Mechanisms, prediction and treatment of ventricular tachyarrhythmias occurring late after myocardial infarction

Studies from the 1980s, refined in the intervening years, have examined the milieu for ventricular tachycardia (VT) and ventricular fibrillation (VF) occurring late after acute myocardial infarction (AMI). The arrhythmogenic substrate appears to be patchy areas of fibrous tissue interdigitating with viable bundles of myocardium which have distorted orientation and tortuous interconnections. These promote conduction delay in sinus rhythm. Factors found to promote induction of VT rather than VF are longer conduction delay in sinus rhythm, larger infarct size, a more ragged infarct edge and longer ventricular extrastimulus coupling intervals. Predictors of spontaneous VT and VF late after AMI include inducible VT at electrophysiological studies (EPS), delayed conduction in sinus rhythm detected as late potentials on signal-averaged surface electrocardiogram (ECG), and low left ventricular ejection fraction (LVEF). Treatments of propensity for VT or VF after AMI include insertion of a defibrillator (ICD), which has the best track record, antiarrhythmic medication (less reliable), and ablation or excision of arrhythmogenic substrate (for refractory VT and VF).     

Measurement of ventricular electrogram amplitude during intraoperative induction of ventricular tachyarrhythmias.

Adequate sensing of ventricular tachycardia (VT) and ventricular fibrillation (VF) is necessary for proper functioning of an implantable cardioverter defibrillator (ICD). Several ICDs currently undergoing investigation have programmable fixed gain sensitivity for tachycardia detection. If intracardiac electrogram amplitude decreases below the programmed sensitivity during VT or VF, detection of a ventricular arrhythmia may be delayed or missed. The mean amplitude of intracardiac electrograms (ICEGM) recorded with bipolar epicardial or transvenous sensing leads was measured in 63 patients during induced VT and VF recorded in the operating room at the time of ICD implantation. The mean amplitude of the ICEGM during 41 episodes of VF in 15 patients decreased from 14.9 +/- 0.9 mV during sinus rhythm to 8.8 +/- 0.7 mV at 1 second, 9.7 +/- 0.7 mV at 5 seconds, and 9.4 +/- 0.7 mV at 10 seconds (p < 0.0001 vs sinus rhythm ICEGM) with endocardial leads. The mean amplitude of the ICEGM recorded during 173 episodes of VF in 43 patients with epicardial leads decreased from 10.4 +/- 0.3 mV in sinus rhythm to 7.8 +/- 0.3 mV at 1 second, 8.3 +/- 0.3 mV at 5 seconds and 8 mV at 10 seconds (p <0.0001 vs sinus rhythm ICEGM). The mean amplitude of epicardial and transvenous ICEGMs recorded during 34 episodes of monomorphic VT decreased from 18.5 +/- 1.8 mV (epicardial) and 14.4 +/- 2.0 mV (transvenous) during sinus rhythm (p = 0.15, epicardial vs transvenous) to 16.0 +/- 1.7 mV (epicardial) and 13.7 +/- 1.9 mV (transvenous) at 10 seconds (< 10% of baseline amplitude).(ABSTRACT TRUNCATED AT 250 WORDS)     

Substrate mapping vs. tachycardia mapping using CARTO in patients with coronary artery disease and ventricular tachycardia: impact on outcome of catheter ablation.

