Multipolar mapping for catheter ablation of premature ventricular complexes originating from papillary muscles in the structurally normal heart: a case series.

BACKGROUND: Previous studies on radiofrequency catheter ablation of premature ventricular complexes (PVCs) arising from the left ventricle (LV) papillary muscles (PM) show a modest procedural success rate with higher recurrence rate. Our study sought to explore the utility of using a multipolar mapping with a steerable linear duodecapolar catheter for ablating the PM PVCs. METHODS: Detailed endocardial multipolar mapping was performed using a steerable linear duodecapolar catheter in 6 consecutive PM PVCs patients with structurally normal heart. The clinical features and procedural data as well as success rate were analysed. RESULTS: LV endocardial electroanatomic mapping was performed in all patients via a retrograde aortic approach using a duodecapolar mapping catheter. All patients displayed a PVC burden with 16.2 ± 5.4%. Duodecapolar catheter mapping demonstrated highly efficiency with an average procedure time (95.8 ± 7.4 min) and fluoroscopy time (14.2 ± 1.5 min). The mean number of ablation applications points was 6.8 ± 1.9 with an average overall ablation duration of 6.1 ± 3.0 min. The values of earliest activation time during mapping using duodecapolar catheter were 37.8 ± 7.2 ms. All patients demonstrated acute successful ablation, and the PVC burden in all patients after an average follow-up of 8.5 ± 2.0 months was only 0.7%. There were no complications during the procedures and after follow-up. CONCLUSIONS: Mapping and ablation of PM PVCs using a duodecapolar catheter facilitated the identification of earliest activation potentials and pace mapping, and demonstrated a high success rate during follow-up.

Compartmentalized Structure of the Moderator Band Provides a Unique Substrate for Macroreentrant Ventricular Tachycardia.

Background Papillary muscles are an important source of ventricular tachycardia (VT). Yet little is known about the role of the right ventricular (RV) endocavity structure, the moderator band (MB). The aim of this study was to determine the characteristics of the MB that may predispose to arrhythmia substrates. Methods Ventricular wedge preparations with intact MBs were studied from humans (n=2) and sheep (n=15; 40-50 kg). RV endocardium was optically mapped, and electrical recordings were measured along the MB and septum. S1S2 pacing of the RV free wall, MB, or combined S1-RV S2-MB sites were assessed. Human (n=2) and sheep (n=4) MB tissue constituents were assessed histologically. Results The MB structure was remarkably organized as 2 excitable, yet uncoupled compartments of myocardium and Purkinje. In humans, action potential duration heterogeneity between MB and RV myocardium was found (324.6±12.0 versus 364.0±8.4 ms; P<0.0001). S1S2-MB pacing induced unidirectional propagation via MB myocardium, permitting sustained macroreentrant VT. In sheep, the incidence of VT for RV, MB, and S1-RV S2-MB pacing was 1.3%, 5.1%, and 10.3%. Severing the MB led to VT termination, confirming a primary arrhythmic role. Inducible preparations had shorter action potential duration in the MB than RV (259.3±45.2 versus 300.7±38.5 ms; P<0.05), whereas noninducible preparations showed no difference (312.0±30.3 versus 310.0±24.6 ms, respectively). Conclusions The MB presents anatomic and electrical compartmentalization between myocardium and Purkinje fibers, providing a substrate for macroreentry. The vulnerability to sustain VT via this mechanism is dependent on MB structure and action potential duration gradients between the RV free wall and MB.

Comparison of robotic magnetic navigation-guided and manual catheter ablation of ventricular arrhythmias arising from the papillary muscles.

