Chronic Pacing Research Articles

The Subcutaneous/Leadless ICD

Since the original demonstration in 1980 by Michel Mirowski that an implantable defibrillator (ICD) could save lives, these devices have become routine therapy. The requirement for a transvenous lead is associated with patient morbidity and, when lead extraction is necessary, mortality. In 2010, Bardy et al. published the first use in humans of a novel system utilising a solely subcutaneous parasternal lead with a laterally placed canister to achieve reliable defibrillation. This landmark study culminated 9 years of intensive research to identify the most effective defibrillating electrode configuration. The guiding principle for the subcutaneous defibrillator (S-ICD) has been operational simplicity. Device settings are automated except for shock therapy (on/off), post-shock pacing (on/off), conditional shock zone (on/off, rate) and shock zone (170–240 beats/min). The S-ICD system automatically selects an appropriate vector for rhythm detection to best avoid double QRS counting and T-wave oversensing. Absence of chronic pacing capability excludes patients requiring anti-bradycardia pacing and a transvenous device is more appropriate for patients with relatively slow VT or demonstrated reliable anti-tachycardia VT termination. The ability to utilise signals more closely approximating the surface ECG electrograms may reduce the incidence of inappropriate shocks, which remain common with transvenous systems irrespective of single or dual chamber sensing. The S-ICD is commercially available in Europe and being assessed by the FDA in the United States. It presently bodes to be an important advance for patients requiring primary prevention against sudden death.

Right ventricular pacing in MADIT-II: A risk factor for increased mortality, or mainly a marker of increased risk

f s a t p w . q n The potential for right ventricular apical (RVA) pacing to impact clinical outcomes adversely in patients with permanent pacemakers and implantable cardioverter-defibrillators (ICDs) has led to substantial changes in implantable device algorithms and the manner in which devices are selected and programmed. In this regard, the largely unanticipated observations of the Dual-Chamber and Implantable Defibrillator (DAVID) trial provided the trigger; however, findings from studies both preceding and subsequent to DAVID support the notion that chronic RVA pacing increases the risk of both new or worsening heart failure (HF) and of mortality in a certain proportion of paced patients. The DAVID trial comprised ICD patients with ejection fraction (EF) 40% and no pacing indication. In terms of radycardia pacing, devices were programmed to either a backup” pacing mode only (VVI 40 bpm) or the DDDR ode with base rate of 70 bpm. At 18-month follow-up, ndividuals in whom pacing had been programmed to VVI 0 bpm had a low (about 1%) RV pacing frequency and a ignificantly lower incidence of the combined endpoint of eath and HF hospitalizations than did DDDR-paced paients in whom RV pacing frequency was approximately 0%. In reexamining DAVID trial data, Sharma et al determined that RV pacing frequency (primarily RVA pacing) was crucial in determining adverse outcome, whereas other possible contributors, such as New York Heart Association (NYHA) functional class and EF were not. The best separation between higher and lower risk occurred with DDDR pacing 40% versus 40%. Initially, it seemed that the adverse RV pacing effect was primarily a problem in the relatively “sick” ICD population given their usual low left ventricular EF and frequent HF history. However, this assumption was not valid. As previously noted, similar observations were already evident in several pacemaker clinical studies in which impaired left ventricular function was not an issue. For instance, a substudy of the Mode Selection Trial (MOST) examined findings in 1,339 patients with normal baseline QRS dura-

Upgrading to Biventricular Pacing Guided by Pressure-Volume Loop Analysis During Implantation

cardiac resynchronization therapy (CRT) may improve prognosis in patients with chronic right ventricular (RV) pacing, and optimal lead position can decrease nonresponders. We evaluated the clinical and echocardiographic response to CRT in patients with previous chronic RV pacing, using pressure-volume loop analyses to determine the optimal left ventricular (LV) lead position during implantation. In this single-blinded, randomized, controlled crossover study, 40 patients with chronic RV apical pacing and symptoms of heart failure, decreased LV ejection fraction (LVEF) or dyssynchrony were included. During implantation, stroke work (SW), LVEF, cardiac output, and LV dP/dt(max) were assessed by a conductance catheter. Clinical and echocardiographic response was studied during a 3-month period of RV pacing (RV period, LV lead inactive) and a 3-month period of biventricular pacing (CRT period). At the optimal LV lead position, SW (37 ± 41%), LVEF (16 ± 13%), cardiac output (29 ± 16%), and LV dP/dt(max) increased (11 ± 11%) significantly during biventricular pacing compared to baseline. Additional benefit could be achieved by pressure-volume loop guided selection of the best left-sided pacing location. RV outflow tract pacing did not improve hemodynamics. During follow-up, symptoms improved during CRT, VO(2,max) increased 10% and significant improvements in LVEF, LV volumes, and mitral regurgitation were observed as compared to the RV period. CRT in patients with chronic RV pacing causes significant improvement of both LV function as measured by pressure-volume loops during implantation and clinical and echocardiographic improvement during follow-up. Pressure-volume loops during implantation may facilitate selection of the most optimal pacing site.

