Effect of standing on ventricular parasystole: shortening of the parasystolic cycle length.

OBJECTIVE: To investigate the effect of standing on the parasystolic cycle length in cases of "true" ventricular parasystole. METHODS: Parasystolic cycle length and sinus cycle length were measured during lying and standing in eight men with true ventricular parasystole. These cycle lengths were also measured after exercise in the lying position. RESULTS: In all cases, parasystolic cycle length and sinus cycle length both shortened on standing, by a mean of 6.4% and 17.8%, respectively, compared to lying. In all cases, the rate of shortening of the parasystolic cycle length was less than that of the sinus cycle length. Parasystolic cycle length was prolonged after exercise, in contrast to a shortening of the sinus cycle length. CONCLUSIONS: Influences on the parasystolic cycle length are not always in the same direction as on the sinus cycle length. This suggests that the effect of autonomic changes on parasystolic rhythm is not always parallel to that on sinus rhythm.     

Influence of sinus impulses on the parasystolic cycle length

Recently, it has been shown that in most clinical cases of parasystole, the parasystolic rhythm is not completely independent of the sinus rhythm. In this study, to disclose the mechanism of such "irregular" parasystole, parasystolic cycles with an intervening sinus QRS complex (XSX) were compared with their immediately adjacent pure parasystolic cycles without any intervening nonparasystolic QRS complexes (XX) in 10 cases of ventricular parasystole. In eight cases, the XSX interval was equal to or nearly equal to the adjacent pure XX interval; in one, the XSX interval was shorter than the XX interval; and in only one, the XSX interval was longer than the XX interval. In six cases in which the XSX interval was almost equal to the XX interval, calculated XSX intervals with a later intervening sinus QRS complex were obtained from the differences between the XSSX interval (ie, interectopic interval with two intervening sinus QRS complexes) and its adjacent XX interval. In five of the six cases, the calculated XSX interval was shorter than the XX interval. These observations suggest that in most cases of parasystole, early intervening sinus impulses do not change the parasystolic cycle, whereas late intervening sinus impulses shorten the parasystolic cycle. This suggests the presence of type I second-degree entrance block as the mechanism of "irregular" parasystole.     

Intermittent sinus bigeminy as an expression of sinus parasystole: A case report

A case of sinus parasystole is reported. The diagnosis of sinus parasystole is relatively difficult because there is no difference between the basic sinus P wave and the parasystolic wave. Sinus parasystole is diagnosed according to the following electrocardiographic criteria: (1) premature P waves having contour identical to P waves of basic beats; (2) intervals between premature P waves mathematically related. In the case reported, the coupling intervals during long phases of intermittent sinus bigeminy were nearly fixed, because there was little variability in the returning cycles, making the diagnosis of sinus parasystole difficult.     

Ventricular parasystole and ventricular couplets: A re-entry within the parasystolic focus?

We report a 62-year-old man with a persistent ventricular rhythm originating in a parasystolic focus associated with frequent ventricular couplets with fixed coupling. Both intravenous (IV) procainamide (1 g) and propafenone (70 mg IV) promptly suppressed only the second component of ventricular couplets, suggesting that re-entry rather than enhanced automaticity was the mechanism of ventricular couplets. On the contrary, the nonresponse of ventricular rhythm and ventricular couplets to verapamil (10 mg IV) suggested that triggered activity should not play a role in the genesis of this ventricular rhythm. The mechanisms of the ventricular couplets (rapidly discharging parasystolic focus vs. re-entry) are discussed.     

Effect of amiodarone on dispersion of atrial refractoriness and cycle length in patients with atrial fibrillation

INTRODUCTION: Amiodarone is effective in preventing the recurrence of atrial fibrillation (AF) after cardioversion (CV). Dispersion of atrial refractoriness may be relevant to the generation of AF. We designed a study to determine the electrophysiologic effects of amiodarone in patients with previous early recurrence of AF after CV. METHODS AND RESULTS: Fifteen patients with previous AF recurrence (without antiarrhythmic drugs) after CV (CV1) were selected for amiodarone therapy and repeat CV (CVamio). Prior to CV1, mean AF cycle length (AFCL) had been recorded at four atrial sites (right atrial appendage [RAA], distal coronary sinus [DCS], right atrial lateral wall [LAT], and interatrial septum [IAS]) and dispersion of AFCL had been calculated. These patients were treated with amiodarone and, prior to CVamio, AFCL was recorded at the four atrial sites as for CV1. Between CV1 and CVamio, AFCL increased at all atrial sites: 153 +/- 13 msec to 179 +/- 14 msec at RAA, 144 +/- 12 msec to 174 +/- 18 msec at DCS, 158 +/- 13 msec to 182 +/- 16 msec at LAT, and 161 +/- 18 msec to 181 +/- 17 msec at IAS. Dispersion of AFCL decreased from 24 +/- 10 msec at CV1 to 15 +/- 11 msec at CVamio (P = 0.01). The median time in sinus rhythm increased from 3.12 hours post CV1 to 28 days post CVamio, (P < 0.02). CONCLUSION: Amiodarone causes a reduction in the dispersion of AFCL. This action may be relevant to the beneficial effects of amiodarone in patients with AF.     

