心房肌复极的电整复性与阵发性心房颤动发生机制的实验研究

目的 研究在体犬左、右心房肌的电整复性即动作电位时程整复性(APDR),观察其与阵发性心房颤动(房颤)发生的潜在机制.方法 使用单相动作电位技术记录14只犬左、右心房复极达90%的动作电位时程(APD_(90)),并通过S_1S_2程序刺激,观察APDR变化,即每一个舒张间期与刺激后发生心房肌复极APD_(90)的关系,并观察房颤的诱发情况.结果 APD_(90)左心房为(157.4±43.5)ms明显小于右心房(170.9±37.9)ms,P<0.05.心房肌在S_1S_2递减程序刺激下,左心房与右心房具有不同斜率的APDR曲线,左心房的APDR曲线斜率1.3±0.4大于右心房0.9±0.3,P<0.05.进行心房快速起搏S_1S_2刺激时,14只犬中共诱发出18阵房颤,其中左心房刺激发作12阵,明显多于右心房6阵(P<0.05).结论 左、右心房间具有单相动作电位时程的异质性及APDR不均一的复极特性,是诱发折返、发生和维持房颤的基质之一.     

Monophasic action potentials of the right atrium in patients with paroxysmal atrial fibrillation

To investigate the mechanism of atrial fibrillation (AF), monophasic action potentials (MAPs) from the atrial myocardium were studied in 7 patients with paroxysmal AF (PAF) and in 7 control individuals. The MAPs were recorded using a contact catheter during sinus rhythm and continuous pacing at the high right atrium (HRA) with pacing cycle lengths of 600, 500 and 400 ms. MAPs were obtained from 6 sites in each participant. The MAPD90 was measured from onset to 90% of MAP repolarization. Average, maximal and minimal MAPD90 (avMAPD90, maxMAPD90 and minMAPD90) were obtained from all participants. The dispersion of MAPD90 (dispMAPD90) was defined as the difference between maxMAPD90 and minMAPD90. The width of each atrial potential (WAP) and the wavelength index (WLI=MAPD90/WAP) were determined. Average, maximal and minimal WLI (avWLI, maxWLI and minWLI) were obtained from all participants. The avMAPD90 and maxMAPD90 did not significantly differ between the 2 groups. The minMAPD90 in the PAF group was significantly smaller than that in the control group at HRA pacing with cycle lengths of 500 and 400 ms (210+/-18ms vs 245+/-14 ms, p<0.05; 207+/-23 ms vs 238+/-20 ms, p<0.05; respectively). The dispMAPD90 was significantly longer in the PAF group than in the control group during sinus and HRA pacing. The WAP value did not differ between the 2 groups. The minWLI in the PAF group was significantly smaller than that in the control group at HRA pacing with cycle lengths of 500 and 400 ms (3.3+/-0.5 vs 3.8+/-0.3, p<0.05; 3.2+/-0.4 vs 3.7+/-0.3, p<0.02). A shortened and widened dispersion of atrial refractoriness may play an important role in the genesis of AF. Furthermore, smaller wavelengths may form in the atrium of patients with PAF.     

心房肌易损性与阵发性心房颤动的发生机制

目的探讨左、右心房肌复极,及其易损性与阵发性心房颤动(AF)的发生与维持机制。方法应用单相动作电位(MAP)技术记录14只犬左、右心房肌的复极达90%动作电位时程(APD90),通过S1S2程序刺激,同时记录心房有效不应期(ERP)及相对不应期(RRP),观察反复心房激动(RAF,在S1S2的早搏刺激后,发生2个以上的连续心房活动,从心房刺激到RAF第一个激动的间期必须小于250 ms)及AF的诱发。结果14只犬S1S2间期递减至130±32 ms时,可出现RAF,随后当S1S2间期缩短为110±28 ms时AF发作。AF发作前大多数可记录到RAF(66.7%);共诱发出15阵RAF,左房11阵,右房4阵,左房RAF的发生率明显多于右房(P<0.05);共诱发出18阵AF,左房诱发出12阵,右房诱发出6阵。左房的AF诱发率明显多于右房(P<0.05)。结论AF发作前多伴有RAF发作;RAF是易发生阵发性AF的特征性表现,代表心房的易损性;左右心房易损性不同。     

Sotalol reverses remodeled action potential in patients with chronic atrial fibrillation but does not prevent arrhythmia recurrence