AIMS: For ablation of ventricular tachycardia (VT) in patients after myocardial infarction, a three-dimensional mapping system is often used. We report on our overall success rate of VT ablation using CARTO in 47 patients, with a subgroup analysis comparing VT mapping with the results of mapping that had to be performed during sinus rhythm or pacing (substrate mapping). METHODS AND RESULTS: A CARTO map was performed and VT ablation attempted using two strategies: Patients in the VT-mapping group had incessant VT (four patients) or inducible stable VT (18 patients) such that the circuit of the clinical VT could be reconstructed using CARTO. During VT, the critical area of slow conduction was identified using diastolic potentials and conventional concealed entrainment pacing. In contrast, patients in the substrate-mapping group had initially inducible VT. However, a complete VT map was not possible because of catheter-induced mechanical block (six patients) or because haemodynamics deteriorated during the ongoing VT (19 patients). Therefore, pathological myocardium was identified by fragmented, late- and/or low-amplitude (<1.5 mV) bipolar potentials during sinus rhythm or pacing, and the ablation site was primarily determined by pace mapping inside or at the border of this pathological myocardium. Acute ablation success in all patients with regard to non-inducibility of the clinical VT or any slower VT was 79% after a single ablation procedure, but increased to 95% after a mean of 1.2 ablation procedures. However, chronic success was 75%, when it was defined as freedom from any ventricular tachyarrhythmia (VT or VF) during a follow-up of 25+/-13 months. In the subgroup analysis, patients in the VT-mapping group were not significantly different from patients in the substrate-mapping group with regard to age (65+/-7 vs. 65+/-9 years), ejection fraction (30+/-7 vs. 30+/-8%), VT cycle length (448+/-81 vs. 429+/-82 ms), number of radiofrequency applications (17+/-9 vs. 14+/-6 applications), use of an irrigated tip catheter (23 vs. 32%), and ablation results. CONCLUSION: When using a CARTO-guided approach for VT ablation in patients with coronary artery disease, the freedom from any ventricular arrhythmia is high (75%), but leaves the patient at a 23% risk of developing fast VT/VF during follow-up. Mapping during sinus rhythm or pacing is as successful as mapping during VT.     

Epicardial Macro-Reentrant Ventricular Tachycardia Exhibiting an Endocardial Centrifugal Activation Pattern in a Case with Arrhythmogenic Right Ventricular Cardiomyopathy

A 55-year-old man with arrhythmogenic right ventricular cardiomyopathy underwent catheter ablation of ventricular tachycardia (VT) with left bundle branch block and left superior axis QRS morphology with an early precordial transition. Endocardial mapping during the VT revealed a focal activation pattern from a small region of low voltage in the left ventricular (LV) septum. Despite earliest endocardial activation in the LV septum, epicardial mapping demonstrated a macro-reentrant circuit with successful catheter ablation at an inferior peritricuspid annular site. Activation from the reentrant circuit propagated through the scar area in the epicardial right ventricle to the remote endocardial LV breakout site.     

Transmural temporospatial left ventricular activation during pacing from different sites: potential implications for optimal pacing

AIMS: Previous studies showed that right ventricular (RV) endocardial pacing can be deleterious even in individuals with initially normal left ventricular (LV) function. The mechanism(s) by which RV endocardial pacing may cause LV dysfunction is unknown. This study compares the temporospatial LV transmyocardial activation profiles during sinus rhythm with normal His/Purkinje conduction vs. currently utilized and proposed cardiac pacing sites. METHODS AND RESULTS: Mongrel dogs were instrumented with transmural electrodes that tracked transmyocardial activation sequences at five sites in the LV. Pacing/recording catheters were positioned in the RV apex and on the RV and LV sides of the ventricular septum. An epicardial pacing electrode was also sewn to the mid-lateral LV epicardium. Electrograms were recorded during sinus rhythm and pacing from the RV endocardium, LV septum, LV epicardium and during biventricular pacing. Compared to normal sinus/His/Purkinje rhythm (NSR), RV endocardial pacing significantly (P < 0.05) prolonged transmural activation (NSR endocardium 6.1 +/- 1 ms vs. RV endocardium 23.0 +/- 2.6 ms). The highly ordered temporospatial pattern of transmural activation during sinus rhythm was replaced with dispersion and intermingling of endo-, mid-, and epicardial activation. LV epicardial and biventricular pacing did not correct these abnormalities. Only LV septal pacing achieved the transmural and transseptal activation sequences similar to sinus rhythm. CONCLUSION: Clinically utilized pacing modalities, including biventricular pacing, cause abnormal transmyocardial activation. LV septal pacing results in transmyocardial activation patterns that closely resemble those seen in sinus rhythm.     

