室性期前收缩性心肌病

频发的室性期前收缩导致心脏结构改变和左心室射血分数下降,称为室性期前收缩性心肌病。消除室性期前收缩后心脏结构和功能可恢复正常。回顾性研究显示,病程长及室性期前收缩负荷高是室性期前收缩性心肌病主要易患因素。其发生机制可能与室性期前收缩发生时心脏无法有效充盈及左右室收缩不同步导致心室腔扩大,心功能下降相关。射频消融术已成为根治室性期前收缩、逆转室性期前收缩性心肌病的唯一方法。     

室性期前收缩性心肌病

室性期前收缩是一种常见的心律失常,频繁发作可导致室性期前收缩性心肌病,但该心肌病目前发病机制及相关风险因素仍不甚明确.现就室性期前收缩性心肌病的研究进展做一综述.     

室性期前收缩性心肌病诊疗进展

频发室性期前收缩可导致心脏结构改变,左心室收缩功能降低,最终发展为心肌病,即室性期前收缩性心肌病。目前还需要进一步研究室性期前收缩性心肌病发病机制以及其发展的危险因素。有效的药物或射频导管消融治疗可预防或逆转室性期前收缩性心肌病,射频导管消融逐渐成为一线治疗方法。     

无症状性室性期前收缩预后和治疗进展

室性期前收缩是临床实践中常见的心律失常之一。大多数室性期前收缩患者没有临床症状。没有器质性心脏病的无症状性室性期前收缩患者预后相对较好,然而,频发的无症状性室性期前收缩可能与多种心血管事件和死亡风险增加有关,而且这类患者可能更倾向于发展成心动过速诱导的心肌病。因此,对无症状性室性期前收缩患者进行合理的临床评估至关重要。决定是否针对无症状性室性期前收缩进行治疗主要基于3个因素:基础心脏疾病、室性期前收缩的负荷、心功能状况。治疗室性期前收缩的方法主要包括药物治疗和导管消融治疗。导管消融治疗已经成为治疗室性期前收缩的安全有效的方法。     

室性期前收缩性心肌病发生及逆转的预测因素

室性期前收缩(PVCs)是临床上最常见的室性心律失常之一,部分频发PVCs可诱发PVCs性心肌病。其发生与否与许多因素相关,如PVCs的负荷、QRS波群时限、起源部位、无昼夜节律、插入性PVCs、联律间期、体重指数、期前收缩后收缩增强、症状、症状持续时间和男性等。PVCs性心肌病的治疗以射频导管消融治疗为主。成功消融后,影响PVCs性心肌病逆转的因素有:基线负荷大、消融后残余负荷小、QRS波群时限短及振幅大、基线左室舒张末期内径相对小以及期前收缩后血压升高等。     

室性期前收缩性心肌病研究进展

室性期前收缩是临床上常见的心律失常之一,而近年来长期频发室性期前收缩引起的心肌病也得到大量研究的证实,即室性期前收缩性心肌病。此类心肌病的发病机制目前尚不明确,其预测因子仍是目前的研究热点。随着诊疗技术的不断发展,有效的药物或射频导管消融治疗能在一定程度上减少或抑制室性期前收缩,并改善心功能,甚至可逆转心室重构。     

消融右室流出遵起源频发室性期前收缩心功能改善2例

一般认为心动过速性心肌病与各种心律失常有关,包括心房纤颤、心房扑动、室上性心动过速和室性心动过速。近来国内外也有少量报道频发性的单形性室性期前收缩（室性早搏,室早）也可导致心肌病的发生。     

具有危险性的急性缺血性室性期前收缩

定义 缺血性室性期前收缩是指急性心肌缺血时发生的室性期前收缩,缺血缓解后室性期前收缩随之消失。急性缺血性室性期前收缩是引起室性心动过速或心室颤动的始动因素,是诱发猝死的主要原因之一。因此,将急性缺血时发生的室性期前收缩称为具有危险性的室性期前收缩。     

