Detection of patients with sick sinus syndrome by use of low amplitude potentials early in filtered P wave

Objectives. This study sought to determine whether patients with sick sinus syndrome could be detected by analyzing the initial portion of the signal-averaged P wave corresponding to the electrical activity of the perinodal atrial myocardial cells.Background. In sick sinus syndrome, pathophysiologic abnormalities have been shown not only in the sinus node, but also in atrial muscle, especially the perinodal portion.Methods. The study included 41 patients with sick sinus syndrome and 140 age-matched control subjects. Eighteen of 41 patients with sick sinus syndrome had paroxysmal atrial fibrillation. Signal-averaged P wave electrocardiograms (ECGs) were recorded through a bandpass filter of 40 to 300 Hz with a P wave-triggering technique. Signals of the orthogonal bipolar leads were combined into a spatial magnitude. The root mean square voltage for the initial 30 ms (EP30) and the duration of initial low amplitude signals <4 μV (ED4) of the filtered P wave were measured. The root mean square voltage for the last 20 ms (LP20) and the duration of the filtered P wave were also measured.Results. EP30 was significantly lower and ED4 was significantly longer in patients with sick sinus syndrome than in the control subjects (EP30 [mean ± SD]: 2.18 ± 0.90 vs. 3.94 ± 1.45 μV, p < 0.0001; ED4: 31.7 ± 14.5 vs. 14.0 ± 7.4 ms, p < 0.0001), although there was no significant difference in LP20 between patients with sick sinus syndrome without paroxysmal atrial fibrillation and the control subjects. The duration of the filtered P wave was significantly but minimally longer in patients with sick sinus syndrome than in the control subjects (139.8 ± 18.8 vs. 127.3 ± 13.6 ms, p < 0.0001). The criteria of EP30 <3.0 μV and ED4 > 22 ms as atrial early potential gave a sensitivity of 76%, a specificity of 91%, a positive predictive value of 74% and a negative predictive value of 93% for identification of patients with sick sinus syndrome.Conclusions. These results suggest that the long, low amplitude signals early in the filtered P wave on the signal-averaged ECGs are characteristic of sick sinus syndrome. Thus, the atrial early potential could be a useful marker to identify patients with sick sinus syndrome.     

Effects of digitalis on the human sick sinus node after pharmacologic autonomic blockade

To study the effects of digitalis on the sinus node and the mechanisms involved, 16 patients with the sick sinus syndrome had electrophysiologic assessment of sinus nodal function during (1) control study, (2) after pharmacologic autonomic blockade with propranolol (0.2 mg/kg body weight and atropine sulfate 0.04 mg/kg intravenously), and (3) 10 minutes after 0.01 mg/kg of intravenous ouabain. The study was completed within 30 minutes of pharmacologic autonomic blockade. During the control study 50 percent of patients had an abnormal corrected sinus nodal recovery time or abnormal sinoatrial conduction time, or both. The effects of ouabain on sinus nodal function were compared with those after pharmacologic autonomic blockade. Ouabain significantly increased both intrinsic sinus cycle length (ouabain 975 ± 194 ms [mean ± standard deviation]; autonomic blockade 1,025 ± 218 ms, probability [p] < 0.001) and corrected sinus nodal recovery time (ouabain 615 ± 503 ms; autonomic blockade 575 ± 536 ms, p < 0.05). In contrast there was no significant change in sinoatrial conduction time after ouabain (ouabain 141 ± 56 ms; autonomic blockade 132 ± 45 ms; difference not significant). The effects of ouabain were similar in patients with both normal and abnormal sinus nodal function.These findings suggest that (1) digitalis in therapeutic doses has a depressant effect on intrinsic sinus nodal automaticity in patients with normal as well as abnormal sinus nodal function; (2) digitalis has no significant effects on sinoatrial conduction; and (3) the effects of digitalis on sinus nodal automaticity are primary and independent of its vagal and antiadrenergic effects.     