Electrophysiological and anatomic differences between canine hearts with inducible ventricular tachycardia and fibrillation associated with chronic myocardial infarction

This study examined electrophysiological and anatomic differences between dogs with ventricular tachycardia (VT) and fibrillation (VF) inducible by programmed ventricular stimulation 7-21 days after left anterior descending coronary artery ligation. Of 106 dogs studied, 40 had inducible VT, 19 had inducible VF, and 47 had no inducible arrhythmias. Differences between these three groups of animals were examined with cardiac mapping (to determine ventricular activation time in sinus rhythm) and post-mortem pathology (to measure infarct size and to reconstruct the anatomy at the infarct edge). Animals with inducible VT had longer maximal epicardial activation time (127 +/- 8 msec) than did animals with inducible VF (91 +/- 8 msec, p less than 0.05) or animals with no inducible arrhythmias (75 +/- 2 msec, p less than 0.001). Delayed epicardial activation occurred in 90% of animals with VT, 42% of animals with VF, and in only 6% of animals with no inducible arrhythmias. Endocardial and myocardial activation times were similar for the VT and VF groups. Infarct size was 18 +/- 2% of the ventricles for the VT group, much higher than for the VF group (11 +/- 2%, p less than 0.001) or for the group with no inducible arrhythmias (9 +/- 1%, p less than 0.001). The maximum diameter of viable muscle bundles interdigitating with scar tissue at the infarct edge was much larger in animals with VT (2.4 +/- 0.2 mm) than in animals with VF (1.8 +/- 0.2 mm, p less than 0.05) or animals with no inducible arrhythmias (1.7 +/- 0.1 mm, p less than 0.01). Thus, when compared with animals with inducible VF, animals with inducible VT had longer epicardial activation time, larger infarct size and viable muscle bundles of larger diameter at the infarct edge.     

Tachycardia-Induced Right Ventricular Cardiomyopathy: Epicardial Radiofrequency Ablation of an Unusual and Unexpected Ventricular Tachycardia

A 38-year-old man without prior medical history was hospitalized for sustained monomorphic ventricular tachycardia (VT) left bundle branch block pattern with inferior QRS axis resistant to beta blockers. Right ventricular (RV) ejection fraction (EF) was 28%. Left ventricular EF was normal. Right and left endocardial ablation failed. Percutaneous epicardial radiofrequency application at the lateral mitral annulus was successful. The RVEF later normalized.
Some VTs originating from the left ventricular epicardium are potential mimickers of benign VTs originating from the ventricular outflow tract (right or left) or arrhythmogenic right ventricular cardiomyopathy VT and they may induce isolated RV dysfunction.     

Intraoperative mapping-guided argon laser ablation of malignant ventricular tachycardia

Intraoperative mapping-guided laser ablation of arrhythmogenic myocardium was performed in 5 patients with refractory sustained ventricular tachycardia (VT). Using a 15-W argon laser coupled to a 300-mu optical fiber, a bloodless laser ventriculotomy was successfully performed in 4 patients with VT. Visually- and mapping-guided endocardial ablation of 7 VT morphologic patterns was performed. Five of the 7 sites of VT origin were unresectable using standard resection techniques. Postoperatively, spontaneous and inducible VT was suppressed in all patients (without antiarrhythmic drugs in 4 patients and with a previously ineffective drug 1 patient). Mean pulmonary capillary wedge pressure, cardiac index and left ventricular ejection fraction were unchanged (p greater than 0.2) from preoperative values. Mean maximal creatinine kinase-MB isoenzyme concentration was 139 +/- 75 IU. All patients were New York Heart Association functional class II at discharge. During follow-up, no spontaneous arrhythmia has recurred in any patient. Thus, intraoperative argon laser ablation is effective for VT ablation alone or in conjunction with standard surgical resection techniques.     