New method of determining the atrial fibrillation cycle length during human atrial fibrillation

INTRODUCTION: The aim of this study was to investigate the usefulness of the autocorrelation function (reversed fast Fourier transform analysis) in determining the atrial fibrillation cycle length (AFCL) during human atrial fibrillation (AF). METHODS AND RESULTS: From 30 episodes of atrial electrograms recorded for 30 seconds from the high right atrium during type I AF in 16 patients, the mean, 5th percentile (p5), and 95th percentile (p95) of the AFCLs were measured by using a computer-picked activation time. The peak, minimum, and maximum AFCLs also were measured by using the autocorrelation function. The mean AFCL was retrieved at the point of the maximum peak of the coefficient of the first positive autocorrelogram. The minimum AFCL (min AFCL) was chosen as the point where the first positive autocorrelogram crossed the baseline from negative to positive, and the maximum AFCL (max AFCL) was chosen as the point where the first positive autocorrelogram crossed the baseline from positive to negative. There was a significantly strong correlation between the mean and peak AFCLs (r = 0.995, P < 0.0001), p5 and min AFCLs (r = 0.953, P < 0.0001), and p95 and max AFCLs (r = 0.98, P < 0.0001). CONCLUSION: The autocorrelation function was useful in determining the AFCLs, at least during type I AF. The min AFCL may be used as an index of the refractory period during AF when the p5 AFCL approximates the refractory period.     

Fluctuations of the atrial cycle length and A-V delay with a universal (DDD) pacemaker

The electronic characteristics of a new universal (DDD) pulse generator can result in significant shortening of the atrial cycle length (A-A interval) and shortening of the atrioventricular (A-V) interval beyond the programmed values. These pacemaker arrhythmias are entirely compatible with normal function and must not be interpreted as malfunctions.     

Non-invasive assessment of magnitude and dispersion of atrial cycle length during chronic atrial fibrillation in man

Aims Atrial fibrillation cycle lengths can be assessed from rightprecordial ECG leads and the unipolar oesophageal ECG usinga non-invasive method called Frequency Analysis of FibrillatoryECG. The purpose of this report is to present the results fromapplication of this method in a large group of patients withlong-term atrial fibrillation and to examine the differencesbetween patients with ‘coarse’ and ‘fine’atrial fibrillation. Methods and Results Simultaneous 15min recordings from V₁, V₂and an oesophageallead at a position behind the posterior atrium were obtainedin 28 patients, aged 41 to 78 years, with long-term (>1 month)atrial fibrillation. In each lead, using the time averagingtechnique, the QRST complexes were suppressed. Thereafter, thefrequency distribution of the residual ECG was estimated bymeans of Fast Fourier Transform. In the 3–12Hz range ofeach lead, the dominant atrial cycle length, the power maximumand the spectral width were calculated. In 26 patients (93%), frequency spectra in the 3–12Hzrange could be obtained. The dominant atrial cycle length rangedfrom 120 to 175ms, mean 150±16 (SD) ms in V₁, and from120 to 190ms, mean 150±16 in an oesophageal lead (ns).The absolute difference in the dominant atrial cycle lengthbetween V₁and the oesophageal lead was 10·4±7·7ms.There was no significant difference in the dominant atrial cyclelength in V₁between patients with coarse and fine atrial fibrillation.The power maximum in V₁was significantly greater in patientswith coarse compared to fine atrial fibrillation (P=0·01).The spectral widths ranged from 10 to 55ms and demonstratedsignificantly higher mean values in lead V₂compared to V₁(P=0·001).Compared to V₁, the mean values tended to be smaller in theoesophageal lead (P=0·05). Conclusions Using the Frequency Analysis of Fibrillatory ECG method, thedominant atrial cycle length, power maximum and spectral widthcan be estimated from the frequency spectra in the majorityof patients with atrial fibrillation. Spatial dispersion ofthe dominant atrial cycle length occurs in some patients andmay be an important proarrhythmic marker. The distinction betweencoarse and fine atrial fibrillation cannot be used as a markerof the atrial cycle length.     