室性期前收缩诱发性心肌病研究进展

<正>室性期前收缩(premature ventricular contractions,PVCs)为临床常见的心律失常,可见于多种器质性及非器质性心脏病患者。对于非器质性心脏病患者,称为特发性PVCs。以往研究认为,特发性PVCs是良性疾病,不需治疗,但近年来国内外多项临床研究及动物实验证明,频发PVCs可诱发可逆性心肌病变~([1-2]),并且提出了室性期前收缩诱发性心肌病(PVC-induced cardiomyopathy,PICMP)这一概念。PICMP被定义为:除外任何潜在心脏疾病,左室射血分数小于50%的     

心脏再同步治疗术中不同起搏模式对室性心律失常诱发的影响

目的 评价心脏再同步治疗(CRT)植入术中不同起搏模式对室性心律失常诱发情况的影响.方法 连续入选植入心脏再同步治疗除颤器(CRT-D)的患者,术中采用3种起搏模式:右心室起搏、双心室同步起搏和双心室顺序起搏(左心室优先50 ms和80 ms,右心室优先50 ms和80 ms).然后分别从左心室或右心室导线引入最多2个期前刺激,评估室性心律失常的诱发情况.结果 共有15例成功植入CRT-D的患者入选,男11例,年龄49 ～72(61±7)岁.缺血性心肌病7例,扩张型心肌病8例.左心室射血分数0.30±0.07.9例患者发生终点事件:5例诱发持续性室性心动过速(VT)/心室颤动(VF),4例诱发非持续性VT.双心室同步起搏时未诱发持续性VT/VF事件,双心室顺序起搏时有5例诱发VT/VF( P＜0.01).结论 双心室顺序起搏模式可能具有潜在致心律失常作用.双心室顺序起搏模式下心脏电生理刺激或自发的室性期前收缩对衰竭心脏电生理稳定性的影响需长期临床研究进一步证实.     

二维斑点追踪成像技术评价频发室性期前收缩患者的左心室功能的应用

目的:探讨二维斑点追踪成像技术评估特发性频发室性期前收缩患者的左心功能。方法:研究纳入50例特发性频发室性期前收缩患者以及20例健康人群对照。两组对照进行基线的普通超声心动图、二维斑点追踪成像技术及24h动态心电图检查。结果:病例组与对照组的左心室射血分数、左心室舒张末内径、左心室收缩末内径的差异无统计学意义(P0.05);病例组的左心室短轴应变、左心室圆轴应变及左心室长轴应变显著低于正常对照组(P0.001)。结论:二维斑点追踪成像技术能够识别频发室性期前收缩患者早期隐匿的左心室功能损害。     

Premature ventricular contraction-induced concealed mechanical bradycardia and dilated cardiomyopathy:

Left ventricular (LV) dysfunction due to frequent isolated premature ventricular contractions (PVCs) has been rarely reported. LV dysfunction and concealed mechanical bradycardia resolved in a patient with idiopathic dilated cardiomyopathy after the focal source of PVCs in the LV was eliminated by radiofrequency ablation (RFA). The patient remained free from PVCs and maintained normal LV function over 36-month follow-up. In a subset of patients with idiopathic dilated cardiomyopathy with frequent isolated PVCs, RFA of the arrhythmic focus restores normal LV function that can be long lasting.     

Radiofrequency ablation of frequent, idiopathic premature ventricular complexes: Comparison with a control group without intervention