Chronic ventricular pacing in children: toward prevention of pacing-induced heart disease

In children with congenital or acquired complete atrioventricular (AV) block, ventricular pacing is indicated to increase heart rate. Ventricular pacing is highly beneficial in these patients, but an important side effect is that it induces abnormal electrical activation patterns. Traditionally, ventricular pacemaker leads are positioned at the right ventricle (RV). The dyssynchronous pattern of ventricular activation due to RV pacing is associated with an acute and chronic impairment of left ventricular (LV) function, structural remodeling of the LV, and increased risk of heart failure. Since the degree of pacing-induced dyssynchrony varies between the different pacing sites, ‘optimal-site pacing’ should aim at the prevention of mechanical dyssynchrony. Especially in children, generally paced from a very early age and having a perspective of life-long pacing, the preservation of cardiac function during chronic ventricular pacing should take high priority. In the perspective of the (patho)physiology of ventricular pacing and the importance of the sequence of activation, this paper provides an overview of the current knowledge regarding possible alternative sites for chronic ventricular pacing. Furthermore, clinical implications and practical concerns of the various pacing sites are discussed. The review concludes with recommendations for optimal-site pacing in children.

Effect of Peri-Infarct Pacing Early After Myocardial Infarction

Background— Left ventricular (LV) remodeling has been attributed to the segmental loss of viable myocardium due to myocardial infarction (MI), which results in redistribution of cardiac workload, with increased regional wall stress in and around the infarct zone. Because ventricular pacing has been shown to reduce regional wall stress and workload in regions near the pacing site, this trial was designed to test whether chronic pacing near the infarct attenuates LV remodeling. Methods and Results— Eighty patients with an anterior MI, peak creatine kinase >2000 mU/mL, ejection fraction ≤35%, wall motion abnormality (WMA) in >5 of 16 segments, and QRS <120 ms, were randomized to either control (implantable cardioverter-defribillator [ICD]) or biventricular pacing with peri-infarct LV lead placement (cardiac resynchronization therapy [CRT]-D) arms between 2 and 14 days after the MI. The primary end point—change in LV end-diastolic volume (LVEDV) from baseline to 12 months—was not significantly different between the 2 groups (CRT, 10.6±27.7 mL; ICD, 11.2±31.2 mL; 2-sample t test P >0.05). In a hypothesis-generating secondary analysis, there was a sustained reduction in the WMA score at 12 months in paced patients (CRT, −0.16±0.28; ICD, −0.01±0.24, 2-sample t test P =0.03). No differences were found in the therapy-related event rate, hospitalizations, or mortality (all P >0.05). Conclusions— Chronic pacing in the infarct region did not alter the primary end point of LV remodeling over 1 year. Clinical Trial Registration— URL: http://www.clinicaltrials.gov . Unique identifier: NCT00605631.

Left ventricular dysfunction due to right ventricular stimulation: is biventricular upgrade really necessary?

Left ventricular (LV) dysfunction can occur due to chronic right ventricular apical pacing. Upgrading of the pacemaker to biventricular pacing is an option to reverse LV dysfunction but reprogramming of the atrioventricular (AV) timing can also be favourable. In this case report we describe the effect of AV-time reprogramming in a patient with LV function deterioration that emerged two years after implantation of a dual chamber system for sick sinus syndrome. Echocardiographc studies demonstrated a tremendous improvement in LV function during two years follow-up whereas the percentage of right ventricular pacing diminished dramatically. Careful analysis of the cause of LV deterioration can avoid unnecessary upgrading to biventricular pacing. (Neth Heart J 2010;18:604-5.).

E0095 The study on the relations between rennin-angiotensin-aldosterone system and atrial structural remodelling and atrial fibrillation

ObjectiveTo investigate the effects of perindopril and/or spironolactone on atrial structural and functional remodelling in atrial fibrillation (AF) dogs induced by chronic rapid atrial pacing, and research the relations between...