Autonomic modulation of the atrial cycle length by the head up tilt test: non-invasive evaluation in patients with chronic atrial fibrillation

Objective—To determine the effects of upright posture compared with supine position on the dominant atrial cycle length (DACL) in patients with chronic atrial fibrillation.
Design—The power/frequency spectrum of QRST suppressed lead V1 ECG was studied in 14 patients in the supine position and during the head up tilt table test. The DACL changes were compared with changes in heart rate and blood pressure.
Results—Compared with the supine position, the upright position reduced the DACL from 160 to 150 ms (p < 0.01). The DACL was increased after returning to the supine position from the upright position, from 147 to 154 ms (p < 0.01). Heart rate increased from 91 beats/min in the supine position to 106 in the upright position (p < 0.01). There was a decrease in heart rate from 109 beats/min in the upright position to 93 after returning to the supine position (p < 0.01). No significant changes were seen in systolic or diastolic blood pressure. There were indications of an inverse relation between DACL and heart rate when comparing the supine position before and after tilt with the upright position (p < 0.001).
Conclusions—The sympathetic stimulation and vagal withdrawal induced by rising to upright body position are associated with a decrease in DACL during chronic atrial fibrillation. Thus a reflex increase in sympathetic discharge after induction of atrial fibrillation could favour the persistence of the arrhythmia.

Keywords: atrial fibrillation;  autonomic nervous system;  atrial cycle length;  heart rate     

Influence of heart rate on systolic time intervals: Effects of atrial pacing versus dynamic exercise

The effects of atrial pacing and dynamic exercise in the supine position on systolic time intervals (STI) were compared in 10 normals. In another group of 13 normals, the effect of exercise alone on STI was tested. A linear shortening of electromechanical systole (QS₂) and left ventricular ejection time (LVET) with increasing heart rate was demonstrated with right atrial pacing and dynamic exercise in the frequency range between 60 and 140 beats/min. However, the shortening of LVET was significantly less (p<0.01) with exercise compared to pacing. This is explained by an increase in left ventricular stroke volume with exercise. The pre-ejection period (PEP) was significantly (p<0.001) shortened with exercise, but there was no change with atrial pacing. Thus, changes in heart rate (HR) alone, without changes in the dynamic state of the heart, did not influence PEP. It is suggested that PEP at rest should not be corrected for heart rate. The supine exercise regression equations for correction of heart rate for LVET and PEP differ from both the resting and the upright exercise regression equations. With exercise a frequency correction of STI using regression equations should be abandoned. Instead, uncorrected STI at standard heart rates (e.g., 100, 110, and 130 beats/min) should be taken for comparison. Heart rate standardization should be employed using the formula     

Effect of cardiac exposure by median sternotomy on atrial fibrillation cycle length.

BACKGROUND: Epicardial mapping is a powerful tool that has enabled us to gain insight into the electrical phenomena perpetuating atrial fibrillation and has guided the design of surgical and catheter-based therapeutic strategies. However, epicardial data are acquired during abnormal physiological conditions; the patients are anaesthetized, their chests opened, dislocating the heart and exposing it to air of room temperature, and the autonomic tone is modulated due to the surgery. The effect of intra-operative conditions on atrial electrophysiological properties have not been investigated before. Thus in the present study we assessed the atrial cycle length, shown to be an index of atrial refractoriness, and the ventricular rate before and during open-heart surgery in 10 patients with chronic atrial fibrillation and an underlying heart disease. METHODS AND RESULTS: Using a newly introduced and validated ECG method known as frequency analysis of fibrillatory ECG (FAF-ECG), the atrial cycle length and the ventricular rate were determined just before surgery. After anaesthesia and median sternotomy, epicardial mapping of the entire right atrial free wall was performed. The mean ventricular rate as well as the dominant atrial fibrillation cycle length consistently increased, the former from 71 to 92 beats x min(-1) (mean of all patients, P<0.05) and the latter from 156 to 172 ms (P<0.05). CONCLUSIONS: Atrial fibrillation cycle length, an index of atrial refractoriness, is increased as an effect of anaesthesia and heart exposure during open-heart surgery in patients with chronic atrial fibrillation, implying that atrial activation might be altered, which must be considered when interpreting data from epicardial conduction analysis.     