Influence of the autonomic nervous system on the Q-T interval in man

Drugs that affect the autonomic nervous system can influence the Q-T interval directly or by changing the heart rate. Bazett's formula to correct for rate may be misleading after certain drug interventions. This hypothesis was tested in 20 patients receiving both propranolol (0.15 mg/kg intravenously) and atropine (0.03 mg/kg intravenously). Six patients received propranolol first, 7 patients received atropine first, and 7 patients received atropine plus propranolol simultaneously. During control and after drug intervention, the Q-T interval was measured directly in sinus rhythm and during a fixed atrial paced rate, and was calculated using Bazett's formula. The ventricular effective refractory period was also determined in 6 patients after administration of atropine plus propranolol. The sinus cycle length (836 ± 156 to 648 ± 84 ms, mean ± standard deviation), measured Q-T interval (367 ± 26 to 329 ± 26 ms), and atrially paced Q-T interval (330 ± 28 to 315 ±27 ms) shortened after atropine plus propranolol (p <0.001), but the corrected Q-T interval with use of Bazett's formula did not change (402 ± 33 to 412 ± 24 ms). The ventricular effective refractory period also shortened from 241 to 20 to 218 ± 21 ms after atropine plus propranolol (p <0.02). The sinus cycle length increased after propranolol (750 ± 97 to 907 ± 108 ms, p <0.001), but no change occurred in the measured Q-T interval or atrial paced Q-T interval although the corrected Q-T interval using Bazett's formula was greatly shortened (428 ± 15 to 391 ±22 ms, p <0.001). The sinus cycle length, measured Q-T interval, and atrially paced Q-T interval decreased after atropine (p <0.01), but the corrected Q-T interval lengthened (375 ± 29 to 418 ± 28 ms, p <0.01).In summary, atropine and atropine plus propranolol shorten the Q-T interval independent of rate, demonstrating a direct vagal effect on the Q-T interval. Bazett's formula inaccurately predicts the Q-T interval after administration of atropine, propranolol, and atropine plus propranolol.     

Age,Gender, and Autonomic Tone Effects on Surface Electrocardiographic Indices of Ventricular Repolarization

Background: Prolonged QT offset dispersion (QToD), an index of heterogeneity of ventricular repolarization, is thought to be an independent predictor of all‐cause and cardiovascular mortality. However the influence of gender and autonomic tone in healthy adults on age‐related changes in measures of ventricular repolarization are not well characterized. Methods: QToD and T wave complexity were measured in 56 healthy subjects with no detectable heart disease (by echo and stress test)—38 young subjects with a mean age of 28 ± 4 years and 18 old subjects with a mean age of 71 ± 7 years. QToD and T wave complexity were computed from 12‐lead ECGs using the GE Marquette QT Guard automated analysis program with manual over‐reading at rest (baseline), following exercise, and double autonomic blockade with atropine and propranolol. Data was analyzed using factorial ANOVA. Results: Young males had a significantly greater QToD than young and old females at baseline (28 ± 5 ms, 23 ± 5 ms, and 22 ± 5 ms, respectively, P < 0.01), an intrinsic effect independent of changes in autonomic tone. In contrast, females had significantly greater T wave complexity than males following exercise and double autonomic blockade with a definite trend at baseline. There was no correlation between T wave complexity and QToD. Conclusions: Age and gender demonstrate a complex interaction on indices of myocardial repolarization with different measures behaving differently. These findings have implications for better understanding age and gender effects on myocardial electrophysiology. A.N.E. 2001;6(4):290–297     

Impact of Pharmacological Autonomic Blockade on Complex Fractionated Atrial Electrograms

Autonomic Blockade During Atrial Fibrillation . Introduction: The influence of the autonomic nervous system on the pathogenesis of complex fractionated atrial electrograms (CFAE) during atrial fibrillation (AF) is incompletely understood. This study evaluated the impact of pharmacological autonomic blockade on CFAE characteristics. Methods and Results: Autonomic blockade was achieved with propanolol and atropine in 29 patients during AF. Three‐dimensional maps of the fractionation degree were made before and after autonomic blockade using the Ensite Navx^® system. In 2 patients, AF terminated following autonomic blockade. In the remaining 27 patients, 20,113 electrogram samples of 5 seconds duration were collected randomly throughout the left atrium (10,054 at baseline and 10,059 after autonomic blockade). The impact of autonomic blockade on fractionation was assessed by blinded investigators and related to the type of AF and AF cycle length. Globally, CFAE as a proportion of all atrial electrogram samples were reduced after autonomic blockade: 61.6 ± 20.3% versus 57.9 ± 23.7%, P = 0.027. This was true/significant for paroxysmal AF (47 ± 23% vs 40 ± 22%, P = 0.003), but not for persistent AF (65 ± 22% vs 62 ± 25%, respectively, P = 0.166). Left atrial AF cycle length prolonged with autonomic blockade from 170 ± 33 ms to 180 ± 40 ms (P = 0.001). Fractionation decreases only in the 14 of 27 patients with a significant (>6 ms) prolongation of the AF cycle length (64 ± 20% vs 59 ± 24%, P = 0.027), whereas fractionation did not reduce when autonomic blockade did not affect the AF cycle length (58 ± 21% vs 56 ± 25%, P = 0.419). Conclusions: Pharmacological autonomic blockade reduces CFAE in paroxysmal AF, but not persistent AF. This effect appears to be mediated by prolongation of the AF cycle length. (J Cardiovasc Electrophysiol, Vol. pp. 766‐772, July 2010)     

