克拉霉素致室性心律失常的观察及部分机制探讨

目的探讨克拉霉素致室性心律失常的机制。方法 30只健康新西兰长耳兔随机分为对照组、常规剂量组(克拉霉素1倍血药浓度)和大剂量组(克拉霉素10倍血药浓度)组,每组各10只制作兔左室楔形心肌块模型。采用浮置玻璃微电极法同步记录各组内、外膜下心肌动作电位和容积心电图,观察在基础周长为2 000 ms电刺激情况下,灌流过程中QT间期、跨室壁离散度(TDR)和T波顶点到终点距离(T_(p-e))及致心律失常危险度。结果相比对照组,常规剂量组的QT间期、TDR、T_(p-e)和致心律失常危险度未见差异(P0.05);相比其他两组,大剂量组QT间期、TDR和T_(p-e)明显延长(P0.05),致心律失常危险度明显增大(5±3.27vs 0,0vs 0,P0.05)。结论慢心率下,正常血药浓度克拉霉素致室性心律失常可能性较低,过高血药浓度克拉霉素易诱发尖端扭转性室性心律失常。     

急性心肌缺血犬心肌细胞瞬时外向钾电流和跨壁复极离散度变化致心律失常机制研究

目的:探讨急性心肌缺血对犬左室心肌楔形组织块瞬时外向钾电流(Ito)、跨壁复极离散度(TDR)变化及其与室性心律失常的关系。方法:建立冠状小动脉灌注犬左室心肌楔形组织块模型,应用浮置玻璃微电极和心电图同步记录技术,观察急性无灌流心肌缺血对内、中、外3层心肌细胞Ito、动作电位时程(APD)、TDR和心律失常的影响。结果:急性心肌缺血早期犬左室内、中、外3层心肌细胞的Ito增大,APD缩短,均以外膜心肌细胞最明显,TDR增加,诱发早期后除极、R-on-T期前收缩和室性心动过速。结论:急性心肌缺血时Ito增大,TDR增加,产生2相位折返,是多型性室性心动过速发生的重要机制。     

急性缺血对兔左心室跨壁复极离散度的影响

急性缺血是导致室性心律失常、心脏性猝死的主要原因之一。本研究以经冠状动脉灌注的兔左心室楔形心肌组织块为对象，着重探讨了急性无灌注缺血过程中兔左心室内外膜心肌动作电位、跨壁复极离散度（transmural dispersion of repolarization，TDR）演变规律及室性心律失常发生机制。     

抗心律失常肽对陈旧性心肌梗死兔室性心律失常的影响

目的观察缝隙连接激动剂抗心律失常肽(AAP10)对陈旧性心肌梗死(OMI)兔室性心律失常的影响,并探讨其作用机制。方法将30只雄性日本大耳白兔随机分为假手术组(Sham)、OMI 组和 AAP10组,每组各10只。Sham 组开胸但不结扎冠状动脉,OMI 组和 AAP10组开胸并结扎冠状动脉左室支制备心肌梗死模型,普通饲料喂养3个月后制备兔左心室楔形心肌块的灌注模型。Sham 组和 OMI 组灌流正常台氏液,AAP10组灌流正常台氏液+AAP10(80 nmol/L)。灌流全程同时采用浮置玻璃微电极法同步记录内膜下心肌、外膜下心肌跨膜动作电位和跨壁心电图,并观察心外膜下心肌的刺激反应间期(stimulus-response-interval,SRI)和室性心动过速(室速)的诱发率。结束试验后测量梗死周边区心室壁的厚度、左室重、全心重。结果 OMI 组和 AAP10组兔均存在显著的心肌重构,并且 OMI 组兔有较高的室速诱发率(80%)。OMI 组与 AAP10组相比,AAP10显著缩短 SRI[SRI-1为(28.71±0.55)ms 与(20.59±0.79)ms;SRI-2为(38.67±0.49)ms 与(30.42±0.74)ms,P<0.01],而且 AAP10明显降低室速的诱发率(20%),但对动作电位形态和时程均无影响。结论AAP10可以在不影响动作电位形态和时程的前提下提高缝隙连接的传导速度,并可降低 OMI 兔室性心律失常的发生率。     