E0018 Vagus nerve-mediated electrical remodelling of pulmonary veins in chronic atrial pacing dogs with or without superior vena cava and aortic root fat pad

ObjectivesWe aim to elucidate the relationship between vagus nerve and the electrical remodelling of pulmonary veins in vagus nerve-mediated atrial fibrillation dogs.Methods24 adult mongrel dogs weighing 15–20 Kg were randomly...

Performance of the Lumenless 4.1‐Fr Diameter Pacing Lead Implanted at Alternative Pacing Sites in Congenital Heart: A Chronic 5‐Year Comparison

United States approval of the Model 3830, 4.1-French (Fr) diameter, lumenless, pacing lead (Medtronic Inc., Minneapolis, MN, USA) in patients under 17 years of age, and those with congenital heart disease (CHD), was in 2005. To date, long-term performance at alternative pacing sites (APS) is limited and chronic efficacy comparisons with more established leads is lacking. The purpose of this study was to evaluate these factors. Implant and follow-up data on leads were compared: group 1 (non-3830 leads) and group 2 (Model 3830 leads). These included acute and chronic sensing and pacing, impedances, implant sites, and complications. Groups were compared using Fischer's exact test, paired, and nonpaired t-tests, with significance defined at P < 0.05. A total of 119 patients (ages 5-48 years) received 171 leads: group 1 (n = 80) and group 2 (n = 91). At implant, there were no differences in patient age, CHD, sensing, or pacing thresholds between groups. Implant lead impedances differed between groups but all were within normal values for each lead design. Chronic data showed no difference in sensing, pacing thresholds, or impedances. There were five (6%) early lead dislodgements in group 1 and one (1%) in group 2. APS were achieved in group 2 with mean 1.6 ± 1.3 minutes fluoroscopy time. The new 4.1-Fr lumenless lead shows similar performance indices to established leads even at APS, yet is thinner and achieves APS with technical ease, permitting more efficient chronic pacing in children and all patients with CHD.

Comparative Mechanical Activation Mapping of RV Pacing to LBBB by 2D and 3D Speckle Tracking and Association With Response to Resynchronization Therapy

The goals of this study were to compare patterns of mechanical activation in patients with chronic right ventricular (RV) pacing with those with left bundle branch block (LBBB) using 2-dimensional and novel 3-dimensional speckle tracking, and to compare ejection fraction (EF) response and long-term survival after cardiac resynchronization therapy (CRT). Several randomized CRT trials have excluded patients with chronic RV pacing, and current guidelines for CRT include patients with intrinsically widened QRS, typically LBBB. We studied 308 patients who were referred for CRT: 227 had LBBB, 81 were RV paced. Dyssynchrony was assessed by tissue Doppler, routine pulsed Doppler, and 2-dimensional speckle-tracking radial strain. 3D strain was assessed using speckle tracking from a pyramidal dataset in a subset of 57 patients for mechanical activation mapping. Survival after CRT was compared with survival in a group of 46 patients with attempted, but failed, CRT. Patients with chronic RV pacing and LBBB had similar intraventricular dyssynchrony, with opposing wall delays by tissue Doppler of 82 +/- 45 ms versus 87 +/- 63 ms and anteroseptum-to-posterior delays by speckle tracking of 225 +/- 142 ms, versus 211 +/- 107 ms, respectively. RV-paced patients, however, had greater interventricular dyssynchrony: 44 +/- 24 ms versus 35 +/- 21 ms (p < 0.01), which correlated with their greater QRS duration (p < 0.001). Sites of latest mechanical activation were most often posterior or lateral in both groups, but RV-paced patients had sites of earliest activation more often from the inferior-septum and apex (p < 0.05). EF response was similar in RV-paced and LBBB groups, and survival free from transplantation or mechanical support after CRT was similarly favorable as compared with failed CRT patients over 5 years (p < 0.01). RV-paced patients, when compared with LBBB patients, had similar dyssynchronous patterns of mechanical activation and greater interventricular dyssynchrony. Importantly, RV-paced patients had similar EF response and long-term outcome as those with LBBB, which supports their candidacy for CRT.