Effects of Atropine and Pirenzepine on Heart Rate Turbulence

Background: It has been shown that mortality risk in patients after myocardial infarction could be estimated by heart rate turbulence (HRT), a short‐term change in heart rate after ventricular premature beat (VPB), presumably caused by baroreceptor mechanism. We sought to determine whether pharmacological blockade with atropine, or augmentation of vagal tone with pirenzepine given in small doses would influence HRT. Methods: In 30 patients with normal echocardiogram, and without signs or symptoms of coronary artery disease, after electrophysiologic examination or radiofrequency ablation for supraventricular arrhythmias was completed, turbulence onset (TO) and turbulence slope (TS) in basal state, after 1.3 mg IV pirenzepine and finally, after atropine in dose of 0.04 mg/kg of body weight were compared. Results: As assessed by Friedman ANOVA test both pirenzepine and atropine caused a significant change in both TO (P < 0.01) and TS (P < 0.01). The mean basal TO of ?3.6 ± 2.9%, changed after pirenzepine to ?5.99 ± 5.6% (P < 0.01), and after atropine it changed to ?3.3 ± 18.1% (P < 0.01). The mean basal TS of 18.6 ± 10.1 ms/R‐R interval increased after pirenzepine to 26.8 ± 19.9 ms/R‐R interval (P < 0.05), and decreased after atropine to 1.2 ± 0.8 ms/R‐R interval (P < 0.01). Mean cycle length increased after pirenzepine from 706.8 ± 106.8 to 830 ± 151.9 ms (P < 0.01), and decreased after atropine to 454.2 ± 58.1 ms (P < 0.01). Conclusion: A conclusion could be drawn that vagomymetic manipulation with intravenous pirenzepine increases HRT; vagal blockade with atropine decreases HRT. This finding suggests that a normal vagal innervation of heart is a prerequisite for the phenomenon of HRT.     

Intracavitary filling pattern in the failing left ventricle assessed by color M-mode Doppler echocardiography

Objectives. The present study aimed to investigate the mechanism of intracavitary changes in filling pattern during acute ischemic left ventricular failure and during beta-adrenergic blockade.Background. Recent clinical studies with color M-mode Doppler imaging have shown abnormal intracavitary filling patterns in the diseased ventricle.Methods. In open chest anesthetized dogs with intracardiac micromanometers and myocardial segment-length crystals, global ischemic left ventricular failure was induced (n = 8) by coronary microembolization. In nonischemic ventricles inotropy was decreased (n = 6) by intravenous propranolol and increased (n = 6) by intravenous isoproterenol. From color M-mode Doppler images we calculated the time difference between peak early diastolic filling velocity at the mitral tip and apex using computer analysis. The time difference of peak velocity was used as an index of the timing of apical filling.Results. There was marked retardation of apical filling with microembolization and propranolol. Time difference of peak velocity increased from 20 ± 6 (mean ± SEM) to 101 ± 17 ms (p < 0.05) and from 21 ± 8 to 80 ± 18 ms (p < 0.05), respectively. Time constant of isovolumic relaxation increased from 34 ± 3 to 43 ± 5 ms (p < 0.05) and from 31 ± 1 to 39 ± 3 ms (p < 0.05) during microembolization and beta-blockade, respectively. Isoproterenol tended to cause the opposite changes. Time difference of peak velocity showed a positive correlation with time constant of isovolumic relaxation (r = 0.89, p < 0.01) and a negative correlation with peak early transmitral pressure gradient (r = 0.88, p < 0.01 ). In the intact left ventricle, peak apical filling velocity coincided with peak early transmitral pressure gradient. During ischemic failure, however, peak apical filling velocity occurred 53 ± 14 ms after peak early transmitral pressure gradient had decreased to zero and at a time when transmitral flow had ceased, suggesting a change in intraventricular flow distribution.Conclusions. Color M-mode Doppler imaging revealed retarded apical filling during depression of myocardial function by global myocardiai ischemia or beta-blockade. The abnormal filling pattern may be a sign of impaired left ventricular relaxation.     

Menstrual Cycle and ST Height

Background: Sex hormones and menstrual cycle effects on ST height have not yet been clearly identified. Methods: Twenty‐two young, healthy women (aged 22–32 years) were included in this study. Twelve‐lead ECGs were registered during menses, follicular and luteal phase of the menstrual cycle at baseline, and after double autonomic blockade (DAB). Chest leads V2–V4 and limb leads I and II were chosen for analysis. ST height was measured manually at J‐Point and 40 ms after the J‐Point, and values were corrected for QRS amplitude (J‐Point/QRS, 40 ms/QRS). Repeated measure ANOVA was used to analyze differences in ST height among the three phases of the menstrual cycle. A P‐value < 0.05 was considered as significant. Results: At baseline, ST height, QTc, and T wave amplitude were not significantly different among the three phases of the menstrual cycle. After double autonomic blockade, ST height at 40 ms, J‐Point/QRS, and 40 ms/QRS was significantly higher during follicular versus luteal phase (0.152 ± 0.413 mm versus ?0.007 ± 0.427 mm, P = 0.0059 at 40 ms; ?0.001 ± 0.030 versus ?0.015 ± 0.032, P = 0.0039 at J‐Point/QRS; 0.013 ± 0.031 versus ?0.004 ± 0.032, P = 0.0005 at 40 ms/QRS) as was the QTc. ST height differences at J‐Point were not significantly different (?0.046 ± 0.395 mm follicular, ?0.167 ± 0.448 mm luteal, and ?0.083 ± 0.492 mm menses, P = 0.1014). Conclusion: ST height and QTc varied among the three phases of the menstrual cycle, predominantly after double autonomic blockade. Female sex hormones that vary throughout the menstrual cycle may modulate measures of repolarization.     