伴右心室出口的左心室起源缺血性室性心动过速的标测和消融

目的折返性的缺血性室性心动过速（VT）绝大多数发生于左心室并表现为右束支阻滞（RBBB）图形。本文报道1组VT折返环位于左心室但出口在右心室且表现为左束支阻滞（LBBB）的病例。方法32例因陈旧性心肌梗死伴VT而接受电生理检查和射频消融的患者,其中4例临床有LBBB形态的VT。使用非接触等电位和虚拟单极标测判断VT起源,结合舒张中期电位（MDP）和拖带标测确定折返关键通路和消融靶点。用盐水冲洗电极导管在折返环的关键峡部行线性消融。结果全部32例患者中,4例临床有LBBB型VT者均成功被诱发,其中1例有两种LBBB型VT,1例同时有RBBB型VT但周长与LBBB型相同;另有1例共有6种形态的VT,包括RBBB和LBBB型。在右心室内的非接触式等电位标测可迅速确定VT在右心室的传出部位,该处的虚拟单极标测显示rS型提示左心室起源。3例在左心室成功拖带并消融成功,靶点均紧邻左心室间隔,其中1例位于下壁,1例在前壁,1例两种LBBB型VT分别在前壁和下壁间隔旁消融成功。随访1～4．2年,未服抗心律失常药无VT发作。而1例诱发出6种单形（包括RBBB和LBBB型）VT患者因巨大室壁瘤及心功能障碍不能耐受而中途放弃消融。结论紧邻室间隔的前壁和下壁心肌梗死后的左心室起源VT可能因在右心室有出口而表现为LBBB型,需要在标测和消融时予以注意。     

Treatment of refractory ventricular tachycardia using cumulative high-energy fulguration

Intracardiac electrode catheter ablation of arrhythmogenic foci, using cumulative high energy, was attempted in 29 patients (mean age 57 +/- 15 years) presenting with ventricular tachycardia (VT) refractory to antiarrhythmic drugs. A heart disease, present in 25 patients, was responsible for severe heart failure in 10 of them; 13 patients had myocardial infarction, 7 had arrhythmogenic dysplasia of the right ventricle, 5 had cardiomyopathy (dilated in 4, hypertrophic in 1). The myocardium was apparently normal in 4 patients, 2 of whom had mitral valve prolapse. Morphologically, VT was single in 20 cases, double in 4 cases and more than triple in 5 cases; arrhythmia was continual or occurred several times a day in 17 cases. In one (20 patients) or several (9 patients) catheter ablation sessions, 1 to 16 cathodic shocks of 160 to 240 Joules (1.180 +/- 1.062 J) were delivered after mapping and focal stimulation without irreversible adverse reaction. The cumulative energy delivered was 840 +/- 558 J in the right ventricle (11 patients) and 1.390 +/- 1.244 J in the left ventricle (18 patients). During a 23.4 +/- 12 months follow-up period, 4 patients died (2 of heart failure, 1 of a hitherto undocumented VT, 1 suddenly of bradycardia-asystole). VT was regarded as being controlled in 23/27 patients, 15 of whom were not taking antiarrhythmic agents. The presystolic potential during VT was -5 + 5 ms in the 4 failure cases versus -41 + 29 ms in the successful cases (p less than 0.05). It is concluded that electrode catheter ablation is an effective curative treatment of VT.(ABSTRACT TRUNCATED AT 250 WORDS)     

The use of unipolar intracardiac impedance for discrimination of haemodynamically stable and unstable arrhythmias in man.

AIMS: To determine the feasibility of discriminating haemodynamically stable from unstable arrhythmias using right ventricular (RV) unipolar intracardiac impedance (Z). METHODS AND RESULTS: A quadrapolar temporary pacing electrode was positioned at the RV apex and unipolar impedance was measured between the tip electrode and a surface patch electrode. Changes in peak-to-peak Z amplitude were measured simultaneously with surface ECG and blood pressure during induced arrhythmias. Haemodynamic instability was defined as a systolic pressure of <90 mmHg. There were 25 episodes of ventricular fibrillation (VF) induced in 15 patients, 18 episodes of ventricular tachycardia in 16 patients, and 33 episodes of supraventricular tachycardia (SVT) in 16 patients. Compared with the baseline rhythm, mean Z amplitude reduced from 51.3+/-7.7 to 11.2+/-7.4 Ohm (P<0.001) during VF, from 52.2+/-6.3 to 21.7+/-10.1 Ohm (P<0.01) during haemodynamically unstable VT, from 55.0+/-6.9 to 39.9+/-11 Ohm (ns) during stable VT, and from 56.4+/-8.4 to 36.9+/-9.3 Ohm during SVT (P<0.001). CONCLUSION: Right ventricular unipolar impedance is an adequate sensor for determining mechanical ventricular contraction and acts as a surrogate marker for a fall in arterial blood pressure during VF. However, for ventricular and supraventricular tachycardias, variations between patients did not allow adequate discrimination between stable and unstable arrhythmias.     