加替沙星致室性心律失常机制的研究

目的:探讨临床广泛使用的第四代氟喹诺酮类抗生素——加替沙星致室性心律失常的机制。方法:制作兔左室楔形心肌块模型,将30只健康新西兰长耳兔随机分为正常组、加替沙星组和低钾低镁组(低钾组),每组各10只。正常组灌流正常台式液,加替沙星组灌流19mmol/L加替沙星30min,低钾组灌流同浓度但溶于低钾低镁液的加替沙星30min。采用浮置玻璃微电极法同步记录各组内、外膜下心肌动作电位和跨壁心电图,观察灌流过程中心律失常发生率,QT间期和TDR(跨室壁离散度)的变化。结果:1与正常组比较,加替沙星组和低钾组的QT明显延长;TDR,EAD(早后除极)和TdP(尖端扭转型室速)的发生率亦明显增大(P0.05)。2与加替沙星组比较,低钾组的QT和TDR差异未见统计学意义(P0.05)。3与加替沙星组比较,低钾组的EAD和TdP的发生率明显增大(P0.05)。结论:在加替沙星合并低钾低镁条件下易诱发Tdp及EAD等恶性心律失常。     

左氧氟沙星对糖尿病兔的致心律失常作用

目的 糖尿病患者QT间期延长反映了心脏的电不稳定性,这与心律失常的发生有关.作为临床常用的抗生素之一,左氧氟沙星可引起QT间期延长,甚至引起致命性尖端扭转性室性心动过速（Tdp）.本研究旨在评估左氧氟沙星对糖尿病兔的致心律失常作用.方法 健康新西兰大白兔30只,体重2.0～2.5 kg,雌雄各半,应用随机数字法分为对照组（n=10）和实验组（n=20）.实验组经耳缘静脉注射5％四氧嘧啶160 mg/kg建立糖尿病兔模型,对照组兔注射相同剂量的生理盐水.72 h后监测兔空腹血糖,若空腹血糖值大于基础血糖值的3倍,视为建模成功.饲养4周后制作冠状动脉灌流的左心室楔形心肌模型,分别灌注左氧氟沙星（1.14 mg/ml）,比较灌注左氧氟沙星前后对照组兔和糖尿病兔跨壁心电图QT间期、左心室心肌内膜、外膜细胞的动作电位时限（APD）、跨壁复极离散度（TDR）及室性心律失常的发生率.结果 与对照组相比,糖尿病兔心肌QT间期延长19％,糖尿病内膜、外膜APD明显延长,跨壁复极离散度增大,早后除极发生率为36％,心室颤动（室颤）发生率18％.灌注左氧氟沙星后,对照组心肌QT间期、内膜、外膜APD均延长,跨壁复极离散度增大,早后除极发生率60％,所有心肌均未发生室颤;糖尿病组心肌QT间期、内膜、外膜APD、跨壁复极离散度均显著增大,早后除极的发生率为63％,心室颤动发生率为45％,室性心律失常发生率显著增加（P＜0.05）.结论 左氧氟沙星引起糖尿病兔QT间期延长,跨壁复极离散度异常增大.与对照组相比,糖尿病组灌注左氧氟沙星后更易发生心律失常.     

急性心肌缺血时瞬时外向钾电流和跨壁复极离散度的变化及其计算机仿真研究

目的探讨急性心肌缺血时犬左室心肌楔形组织块瞬时外向钾电流(Ito)、跨壁复极离散度(TDR)的变化及其计算机仿真研究。方法建立冠状小动脉灌注犬左室心肌楔形组织块模型,应用浮置玻璃微电极和心电图同步记录技术,观察急性无灌流心肌缺血对内中外三层心肌细胞Ito、动作电位时程(APD)、TDR和心律失常的影响,并结合急性心肌缺血Ito离子流和TDR的变化,应用修正Luo-Rody参数进行计算机仿真。结果急性心肌缺血早期犬左室内中外三层心肌细胞的Ito离子流增大,APD缩短,均以心外膜层细胞最明显,TDR增加,诱发R-on-T早搏和室性心动过速,并经计算机仿真可以证实与临床一致的心电图特点。结论急性心肌缺血时Ito离子流增大,TDR增加,产生2位相折返,是多型性室性心动过速发生的重要机制,计算机仿真可以显示这些特点。     

