- Email: [email protected]
Effects of acute atrial dilatation on heterogeneity in conduction and arrhythmia vulnerability in the human atrium
Abstracts / Journal of Electrocardiology 44 (2011) e1–e64 Background: In patients with ST-elevation myocardial infarction (STEMI), presence of microvascular obstruction (MVO) confers a higher risk of left ventricular dysfunction, adverse left ventricular remodeling and clinical outcomes. We compared 2 different measures of ST-segment recovery for prediction of MVO following primary percutaneous coronary intervention (PPCI) for STEMI. Methods: A total of 144 patients were included in a post hoc analysis of the Efficacy of FX06 in Ischemia-Reperfusion Injury trial. Microvascular obstruction determined by contrast-enhanced cardiac magnetic resonance imaging at 5 to 7 days after the index event. Electrocardiograms obtained at baseline and 90 minutes after PPCI. Two methods for calculating and categorizing ST-segment recovery were used: (1) sum ST-segment deviation (STD) resolution (percent resolution of STD from baseline to post-PCI) analyzed in 3 categories (70%, 30% to b70%, 30%); (2) worst-lead residual STD (the absolute magnitude of residual STD in the most affected lead on the post-PCI ECG, without reference to the baseline ECG) analyzed in 3 categories (b1, 1 to b2, and ≥2 mm). Results: For prediction of MVO, worst-lead residual defined the highest risk group (Table 1). In addition, this group was more than twice as large as the highest risk group defined by STD resolution. By multivariable logistic regression analysis, STD resolution was not associated with presence of MVO (adjusted for age, sex, infarct location, TIMI flow, time to therapy). In same analysis, worst-lead residual STD of 2 mm or greater was strongly associated with presence of MVO (odds ratio [95% confidence interval], 9.2 [2.5-33.4]; P = .001). Conclusion: Following PPCI, worst-lead residual STD defines a wider spectrum of risk for MVO than STD resolution, and worst-lead residual 2 mm or greater at 90 minutes is strongly associated with MVO determined by CMR. doi:10.1016/j.jelectrocard.2010.12.069
O62 Effects of acute atrial dilatation on heterogeneity in conduction and arrhythmia vulnerability in the human atrium Flavia Ravelli a, Michela Masè a, Maurizio Del Greco b, Massimiliano Marini b, Marcello Disertori b a Department of Physics, University of Trento, Povo - Trento, Italy b Division of Cardiology, S. Chiara Hospital, Trento, Italy Introduction: The mechanisms by which atrial stretch favors the development of a substrate for atrial fibrillation (AF) are not fully understood. Although several experimental and clinical studies have investigated the effect of stretch on atrial refractoriness, only few experimental studies have been performed to investigate its effects on atrial conduction properties. In the present study, the role of stretch-induced conduction changes in the creation of a substrate for atrial fibrillation was investigated by quantifying the spatial distribution of local conduction velocities in the human right atrium during acute atrial dilatation. Methods: Ten patients (6 men; age, 55 ± 15 years) undergoing clinically indicated electrophysiological studies were studied. An electroanatomical mapping of the right atrium was performed during coronary sinus pacing in control condition and during acute atrial dilatation. Atrial stretch was obtained by simultaneous atrioventricular (AV) pacing at a cycle length of 450 to 500 milliseconds. Local conduction velocities (CVs) in the direction of wavefront propagation were accurately estimated applying the principle of triangulation and spatially mapped over the whole right atrial endocardial surface. Results: Simultaneous AV pacing significantly increased right atrial volume from 72 ± 29 to 86 ± 31 mL (P b .001). This 23% increase in atrial volume determined an overall decrease in atrial conduction velocity from 65.8 ± 5.9 to 55.2 ± 7.2 cm/s (P b .001) and an increased heterogeneity in atrial conduction, characterized by a higher incidence of slow conduction and local conduction blocks (CV b30 cm/s) from 10% ± 4% to 16% ± 8% (P b .01). Acute atrial dilatation by simultaneous AV pacing increased AF vulnerability, with 6 of 10 patients developing AF episodes during the stretch condition. Conclusion: Quantification of stretch-induced conduction changes in the human atrium is feasible by the combined use of simultaneous AV pacing and CV map construction. Acute atrial dilatation of the human atrium resulted in a