Aims: Due to the complex anatomy of the left ventricular (LV) and right ventricular (RV) papillary muscles (PMs), PM ventricular arrhythmias (VAs) can be challenging to target with ablation. We sought to compare the outcomes of robotic magnetic navigation-guided (RMN) ablation and manual ablation of VAs arising from the LV and RV PMs. Methods and results: We evaluated 35 consecutive patients (mean age 65 ± 12 years, 69% male) who underwent catheter ablation of 38 VAs originating from the LV and RV PMs as confirmed by intracardiac echocardiography. Catheter ablation was initially performed using RMN-guidance in 24 (69%) patients and manual guidance in 11 (31%) patients. Demographic and procedural data were recorded and compared between the two groups. The VA sites of origin were mapped to 20 (53%) anterolateral LV PMs, 14 (37%) posteromedial LV PMs, and 4 (11%) RV PMs Acute successful ablation was achieved for 20 (74%) VAs using RMN-guided ablation and 8 (73%) VAs using manual ablation (P = 1.000). Fluoroscopy times were significantly lower among patients undergoing RMN ablation compared to patients undergoing manual ablation [median 7.3, interquartile range (IQR) 3.9-18 vs. 24 (16-44) min; P = 0.005]. Retrograde transaortic approach was used in 1 (4%) RMN patients and 5 (46%) manual patients (P = 0.005). No procedural complications were seen in study patients. Conclusion: Use of an RMN-guided approach to target PM VAs results in comparable success rates seen with manual ablation but with lower fluoroscopy times and decreased use of transaortic retrograde access.

Usefulness of pace mapping in catheter ablation of left ventricular papillary muscle ventricular arrhythmias with a preferential conduction.

INTRODUCTION: Preferential conduction from an origin to breakout sites can occur during ventricular arrhythmias (VAs) originating from the left ventricular papillary muscles (LVPMs). The purpose of this study was to investigate the incidence, electrophysiological characteristics, and relevance to radiofrequency catheter ablation (RFCA) of such a preferential conduction demonstrated by pace mapping. METHODS AND RESULTS: We studied 34 consecutive patients undergoing RFCA of 40 LVPM VAs. Among 78 QRS morphologies during these VAs, pace mapping was performed for 67 QRS morphologies during 37 VAs, and revealed VA-matched pace maps (M-PMs) with a latency for 14 QRS morphologies during 11 VAs (30%). Among 47 QRS morphologies with activation mapping, RFCA at the earliest activation site (EAS) was successful in 39, but not successful in 8 despite M-PMs with no latency. In these cases, RFCA was successful at remote sites of the M-PMs with latency (n = 6) and a site located between the EAS and site of that with latency (n = 1). Among the remaining 31 QRS morphologies with pace mapping only, RFCA was successful at M-PM sites with no latency in 17, and at M-PMs sites with latency in 7. In 3 of those 7 QRS morphologies, M-PMs were recorded at multiple remote sites, and RFCA was not successful at M-PM sites with no latency (n = 2) or a shorter latency (n = 1). CONCLUSIONS: When an M-PM with latency was recorded in LVPM VAs, RFCA at that site was highly successful. Attention should be paid to latency as well as the score during pace mapping of LVPM VAs.

Surface electrocardiography characteristics and radiofrequency catheter ablation of idiopathic ventricular arrhythmias originating from the left infero-septal papillary muscles: differences from those originating from the left posterior fascicle.