Comparison of Effectiveness of Right Ventricular Septal Pacing Versus Right Ventricular Apical Pacing

Chronic right ventricular apical pacing (RVAP) has been associated with negative hemodynamic and clinical effects. The aim of the present study was to compare RVAP with right ventricular septal pacing (RVSP) in terms of echocardiographic features and clinical outcomes. A total of 93 patients without structural heart disease and with an indication for a permanent pacemaker were randomly assigned to receive a screw-in lead either in the RV apex (n = 46) or in the RV mid-septum (n = 47). The patients were divided into 3 subgroups according to the percentage of ventricular pacing: control group (n = 21, percentage of ventricular pacing < or =10%), RVAP group (n = 28), or RVSP group (n = 32; both latter groups had a percentage of ventricular pacing >10%). The RVAP group had more intraventricular dyssynchrony and a trend toward a worse left ventricular ejection fraction compared to the RVSP and control groups at 12 months of follow-up (maximal delay to peak systolic velocity between any of the 6 left ventricular basal segments was 57.8 +/- 38.2, 35.5 +/- 20.6, and 36.5 +/- 17.8 ms for RVAP, RVSP, and control group, respectively; p = 0.006; mean left ventricular ejection fraction 62.9 +/- 7.9%, 66.5 +/- 7.2%, and 66.6 +/- 7.2%, respectively, p = 0.14). Up to 48.1% of the RVAP patients showed significant intraventricular dyssynchrony compared to 19.4% of the RVSP patients and 23.8% of the controls (p = 0.04). However, no overt clinical benefits from RVSP were found. In conclusion, RVAP was associated with increased dyssynchrony compared to the RVSP and control patients. RVSP could represent an alternative pacing site in selected patients to reduce the harmful effects of traditional RVAP.

Effects of spironolactone on atrial structural remodelling in a canine model of atrial fibrillation produced by prolonged atrial pacing

Suppression of the renin-angiotensin-aldosterone system can prevent atrial fibrillation (AF) by attenuating atrial structural remodelling but the role of aldosterone in AF prevention has not been investigated thoroughly. We explored whether the aldosterone antagonist, spironolactone, could improve atrial structural remodelling in long-term rapid pacing-induced AF. Three groups of dogs were used, sham-operated, control and spironolactone-treated groups. Dogs in the control and spironolactone groups had right atrial pacing for 6 weeks. The spironolactone group was given spironolactone 1 week before and during the atrial pacing. After 6 weeks of pacing, atrial structural and functional changes were assessed by echocardiography, haemodynamic parameters by cardiac catheterization, histopathological changes by light and electron microscopy and cardiomyocyte apoptosis by TUNEL. Caspase-3, Bcl-2, bax, calpain I, calpastatin, matrix metalloproteinase (MMP)-9 and tissue inhibitors of metalloproteinase (TIMP)-1 were analysed by immunohistochemistry and Western blotting. The inducibility and duration of AF were measured by atrial burst pacing. After atrial pacing, the proportion of TUNEL positive cells, myolysis, atrial fibrosis and dilatation were all significantly increased and these changes were inhibited by spironolactone. Spironolactone treatment reversed the increased expression of caspase-3, bax, calpain I and MMP-9 and the decreased level of Bcl-2, calpastatin and TIMP-1, induced by chronic atrial pacing. Also spironolactone prevented the increased inducibility and duration of AF, induced by tachypacing. Treatment with spironolactone prevented myocardial apoptosis, myolysis, atrial fibrosis and dilatation, suggesting a possible beneficial effect of aldosterone antagonism on atrial structural remodelling in AF.

Upgrading to resynchronization therapy after chronic right ventricular pacing improves left ventricular remodelling

Chronic right ventricular (RV) pacing may impose ventricular dyssynchrony leading to LV remodelling and is associated with increased morbidity and mortality. Upgrading patients with chronic RV pacing to cardiac resynchronization therapy (CRT) may be considered to restore synchronicity and prevent these deleterious effects. A total of 172 patients from two tertiary centres were analysed over a mean follow-up of 21.7 and 23.5 months after primary CRT implantation (n = 102) and CRT upgrade (n = 70), respectively. In the latter group, mean duration of RV pacing before CRT upgrade was 80.3 months, and ventricular stimulation was >95%. A significant improvement in left ventricular (LV) ejection fraction (10 and 11% absolute increase in primary CRT vs. upgrades, respectively), LV end-diastolic diameter index (-0.15 cm/m(2) vs. -0.2 cm/m(2)), and LV end-systolic diameter (-6.0 vs. -7.0 mm) was observed in both groups, which did not differ between primary CRT recipients and CRT upgrades. Response to CRT upgrade was independent of the underlying rhythm, QRS duration, duration of prior RV pacing, or LV function and size at baseline. Of note, even seven of nine patients with RV pacing >12 years responded favourably to CRT. The current study demonstrates that CRT reverses LV remodelling in heart failure patients with chronic RV pacing in a similar way as in primary CRT recipients, even after very long periods of RV pacing. Our data, therefore, may have important implications for the treatment of pacemaker-dependent patients with heart failure, and support the use of CRT in this setting.