INTRODUCTION: Recurrence of atrial fibrillation (AF) may be related to AF-induced electrical remodeling characterized by shortening of the atrial action potential duration (APD) and loss of its rate adaptation. We investigated the effects of pretreatment with oral d,l-sotalol on rate-dependent changes in atrial monophasic action potential (MAP) duration after cardioversion of chronic AF with reference to the efficacy in preventing the arrhythmia recurrence. METHODS AND RESULTS: MAPs were recorded from the right atrium at six pacing cycle lengths (CLs) from 300 to 750 ms in 19 chronic AF patients after electrical cardioversion; 9 had been pretreated with oral d,l-sotalol (196 +/- 42 mg/day) for 7 days and 10 were untreated. MAP duration at 90% repolarization (MAPD90) in 11 control patients increased progressively with increases in CLs from 209 +/- 19 ms at CL = 300 ms to 264 +/- 28 ms at CL = 750 ms. In AF patients without sotalol, the CL-MAPD relation was shifted downward and flattened at longer CLs; MAPD90 values were 206 +/- 11 ms and 227 +/- 16 ms at CLs of 300 and 750 ms, respectively. MAPD90 values at CLs > or =500 ms in AF were significantly shorter than controls. In AF patients with sotalol, the normal CL-MAPD relation was preserved; MAPD90 increased from 226 +/- 19 ms to 282 +/- 46 ms in the CL range. AF recurred within 2 weeks after cardioversion in 14 of 24 patients pretreated with d,l-sotalol (216 +/- 51 mg/day) despite of continuation of sotalol treatment. CONCLUSION: Sotalol reverses AF-induced decrease in MAPD adaptation to rate in the atria of chronic AF patients, but this effect does not lead to prevention of AF recurrence.     

Monophasic action potential mapping in human subjects with normal electrocardiograms: direct evidence for the genesis of the T wave

T wave concordance in the normal human electrocardiogram (ECG) generally is explained by assuming opposite directions of ventricular depolarization and repolarization; however, direct experimental evidence for this hypothesis is lacking. We used a contact electrode catheter to record monophasic action potentials (MAPs) from 54 left ventricular endocardial sites during cardiac catheterization (seven patients) and a new contact electrode probe to record MAPs from 23 epicardial sites during cardiac surgery (three patients). All patients had normal left ventricular function and ECGs with concordant T waves. MAP recordings during constant sinus rhythm or right atrial pacing were analyzed for activation time (AT) = earliest QRS deflection to MAP upstroke, action potential duration (APD) = MAP upstroke to 90% repolarization, and repolarization time (RT) = AT plus APD. AT and APD varied by 32 and 64 msec, respectively, over the left ventricular endocardium and by 55 and 73 msec, respectively, over the left ventricular epicardium. On a regional basis, the diaphragmatic and apicoseptal endocardium had the shortest AT and the longest APD, and the anteroapical and posterolateral endocardium had the longest AT and the shortest APD (p less than .05 to less than .0001). RT was less heterogeneous than APD, and no significant transventricular gradients of RT were found. In percent of the simultaneously recorded QT interval, epicardial RT ranged from 70.8 to 87.4 (mean 80.7 +/- 3.9) and endocardial RT ranged from 80 to 97.8 (mean 87.1 +/- 4.4) (p less than .001).(ABSTRACT TRUNCATED AT 250 WORDS)     

High-density activation mapping of fractionated electrograms in the atria of patients with paroxysmal atrial fibrillation