Aims: Distinguishing between ventricular arrhythmias originating from the left ventricular infero-septal papillary muscles (PM) and those from the left posterior fascicle (LPF) by surface electrocardiography (ECG) is very difficult. This study aimed to report the ECG characteristics and radiofrequency catheter ablation of PM and LPF ventricular arrhythmias. Methods and results: A total of 127 patients underwent catheter ablation of idiopathic ventricular arrhythmias originating from the LPF (n = 106; 85 males; 10-70 years) or PM (n = 21; 14 males; 4-68 years) were studied. A three-dimensional electroanatomic system (3D-EAS) was used to aid ablation. PM ventricular arrhythmias had a longer QRS duration (154.4 ± 18.0 vs. 119.7 ± 12.6 ms, P < 0.001) than LPF ventricular arrhythmias. All 7 ventricular arrhythmias with QRS duration >160 ms originated from the PM, whereas all 87 ventricular arrhythmias with QRS duration <130 ms arose from the LPF. In 33 ventricular arrhythmias with QRS 130-160 ms, all 13 with Vi/Vt ≤ 0.85 originated from the PM, and 19 of 20 with Vi/Vt > 0.85 arose from the LPF. Of the 8 PM ventricular arrhythmias patients whose initial ablation was undertaken using a non-irrigated 4 mm-tip catheter, 1 failed and 6 recurred. However, of the remaining 13 ones using an irrigated catheter and the 3D-EAS, all succeeded and 2 recurred. No complications were noted in any patient. Conclusion: PM ventricular arrhythmias could be identified from LPF ventricular arrhythmias by calculation of QRS duration combined with Vi/Vt using ECG.

Imaging characteristics of papillary muscle site of origin of ventricular arrhythmias in patients with mitral valve prolapse.

BACKGROUND: Mitral valve prolapse has been associated with increased risk of ventricular arrhythmias. We aimed to examine whether certain cardiac imaging characteristics are associated with papillary muscle origin of ventricular arrhythmias in these patients. METHODS AND RESULTS: We screened electronic medical records of all patients documented to have mitral valve prolapse on either transthoracic echocardiogram (TTE) or cardiac magnetic resonance imaging (CMR) in our center, who also underwent an electrophysiologic study (EPS) between 2007 and 2016. Anterior and posterior mitral leaflet thickness and prolapsed distance were measured on TTE and late gadolinium enhancement (LGE) was assessed on CMR. Patients were categorized as papillary muscle positive (pap (+)) or negative (pap (-)) using EPS. Eighteen patients were included in this study. Of the 15 patients who underwent TTE, a significantly higher proportion of patients in the pap (+) group had an anterior to posterior leaflet prolapse ratio of >0.45 indicating more symmetric leaflet prolapse. There were no differences in anterior or posterior leaflet thickness or prolapse distance between the groups. Patients in the pap (+) group were more likely to be women. Of the 7 patients who underwent CMR, those who were pap (+) were more likely to have LGE in the region of the papillary muscles than those who were pap (-). CONCLUSION: Female gender, more symmetric bileaflet prolapse on TTE, and the presence of papillary muscle LGE on CMR may be associated with papillary muscle origin of ventricular arrhythmias in patients with mitral valve prolapse.

The tip of the muscle is a dominant location of ventricular ectopy originating from papillary muscles in the left ventricle.

INTRODUCTION: Frequent ventricular premature complexes (VPCs) may cause symptoms and/or lead to deterioration of LV systolic function. Although frequent VPCs may be abolished by catheter ablation, it may be challenging in case of their origin from the LV papillary muscles (PMs). Our collaborative study aimed to analyze in detail the site of origin and the outcome of ablation. METHODS: Consecutive 34 patients (males: 68%; aged 62 ± 12 years; LV ejection fraction: 50 ± 9%) undergoing catheter ablation of VPCs originating from PMs were included. All procedures were guided by intracardiac echocardiography. RESULTS: The size and shape of PMs were highly variable. The length of anterolateral and posteromedial PM was 23 ± 4 mm and 28 ± 7 mm, respectively. In about one-third of patients, the PM was formed by two distinctly separate heads. The ectopic foci were located on anterolateral, posteromedial or both PM in 35%, 56% and 9% of cases, respectively. Their location was found within the distal, mid, or proximal (basal) third of PM in the 67%, 19%, and 14%, respectively. A total of 86% of PM foci were acutely abolished and long-term success was achieved in 65% of patients. Absence of VPCs of other morphologies and a high burden of ectopic activity before ablation were associated with favorable clinical outcome. CONCLUSION: VPCs originate predominantly from the distal portion of the PM. This knowledge may facilitate the mapping in patients with infrequent ectopic beats. Intracardiac echocardiography is of crucial importance for navigation of the ablation catheter and for assessment of its stability at PM target sites.