BACKGROUND: Idiopathic premature ventricular complexes (PVCs) usually are considered benign, even when frequent. However, case reports have demonstrated a possible link between frequent PVCs and left ventricular (LV) dysfunction. In addition, frequent PVCs recently were demonstrated to be associated with increased LV dimensions and cardiomyopathy. METHODS: Among 60 consecutive patients with idiopathic, frequent PVCs (>10/hour), a reduced LV ejection fraction (EF; mean 34% +/- 13%) was present in 22 (37%) patients. Patients with decreased LV function had a greater PVC burden on a 24-hour Holter monitor than patients with normal EF (37% +/- 13% vs. 11% +/- 10% of all QRS complexes; P <.0001). There was a significant inverse correlation between the PVC burden and the EF before ablation (r = 0.73, P <.0001). RESULTS: The PVCs originated in the right ventricular outflow tract in 31 (52%) of 60 patients, the LV outflow tract in 9 (15%) of 60 patients, and in other sites in 13 (22%) of 60 patients. The site of PVC origin could not be determined in seven patients. Ablation was completely successful in 48 (80%) patients. In patients with an abnormal EF before ablation, LV function normalized in 18 (82%) of 22 patients from a baseline of 34% to 59% +/- 7% (P <.0001) within 6 months. In the four patients in whom ablation was ineffective, the EF further declined from 34% +/- 10% to 25% +/- 7% (P = .06) during follow-up. In a control group of 11 patients with a similar PVC burden (30% +/- 8%) and a reduced EF (28% +/- 13%) who did not undergo ablation, the EF remained unchanged in 10/11 patients over 19 +/- 17 months of follow-up and one patient underwent heart transplantation. CONCLUSION: LV dysfunction in the setting of frequent, idiopathic PVCs may represent a form of cardiomyopathy that can be reversed by catheter ablation of the PVCs.     

Frequent Premature Ventricular Complexes Originating from the Right Ventricular Outflow Tract Are Associated with Left Ventricular Dysfunction

Background : Recent case series have shown reversal of left ventricular (LV) dysfunction after catheter ablation of frequent premature ventricular complexes (PVCs) originating from the right ventricular outflow tract (RVOT). We conducted a retrospective study to evaluate the prevalence of patients with frequent RVOT PVCs (≥10 per hour) and LV dysfunction. Methods : RVOT PVC was defined as PVC with left bundle branch block morphology and inferior axis on a 12‐lead ECG. We included patients with frequent RVOT PVCs on 24‐hours Holter monitor who had a recent evaluation of LV function. Patients with structural heart disease, including obstructive coronary artery disease, were excluded. Patients were divided into three groups based on the number of PVCs (<1000/24 hour, 1000–10,000/24 hour, ≥10,000/24 hour), and the prevalence of LV dysfunction was evaluated in each group. Results : Our analysis included 108 patients: 24 patients had <1000PVCs/24 hour, 55 patients had 1000–10,000PVCs/24 hour, and 29 patients had ≥10,000PVCs/24 hour. The prevalence of LV dysfunction was 4%, 12%, and 34%, respectively (P = 0.02). With logistic regression analysis, non‐sustained ventricular tachycardia was an independent predictor of LV dysfunction with odds ratio of 3.6 (1.3–10.1). Conclusion : We demonstrated a significant association between frequent RVOT PVCs and LV dysfunction in patients without structural heart disease.     

特发性右室流出道心律失常患者J波的发生率及其临床特征

目的 调查J波在特发性右室流出道室性心动过速或室性早搏（RVOT-VT/PVCs）病人的发生率及其临床特征。方法 该研究纳入143例特发性 RVOT-VT/PVCs的患者和285例年龄和性别匹配的健康体检者作为对照组。 评估、比较两组间 J-波的发生率。 依据J波的存在与否,将患者分为伴有J波的 RVOT-VT/PVCs组（J-VT/PVCs组）和不伴有J波的 RVOT-VT/PVCs组（non-J-VT/PVCs组）,对两组的临床和电生理数据进行比较。 结果 与对照组比较,J波在特发性 RVOT-VT/PVCs患者中更为常见（39. 9% vs 16. 1% ,P〈0. 01）。 与 non-J-VT/PVCs组比较,J-VT/PVCs组持续性VT、晕厥有较高的发生率,分别为24. 6% vs 4. 7% ;26. 3% vs 2. 3% ,P均〈0.01。 而且VT的周期更短[（304±56）ms vs（350±56）ms,P〈0. 01]。 两组中无心室颤动或心脏猝死发生。 结论 特发性RVOT-VT/PVCs患者,有较高的J波发生率;有J波的患者伴随有较严重的心律失常 。     