自主神经对左上肺静脉电生理特征的影响

目的研究迷走神经刺激和心脏自主神经阻断对左上肺静脉(LSPV)电生理特征影响。方法用7只成年杂种犬自身对照,观察基础状态、左侧迷走神经干刺激、阻断迷走神经和阻断自主神经等不同状态下犬的心房和LSPV远端(LSPV-D)、中端(LSPV-M)、近端(LSPV-P)有效不应期(ERP)的变化,以及起搏肺静脉时心房颤动(简称房颤)诱发率的变化。结果①迷走神经刺激时LSPV的ERP均较基础状态下缩短,房颤的诱发率最高(71.4%)。②单用阿托品阻断迷走神经时LSPV-M的ERP较基础状态下延长(125.8±9.1msvs112.9±13.8ms,P<0.05),LSPV-P和LSPV-D无变化,但房颤诱发率较基础状态下和迷走神经刺激时下降(17.1%vs24.8%,71.4%,P<0.05)。③联合应用阿托品和普奈洛尔阻断自主神经时LSPV-D、LSPV-M和LSPV-P的ERP均显著延长,房颤的诱发率最低(7.6%)。④基础状态下LSPV-D的ERP长于LSPV-P(118.6±17.5msvs106.4±10.7ms,P<0.05),阻断自主神经时LSPV-D的ERP短于LSPV-P(135.0±8.2msvs151.4±12.1ms,P<0.05)。结论LSPV的电生理特征存在“异质性”,对阻断自主神经的药物反应性也不同,对房颤的发生和维持有重要作用。而自主神经张力的变化可以改变LSPV的电生理特性,其中交感神经也是主要原因之一。     

Vasodilator Capacity of Forearm Vessels in Hypertension

Factors determining vascular resistance were examined in 6 normotensive subjects (NT), 5 with established hypertension (EH) and diastolic pressures > 90 mmHg and 7 with borderline hypertension (BH) having pressures intermittently > 140/90 mmHg. Using plethysmography, we measured forearm blood flow (FBF), arterial resistance (FAR) and venous compliance (FVC) before and after autonomic blockade with propranolol 0.2 mg/kg, atropine 0.04 mg/kg and phentolamine 15 mg I.V. Subjects with EH had the highest baseline FBF. MAP was increased 18–22% after atropine and propranolol in all 3 groups. Phentolamine decreased MAP -8.9 ± 2.1% in NT, -6.9 ± 1.2% in BH and -16.5 ± 1.9% in EH (p<0.05). After total blockade, FAR in EH (32.4 ± 4.8 units) was similar to FAR in NT (31.0 ± 3.6 units) whereas that in BH remained high (50.2 ± 3.8 units; p<0.01). Baseline FVC was highest in NT, intermediate in BH and lowest in EH and was not altered by autonomic blockade. Non-gravitational exercise for 6 min during upper arm arterial occlusion after autonomic blockade resulted in a residual FAR of 2.3 ± 0.1 units in NT, 3.8 ± 0.3 units in BH and 4.2 ± 1.7 units in EH (p<0.01) during reactive hyperemia. Increased FAR in our subjects with BH and EH was probably due to structural vascular alterations. The greater increase in FAR and MAP in EH over that observed in BH has a sympathetic nervous system component.     

Electrocardiographic P wave changes after thoracoscopic pulmonary vein isolation for atrial fibrillation

Background

Changes in P wave duration (PWD) and P wave area (PWA) have been described following catheter ablation for atrial fibrillation (AF). We hypothesize that video-assisted thoracoscopic pulmonary vein isolation (VATS-PVI) for AF results in decrease of PWD, PWA and P wave dispersion, which may resemble reverse electrical remodeling of the atrium after restoration of sinus rhythm.

Methods

VATS-PVI consisted of PVI and ganglionic plexus ablation in 29 patients (mean age, 59?±?7 years; 23 males; 17 paroxysmal AF) and additional left atrial lesions in patients with persistent AF. PWD and PWA were measured in ECG lead II, aVF and V2 of ECGs during sinus rhythm before, directly after, and 6 months postprocedure. P wave dispersion was derived from the 12 lead ECG.