BACKGROUND: Areas of complex fractionated atrial electrograms (CFAEs) have been implicated in the atrial substrate of atrial fibrillation (AF). The mechanisms underlying CFAE in humans are not well investigated. OBJECTIVES: The purpose of this study was to investigate the regional activation pattern associated with CFAE using a high-density contact mapping catheter. METHODS: Twenty patients with paroxysmal AF were mapped using a high-density multielectrode catheter. CFAE were mapped at 10 different sites (left atrium [LA]: inferior, posterior, roof, septum, anterior, lateral; right atrium [RA]: anterior, lateral, posterior, septum). Local atrial fibrillation cycle length (AFCL) was measured immediately before and after the occurrence of CFAE, and the longest electrogram duration (CFAEmax) was assessed. RESULTS: Longer electrogram durations were recorded in the LA compared with the RA (CFAEmax 118 +/- 21 ms vs 104 +/- 23 ms, P = .001). AFCL significantly shortened before the occurrence of CFAEmax compared with baseline (LA: 174 +/- 32 ms vs 186 +/- 32 ms, P = .0001; RA: 177 +/- 31 ms vs 188 +/- 31 ms, P = .0001) and returned to baseline afterwards. AFCL shortened by >or=10 ms in 91% of mapped sites. Two different local activation patterns were associated with occurrence of CFAEmax: a nearly simultaneous activation in all spines in 84% indicating passive activation, and a nonsimultaneous activation sequence suggesting local complex activation or reentry. CONCLUSION: Fractionated atrial electrograms during AF demonstrate dynamic changes that are dependent on regional AFCL. Shortening of AFCL precedes the development of CFAE; thus, cycle length is a major determinant of fractionation during AF. High-density mapping in AF may help to differentiate passive activation of CFAE from CFAE associated with an active component of the AF process.     

Dispersion of refractoriness in patients with paroxysmal atrial fibrillation. Evaluation with simultaneous endocardial recordings from both atria

This article studies the role of dispersion of atrial refractoriness (DAR) in the genesis of atrial fibrillation (AF). A 20-polar Halo catheter or a 40-polar basket catheter was placed in the right atrium and a 10-polar catheter in the coronary sinus in 21 patients with paroxysmal AF. Bipolar electrograms during AF were recorded from 7 to 16 sites in both atria. As control, electrograms during AF induced by extra-stimulation or burst pacing were also recorded from 4 to 14 sites in both atria in 12 patients with supraventricular tachycardias but without history of AF. The local atrial fibrillation intervals (AFI) during a period of 10 s or 20 s were measured and the mean, median and the 5th, 10th and 15th percentile AFIs at each site were calculated as estimates of the local effective refractory period (AERP). The maximum dispersion and variance of the estimated AERP among the 7-16/4-14 sites were used as measures of the DAR. The maximum dispersion and variance of the 5th and 10th percentile AFIs were significantly greater in the AF group than those in the control group, which were mainly due to the shortening of the minimum 5th and 10th percentile AFIs. No significant differences in dispersion and variance of the mean and median AFIs were shown between the 2 groups. The dispersion and variance of atrial refractoriness during AF estimated from the measurement of short AFIs were significantly greater in patients with paroxysmal AF than in those without clinical AF. The increased dispersion of refractoriness in patients with AF was mainly due to the shortening of the minimum AFIs. These findings suggest the involvement of an increased dispersion of atrial refractoriness in the genesis of paroxysmal AF.     

Immediate recurrence of atrial fibrillation after internal cardioversion: importance of right atrial conduction variations

This study investigates the importance of right atrial conduction features in predicting of immediate recurrence of atrial fibrillation (AF) after internal cardioversion (IC). Patients with chronic AF who were resistant to external cardioversion were studied. Twenty-four patients (16 female, 8 male mean age 58 +/- 7 years) who were successfully converted to sinus rhythm (SR) by IC, and experienced recurrence of AF within 1 minute of restoration of SR were enrolled in group A. Thirty-four patients, who were converted to SR by IC and in whom SR was maintained at least 1 minute after IC, were enrolled in group B (24 female, 10 male mean age 56 +/- 6 years) as control. There was no difference in age, left atrial diameter, use of antiarrhythmic drug, etiology and duration of AF between the groups. After successful IC, His bundle electrocardiograms via placed electrode catheters, and surface electrocardiograms were recorded for 1 minute. P-A interval duration, as a marker of right atrial conduction, was measured from the onset of the earliest registered surface P wave to the onset of the atrial deflection on His-bundle catheter recording. The difference between the recorded maximum P-A duration and minimum P-A duration obtained in 1 minute after IC was described as P-A interval absolute difference. There were no differences in the maximum P-A duration and minimum P-A duration between two groups. But, the P-A absolute difference was more pronounced in group A compared to group B (16.9 +/- 7.7 ms versus 10.3 +/- 6.4 ms, P < .001) and was significantly correlated with P wave dispersion derived from the surface electrocardiogram (r = .72, P < .001) In conclusion, variations in right atrial conduction might play an important role in predicting immediate recurrence of AF in patients converted to SR by IC.     