Conventional Versus Biventricular Pacing in Heart Failure and Bradyarrhythmia: The COMBAT Study

Background Worsening in clinical and cardiac status has been noted after chronic right ventricular pacing, but it is uncertain whether atriobiventricular (BiVP) is preferable to atrio-right ventricular pacing (RVP). Conventional versus Multisite Pacing for BradyArrhythmia Therapy study (COMBAT) sought to compare BiVP versus RVP in patients with symptomatic heart failure (HF) and atrioventricular (AV) block. Methods and Results COMBAT is a prospective multicenter randomized double blind crossover study. Patients with New York Heart Association functional class (FC) II-IV, left ventricular ejection fraction (LVEF) <40%, and AV block as an indication for pacing were enrolled. All patients underwent biventricular system implantation and then were randomized to receive successively (group A) RVP-BiVP-RVP, or (group B) BiVP-RVP-BiVP. At the end of each 3-month crossover period, patients were evaluated according to Quality of Life (QoL), FC, echocardiographic parameters, 6-Minute Walk Test (6MWT), and peak oxygen consumption (VO 2max). Sixty patients were enrolled, and the mean follow-up period was 17.5 ± 10.7 months. There were significant improvements in QoL, FC, LVEF, and left ventricular end-systolic volume with BiVP compared with RVP. The effects of pacing mode on 6MWT and VO 2max were not significantly different. Death occurred more frequently with RVP. Conclusion In patients with systolic HF and AV block requiring permanent ventricular pacing, BiVP is superior to RVP and should be considered the preferred pacing mode.

The story of an active fixation coronary sinus lead: Promise and peril

The benefits of cardiac resynchronization therapy are well established. Patient outcomes depend on successful implantation of a left ventricular lead in a physiologically advantageous site that is stable with an acceptable acute and chronic pacing threshold and shows short- and long-term freedom from diaphragmatic or chest wall stimulation. The currently available passive fixation coronary sinus (CS) leads rely on their characteristic shape and size to remain stable in a CS branch. As such, anatomy dictates lead selection.

Down to the Wire: Tricuspid Stenosis in the Setting of Multiple Pacing Leads

Tricuspid stenosis in the setting of endocardial pacing leads is a rare entity, attributed to infection or lead malposition. We report the case of a 37-year-old man without these risk factors, who presented with new onset severe tricuspid stenosis in the setting of multiple chronic pacing leads.

Cardiac Resynchronization Therapy for Left Ventricular Dysfunction Induced by Chronic Right Ventricular Pacing in a Child

Cardiac resynchronization therapy (CRT) has been proven its value in adult patients with congestive heart failure of low ejection fraction and wide QRS duration. Contrast to adult patients, CRT has been rarely applied for young patients. We report on a 9-yr-old boy with progressive left ventricular (LV) dilatation and dysfunction following chronic VVI pacemaker therapy for congenital complete atrioventricular block associated with maternal anti-SSA/Ro and SSB/La antibody. His LV dysfunction was improved after epicardially established CRT.

Atrial Fibrillation in Congestive Heart Failure

Atrial fibrillation (AF) and heart failure (HF) are common and interrelated conditions, each promoting the other, and both associated with increased mortality. HF leads to structural and electrical atrial remodeling, thus creating the basis for the development and perpetuation of AF; and AF may lead to hemodynamic deterioration and the development of tachycardia-mediated cardiomyopathy. Stroke prevention by antithrombotic therapy is crucial in patients with AF and HF. Of the 2 principal therapeutic strategies to treat AF, rate control and rhythm control, neither has been shown to be superior to the other in terms of survival, despite better survival in patients with sinus rhythm compared with those in AF. Antiarrhythmic drug toxicity and poor efficacy are concerns. Catheter ablation of AF can establish sinus rhythm without the risks of antiarrhythmic drug therapy, but has important procedural risks, and data from randomized trials showing a survival benefit of this treatment strategy are still lacking. In intractable cases, ablation of the atrioventricular junction and placement of a permanent pacemaker is a treatment alternative; and biventricular pacing may prevent or reduce the negative consequences of chronic right ventricular pacing.