Results

Prior to VATS-PVI, PWD did not correlate with left atrial size and no difference in left atrial size was found between patients with paroxysmal or persistent AF (p?=?0.27). Following VATS-PVI, PWD initially prolonged in all patients from 115?±?4.6 ms to 131?±?3.6 ms (p?<?0.01) but shortened to 99?±?3.2 ms after 6 months (p?<?0.01). PWA was 5.60?±?0.32 mV*ms at baseline, 6.44?±?0.32 mV*ms post-VATS-PVI (P?=?NS), and 5.40?±?0.28 mV*ms after 6 months (p?=?NS vs. baseline, p?<?0.05 vs. post-VATS-PVI). P wave dispersion decreased in the persistent AF group from baseline 67?±?3.3 to 64?±?2.5 ms post-VATS-PVI (p?=?0.30) and to 61?±?3.4 ms after 6 months (p?<?0.05).

Conclusions

PWD increases significantly directly after successful VATS-PVI in both groups. There was significant decrease in PWD after 6 months. Similarly, P wave dispersion decreased in the persistent group. These changes suggest an immediate procedure related effect, but the later changes may represent reverse electrical atrial remodeling following cessation of AF.     

Differential effects of functional autonomic blockade on the variables of sinus nodal automaticity in sick sinus syndrome

To study the pathophysiologic mechanism of sick sinus syndrome and to establish the relation of intrinsic heart rate, corrected sinus nodal recovery time and sinoatrial conduction time in this syndrome, electrophysiologic studies were conducted in 22 men (mean age 60 ± 12 years) with the clinical diagnosis of sick sinus syndrome. Measurements were determined before and after autonomic blockade with propranolol (0.2 mg/kg body weight) and atropine sulfate (0.04 mg/kg). Fifty-nine percent of patients (Group I) had an abnormal intrinsic heart rate, suggesting intrinsic abnormality of sinus nodal automaticity; 41 percent (Group II) had a normal intrinsic heart rate after autonomic blockade, suggesting disturbed autonomic regulation. One patient with an observed intrinsic heart rate higher than the upper limit of predicted intrinsic heart rate was also included in Group II. The mean corrected sinus nodal recovery time before autonomic blockade was 751 ± 502.8 ms and was abnormal (more than 450 ms) in 10 of the 13 patients in Group I and 2 of the 9 patients in Group II. After autonomic blockade this interval was 694 ± 638.7 ms and was abnormal in 12 of the 13 patients in Group I and in 2 of the 9 patients in Group II. The patients in each group could be further classified into three groups on the basis of normal or abnormal corrected sinus nodal recovery time before or after autonomic blockade. Not all patients with abnormal intrinsic heart rate (Group I) had abnormal corrected sinus nodal recovery time and vice versa. Patients in Group II were younger in age, had a lesser incidence of organic heart disease and were more severely symptomatic.Mean sinoatrial conduction time during control studies was 210.4 ±96.3 ms and decreased significantly (143.2 ± 59.6 ms, p < 0.005) after autonomic blockade. This interval was abnormal in 3 of the 13 patients in Group I and in 6 of the 9 patients in Group II during control studies; after autonomic blockade it remained abnormal in 3 patients in Group I and in 1 patient in Group II.It is concluded that determination of heart rate and corrected sinus nodal recovery time after autonomic blockade increases the sensitivity of electrophysiologic testing and offers some insight into the pathophysiology of sick sinus syndrome. Patients with sick sinus syndrome who have a normal intrinsic heart rate have a greater incidence of abnormal sinoatrial conduction time than do those with an abnormal intrinsic heart rate. Thus, abnormal sinoatrial conduction time is usually due to extrinsic autonomic influences.     

自主神经系统对窦性心律震荡的影响

目的通过心室起搏诱发窦性心律震荡(HRT)模型,观察自主神经对HRT指标的影响。并探讨诱发室性早搏的不同联律间期(CI)及代偿间期(CP)与HRT指标之间的关系。方法15例无器质性心脏病患者,在不使用自主神经阻断药物情况下(基础状态),采用右室心尖部V-S2刺激,联律间期以刺激前平均心动周期的60%感知V波,并逐渐2%递减,直至连续发出10个V-S2刺激,每个S2刺激之间至少间隔有20个VV间期;然后静脉注入艾司洛尔(艾司洛尔状态),待药物作用至高峰后重复上述V-S2刺激;静脉注入阿托品(阿托品状态),待其作用至高峰后再次重复上述刺激;随即再次注入艾司洛尔(联合用药状态)后重复发出10个V-S2刺激。测量并分析四种状态下体表心电图及腔内心电图数据。结果基础状态下RR间期是698.91±75.70ms,震荡初始(TO)为-1.65%±2.29%,震荡斜率(TS)为8.16±4.63ms。而在使用不同的自主神经阻滞药物后,TO显著性增加发生在阿托品状态和联合用药状态,而在艾司洛尔状态无显著变化。TS显著性降低发生在阿托品状态和联合用药状态(P均<0.01),而在艾司洛尔状态无显著变化。基础状态诱发的室性早搏,它的CI与HRT指标并没有相关性(所有的P>0.05),而CP则与HRT指标相关。结论自主神经系统对HRT的影响中,迷走神经起着主导作用;基础状态下CI和HRT指标之间不相关,而CP与之相关。     