Recording of the right atrial monophasic action potential in humans. I. Subjects not affected by arrhythmia

Using a bipolar suction electrode technique, right atrial monophasic action potential (RA MAP) was recorded in 18 patients surely free from any kind of arrhythmia. Two morphologically different kinds of RA AMP were obtained: the former exhibiting an evident transition between phase 1-2 (plateau) and phase 3 of repolarization (FP), the latter without any appreciable palteau (FL). Electrophysiological properties of human myocardial atrial tissue have been investigated by microelectrode technique. The two types of MAP recorded by us resemble the former the action potential obtained from conducting specialized fiber, the latter the action potential of contractile fibers. A statistically significant difference in RA MAP duration measured at 90% level of repolarization (D 90%) was found between the two kinds of MAP: therefore we suggest to perform quantitative evaluations and pharmaco-ogical investigations only including MAPs of similar morphology. The intraindividual variation coefficient of D 90% may be considered an expression of the range of variability of repolarization duration in man; we suggest that only MAPs of similar configuration should be accepted for its calculation in order to avoid errors of evaluation.     

正常心室肌复极离散度初步研究

目的     

Prolonged and fractionated right atrial electrograms during sinus rhythm in patients with paroxysmal atrial fibrillation and sick sinus node syndrome

Intraatrial catheter mapping of the right atrium was performed during sinus rhythm in 92 patients: Group I = 43 control patients without paroxysmal atrial fibrillation or sick sinus node syndrome; Group II = 31 patients with paroxysmal atrial fibrillation but without sick sinus node syndrome; and Group III = 18 patients with both paroxysmal atrial fibrillation and sick sinus node syndrome. Atrial electrograms were recorded at 12 sites in the right atrium. The duration and number of fragmented deflections of the atrial electrograms were quantitatively measured. The mean duration and number of fragmented deflections of the 516 atrial electrograms in Group I were 74 +/- 11 ms and 3.9 +/- 1.3, respectively. The criteria for an abnormal atrial electrogram were defined as a duration of greater than or equal to 100 ms or eight or more fragmented deflections, or both. Abnormal atrial electrograms were observed in 10 patients (23.3%) in Group I, 21 patients (67.7%) in Group II and 15 patients (83.3%) in Group III (Group II versus Group I, p less than 0.001; Group III versus Group I, p less than 0.001). The mean number of abnormal electrograms per patient with an abnormal electrogram was 1.3 +/- 0.7 in Group I, 2.5 +/- 1.9 in Group II and 3.5 +/- 2.5 in Group III (Group I versus Group II, p less than 0.01; Group II versus Group III, p less than 0.05). A prolonged and fractionated atrial electrogram characteristic of paroxysmal atrial fibrillation can be closely related to the vulnerability of the atrial muscle.(ABSTRACT TRUNCATED AT 250 WORDS)     

Age-associated changes in electrophysiologic remodeling: a potential contributor to initiation of atrial fibrillation

OBJECTIVE: Although the incidence of atrial fibrillation (AF) increases with age, the cellular electrophysiological changes that render the atria of aged individuals more susceptible to AF remain poorly understood. We hypothesized that dispersion of atrial repolarization increases with aging, creating a substrate for initiation of AF. METHODS: Four groups of dogs were studied: adult and old dogs in normal sinus rhythm (SR) and adult and old dogs with chronic AF (CAF) induced by rapid atrial pacing. In each dog, action potentials (AP) were recorded with microelectrodes from isolated endocardial preparations of four regions of right atrium and three regions of left atrium. Two indices of AP duration (APD) heterogeneity were obtained in each dog by calculating standard deviation (SD) and the coefficient of variation (COV=[SD/mean] x 100%). RESULTS: In SR groups, APD averaged across all regions was significantly longer in old than in adult tissues. Both indices of APD heterogeneity were higher in old dogs in comparison to adult. At both ages, CAF was associated with significant APD shortening and a decrease in APD adaptation to rate. While CAF significantly increased both indices of APD heterogeneity in adult dogs, it significantly decreased them in old dogs. CONCLUSIONS: The increase of spatial variability in repolarization in old atria may contribute to the initiation of AF in the aged. CAF-induced APD shortening and a decrease in APD adaptation appear to be important for the maintenance of sustained AF in both adult and old atria. The CAF-induced increase in dispersion of repolarization may be important for AF stabilization in adults, while previously reported fibrosis and slowed conduction of premature beats may be important in the old for both AF initiation during SR and subsequent stabilization of AF.     