运动康复在心房颤动中作用的研究进展

心房颤动是临床常见的心律失常,且成为威胁国民健康的慢性病之一。但当前其治疗方案局限于下游,缺少上游干预及预防。心脏运动康复已被证实可提高冠心病、心力衰竭等多种心血管病患者的运动能力并改善症状。但运动训练在心房颤动管理中的作用尚不明确,且存在很多争议。本文通过阐述运动在心房颤动预防中的作用,及对非永久性房颤和永久性房颤的影响,系统回顾了运动康复在心房颤动中作用的最新研究进展。     

心房颤动周长与导管消融效果的关系

目的分析不同类型以及不同因素心房颤动(简称房颤)患者房颤周长(AFCL)的特点以及与导管消融效果的关系。方法选取本院行导管消融的房颤患者35例,其中阵发性房颤和持续性房颤分别为20例和15例。所有患者术前房颤心律下行食管电生理检查,记录左房后壁电活动,测量房颤周长。结果持续性房颤AFCL显著短于阵发性房颤患者(143±33 ms vs 151±31 ms,P<0.05)。AFCL与性别、是否合并高血压、糖尿病等因素无关,但AFCL在老龄、房颤病史较长、左房较大的患者中明显缩短。房颤消融术后无复发的患者AFCL明显长于复发患者(152±28 ms vs 133±22 ms,P<0.05)。左房直径和AFCL是房颤消融效果的独立预测因素。结论房颤周长可作为预测房颤预后的重要指标。     

Paroxysmal cycle length shortening in the pulmonary veins during atrial fibrillation correlates with arrhythmogenic triggering foci in sinus rhythm

INTRODUCTION: The focal origin of atrial fibrillation (AF) is identified by recording atrial ectopic beats or the ectopic activity that precedes AF. We hypothesized that arrhythmogenic pulmonary veins (PVs) also could be identified during persistent AF. METHODS AND RESULTS: Patients with persistent AF referred for focal ablation were enrolled prospectively. During AF, bipolar electrograms were recorded from each PV for a minimum of 120 seconds, as well as from the right atrium and coronary sinus. The cycle length of activity in each PV was measured during AF and plotted on a frequency histogram. Following cardioversion to sinus rhythm, arrhythmogenic PVs were identified from reinitiation of AF or from ectopic beats. Ten patients were enrolled and 37 PVs analyzed. During AF, 17 PVs demonstrated bimodal cycle length frequency histograms, with periods of paroxysmal short cycle length recording. Following cardioversion, 14 PVs were identified as arrhythmogenic as defined earlier. Each of these arrhythmogenic PVs showed paroxysmal short cycle length recording during AF. Sensitivity was 87%, specificity 91%, positive predictive value 87%, and negative predictive value 100%. CONCLUSION: The arrhythmogenic PVs responsible for the focal activity that triggers AF also demonstrate paroxysmal short cycle length recording during sustained AF. These results demonstrate that arrhythmogenic PVs still can be identified reliably, even during sustained AF.     

Role of dispersion of atrial refractoriness in the recurrence of clinical atrial fibrillation; a manifestation of atrial electrical remodelling in humans?

AIMS: The mechanism of atrial fibrillation recurrence following cardioversion is unknown, although experimental studies have indicated that changes in dispersion of atrial refractoriness may play a role. The aims of this study were to assess (1) if dispersion of atrial refractoriness is relevant to atrial fibrillation recurrence and (2) if dispersion of refractoriness is part of the atrial electrical remodelling process in humans. METHODS AND RESULTS: Thirty-seven consecutive patients underwent internal cardioversion (CV1) of persistent atrial fibrillation. Patients were monitored by daily transtelephonic recordings following discharge and if there was spontaneous atrial fibrillation recurrence they were rapidly admitted for repeat cardioversion (CV2). We used the 5th percentile of 100 consecutive atrial fibrillation cycle lengths (AFCL(P5)) and the atrial effective refractory period (AERP) as measures of atrial refractoriness at four different atrial sites. Dispersion of AFCL(P5)at CV1 was significantly higher in those who had subsequent recurrence of atrial fibrillation than in those who remained in sinus rhythm for at least 1 month after cardioversion (35+/-17 ms vs 9+/-13 ms;P<0.02). Dispersion of AFCL(P5)measured at CV2 was significantly lower than that measured in the same patients at CV1 (19+/-8 ms vs 35+/-11 ms;P=0.02). i.e. dispersion of AFCL(P5)had reduced following a period of sinus rhythm. In contrast, there was no difference in dispersion of AERP between the recurrers and non-recurrers. Dispersion of AERP between CV1 and CV2 did not change following a period of sinus rhythm. CONCLUSION: Dispersion of AFCL is relevant to atrial fibrillation recurrence and may represent a manifestation of atrial electrical remodelling in humans. Treatment directed at AFCL dispersion may be useful in the suppression of atrial fibrillation recurrence following cardioversion.     