The Value of P Dispersion on Predicting Atrial Fibrillation After Coronary Artery Bypass Surgery: Effect of Magnesium on P Dispersion

Background: AF is a frequent arrhythmia complicating CABG, and it is well known that dispersion and prolongation of P wave increases the risk of AF. The aim of this study was to investigate the effect of magnesium (Mg) treatment on P‐wave duration and dispersion in patients undergoing CABG. Method: The study included 148 consecutive patients (33 women, 115 men; mean age 62.1 ± 7.0 years) undergoing CABG who were randomly allocated to two groups. Group A consisted of 93 patients to whom 1.5 g daily MgSO₄ infusion was applied the day before surgery, just after operation, and 4 days following surgery, and group B consisted of 55 control patients. From the preoperative and postoperative fourth day, 12‐lead ECG recordings, duration of the P waves, and P‐wave dispersions were calculated. Results: There were no differences between the two groups with regard to age, sex, and blood Mg level. Comparison of the baseline and day 4 ECG measurements showed no difference as far as heart rates, duration of PQ, and QRS intervals were concerned. AF developed in 2 (2%) cases in group A and in 20 (36%) cases in group B (P < 0.001). There was no difference between the two groups when average basal P max, P min, P dispersion, and day 4 P min values were compared. In group A, fourth day P max (94.3 ± 11.8 vs 101.0 ± 13.2 ms; P = 0.0025) and P dispersion (38.2 ± 9.2 vs 44.9 ± 10.9 ms; P = 0.0002) were significantly lower as compared to group B. Comparing the patients who developed AF, and who did not, no difference was detected with regard to baseline P max, P min, P dispersion, and day 4 P min. Day 4 P max (95.1 ± 11.8 vs 106.4 ± 14.0 ms, P = 0.0015) and P dispersion (38.9 ± 8.8 vs 50.7 ± 13.0 ms, P = 0.001) of patients who developed AF were significantly higher. Baseline Mg levels were similar in patients who developed AF, and who did not, but the day 4 Mg level was significantly lower in AF group (2.0 ± 0.23 vs 2.15 ± 0.26 mg/dL, P < 0.001). Conclusion: Perioperative Mg treatment reduces P dispersion and the risk of developing AF in patients undergoing CABG. A.N.E. 2002;7(3):211–218     

Differential effect of pharmacological autonomic blockade on some electrophysiological properties of the human ventricle and atrium.

OBJECTIVE--This study investigated the dominance of each limb of the autonomic nervous system and tested sympathetic-vagal interactions in the human ventricle and atrium after administration of propranolol and atropine. PATIENTS AND METHODS--The 90% monophasic action potential duration (MAPD90) and the effective refractory period (ERP) at the right ventricular apex (RV) and the right lateral atrium (RA) were measured in 14 patients. The MAPD90 was measured during constant RV and RA pacing (cycle length 600 ms) and the ERP was measured at a driven cycle length of 600 ms. Electrophysiological variables were measured during a control period, after propranolol (0.15 mg/kg loading dose followed by 0.1 mg/min infusion), and after autonomic blockade (atropine 0.04 mg/kg). RESULTS--Both RV MAPD90 and RV ERP increased after propranolol (RV MAPD90 from 268 (26) ms to 275 (26) ms, p < 0.005; RV ERP from 252 (25) ms to 258 (26) ms, p < 0.0005) and then decreased to below the control values after autonomic blockade (RV MAPD90 256 (24) ms; RV ERP 239 (25) ms, p < 0.0005 v propranolol, p < 0.0005 v control). In contrast, both RA MAPD90 and RA ERP increased after propranolol (RA MAPD90 from 242 (19) ms to 260 (19) ms; RA ERP from 216 (21) ms to 230 (18) ms, p < 0.0005), and then increased slightly more after autonomic blockade (RA MAPD90 265 (16) ms, p = 0.09; RA ERP 235 (16) ms, p = 0.07), thus remaining above control values (p < 0.0005). CONCLUSIONS--The results indicate (a) that in the human ventricle vagal stimulation and sympathetic beta stimulation are antagonistic and that direct vagal stimulation predominates over beta stimulation, with sympathetic-vagal interaction being minimal and (b) that in the human atrium vagal stimulation and beta stimulation are synergistic and beta stimulation predominates over vagal stimulation, with direct vagal stimulation having a minimal effect.     