e25
slowing of conduction and in a significant increase in vulnerability to AF. These stretch-related changes in atrial conduction are likely to be an important factor in the creation of a substrate for atrial fibrillation. doi:10.1016/j.jelectrocard.2010.12.070
O63 Evaluation of anesthetic effects with propofol during atrial fibrillation Raquel Cervigón a, Javier Moreno b, Julián Pérez-Villacastín b, José Millet c, Francisco Castells c a Universidad de Castilla-La Mancha, Spain b Hospital Clínico San Carlos, Spain c Universitat Politècnica de València, Spain Background: The effects of the autonomic nervous system (ANS) on atrial fibrillation (AF) have been reported in previous studies such as circadian rhythms and stress tests. On the hand, previous to an AF ablation procedure, an anesthetic agent (usually propofol) is given to the patients for procedural sedation. Because propofol affects the ANS, this study, attemps to respond if propofol exerts any significant influence on AF. Methods: The study includes 27 AF patients (21 paroxysmal AF and 6 persistent AF) submitted to an AF ablation procedure. Previous to the ablation procedure, propofol was administered to each patient. Recordings were acquired both in basal state and under the effects of propofol. For each patient, a set of 12 intra-atrial recordings (at the right atrium [RA], left atrium [LA], and septum) and 3 surface electrocardiograms (ECGs) were registered. The effects of propofol were evaluated using different parameters: (1) dominant rate of the atrial electrical activity, (2) Shannon entropy, (3) delay and synchronization indexes between adjacent sites, and (4) atrioventricular conduction ratio (in terms of the ratio between the atrial rate at the septum and the RR rate). These parameters were computed at both RA and LA and compared before and after propofol infusion. Results: The dominant atrial rate exhibited a slight but significative decrease in the RA from 5.85 ± 0.54 Hz in basal to 5.71 ± 0.61 Hz during propofol infusion (P = .045). However, no significative differences were found in the LA. The Shannon entropy showed a downward trend in the RA (ie, more organized) from 3.56 ± 0.19 to 3.51 ± 0.19 and an upward trend in the LA from 3.62 ± 0.19 to 3.67 ± 0.16 (P = .001). Furthermore, the delay index decreased in the RA from 33.56 ± 16.51 to 26.61 ± 10.32 milliseconds but increased in the LA from 27.32 ± 11.34 to 31.19 ± 15.17 milliseconds (P = .018). Consistently, the synchronization index increased in the RA from 0.58 ± 0.27 to 0.69 ± 0.20, whereas decreased in the LA from 0.67 ± 0.21 to 0.62 ± 0.28 (P = .022). Finally, the mean RR interval decreased from 579 ± 140 to 554 ± 131 milliseconds (P = .045), and the atrioventricular conduction ratio decreased from 3.31 ± 0.83 to 3.17 ± 0.75 (P = .033). Conclusion: This study shows that propofol causes opposite effects on the RA and LA. Specifically, the atrial electrical activity at the RA becomes more organized, whereas at the LA, it becomes more disorganized. Although only slight differences were observed, the fact that all parameters behaved consistently reinforces this conclusion. This study may contribute to a better knowledge about the effects of the ANS on the electrophysiological properties during AF. doi:10.1016/j.jelectrocard.2010.12.071
O64 A new algorithm for estimating the atrial activity in the frequency domain Raul Llinares a,b, Jorge Igual a,b, Julio Miro-Borras a,b, Andres Camacho a,b a Universidad Politecnica de Valencia, Valencia, Spain b Departamento de Comunicaciones, Spain Background: In this work, we present a fixed point algorithm to extract the atrial rhythm in atrial tachyarrhythmias from the surface 12-leads electrocardiogram (ECG).