Endothelin receptor--a blockade decreases ventricular arrhythmias after myocardial infarction in rats

OBJECTIVE: Endothelin-1 (ET-1) production increases during acute myocardial infarction (MI) and may contribute to the genesis of ventricular tachycardia (VT) and ventricular fibrillation (VF). However, the antiarrhythmic effects of ET-1 receptor blockade, examined shortly after MI, have been debated. In the present study, we examined the effects of such treatment on VT/VF during the first 24 h post-MI. METHODS: Thirty-five Wistar rats (223+/-22 g) were randomly allocated to either the ET-1 receptor-A (ETA) antagonist BQ-123 (0.4 mg/kg, BQ-123 group, n=17), or normal saline (control group, n=18) and were subjected to coronary artery ligation. A single-lead electrocardiogram was continuously recorded for 24 h post-MI, using an implanted telemetry system, and episodes of VT/VF were analyzed. Monophasic action potential (MAP) recordings were obtained from the left (LV) and right (RV) ventricular epicardium at baseline, 5 min after treatment and 24 h post-MI. RESULTS: There were 15.94+/-19.35 episodes/h/rat of VT/VF in the control group and 1.66+/-2.22 in the BQ-123 group (p=0.010), resulting in a lower (p=0.030) arrhythmic mortality in treated animals. The mean episode duration was 7.40+/-7.16 s for the control group and 2.30+/-1.37 s for the BQ-123 group (p=0.011). The maximum decrease in VT/VF was observed during the 1st, 5th and 6th hours post-MI. In the control group, LV MAP duration increased 24 h post-MI, displaying an increased beat-to-beat variation, but remained unchanged in the BQ-123 group. CONCLUSION: Acute ETA blockade reduces the incidence of VT/V F during the first 24-h post-MI in the rat, through a decrease in the dispersion of repolarization.     

Antidysrhythmic actions of meobentine sulfate

The antiarrhythmic efficacy of meobentine sulfate, a bethanidine derivative lacking inhibitory effects on adrenergic neuronal function, was assessed in three canine models. Intravenous meobentine sulfate, administered in dosages of 5.0, 10,0, and 20.0 mg/kg, produced a dose-related increase in the ventricular fibrillation threshold (VFT) under nonischemic conditions (7.6 +/- 1.8 mA vs 37.8 +/- 8.6 mA) (20 mg/kg; p less than 0.05) and during regional myocardial ischemia (5.6 +/- 1.5 mA vs 41.8 +/- 9.1 mA) (20 mg/kg; p less than 0.05). The VFT was also increased in the presence of chronic ischemic injury (6.4 +/- 1 mA to 31 +/- 10 mA) (20 mg/kg; p 0.05). In the conscious dog, 4 days after an anterior myocardial infarction, programmed electrical stimulation (PES) produced nonsustained ventricular tachycardia (VT) in five dogs. After meobentine sulfate administration, eight of nine animals had sustained VT and one animal developed ventricular fibrillation (VF). At a dose of 20 mg/kg, there was prolongation of the cycle length of the VT (169 +/- 11 msec to 237 +/- 20 msec), prolongation of the QRS duration (58 +/- 2.6 msec to 71 +/- 3.7 msec), and prolongation of the delay in epicardial activation. There was an enhanced potential after meobentine administration for programmed stimulation to produce ventricular arrhythmias with the introduction of fewer premature impulses. In the third canine model, conscious dogs with a previous anterior myocardial infarction developed VF in response to electrically induced left circumflex coronary artery injury. Meobentine (20 mg/kg) failed to prevent VF in eight of eight dogs. These results suggest that while meobentine sulfate significantly increases the electrical VFT, it does not protect the conscious canine from the induction of ventricular tachyarrhythmias in response to PES, and it does not prevent VF in a conscious canine model of sudden coronary death.(ABSTRACT TRUNCATED AT 250 WORDS)     

Radiofrequency catheter ablation of ventricular tachycardia guided by intracardiac echocardiography.