Long-term recording of monophasic action potentials from human endocardium

In 36 patients undergoing routine cardiac catheterization, a new “contact electrode” catheter technique was used to record monophasic action potentials (MAPs) from right atrial and right and left ventricular endocardial sites without the application of suction. Although of smaller amplitude, typically ranging from 15 to 40 mV, and of different reversal ratio (33 ± 3%), MAP recordings closely resembled transmembrane action potentials in configuration and duration. Continuous MAP recordings of stable amplitude and, during regular pacing, of constant duration (± 1% at 90% repolarization) could be made from the same endocardial site for test periods of 1 hour (n = 4), permitting direct evaluation of the effect of cycle length alterations on local myocardial repolarization. A linear relation was found between MAP duration and basic cycle length varying from 350 to 700 ms. These rate-dependent changes in MAP duration were caused by a change in the slow phase of repolarization (phase 2), whereas the slope of rapid repolarization (phase 3) was unaltered. Single premature MAPs or MAPs after a pause showed changes in both phases. No MAPs could be recorded in areas of infarcted, aneurysmal myocardium, indicating that local viable myocardium is a prerequisite for the generation of the monophasic signal. Thus, in human subjects this catheter permits safe, long-term recording of MAPs which, although of smaller amplitude than transmembrane action potentials, bear appropriate and predictable phase relations. Such recordings may be useful in evaluating changes in local myocardial electrical activity induced by pacing or resulting from myocardial disease, or both.     

Dispersion of ventricular repolarization and arrhythmia: study of two consecutive ventricular premature complexes

The effect of two consecutive ventricular premature stimuli (S1S2) during atrial pacing on dispersion of repolarization and inducibility of ventricular arrhythmias was studied in 16 dogs under control conditions and in four dogs in the presence of an increased dispersion of repolarization during atrial pacing induced by general hypothermia and regional warm blood perfusion via selective cannulation of the distal branch of left anterior decending coronary artery. Dispersion of repolarization was measured as the maximal difference between the ends of six simultaneously recorded monophasic action potentials (MAPs) from anterior ventricular surface, and consisted of MAP duration difference and activation time difference. Dispersion of repolarization during atrial pacing at control was 29 +/- 7 msec (activation time difference 4 +/- 6 msec, MAP duration difference 25 +/- 8 msec), that after S1 at paraseptal the site was 81 +/- 8 msec (activation time difference 73 +/- 12 msec, MAP duration difference 8 +/- 5 msec), and that after S1S2 was 148 +/- 27 msec (activation time difference 103 +/- 21, MAP duration difference 44 +/- 26 msec). Neither S1 nor S1S2 induced ventricular arrhythmia. Hypothermia and regional warm blood reperfusion increased dispersion of repolarization during atrial pacing to 70 +/- 22 msec (activation time difference 9 +/- 3 msec, MAP duration difference 61 +/- 19 msec). During hypothermia and regional warm blood reperfusion, S1 produced a dispersion of repolarization of 149 +/- 29 msec (activation time difference 85 +/- 8 msec, MAP duration difference 64 +/- 23 msec) and did not induce ventricular arrhythmia.(ABSTRACT TRUNCATED AT 250 WORDS)     

Prediction of terminal atrial myocardial repolarisation from incomplete phase 3 data

The duration of the monophasic action potential (MAP) carries prognostic antiarrhythmic information when the recording is done during sinus rhythm (SR) after DC conversion of atrial fibrillation (AF). This study analyses whether it is possible to predict MAP duration during sinus rhythm by analysing the atrial MAP during AF, even though complete myocardial repolarisation is never reached during this arrhythmia. We have therefore evaluated the estimated duration of the action potential (AP) and MAP by exponential extrapolation of phase 3 data. (1) AP studies were done on 11 human atrial myocardial specimens. Resting membrane potential (RMP) and AP duration were better identified when more data obtained during repolarisation were used for prediction. Thus the predicted RMP deviated on average by -0.4% of AF amplitude from the real RMP level when data to 90% repolarisation were used for extrapolation. AP duration at 90% repolarisation correlated well with the real AP duration (r = 0.88) at this level of data aquisition. (2) Continuous recording of atrial MAPs was done in 15 patients during AF and in 12 of these during SR after DC conversion. Resting myocardial repolarisation level during AF, RP(EST), and estimated MAP duration, MAPD(EST), could be calculated by exponential extrapolation in 12 patients. The actual repolarisation during fibrillation reached below 90% of the RP(EST) level in eight patients and below 70% in all 12. The MAP duration during SR could be predicted with increasing precision when data closer to the RP(EST) were used for calculation of MAPD(EST). Thus MAPD(EST) correlated well with SR MAP duration when data reaching at least 90% of RP were used (r = 0.85).(ABSTRACT TRUNCATED AT 250 WORDS)     