Novel electrocardiogram and electrophysiological findings for differentiating idiopathic left posterior papillary muscle and left posterior fascicular ventricular arrhythmias.

PURPOSE: Differentiation between idiopathic left posterior fascicular ventricular arrhythmias (LPF-VAs) and posterior papillary muscle (PPM) VAs is of clinical value. This study aimed to develop an algorithm to distinguish PPM-VAs from LPF-VAs. METHODS: This study enrolled 73 consecutive cases, including 31 with PPM-VAs and 42 with LPF-VAs, undergoing successful ablation by using 3D mapping and intracardiac echography to confirm the origin of the VAs. Electrocardiographic and electrophysiological parameters were compared between two groups. RESULTS: The 12-lead electrocardiography of the PPM-VAs was characterized by a longer QRS duration than that in LPF-VAs (154.4 ± 14.5 vs. 132.3 ± 13.1 ms, P < 0.001). A QRS duration ≥133 ms was observed in all patients (100%) with PPM-VAs and 13/42 (31.0%) patients with LPF-VAs. The conduction duration from the earliest left ventricular activation site of the VA to the proximal right bundle branch (VA-RBB) was longer in patients with PPM-VAs than LPF-VAs (51.3 ± 12.2 vs. 23.6 ± 7.7 ms, P < 0.001). Based on the ROC analysis, a VA-RBB >36 ms was recognized in 28/31 patients with PPM-VAs (90.3%) and 2/42 with LPF-VAs (4.8%). An algorithm incorporating a QRS duration of ≥133 ms with a conduction duration of a VA-RBB of >36 ms could yield a sensitivity of 90.3% and specificity of 100% for discriminating PPM-VAs from LPF-VAs. CONCLUSIONS: The novel algorithm incorporating a QRS duration of ≥133 ms with a conduction duration of the VA-RBB of >36 ms could be useful in differentiating PPM-VAs from LPF-VAs.

Intracardiac echo-facilitated 3D electroanatomical mapping of ventricular arrhythmias from the papillary muscles: assessing the 'fourth dimension' during ablation.

AIMS: Ventricular arrhythmias (VA) originating from a papillary muscle (PM) have recently been described as a distinct clinical entity with peculiar features that make its treatment with catheter ablation challenging. Here, we report our experience using an intracardiac echo-facilitated 3D electroanatomical mapping approach in a case series of patients undergoing ablation for PM VA. METHODS AND RESULTS: Sixteen patients who underwent catheter ablation for ventricular tachycardia (VT) or symptomatic premature ventricular contractions originating from left ventricular PMs were included in the study. A total of 24 procedures (mean 1.5 per patient) were performed: 15 using a retrograde aortic approach and 9 using a transseptal approach. Integrated intracardiac ultrasound for 3D electroanatomical mapping was used in 15 of the 24 procedures. The posteromedial PM was the most frequent culprit for the clinical arrhythmia, and the body was the part of the PM most likely to be the successful site for ablation. The site of ablation was identified based on the best pace map matching the clinical arrhythmia and the site of earliest the activation. At a mean follow-up of 10.5 ± 7 months, only two patients had recurrent arrhythmias following a repeat ablation procedure. CONCLUSION: An echo-facilitated 3D electroanatomical mapping allows for real-time creation of precise geometries of cardiac chambers and endocavitary structures. This is useful during procedures such as catheter ablation of VAs originating from PMs, which require detailed representation of anatomical landmarks. Routine adoption of this technique should be considered to improve outcomes of PM VA ablation.

Differentiation of papillary muscle from fascicular and mitral annular ventricular arrhythmias in patients with and without structural heart disease.