急性心肌缺血时瞬时外向钾电流和跨壁复极离散度的变化及其计算机仿真研究

目的探讨急性心肌缺血时犬左室心肌楔形组织块瞬时外向钾电流（Ito）、跨壁复极离散度（TDR）的变化及其计算机仿真研究。方法建立冠状小动脉灌注犬左室心肌楔形组织块模型，应用浮置玻璃微电极和心电图同步记录技术，观察急性无灌流心肌缺血对内中外三层心肌细胞Ito、动作电位时程（APD）、TDR和心律失常的影响，并结合急性心肌缺血Ito离子流和TDR的变化，应用修正Luo-Rody参数进行计算机仿真。结果急性心肌缺血早期犬左室内中外三层心肌细胞的Ito离子流增大，APD缩短，均以心外膜层细胞最明显，TDR增加，诱发R-on-T早搏和室性心动过速，并经计算机仿真可以证实与临床一致的心电图特点。结论急性心肌缺血时Ito离子流增大，TDR增加，产生2位相折返，是多型性室性心动过速发生的重要机制，计算机仿真可以显示这些特点。     

胺碘酮对家兔急性心肌缺血左室跨壁复极离散度的影响

目的:探讨胺碘酮对家兔急性缺血左室心肌楔形组织块电生理特性和跨壁复极离散度（TDR）的影响及其抗缺血心律失常的机制。方法: 建立冠状小动脉灌注家兔左室心肌楔形组织块模型,应用浮置玻璃微电极和心电图同步记录技术,观察急性无灌流心肌缺血时,胺碘酮对内外层心肌细胞的动作电位时程（APD）、TDR和心律失常的影响。结果: ①左心室楔形组织块停止灌注后,胺碘酮组内、外膜心肌细胞的APD较对照组明显延长[(228±19) ms vs.(212±6) ms,P<0.05］,且外膜APD的延长更明显[(203±15) ms vs.(180±5) ms,P<0.05］。②急性缺血各时间段,APD较缺血前均缩短,以外膜APD缩短更明显,导致TDR增大。用药后TDR明显短于对照组。结论: 胺碘酮可延长内、外膜心肌细胞的APD,且外膜APD的延长明显,并可减小急性缺血心肌的TDR,这可能是其抗心律失常机制的细胞电生理基础。     

阻断Ryanodine受体对兔儿茶酚胺敏感性室速模型心律失常发生的抑制作用

目的:观察阻断Ryanodine受体对兔儿茶酚胺敏感性室速(CPVT)模型心律失常发生的抑制作用。方法:将40只日本长耳兔随机分为4组:正常对照组、模型组、钙调蛋白激酶Ⅱ抑制剂KN-93组、Ryanodine受体阻滞剂兰尼碱组,每组10只。制备兔左室楔形心肌块的灌流模型,同步记录心内、外膜动作电位及跨壁心电图。正常组灌流台氏液,模型组灌流咖啡因和异丙肾上腺素建立CPVT模型,KN-93组和兰尼碱组预先给予各自药物预灌,然后灌流咖啡因和异丙肾上腺素,观察在快频率程序刺激下各组触发活动和室性心动过速的发生率。结果:对照组、模型组、KN-93(1μmol/L)和兰尼碱组(10μmol/L)触发活动的发生率分别为0/10、10/10、4/10和2/10,多形性室速或室颤的发生率分别为0/10、9/10、3/10、1/10;提示KN-93和兰尼碱均可减少CPVT模型的触发活动和室性心律失常的发生(均P<0.05)。结论:阻断Ryanodine受体能够有效抑制CPVT模型的触发性室性心律失常,Ryanodine受体有望成为防治该类心律失常新的重要靶点。     