Monophasic Action Potentials:

Monophasic Action Potentials. Monophaisc action potential (MAP) recordings reproduce the repolarization time course of intrucellular action potentials with high accuracy and provide precise information on the local activation time. With the advantage of in vivo application and the development of the safer and simpler contact catheter technique, MAP recording has become the method of choice for evaluating myocardial repolarization changes. This review aims to provide information on practical application of MAP recording in the clinical setting. MAPs can easily be recorded from the endocardium with the contact catheter technique in the electrophysiology laboratory and from the epicardium with electrode probes during open heart surgery. The technical aspects are described in detail. The rate dependence of myocardial excitability and repolarization and the effect of antiarrhythmic drugs on MAP duration and effective refractory period are thoroughly reviewed. The use of MAPs in detecting myocardial ischemia, in studying early afterdepolarization and triggered arrhythmias, in measuring dispersion of repolarization, in identifying intracardiac conduction and the development of the T wave, and in verifying the arrhythmogenic effect of mechanoelectric feedback are presented. Computerized automatic analysis of MAPs and the limitations of the MAP technique are also discussed.     

Global and local dispersion of ventricular repolarization: endocardial monophasic action potential mapping in swine and humans by using an electro-anatomical mapping system

This article evaluates whether the global dispersion of ventricular repolarization (DVR) can be estimated from measurements between a few adjacent or remote sites. Monophasic action potentials (MAP) were recorded from 61 +/- 18 left (LV) or right ventricular (RV) sites in 10 pigs and 44 +/- 16 LV, or RV sites in 8 patients by using the CARTO mapping system. MAP duration (MAPd) and end-of-repolarization time were calculated at each site and 13 repolarization maps from pigs and 10 from patients were reconstructed. Global dispersions in MAPd and EOR over the LV or RV were compared with the adjacent DVR among 3 - 7 MAPs in areas > or = 0.7 and < or = 1 cm(2) and with the remote DVRs between 2 MAPs with the greatest activation time difference (remote DVR1) and between the apical and laterobasal LV or RV (remote DVR2). The adjacent dispersions in end-of-repolarization and MAPd were significantly smaller than the global ones, 13 +/- 3 and 12 +/- 3 ms vs. 44 +/- 9 and 42 +/- 12 ms in pigs and 13 +/- 7 and 14 +/- 8 ms vs. 72 +/- 24 and 66 +/- 22 ms in patients. The remote DVR1 (30 +/- 8 and 17 +/- 10 ms in pigs and 40 +/- 28 and 28 +/- 17 ms in patients) and remote DVR2 (16 +/- 7 and 11 +/- 10 ms in pigs and 35 +/- 24 and 21 +/- 21 ms in patients) were also significantly smaller than the global DVRs. In conclusion, global DVR is poorly estimated from MAP recordings from a few adjacent or remote sites, suggesting the importance of obtaining global information in evaluating DVR.     

Dispersion of the monophasic action potential duration in patients with polymorphic ventricular tachycardia.

The mechanism of polymorphic ventricular tachycardia (PMVT) remains unclear. To investigate the electrophysiologic mechanism of PMVT, monophasic action potentials (MAPs) were recorded with a contact electrode technique from right ventricular sites during sinus rhythm and right ventricular pacing. MAPs were obtained from 6 patients with PMVT (PMVT group) and 11 patients without PMVT (control group). The duration from the onset of the upstroke to 90% repolarization of the MAP (MAPD90) during right ventricular pacing at both pacing cycle lengths of 600 and 400 ms was significantly longer in the PMVT group than in the control group (332+/-60 ms vs 279+/-33 ms [P < .005] and 276+/-32 ms vs 229+/-23 ms [P < .0001], respectively). Dispersion of the MAPD90 in sinus rhythm was significantly larger in the PMVT group than in the control group (52.5+/-34.6 ms vs 26.1+/-12.0 ms [P < .005]), and dispersion of the MAPD90 during right ventricular pacing at both pacing cycle lengths of 600 and 400 ms was also significantly larger in the PMVT group than in the control group (86.0+/-44.2 ms vs 37.4+/-28.6 ms [P < .005], and 48.8+/-19.3 ms vs 27.1+/-7.1 ms [P < .05], respectively). Dispersion of repolarization time (activation time plus MAPD90) at a pacing cycle length of 600 ms was longer in the PMVT group than in the control group (104.3+/-38.9 ms vs 49.4+/-31.2 ms [P < .05]). These results suggest that the patients with PMVT have a greater regional dispersion of ventricular repolarization time and that the heterogeneity of ventricular repolarization may play an important role in the genesis of PMVT.     