BACKGROUND: Idiopathic left ventricular arrhythmias (VAs) and those caused by structural heart disease can originate from the papillary muscles, fascicles, and mitral annulus. Differentiation of these arrhythmias can be challenging because they present with a right bundle branch block morphology by electrocardiography. We sought to identify clinical, electrocardiographic, and electrophysiological features that distinguish these left VAs in patients with and without structural heart disease. METHOD AND RESULTS: Patients undergoing catheter ablation for papillary muscle, fascicular, or mitral annular VAs were studied. Demographic data and electrocardiographic and electrophysiological findings were analyzed. Fifty-two VAs in 51 patients (32 [63%] male; mean age 61±15 years) with papillary muscle (n=18), fascicular (n=15), and mitral annular (n=19) origins were studied. Patients with papillary muscle VAs were older and had higher prevalence of left ventricular dysfunction (67% versus 13% of fascicular VA patients [P=0.009]) and coronary artery disease (78% versus 37% of mitral annular VA patients [P=0.036]). Papillary muscle VAs were distinguished electrocardiographically from fascicular VAs by longer QRS durations and lower prevalence of r

Ventricular tachycardia originating from the septal papillary muscle of the right ventricle: electrocardiographic and electrophysiological characteristics.

INTRODUCTION: Premature ventricular complexes (PVCs) and ventricular tachycardia (VT) arising from papillary muscles of both ventricles have recently been described. There is a lack of data on VT originating from the right ventricular papillary (RV PAP) muscles. There have been no prior studies focused on the electrocardiogram (ECG) features and ablation of PVC/VT arising from the septal papillary muscle of the right ventricle. METHODS: Among 155 consecutive patients with normal structural heart who underwent catheter ablation of PVC/VT, 8 patients with PVC/VT from the septal RV PAP muscle were identified. The site of origin of the arrhythmias was identified through activation/pace mapping and intracardiac echocardiography. All patients underwent radiofrequency ablation of the arrhythmia. RESULTS: Data on 8 consecutive patients (2 men, age 42 ± 13 years old) were collected. All patients had a preserved ejection fraction (60 ± 4%). Septal RV PAP arrhythmias had a left superior axis and negative concordance or late R-wave transition in precordial leads. PVCs were spontaneous in 5 cases, were induced by isoprotenerol in 2 cases and by isoproterenol plus phenylephrine in another one. PVCs were never induced with calcium bolus and only rarely with burst pacing. Adenosine never terminated VT or suppressed the VT/PVCs. Radiofrequency, fluoroscopic, and procedural time were, respectively, 10.3 ± 3, 36.4 ±11.3, and 76.3 ± 27.5 minutes. During a mean follow-up of 8 ± 4 months, mean PVC burden was reduced from 14 ± 3% preablation to 0.1 ± 0.2% postablation. CONCLUSION: PVCs and VT originating from septal RV papillary muscle could have a typical ECG pattern due to the site of the muscle involved. Radiofrequency ablation of this anatomic area is feasible and effective.

[Effects of Shenmai injection on afterdepolarization and triggered activities in left ventricular papillary muscle in rat cardiac hypertrophy].

This study is to evaluate the effects of Shenmai injection on the temporal alterations of action potential (AP), early afterdepolarization (EAD) and delayed afterdepolarization (DAD) in papillary muscles. The action potentials were recorded by a glass electrode. APD at 90% repolarization (APD9 ) was measured, and spontaneous EAD and DAD were observed. The results show APD90 was significantly prolonged in model group compared with sham-operated group, whereas it was remained unchanged in Shenmai injec- tion treatment group and amiodarone group. The spontaneous EADs and DADs were frequently visible in model group. In conclusion, EAD, DAD and trigger activities increase gradually during pathological progression of rat cardiac hypertrophy, and Shenmai injection could improve the action potential change in rat cardiac hypertrophy.

Architectural correlates of myocardial conduction: changes to the topography of cellular coupling, intracellular conductance, and action potential propagation with hypertrophy in Guinea-pig ventricular myocardium.