Effect of exercise on cycle length in atrial flutter.

OBJECTIVE--To examine the effect of exercise on cycle length in atrial flutter. PATIENTS--15 patients with chronic atrial flutter. Seven patients were taking digoxin and six verapamil; two were not taking medication. METHODS--All patients underwent bicycle ergometry. Flutter cycle length was measured at rest and at peak exercise. RESULTS--Mean flutter cycle length increased from 245 ms to 256 ms (P = 0.002). Six patients developed 1:1 atrioventricular conduction. Significant increases in flutter cycle length were observed irrespective of development of 1:1 atrioventricular conduction and use of digoxin and verapamil. CONCLUSION--Exercise prolongs flutter cycle length. This effect would promote development of 1:1 atrioventricular conduction during exercise, causing inordinately high ventricular rates.     

The interrelation between the monophasic action potential duration, cycle length and ischaemia in the human left ventricle.

Steady state monophasic action potentials were recorded from a single site in the left ventricular endocardium during incremental atrial pacing to the point of angina in 25 patients. Ischaemic areas of the left ventricle were documented using a perfusion marker (99mTc-MIBI) simultaneously with the action potential recording procedure. Recordings were obtained from an ischaemic area in 13 patients and from a non-ischaemic area in 12. A linear correlation between action potential duration and cycle length changes was demonstrated for both ischaemic and non-ischaemic zone recordings between cycle length changes of 750 and 428 ms. Ischaemia induced a shortening of the action potential duration significantly greater than that produced by cycle length changes (P less than 0.0001). Mean action potential duration shortening corrected for 100 ms change in cycle length for ischaemic zone recordings was 31.4 +/- 4.2 (SD) compared to 23.3 +/- 3.1 ms for non-ischaemic zone recordings. A range of values of action potential duration shortening in unit time was analysed for sensitivity and specificity for the detection of ischaemia. A value of 26.5 ms per 100 ms change in cycle length provided the optimum compromise with 88% sensitivity and specificity. Our data provide a means of employing the monophasic action potential duration to quantify early localized ischaemia in the presence of an alteration in cycle length.     

Effects of cycle length on atrial vulnerability.

The effect of cycle length on atrial vulnerability was studied in 14 patients manifesting reproducible repetitive atrial firing during atrial extra-stimulus (A2) testing. Repetitive atrial firing was defined as the occurrence of two or more premature atrial responses with return cycle (A2-A3) of 250 msec or less and subsequent mean cycle length of 300 msec or less, following A2. The zone of repetitive atrial firing could be defined in terms of its longest and shortest A1-A2 coupling intervals. Each patient was tested at a long cycle length (CL1) (mean 884 msec) and a short cycle length (CL2) (mean 557 msec). CL1 was sinus rhythm and CL2, an atrial paced rhythm. Repetitive atrial firing occurred in two patients at CL1 and in all patients at CL2. Of the former two patients (group 2), the zone of repetitive atrial firing was markedly widened in one at CL2 due to a shortening of atrial functional refractory period (FRP) at CL2. In the other, zone of repetitive atrial firing could not be totally defined due to induction of sustained atrial flutter preventing definition of atrial FRP. The occurrence of repetitive atrial firing at only CL2 in 12 patients (group 1) reflected: 1) a shortening of atrial FRP from 294 +/- 11 msec at CL1 to 242 +/- 10 msec at CL2 (mean +/- SEM; P less than 0.01), allowing delivery of A2 at shorter coupling intervals (9); 2) the new occurrence of repetitive atrial firing at A1-A2 coupling intervals achievable at both cycle lengths (1); or 3) both effects (2). In conclusion, decrease of cycle length potentiated atrial vulnerability. This demonstration implies that atrial pacing could potentiate occurrence of paroxysmal atrial fibrillation or flutter.