Stepwise linear approach to catheter ablation of atrial fibrillation

BACKGROUND: This study attempted to convert atrial fibrillation (AF) to sinus rhythm using a stepwise linear catheter ablation approach. METHODS: One hundred and ninety-six patients (43 with persistent AF) were enrolled in the study. A multiple electrode array was used for anatomical navigation and activation mapping. Continuously incremental stimulation was used to induce AF if spontaneous AF was not present. Stepwise linear ablation was applied until AF was converted to sinus rhythm or atypical atrial flutter (AAFL) or atrial tachycardia (AT). The stepwise approach initially utilized a figure-7 lesion line between the right and left superior pulmonary vein on the roof of the left atrium and then extended along the ridge between the left appendage and the left pulmonary veins until the mitral valve annulus, as the primary lesions. If AF still persisted, high-frequency potentials in the inferior left atrium, coronary sinus, or right atrium were targeted. Noninducibility of AF was used as the end point. RESULTS: AF was converted to sinus rhythm in 81.6% of patients (90.8% of paroxysmal and 51.1% of persistent AF, P<.01). The remainders of patients were converted to AAFL or AT. AF was terminated after ablation in right atrium in 7 patients. During an 18.2+/-7.3 month follow-up, 88.3% of patients were free of atrial tachyarrhythmias without medication, 9.7% of patients had refractory AAFL/AT, and only 2.1% of patients had paroxysmal AF. CONCLUSION: Stepwise linear ablation is effective in converting AF to sinus rhythm and the figure-7 lesion line should be the basic lesion. Right atrium ablation is necessary in some patients.     

Detection of hypertensive patients at risk for paroxysmal atrial fibrillation during sinus rhythm by computer-assisted P wave analysis.

OBJECTIVE AND METHODS: To determine whether hypertensive patients at risk for paroxysmal atrial fibrillation (AF) could be detected while in sinus rhythm, a computer-based 12-lead surface electrocardiogram was recorded in 50 hypertensive patients with history of paroxysmal AF (group A) and in 60 hypertensive patients without history of AF (group B). The maximum P-wave duration (P(maximum)), the minimum P-wave duration (P(minimum)), P-wave dispersion (Pdispersion = Pmaximum Pminimum), adjusted P-wave dispersion (APdispersion = Pdispersion/square root of the number of measurable leads), mean P-wave duration (mean P) and the standard deviation of the P-wave duration in all measured leads (SDP) were calculated. RESULTS: Pdispersion, APdispersion and SDP were significantly higher in group A than in group B (Pdispersion, 52 +/- 19 versus 41 +/- 15 ms, P< 0.001; APdispersion, 15.2 +/- 5.5 versus 11.9 +/- 4.6 ms, P< 0.001; SDP, 16 +/- 5 versus 13 +/- 5 ms, P < 0.001). P(minimum), mean P and left ventricle ejection fraction (LVEF) were significantly lower in group A than in group B (Pminimum, 79 +/- 18 versus 91 +/- 13 ms, P < 0.001; mean P, 108 +/- 18 versus 116 +/- 13 ms, P= 0.005; LVEF, 64 +/- 5 versus 69 +/- 8%, P< 0.001). Pminimum, Pdispersion, mean P, SDP, APdispersion and LVEF were found to be significant univariate predictors of paroxysmal AF, whereas only Pminimum (P< 0.001) remained a significant independent predictor of paroxysmal AF in the multivariate analysis. CONCLUSION: Hypertensive patients at risk for paroxysmal AF could be detected while in sinus rhythm by computer-assisted electrocardiographic P-wave analysis.