AIMS: Ventricular tachycardia (VT) frequently has an anatomical substrate. Identification of areas prone to arrhythmogenicity facilitates radiofrequency catheter ablation (RFCA). Furthermore, direct monitoring of complications potentially increases safety of RFCA. The aim of this study was to evaluate the feasibility of guiding RFCA of VT with intracardiac echocardiography (ICE), in order to improve outcome and procedural safety. METHODS AND RESULTS: Eleven patients (age 59 +/- 15 years) with drug-refractory VT of various etiologies were studied. VT mapping and ablation were performed using standard techniques. ICE was performed with a multifrequency (5-10 MHz) phased-array transducer positioned in the right ventricle. Twenty different VTs were treated (CL 352 +/- 120 ms, 2.0 +/- 0.9 VT per patient). LV a- or dyskinesia was identified in all post-infarct patients. In patients with arrhythmogenic right ventricular dysplasia, right ventricular aneurysms and dyskinesia could be identified. In all patients catheter position and tip-tissue contact could easily be monitored with ICE. Procedural success (non-inducibility of hemodynamically stable VT) was achieved in all patients. Complications did not occur. CONCLUSION: ICE is feasible in guiding RFCA of VT of different etiologies. The use of ICE in adjunction with fluoroscopy and mapping procedures will facilitate treatment of VT and may contribute to the safety of the procedure.     

Left bundle branch block-type ventricular tachycardia originating from the left ventricular septum in a patient with cardiac sarcoidosis

This case report describes a left bundle branch block (LBBB)-type ventricular tachycardia (VT) with a unique reentrant circuit in a patient with cardiac sarcoidosis. The VT morphology and pace mapping supported an exit site of the VT from the basal posterior right ventricle (RV) septum. Nonetheless, concealed entrainment was established by pacing from a septal left ventricular (LV) site recording a diastolic potential, opposite site to the RV site. A point ablation at that LV site could successfully terminate the VT, suggesting that a critical isthmus was located on the LV side of the interventricular septum despite the demonstration of an LBBB-type VT.     

致心律失常性右室发育不良症的室性心动过速的低能量电消融治疗

本文报告4例致心律失常性右室发育不良患者,因为反复出现室性心动过速药物治疗无效,而经心内膜起搏标测,在右室心尖部(3例)与右室流出道(1例)找出室性心动过速起源灶,用70～100J直流电进行经导管电消融。术中无心包填塞及肺水肿等并发症。术后不再能诱发出临床型室性心动过速。随访半年,其中2例无心律失常出现,另2例分别在1周与3个月后复发。     

Symptomatic ventricular tachyarrhythmia is associated with delayed gadolinium enhancement in cardiac magnetic resonance imaging and with elevated plasma brain natriuretic peptide level in hypertrophic cardiomyopathy