Beneficial effects of biventricular pacing in chronically right ventricular paced patients with mild cardiomyopathy

To investigate whether cardiac resynchronization therapy (CRT) by means of biventricular (BiV) pacing can improve left ventricular (LV) function, remodelling and clinical status in chronically right ventricular (RV) paced patients with mild cardiomyopathy. Thirty-six chronically (10 +/- 7 years) RV paced patients with left ventricular ejection fraction (LVEF) < 40% or LVEDD > 55 mm, without an established indication for CRT, were subjected to 6 months RV and BiV pacing in a patient-blinded, randomized crossover design. Treatment-effects of BiV pacing were evaluated for LV function, LV remodelling and clinical status. As compared with RV pacing, BiV pacing significantly improved LV function (LVEF 46 +/- 12 vs. 39 +/- 12% and LVFS 24 +/- 7 vs. 21 +/- 7%) and reduced LV end-diastolic and end-systolic diameters and volumes (LVEDD 56 +/- 8 vs. 59 +/- 8 mm, LVESD 43 +/- 8 vs. 47 +/- 9 mm, LVEDV 132 +/- 65 vs.144 +/- 62 mL and LVESV 77 +/- 56 vs. 92 +/- 55 mL, respectively). In 19 patients (53%) response to BiV pacing was clinically relevant, defined as LVESV reduction >15%. BiV pacing also significantly improved NYHA classification. BiV pacing following chronic RV pacing may improve LV function and reverse LV remodelling in patients with relatively mild LV dysfunction or remodelling. Hence, upgrade to BiV pacing might be considered in chronically RV paced patients with mild cardiomyopathy.

Effect of benazepril on atrial cytoskeleton remodeling in the canine atrial fibrillation models

To investigate the effect of benazepril on atrial cytoskeleton remodeling in atrial fibrillation (AF) canines induced by chronic rapid atrial pacing (RAP). Twenty canines were randomly divided into 3 groups: (1) Sham-operated group without RAP; (2) AF group: AF established by RAP at 600 beats per minute for 6 weeks; (3) Benazepril group: benazepril was dosed from 1 week pre-pacing to 6 weeks post-pacing. The diameter of atrial cardiomyocyte was measured, collagen volume fraction (CVF) analyzed by Masson staining and the expression and distribution of desmin were assayed by immunohistochemistry. RT-PCR method was used to semi-quantify the mRNA expression of beta-tubulin and desmin. The diameter of atrial cardiomyocyte increased in AF group [LA:(27.9 +/- 3.8) microm; RA: (26.8 +/- 3.2) microm] and benazepril group[LA: (25.1 +/- 3.4) microm; RA: (25.2 +/- 3.5) microm] than sham-operated group [LA: (19.6 +/- 2.9) microm; RA: (18.7 +/- 2.6) microm] (P < 0.01). CVF increased in AF group than sham-operated group [LA: (16.9 +/- 1.1)% vs (9.2 +/- 0.9)%, RA: (15.7 +/- 2.3)% vs (9.3 +/- 0.8)%, P < 0.01] and it decreased in benazepril group than AF group [LA: (11.3 +/- 0.8)% vs (16.9 +/- 1.1)%, RA: (10.9 +/- 0.8)% vs (15.7 +/- 2.3)%, P < 0.01]. Normal desmin cross-striations were lost in atrial cardiomyocyte and the desmin organization became irregular in AF group. The A values analyzed by immunohistochemistry of desmin increased in AF group than sham-operated group and they decreased in benazepril group than AF group (P < 0.01). The expression of mRNA level of desmin and beta-tubulin were up-regulated in AF group than sham-operated group, (LA:1.0 +/- 0.3 vs 0.6 +/- 0.3, 0.9 +/- 0.4 vs 0.6 +/- 0.3; RA: 1.0 +/- 0.6 vs 0.6 +/- 0.2, 1.1 +/- 0.3 vs 0.7 +/- 0.4, P < 0.01) and they were down-regulated in benazepril group than AF group (LA:0.8 +/- 0.4 vs 1.0 +/- 0.3, 0.7 +/- 0.3 vs 0.9 +/- 0.4; RA:0.7 +/- 0.3 vs 1.0 +/- 0.6, 0.7 +/- 0.3 vs 1.1 +/- 0.3, P < 0.01). Benazepril can favorably improve atrial cytoskeleton remodeling in the canine atrial fibrillation model.