BACKGROUND: We tested the hypothesis that alterations to action potential conduction velocity (CV) and conduction anisotropy in left ventricular hypertrophy are associated with topographical changes to gap-junction coupling and intracellular conductance by measuring these variables in the same preparations. METHODS AND RESULTS: Left ventricular papillary muscles were excised from aortic-banded or sham-operated guinea-pig hearts. With intracellular stimulating and recording microelectrodes, CV was measured in 3 dimensions with simultaneous conductance mapping with subthreshold stimuli and correlated with quantitative histomorphometry of myocardial architecture and connexin 43 distribution. In hypertrophied myocardium, CV in the longitudinal axis was smaller and transverse velocity was greater compared with control; associated with similar differences of intracellular conductance, consistent with more cell contacts per cell (5.7 ± 0.2 versus 8.1 ± 0.5; control versus hypertrophy), and more intercalated disks mediating side-to-side coupling (8.2 ± 0.2 versus 10.2 ± 0.4 per cell). Intercalated disk morphology and connexin 43 immunolabelling were not different in hypertrophy. Hypertrophied preparations showed local submillimeter (≈250 µm) regions with slow conduction and low intracellular conductance, which, although not affecting CV on the millimeter scale, were consistent with discontinuities from increased microscopical connective tissue content. CONCLUSIONS: With myocardial hypertrophy, altered longitudinal and transverse CV, and greater nonuniformity of CV anisotropy correspond to changes of intracellular conductance. These are associated with alteration of myocardial architecture, specifically the topography of cell-cell coupling and gap-junction connectivity.

Cardiac contractility modulation therapy in advanced systolic heart failure.

Cardiac contractility modulation (CCM) is the application of nonexcitatory electrical signals to the myocardium, during the absolute refractory period of the action potential, to elicit a positive inotropic effect without increasing myocardial oxygen consumption. These effects are independent of QRS duration; consequently, CCM device therapy might benefit symptomatic patients with reduced left ventricular ejection fraction who are not candidates for cardiac resynchronization therapy. Preclinical studies have demonstrated a rapid positive inotropic effect of CCM, which seems to be mediated by modulation of cardiomyocyte Ca(2+) fluxes and alterations in the phosphorylation of cardiac phospholamban. In vivo translational and clinical studies that utilized double biphasic voltage pulses to the right ventricular aspect of the interventricular septum have demonstrated positive global effects on cardiac reverse remodelling and contractility. Long-term application of CCM seems to improve patients' exercise tolerance and quality of life. These benefits are apparently accomplished with an acceptable safety profile; however, to date, no data have demonstrated reductions in hospitalizations for heart failure or mortality. CCM is currently available in Europe and ongoing studies are attempting to identify the ideal target population and accumulate additional outcome data.

Confirmation of a proarrhythmic risk underlying the clinical use of common Chinese herbal intravenous injections.