特发性室性心律失常的射频消融

目的特发性室性心律失常（IVA）是指不伴有明显器质性心脏病的室性心动过速（室速）或室性早搏（室早）,约占所有室性心律失常的10％左右。本文系统分析925例IVA病例,探讨IVA的临床、电生理和射频消融的特点。方法本文回顾性分析了从1994年3月至2009年2月,925例IVA患者的临床特点,射频消融治疗的过程和结果。925例病人,男性500例,女性425例,平均年龄（36．65±14．81）岁。临床证实为IVA患者,并且排除了器质性心脏病。在停用抗心律失常药物5个半衰期后,进行电生理检查和射频消融治疗。结果特发性右心室室性心律失常（IRVA）516例,特发性左心室室性心律失常（ILVA）409例,IRVA多发生于女性,发病的平均年龄40岁,大多数表现为频发室早伴有反复单形室性心动过速,出现黑喙症状为14．3％;ILVA多发生于男性,发病的平均年龄33岁,多表现为持续性室速,出现黑矇症状为5．9％。IRVA有486例（94．2％）起源于右心室流出道,而在右心室流出道起源的室速／室早里,又以起源于间隔面的多见,占78％左右,起源于游离壁的占10％左右,其余的12％起源于二者之间的部位。射频消融多采用寻找心内膜最早激动点结合起搏标测来寻找合适的靶点。ILVA最多见的类型是左心室特发室速（ILVT）,有272例（66．5％）,ILVT主要起源于左后分支区域,也可以起源于左前分支区域和临近希氏束部位。主要用激动顺序标测结合浦肯野电位的方法确定消融靶点。IRVA的516例患者射频消融即刻成功率为89．3％。ILVA射频消融即刻成功率为93．7％。结论IVA患者虽然没有器质性心脏病,但是伴有多种临床症状,少部分病人甚至出现黑矇、晕厥,应积极行射频消融治疗,预防出现心室颤动危及生命。     

原发性高血压左心室不同构型民律失常的比较

目的 研究原发性高血压患者左心室重构不同构型间心律失常的差异。方法 179例原发性高血压患者均进行了24h动态心电图，动态血压监测，超声心动图等检查，根据检查结果划分左心室构型，判定心律失常，比较左心室重构组与正常构型组心律失常的发生率；通过多元逐步回归分析，甄选出对心律失常有独立影响的因素。并在校正这些影响因素后，比较左心室不同构型间心律失常严重程度的差异。结果 左心室重构组的房性心律失常，室性心律失常，复杂室性心律失常的发生率均显著高于正常构型组，而影响原发性高血压心律失常的相对独立因素很多，其中部分左心室解剖结构指标，高血压分级，左心房内径，E/A值，夜间舒张压负荷值以及日平均心率等占重要地位；校正上述影响因素后，不同构型两两比较时，部分构型之间心律失常分级级别仍存在差异，且差异为构型本知差异所致。结论 原发性高血压心律失常的影响因素很多（例如高血压分级、左心室重量指数，左心房内径，左心室后壁厚度等），不同构型间心律失常的严重程度存在差异。     

Terapêutica de ressincronização cardíaca e efeito pró‐arrítmico: um problema que deve ser lembrado

The demonstrated benefits of cardiac resynchronization therapy (CRT) in reducing mortality and hospitalizations for heart failure, improving NYHA functional class and inducing reverse remodeling have led to its increasing use in clinical practice. However, its potential contribution to complex ventricular arrhythmias is controversial.We present the case of a female patient with valvular heart failure and severe systolic dysfunction, in NYHA class III and under optimal medical therapy, without previous documented ventricular arrhythmias. After implantation of a CRT defibrillator, she suffered an arrhythmic storm with multiple episodes of monomorphic ventricular tachycardia (VT), requiring 12 shocks. Subsequently, a pattern of ventricular bigeminy was observed, as well as reproducible VT runs induced by biventricular pacing.Since no other vein of the coronary sinus system was accessible, it was decided to implant an epicardial lead to stimulate the left ventricle, positioned in the left ventricular mid‐lateral wall. No arrhythmias were detected in the following six months.This case highlights the possible proarrhythmic effect of biventricular pacing with a left ventricular lead positioned in the coronary sinus venous system.     

Ventricular arrhythmias are related to the presence of autoantibodies with adrenergic activity in chronic chagasic patients with preserved left ventricular function

BackgroundThe presence of G-type immunoglobulins with functional activity was previously demonstrated in chronic chagasic patients (CChP) with heart failure. Here we evaluated the profile and the arrhythmogenic effects of sera from CChP with preserved ventricular function.MethodsElectrocardiography (ECG), Holter monitoring, exercise testing, and left ventricular ejection fraction of 40 CChP were measured. Serum from each patient was characterized in isolated rabbit hearts where ECG parameters were analyzed.ResultsFrom the total sera of the 40 CChP tested in rabbit hearts, 42.5% activated β-adrenergic receptors (Ab-β), 5% activated muscarinic receptors (Ab-M), and 30% activated both muscarinic and β-receptors (Ab-Mβ). In addition, 22.5% of the sera were not reactive (Ab-NR). Ab-β patients presented more cases of arrhythmias in exercise testing (P < .001). In Holter, ventricular arrhythmias appeared more than twice as often in the Ab-β group than in the Ab-NR group and in numbers similar to the Ab-Mβ group (Ab-NR: 2; Ab-β: 5; Ab-Mβ: 3). Arrhythmias were induced by Ab-Mβ in isolated rabbit hearts. Sera from patients with Ab-Mβ, who had longer PR intervals, were able to reversibly prolong PR when perfused in isolated rabbit heart (r² = 0.74; P = .02).ConclusionsHigh prevalence of Ab-β in CChP with preserved left ventricular function led to a greater incidence of ventricular arrhythmias in the patients.     