Effects of Right Coronary Artery PTCA on Variables of P‐Wave Signal Averaged Electrocardiogram

Background: P‐wave signal averaged ECG has been used to detect atrial late potentials that were found in paroxysmal atrial fibrillation. Ischemia is supposed to trigger ventricular late potentials, which indicate an elevated risk for ventricular tachycardia. Preexistent ventricular late potentials measured by ventricular signal averaged ECG is supposed to be eliminated by successful PTCA. Methods: We examined the incidence of atrial late potentials in patients with a proximal stenosis of the right coronary artery and new onset of atrial fibrillation. Furthermore, we investigated the anti‐ischemic effect of a successful percutaneous transluminal coronary angioplasty.(PTCA) of the right coronary artery. P‐wave signal averaged ECG from 23 patients who had a PTCA of the right coronary artery (group A) were compared to age, sex, and disease‐matched control subjects (group B) one day before, one day after, and one month after PTCA. Results: A new appearance of paroxysmal atrial fibrillation was presented in eight patients before PTCA (group A1) of group A. Patients with a stenosis of the right coronary artery had a significantly higher incidence of supraventricular extrasystoles in a 24‐hour‐Holter ECG (131.1 ± 45.4 vs 17.1 ± 18.9, P < 0.0002 ). The duration of the filtered P wave was longer (124.8 ± 11.9 vs 118.5 ± 10.1 ms, P < 0.04 ) and the root mean square of the last 20 ms (RMS 20) was significantly lower in group A than in group B (2.87 ± 1.09 vs 3.97 ± 1.12 μV, P < 0.01 ). A successful PTCA caused an increase in RMS 20 (2.87 ± 1.11 vs 4.19 ± 1.19 μV, P < 0.02 ) and a decrease in filtered P‐wave duration (124.8 ± 11.9 vs 118.4 ± 10.4 ms, P < 0.04 ). Preexistent atrial late potentials were found among 15 patients before PTCA. After successful PTCA only 3 out of 15 patients were affected (P < 0.0004) after one day, as well as after one month. All patients with a history of atrial fibrillation did not suffer from an arrhythmic recurrence within the following six months after successful PTCA. Conclusion: A stenosis of the right coronary artery is associated with atrial late potentials. A successful PTCA of the right coronary artery eliminates preexistent atrial late potentials and may reduce the risk of atrial fibrillation.     

A Prospective Study of Atrial Fibrillation After Cardiac Surgery

Background: Atrial fibrillation (AF) is a commonly encountered arrhythmia following cardiac surgery and when sustained, may be associated with significant morbidity. Methods: This large prospective investigation examined a variety of clinical and P wave signal-averaged electrocardiogram (SAECG) parameters to identify independent predictors of AF following cardiac surgery. A total of 272 patients underwent P wave SAECG recording and analysis prior to surgery. Information on their clinical, surgical, and hemodynamic characteristics as well as hospital course was collected. Patients were followed during their postoperative course with telemetry and ECGs. Results: During an observation period of up to 14 days, 79 patients (29%) developed AF 2.5 ± 1.9 days after surgery. Patients who developed AF following cardiac surgery were more likely to be older, undergo valve surgery, to have ejection fraction (EF) < 40%, to have P wave duration on SAECG >140 ms (all P < 0.01), and to take digoxin preoperatively (P < 0.05). A multivariate analysis found that only P wave duration on SAECG >140 ms and EF < 40% were independent predictors of AF following cardiac surgery. The odds ratio of P wave duration on SAECG >140 ms and EF < 40% for the development of AF following cardiac surgery was 3.1 and 2.8, respectively, and 8.7 when combined. Conclusions: Thus, the presence of preexisting abnormal atrial substrate as detected by P wave prolongation on SAECG, and implicated by EF < 40%, clearly predicted a higher risk of AF following cardiac surgery and may provide clinicians with an effective means of identifying those at greatest risk.     

Abnormalities of Ventricular Repolarization in Mitral Valve Prolapse

Objectives: Mitral valve prolapse (MVP) is associated with arrhythmias and sudden death. Some studies suggest that abnormalities of the autonomic nervous system (ANS) may contribute to these arrhythmias. In a family investigation with genetic analysis of patients carrying a MVP, we performed a Holter study to define the autonomic profile of MVP. Methods and Results: A 24‐hour digitized 3‐lead Holter ECG was recorded in 30 patients with MVP and in two control groups, a group of 30 healthy relatives and a group of 31 healthy volunteers. We studied especially heart rate variability (HRV) and QT dynamicity. The slope of the relationship between ventricular repolarization and heart rate was studied separately during day and night. There was no difference in HRV (SDNN, rMSSD) among the three groups. On the contrary, QT interval duration was increased in patients with MVP as compared to healthy relatives (QT end: 409 ± 52 ms vs 372 ± 23 ms, P < 0.05; QT apex: 319 ± 42 ms vs 286 ± 23 ms, P < 0.01) and to healthy volunteers (QT end: 409 ± 52 ms vs 376 ± 25 ms, P = 0.004; QT apex: 319 ± 42 ms vs 289 ± 23 ms, P < 0.01). Nocturnal ventricular repolarization rate dependence was increased in MVP as compared to healthy relatives (0.16 ± 0.06 vs 0.13 ± 0.04, P < 0.05) and to healthy volunteers (0.16 ± 0.06 vs 0.11 ± 0.06, P < 0.001) whereas the 24‐hour and diurnal QT–R‐R slope was not disturbed. Conclusion: In MVP, QT is increased and the circadian modulation of QT end/RR slope is disturbed with an increased nocturnal rate dependence. These abnormalities of ventricular repolarization might explain the risk of arrhythmic events in MVP.     