ETHNOPHARMACOLOGICAL RELEVANCE: The Chinese herbal intravenous injections (CHI) which are extracted from herb(s) are used clinically in China as putative therapies for a variety of diseases. AIM OF THE STUDY: The mechanism(s) which underline findings of severe adverse drug reactions (ADR) noted in more than a thousand published articles on CHIs, are still poorly understood. With 109 CHIs currently in clinical use, we investigated the proarrhythmic effects of three specific CHIs, Shuanghuanglian (SHL), Qingkailing (QKL) and Yinzhihuang (YZH), using in vivo and in vitro ion channel models. MATERIALS AND METHODS: In vivo and in vitro guinea pig electrocardiogram, intracellular action potential and patch clamp recording techniques were carried out. RESULTS: Both SHL and QKL (both in one, five and ten times clinically relevant doses (CRD) for in vivo and clinically relevant concentrations (CRC) for in vitro) prolonged P-R intervals in a dose or concentration-dependent manner and SHL also prolonged QTc. YZH (ten and 20 times CRD and CRC) prolonged P-R intervals without changing QTc. Intracellular action potential recordings from guinea pig papillary muscle indicated SHL and QKL abolished the firing of action potentials at ten and 30 times CRC respectively. SHL significantly suppressed L-type Ca(2+) current from left ventricular myocytes of guinea pig, hNav1.5 current and hERG current with 50% inhibiting concentrations (IC(50)) of 6.0, 3.0 and 10.7 times CRC, respectively. Also, QKL significantly suppressed L-type Ca(2+) and hNav1.5 currents with IC(50)s of 10.7 and 13.8 times CRC. YZH significantly suppressed L-type Ca(2+), hNav1.5 and hERG currents with IC(50)s of 12.1, 32.9 and 141.7 times CRC, respectively. CONCLUSIONS: The three CHIs studied caused bradyarrhythmia mainly by inhibiting Na(+) current and L-type Ca(2+) current.

Mechanism of prolonged electromechanical delay in late activated myocardium during left bundle branch block.

During left bundle branch block (LBBB), electromechanical delay (EMD), defined as time from regional electrical activation (REA) to onset shortening, is prolonged in the late-activated left ventricular lateral wall compared with the septum. This leads to greater mechanical relative to electrical dyssynchrony. The aim of this study was to determine the mechanism of the prolonged EMD. We investigated this phenomenon in an experimental LBBB dog model (n = 7), in patients (n = 9) with biventricular pacing devices, in an in vitro papillary muscle study (n = 6), and a mathematical simulation model. Pressures, myocardial deformation, and REA were assessed. In the dogs, there was a greater mechanical than electrical delay (82 ± 12 vs. 54 ± 8 ms, P = 0.002) due to prolonged EMD in the lateral wall vs. septum (39 ± 8 vs.11 ± 9 ms, P = 0.002). The prolonged EMD in later activated myocardium could not be explained by increased excitation-contraction coupling time or increased pressure at the time of REA but was strongly related to dP/dt at the time of REA (r = 0.88). Results in humans were consistent with experimental findings. The papillary muscle study and mathematical model showed that EMD was prolonged at higher dP/dt because it took longer for the segment to generate active force at a rate superior to the load rise, which is a requirement for shortening. We conclude that, during LBBB, prolonged EMD in late-activated myocardium is caused by a higher dP/dt at the time of activation, resulting in aggravated mechanical relative to electrical dyssynchrony. These findings suggest that LV contractility may modify mechanical dyssynchrony.

[Effect of GBE50 on action potentials in normal and simulated ischemic guinea pig papillary muscles].

OBJECTIVE: To study the effect of Ginkgo biloba extract 50 (GBE50), a new multicomponent drug with a polyvalent action extracted from the leave of Ginkgo biloba, on the action potentials in normal and simulated ischemic guinea pig papillary muscles. METHOD: Standard intracellular microelectrode technique was used to examine the effects of GBE50 on the action potential parameters [action potential amplitude (APA), overshoot, rest potential, action potential amplitude at 20%, 50%, 90% of repolarization (APD20, APD50, APD90)]. RESULT: In normal guinea pig cardiac papillary muscles, GBE50 (20, 50, 100 mg x L(-1)) shortened APD50 and APD90, and did not affect the rest potential parameters. In simulated ischemic guinea pig cardiac papillary cells, action potential duration was significantly shortened, resting potential and action potential amplitude were reduced. 100 mg x L(-1) GBE50 partly attenuated the change induced by ischemia. CONCLUSION: GBE50 shortened APD of normal guinea pig cardiac papillary cells in a concentration-dependent manner. Under ischemia, all action potential parameters were reduced . GBES0 could alleviate the electrophysiological heterogeneity of ischemic myocardium, which may attenuate myocardial ischemia and block the onset of arrhythmia.