O62 Effects of acute atrial dilatation on heterogeneity in conduction and arrhythmia vulnerability in the human atrium Flavia Ravelli a, Michela Masè a, Maurizio Del Greco b, Massimiliano Marini b, Marcello Disertori b a Department of Physics, University of Trento, Povo - Trento, Italy b Division of Cardiology, S. Chiara Hospital, Trento, Italy Introduction: The mechanisms by which atrial stretch favors the development of a substrate for atrial fibrillation (AF) are not fully understood. Although several experimental and clinical studies have investigated the effect of stretch on atrial refractoriness, only few experimental studies have been performed to investigate its effects on atrial conduction properties. In the present study, the role of stretch-induced conduction changes in the creation of a substrate for atrial fibrillation was investigated by quantifying the spatial distribution of local conduction velocities in the human right atrium during acute atrial dilatation. Methods: Ten patients (6 men; age, 55 ± 15 years) undergoing clinically indicated electrophysiological studies were studied. An electroanatomical mapping of the right atrium was performed during coronary sinus pacing in control condition and during acute atrial dilatation. Atrial stretch was obtained by simultaneous atrioventricular (AV) pacing at a cycle length of 450 to 500 milliseconds. Local conduction velocities (CVs) in the direction of wavefront propagation were accurately estimated applying the principle of triangulation and spatially mapped over the whole right atrial endocardial surface. Results: Simultaneous AV pacing significantly increased right atrial volume from 72 ± 29 to 86 ± 31 mL (P b .001). This 23% increase in atrial volume determined an overall decrease in atrial conduction velocity from 65.8 ± 5.9 to 55.2 ± 7.2 cm/s (P b .001) and an increased heterogeneity in atrial conduction, characterized by a higher incidence of slow conduction and local conduction blocks (CV b30 cm/s) from 10% ± 4% to 16% ± 8% (P b .01). Acute atrial dilatation by simultaneous AV pacing increased AF vulnerability, with 6 of 10 patients developing AF episodes during the stretch condition. Conclusion: Quantification of stretch-induced conduction changes in the human atrium is feasible by the combined use of simultaneous AV pacing and CV map construction. Acute atrial dilatation of the human atrium resulted in a
e25
slowing of conduction and in a significant increase in vulnerability to AF. These stretch-related changes in atrial conduction are likely to be an important factor in the creation of a substrate for atrial fibrillation. doi:10.1016/j.jelectrocard.2010.12.070
O63 Evaluation of anesthetic effects with propofol during atrial fibrillation Raquel Cervigón a, Javier Moreno b, Julián Pérez-Villacastín b, José Millet c, Francisco Castells c a Universidad de Castilla-La Mancha, Spain b Hospital Clínico San Carlos, Spain c Universitat Politècnica de València, Spain Background: The effects of the autonomic nervous system (ANS) on atrial fibrillation (AF) have been reported in previous studies such as circadian rhythms and stress tests. On the hand, previous to an AF ablation procedure, an anesthetic agent (usually propofol) is given to the patients for procedural sedation. Because propofol affects the ANS, this study, attemps to respond if propofol exerts any significant influence on AF. Methods: The study includes 27 AF patients (21 paroxysmal AF and 6 persistent AF) submitted to an AF ablation procedure. Previous to the ablation procedure, propofol was administered to each patient. Recordings were acquired both in basal state and under the effects of propofol. For each patient, a set of 12 intra-atrial recordings (at the right atrium [RA], left atrium [LA], and septum) and 3 surface electrocardiograms (ECGs) were registered. The effects of propofol were evaluated using different parameters: (1) dominant rate of the atrial electrical activity, (2) Shannon entropy, (3) delay and synchronization indexes between adjacent sites, and (4) atrioventricular conduction ratio (in terms of the ratio between the atrial rate at the septum and the RR rate). These parameters were computed at both RA and LA and compared before and after propofol infusion. Results: The dominant atrial rate exhibited a slight but significative decrease in the RA from 5.85 ± 0.54 Hz in basal to 5.71 ± 0.61 Hz during propofol infusion (P = .045). However, no significative differences were found in the LA. The Shannon entropy showed a downward trend in the RA (ie, more organized) from 3.56 ± 0.19 to 3.51 ± 0.19 and an upward trend in the LA from 3.62 ± 0.19 to 3.67 ± 0.16 (P = .001). Furthermore, the delay index decreased in the RA from 33.56 ± 16.51 to 26.61 ± 10.32 milliseconds but increased in the LA from 27.32 ± 11.34 to 31.19 ± 15.17 milliseconds (P = .018). Consistently, the synchronization index increased in the RA from 0.58 ± 0.27 to 0.69 ± 0.20, whereas decreased in the LA from 0.67 ± 0.21 to 0.62 ± 0.28 (P = .022). Finally, the mean RR interval decreased from 579 ± 140 to 554 ± 131 milliseconds (P = .045), and the atrioventricular conduction ratio decreased from 3.31 ± 0.83 to 3.17 ± 0.75 (P = .033). Conclusion: This study shows that propofol causes opposite effects on the RA and LA. Specifically, the atrial electrical activity at the RA becomes more organized, whereas at the LA, it becomes more disorganized. Although only slight differences were observed, the fact that all parameters behaved consistently reinforces this conclusion. This study may contribute to a better knowledge about the effects of the ANS on the electrophysiological properties during AF. doi:10.1016/j.jelectrocard.2010.12.071
O64 A new algorithm for estimating the atrial activity in the frequency domain Raul Llinares a,b, Jorge Igual a,b, Julio Miro-Borras a,b, Andres Camacho a,b a Universidad Politecnica de Valencia, Valencia, Spain b Departamento de Comunicaciones, Spain Background: In this work, we present a fixed point algorithm to extract the atrial rhythm in atrial tachyarrhythmias from the surface 12-leads electrocardiogram (ECG).