhythmia recurrence in the parent study. By 3 months global well-being was significantly worse for patients who had recurrent atrial fibrillation compared to those who did not (6.9 +/- 1.8 versus 7.4 +/- 1.8, p = 0.04). Similarly, symptom severity at 3 months was 11.8 +/- 7.4 for patients without recurrence, compared to 14.8 +/- 7.4 for those with recurrence ( p = 0.001). Interestingly, none of the usual clinical variables that might be perceived to be associated with quality of life, e.g., male versus female sex, age, NYHA class, beta blocker use, and ejection fraction, had much impact on subjective quality of life measures. Quality of life improves with treatment atrial fibrillation and at least some of these improvements are related to the restoration and maintenance of sinus rhythm.
Amiodarone is one of the most frequently used antiarrhythmic drugs in clinical practice. In patients with atrial fibrillation, in whom rhythm control is judged desirable, amiodarone is the most effective therapy. Amiodarone effectively prevents atrial fibrillation and may improve quality of life, but there is no evidence that it decreases mortality or severe morbidity in atrial fibrillation. In patients at risk for life-threatening ventricular arrhythmias, amiodarone may decrease mortality to a small degree, but the evidence for this benefit is incomplete. Patients with implantable cardioverter defibrillators frequently require antiarrhythmic drug therapy, especially to treat electrical storm. Amiodarone is useful in these patients; however, it may increase defibrillation thresholds in some patients. In patients with out-of-hospital DC shock-resistant VF, amiodarone is the most effective antiarrhythmic drug available to assist in resuscitation. Amiodarone is a complicated drug, and its optimal use requires careful patient surveillance with respect to potential adverse effects.
BACKGROUND: Population studies have identified the presence of bundle branch block (BBB) as a risk factor for increased mortality in patients with known cardiac disease. It is unknown how chronic ventricular dyssynchrony resulting solely from conduction delay affects ventricular function. METHODS AND RESULTS: Subjects were retrospectively identified from the University of California, San Francisco, electrocardiogram database with QRS prolongation. Subjects who had no evidence of heart disease and had baseline and serial studies evaluating ongoing risk of coronary artery disease status and left ventricular function were followed over time. Documentation of a minimum of 2 serial evaluations of cardiac status were present in a total of 51/176 (20%) subjects with isolated BBB who constitute the study population. After a mean follow-up of 52 +/- 45 months-adjusting for differences due to age, sex, the presence of hypertension, hyperlipidemia, and diabetes mellitus-left ventricular ejection fraction diminished by -7.3 +/- 12% per year in the isolated left BBB cohort versus -1.9 +/- 4% in isolated right BBB cohort and -1.1 +/- 3% reduction in the isolated nonspecific intraventricular conduction delay cohort (P =.019). CONCLUSIONS: Left bundle branch block itself may be a cause of ventricular dysfunction.