Refractory Ventricular Tachycardia in a Patient With a Left Ventricular Assist Device Successfully Treated With Stellate Ganglion Phototherapy

Neuraxial modulation therapies, such as stellate ganglion block, thoracic epidural anaesthesia, and cardiac sympathetic denervation, are effective for ventricular arrhythmias. However, these treatments can increase the risk of bleeding and infection. In this case report, stellate ganglion phototherapy was safely and effectively performed for refractory ventricular tachycardias in a patient with a history of left ventricular assist device implantation. Stellate ganglion phototherapy may have the potential to treat refractory ventricular arrhythmias as an additive therapy or bridge therapy.     

钙调蛋白抑制剂对陈旧性心肌梗死兔室性心律失常的影响

探讨钙调蛋白抑制剂W 7对陈旧性心肌梗死(HMI)兔室性心律失常的影响,将 30只雄性日本大耳白兔随机分假手术组(Sham)、HMI组和W 7干预组。Sham组开胸但不结扎冠状动脉;HMI组和W 7干预组开胸并结扎冠状动脉左室支制备心肌梗死模型,喂养 3个月后进行研究。W 7干预组在程序刺激前以 50μmol/kg的剂量溶于20ml生理盐水中,在 10min内静脉推注,HMI组和Sham组静脉推注生理盐水。将双极电极刺入左室梗死周边部位及Sham组的相应部位,程序刺激诱发心律失常,记录室性心动过速的发生率,测定心室颤动阈值。结束实验后取出心脏并称量左室重量。结果:Sham组、HMI组和W 7组诱发室性心动过速的发生率分别为 0 /10、8 /10和 3 /10。Sham组与HMI组差异有显著性(P<0. 01);W 7组与HMI组相比较室性心律失常发生率降低,差异有统计学意义(P<0. 05)。三组的心室颤动阈值分别为 13. 30±0. 95V、8. 90±1. 37V和 11. 80±1. 14V,三组之间差异均有显著性(P<0. 01)。结论:钙调蛋白抑制剂能提高HMI兔的心室颤动阈值,降低室性心律失常的发生率。     

Impact of left ventricular hypertrophy on ventricular arrhythmias in the absence of coronary artery disease

Left ventricular hypertrophy has a grave prognosis. Ventricular arrhythmias may account for a large portion of this poor prognosis, but the contribution of coronary artery disease has not been excluded. The occurrence of ventricular arrhythmias was investigated by 24 h ambulatory electrocardiographic (ECG) monitoring in 49 hypertensive patients who had normal findings on coronary arteriography. The presence of left ventricular hypertrophy was assessed by both ECG and echocardiography. The frequency and complexity of ventricular arrhythmias were significantly related to the presence of left ventricular hypertrophy whether it was defined by wall thickness (interventricular septum or posterior wall greater than or equal to 1.2 cm) or by left ventricular mass indexed to height (left ventricular mass/height greater than or equal to 163 g/m in men and greater than or equal to 121 g/m in women). The relation between left ventricular mass or wall thickness to ventricular arrhythmia was graded and continuous; for every 1 mm increase in the thickness of interventricular septum or posterior wall there was an associated two- to threefold increase, respectively, in the occurrence and complexity of ventricular arrhythmias. In conclusion, left ventricular hypertrophy is associated with an increase in the frequency and complexity of ventricular arrhythmias in the absence of coronary artery disease, and the relation is graded and continuous.     