BACKGROUND: Delayed gadolinium enhancement (DGE) in cardiac magnetic resonance (CMR) imaging indicates the areas with myocardial fibrosis, which are suggested to be arrhythmogenic substrate in hypertrophic cardiomyopathy (HCM). Elevated brain natriuretic peptide (BNP) is associated with cardiovascular events in HCM. We investigated the grade of DGE in CMR and plasma BNP levels in HCM patients with or without symptomatic ventricular tachycardia (VT) or ventricular fibrillation (VF). METHODS AND RESULTS: We recruited 26 consecutive untreated HCM patients without any symptoms of heart failure. They were divided into 2 groups: (1) patients with symptomatic VT/VF [VT/VF(+) group, n=6]; (2) patients without symptomatic VT/VF [VT/VF(-) group, n=20]. CMR was performed to evaluate left ventricular geometry and the grade of DGE. Plasma BNP levels, left ventricular mass index, and the number of segments with positive DGE were greater in the VT/VF(+) group than in the VT/VF(-) group (698.1+/-387.6 vs. 226.9+/-256.8pg/ml, p=0.006; 152.3+/-49.5 vs. 89.5+/-24.1g/m(2), p=0.003; 9.7+/-5.7 vs. 3.5+/-3.3, p=0.013). On logistic regression, adjusted odds ratio for symptomatic VT/VF was 214 for logBNP (95% confidence interval [CI] 1.2-37,043, p=0.04) and 1.54 for DGE score (95% CI 1.01-2.34, p=0.04). CONCLUSIONS: High plasma BNP levels and the enlarged area of DGE in CMR were associated with symptomatic ventricular tachyarrhythmia. These factors may be useful markers for detecting high-risk patients of sudden cardiac death in HCM.     

Left ventricular septal and apex pacing for optimal pump function in canine hearts

OBJECTIVES: The goal of this study was to test the hypothesis that left ventricular (LV) pump function is optimal when pacing is performed at the LV near the sites where the impulses exit the Purkinje system. BACKGROUND: Pacing at the conventional site, the right ventricular (RV) apex, adversely affects hemodynamics. During normal sinus rhythm (SR), electrical activation of the working myocardium starts at the LV septal endocardium and spreads from apex to base. METHODS: Experiments were conducted in anesthetized open-chest dogs with normal ventricular conduction to investigate hemodynamic effects of pacing at various epicardial LV sites, the RV apex, and combinations of these sites (n = 11) and of RV and LV septal pacing (n = 8). The LV septal endocardium was reached via the RV by puncturing through the septum with a barbed electrode. Left ventricular systolic (LVdP/dtpos and stroke work) and diastolic (LVdP/dtneg and Tau) function were assessed using pressure-volume relations (conductance catheter technique). RESULTS: Left ventricular systolic and diastolic function were highly dependent on the site of pacing, but not on QRS duration. Left ventricular function was maintained at SR level during LV septal, LV apex, and multisite pacing, was moderately depressed during pacing at epicardial LV free wall sites, and was most severely depressed during RV apex pacing. On average, RV septal pacing did not improve LV function, compared with RV apex pacing, but in each experiment one (variable) RV pacing site was found, which only moderately reduced LV function. CONCLUSIONS: During ventricular pacing, LV pump function is maintained best (i.e., at SR level) when pacing at the LV septum or LV apex, potentially because pacing from these sites creates a physiological propagation of electrical conduction.     

Ablation Approaches for Ventricular Fibrillation

Invasive electrophysiology (EP) mapping and catheter ablation has increasingly become the standard of care for many cardiac arrhythmias like supraventricular tachycardias, atrial fibrillation, premature ventricular complexes (PVC), and monomorphic ventricular tachycardia. In this review, we discuss the recent progress made in the mapping and ablation of ventricular fibrillation (VF). Ventricular activation during VF is apparently disorganized, making mapping and interpretation difficult. Prolonged mapping during VF would require mechanical circulatory support as VF causes complete hemodynamic collapse. These limitations have been addressed by the realization that there is often a reliable trigger arrhythmia that initiates the clinical VF episodes, and an approach to map and ablate this trigger can be successful. Such triggers can be PVCs localizing to the Purkinje/fascicular system, and in other cases can be ectopy from outflow tracts or intracavitary structures like papillary muscles, false tendons or moderator band, or can be monomorphic VT or preexcited atrial fibrillation that degenerate into VF. More recently, approaches beyond trigger elimination directly targeting the VF substrate have been devised. This includes elimination of the arrhythmogenic substrate localizing to the epicardial right ventricular outflow tract in patients with Brugada syndrome, akin to elimination of the arrhythmogenic substrate harbored by regions within scar in ischemic and non-ischemic cardiomyopathies. Further, recent attempts have been made to try to identify and ablate rotors during VF that may be important in perpetuating the VF episode. Such exciting advances in “curing” VF are proving to be life saving for resuscitated survivors of arrhythmic death.