Long-term captopril treatment improves diastolic filling more than systolic performance in rats with large myocardial infarction

Objectives. This study sought determine the effects of long-term angiotensin-converting enzyme (ACE) inhibition on left ventricular (LV) diastolic filling in postinfarction heart failure.Background. Long-term treatment with ACE inhibitors is beneficial in experimental animals and patients with heart failure. Because this treatment typically produces only small improvements in LV systolic function, we hypothesized that improvements in LV diastolic filling might contribute to the overall beneficial effects of ACE inhibitors after myocardial infarction (MI).Methods. We performed transthoracic echocardiographic-Doppler examinations in rats 1 and 6 weeks after transmural MI or sham operation. Rats with MI were randomized to no treatment (n = 10) or captopril (2 g/liter in drinking water, n = 8) after the baseline echocardiogram.Results. Six weeks after MI, untreated rats bad significant LV dilation compared with sham-operated rats (LV diastolic dimension [mean ± SEM] 10.7 ± 0.3 vs. 8.5 ± 0.3 mm, p < 0.05). Rats with untreated MI also had impaired fractional shortening (9 ± 1% vs. 34 ± 2%, p < 0.05) and depressed systolic thickening of the noninfarcted posterior wall (37 ± 3% vs. 65 ± 9%, p < 0.05). Rats with MI showed progressively restricted LV diastolic filling as assessed by transmitral Doppler recordings. At 6 weeks, peak early filling velocity (E) was increased (97 ± 3 vs. 77 ± 2 cm/s, p < 0.05), E wave deceleration was more rapid (23 ± 3 vs. 12 ± 1 m/s², p < 0.05), isovolumetric relaxation time was decreased (18 ± 1 vs. 24 ± 1 ms, p < 0.05), and late filling velocity was lower (26 ± 7 vs. 34 ± 1 cm/s, p < 0.05) in rats with MI versus sham-operated rats. Compared with rats with untreated MI, rats receiving captopril had similar LV diastolic dimensions (10.5 ± 0.35 vs. 10.7 ± 0.35 mm), slightly higher fractional shortening (16 ± 2% vs. 9 ± 1%, p < 0.05 [captopril MI vs. untreated MI]) and unchanged posterior wall thickening (49 ± 12% vs. 37 ± 3%, p = 0.3). In contrast, captopril almost completely normalized diastolic filling abnormalities (E velocity 82 ± 5 cm/s, p < 0.05 [captopril MI vs. untreated MI]; E wave deceleration rate 15 ± 2 m/s², p < 0.05 [captopril MI vs. untreated MI]; isovolumetric relaxation time 20 ± 1 ms).Conclusions. Long-term captopril treatment in rats with a large MI modestly limits LV remodeling and the development of systolic dysfunction but markedly improves the restrictive diastolic filling abnormalities that are seen in untreated rats.     

Prediction of the Recurrence of Atrial Fibrillation After Successful Cardioversion with P Wave Signal‐Averaged ECG

Background: The recurrence of atrial fibrillation (AF) was often observed after cardioversion. Methods: In our study, a P wave triggered P wave signal‐averaged ECG (P‐SAECG) was performed on 118 consecutive patients 1 day after successful electrical cardioversion in order to evaluate the utility of this method to predict AF after cardioversion. We measured the filtered P wave duration (FPD) and the root mean square voltage of the last 20 ms of the P wave (RMS 20). Results: During a 1‐year follow‐up, a recurrence was observed in 57 patients (48%). Patients with recurrence of AF had a larger left atrial size (41.9 ± 4.0 vs 39.3 ± 3.1 mm, P < 0.0003), a longer FPD (139.6 ± 16.0 vs 118.2 ± 14.1 ms, P < 0.0001), and a lower RMS 20 (2.57 ± 0.77 vs 3.90 ± 0.99 μV, P < 0.0001). A cutoff point (COP) of FPD ≥126 ms and RMS 20 ≤3.1 μV could predict AF with a specificity of 77%, a sensitivity of 72%, a positive value of 75%, a negative predictive value of 75%, and an accuracy of 75%. A stepwise logistic regression analysis of variables identified COP (odds ratio 9.97; 95% CI, 4.10–24.24, P < 0.0001) as an independent predictor for recurrence. Conclusions: We conclude that the probability of recurrence of AF after cardioversion could be predicted by P‐SAECG. This method seems to be appropriate to demonstrate a delayed atrial conduction that might be a possible risk factor of reinitiation of AF.