Treatment of arrhythmias in patients with congestive heart failure

Both ventricular and atrial arrhythmias are commonly encountered in patients with ventricular dysfunction. In fact, roughly half of the deaths occurring in patients with ventricular dysfunction are caused by ventricular arrhythmias. Atrial arrhythmias in this patient population compromise left ventricular filling and if uncontrolled can exacerbate (and in some cases cause) the underlying myopathic process. Consequently, the diagnosis and treatment of these complex, and often life-threatening, arrhythmias is a critical component in the management of congestive heart failure (CHF). As the complexity of pharmacologic and nonpharmacologic antiarrhythmic therapy evolves, it has become increasingly important to understand the potential benefits and limitations of the various treatment modalities in the setting of patients with CHF. The management of arrhythmias in patients with CHF includes conventional drug therapies, as well as therapies directed specifically at treating the arrhythmias that are encountered. The treatment of atrial arrhythmias may include anticoagulation, drugs for rate control, rhythm control, or radiofrequency ablation. The treatment of ventricular arrhythmias, conversely, uses the implantable cardioverter-defibrillator to prevent sudden death, with adjuvant drug therapy or ablation for refractory ventricular tachycardia. This article provides an overview of the current state-of-the-art arrhythmia management in patients with CHF.     

Alternans of action potential duration and amplitude in rabbits with left ventricular dysfunction following myocardial infarction

T-wave alternans may predict the occurrence of ventricular arrhythmias in patients with left ventricular dysfunction and experimental work has linked discordant repolarization alternans to the induction of re-entry. The aim of this study was to examine the occurrence of transmural repolarization alternans and to investigate the link between alternans and ventricular arrhythmia in rabbits with left ventricular dysfunction following myocardial infarction. Optical mapping was used to record action potentials from the transmural surface of left ventricular wedge preparations from normal and post-infarction hearts during a progressive reduction in pacing cycle length at 30 and 37°C. Data were analyzed using custom software, including spectral analysis. There were no significant differences in baseline transmural electrophysiology between the groups. Post-infarction hearts had a lower threshold for both repolarization alternans (286 vs. 333 bpm, p<0.05) and ventricular arrhythmias (79 vs. 19%, p<0.01) during rapid pacing, which was not accounted for by increased transmural discordant alternans. In VF-prone hearts, alternans in optical action potential amplitude was observed and increased until 2:1 block occurred. The degree of optical action potential amplitude alternans (12.0 ± 7.0 vs. 1.8 ± 0.3, p<0.05), but not APD(90) alternans (1.4 ± 0.6 vs. 1.1 ± 0.1, p>0.05) was associated with VF inducibility during rapid pacing. Post-infarction hearts are more vulnerable to transmural alternans and ventricular arrhythmias at rapid rates. Alternans in optical action potential amplitude was associated with conduction block and VF. The data suggest that changes in optical action potential amplitude may underlie a mechanism for alternans-associated ventricular arrhythmia in left ventricular dysfunction.     

Electrophysiological effects of acute ventricular dilatation in the isolated rabbit heart

We examined the effects of left ventricular dilatation on epicardial pacing threshold, conduction velocity, and effective refractory period (ERP) in the isolated, retrograde perfused rabbit heart. Left ventricular size was modified by acutely changing the volume of a fluid-filled balloon anchored within the vented left ventricle. Increases in left ventricular volume, associated with increases in left ventricular end-diastolic pressure from 0 +/- 1 to 35 +/- 2 mm Hg, were not associated with significant changes in pacing threshold or conduction velocity. The left ventricular ERP decreased significantly with an added volume of 1.5 ml (91.4 +/- 5.5 msec) compared with starting volume (117.7 +/- 3.8 msec, p less than 0.01). Right ventricular ERP did not change significantly with increases in left ventricular volume. The left and right ventricular ERPs were comparable at starting volume (117.7 +/- 3.8 and 117.6 +/- 3.5 msec, respectively; p = NS) but were significantly different with an added volume of 1.5 ml (91.4 +/- 5.5 and 112 +/- 5.6 msec, p less than 0.05). These changes were independent of coronary perfusion pressure and paced cycle length, suggesting that ischemia is an unlikely explanation for the observed effects. Changes in left ventricular volume decreased left ventricular ERP in a regionally heterogeneous manner, increasing the temporal dispersion of recovery over the left ventricle nearly twofold. Induced ventricular arrhythmias (ventricular tachycardia or fibrillation) were significantly more frequent at high (35%) than at low (3%) volumes during left ventricular pacing. We conclude that ventricular dilatation is associated with increased dispersion of refractoriness in this model, a finding that correlates with propensity for reentrant arrhythmias.