First evidence of premature ventricular complex-induced cardiomyopathy: a potentially reversible cause of heart failure

Tachycardia-induced cardiomyopathy is a well-recognized and reversible condition, but left ventricular dysfunction due to frequent isolated premature ventricular complexes (PVCs) has not been reported. We observed resolution of dilated cardiomyopathy in a patient after a focal source of PVCs was eliminated by radiofrequency ablation. In a subset of patients with heart failure, PVC-induced cardiomyopathy may be a potentially reversible cause of left ventricular dysfunction.     

Ventricular Tachycardia Originating from the Posterior Papillary Muscle in the Left Ventricle A Distinct Clinical Svndrome

1．focal mechanism通常出现在有关地震学研究中,译为“震源机制”。在有关心律失常机制研究的文献中,focal mechanism是指一种有别于折返（reentry）机制的机制,确切的机制尚不完全清楚,认为与自律性异常、促发活动和微折返（microreentry）有关,通译为“局灶机制”。     

Advances in management of premature ventricular contractions

Premature ventricular complexes (PVCs) are a common occurrence in clinical practice. The clinical presentation may range from asymptomatic to left ventricular (LV) dysfunction with congestive heart failure. The decision to suppress PVCs is largely based on the presence of symptoms, interference with other therapy (e.g., cardiac resynchronization therapy), or suspicion of PVC-mediated cardiomyopathy. Catheter ablation has emerged as a safe and effective option for the treatment of frequent PVCs. Careful attention to PVC characteristics on surface electrocardiogram has proven useful for the initial localization of the ectopic focus, which may then serve as a guide to procedural planning. The point of interest is often identified with activation mapping, and the ablation site can be further defined with pace mapping techniques. Clinical experience with PVC ablation has been successful in ≥80 % of cases, and the literature reports multiple cases of marked improvement in LV function after eradicating the culprit ectopic focus in patients with PVC-mediated cardiomyopathy.     

‘Frequent’ ventricular bigeminy – A reversible cause of dilated cardiomyopathy. How frequent is ‘frequent’?

An interesting development in the field of heart failure has been the link between frequent premature ventricular contractions and cardiomyopathy. We report a patient whose frequent ventricular bigeminy resulted in left ventricular impairment that resolved after the use of non-contact mapping during radiofrequency ablation. A review of the literature regarding possible mechanisms is discussed. For the practicing clinician, the question of 'frequent' should be taken in context of symptoms and LV function. A single 24-h Holter monitor may not truly reflect the ectopic load. We recommend that if there is associated LV dysfunction and a causal link to frequent PVCs then suppression with radiofrequency ablation is a safe and effective treatment strategy.     

射频导管消融治疗特发性室性期前收缩触发的心室颤动／多形性室性心动过速

目的：探讨特发性室性期前收缩（早搏,PVC）触发心室颤动和（或）多形性室性心动过速（VF／PVT）的临床特点及射频导管消融治疗效果。方法：313例无器质性心脏病接受射频导管消融治疗的特发性PVC患者,其中6例发生了由PVC触发的VF／PVT,分析该6例患者的临床资料及射频导管消融治疗效果。结果：该6例患者动态心电图可记录到频发PVC[（16303±5854）次／d],PVC联律间期及基础QT间期分别为（412±44）ms和（407±10）ms。这些参数值在另外307例特发性PVC患者中分别为（15570±4743）次／d、（419±36）ms和（404±8）ms,两组间无显著性差异。313例患者中,有88例记录到由PVC触发的单形态室性心动过速（VT）。PVC触发VF／PVT患者中晕厥发生率（3／6）高于由PVC触发的单形态VT患者（4／88,4．5％,P〈0．05）,PVT的周长[（235±22）ms]则短于单形态VT组[（324±29）ms,P〈0．05]。针对触发VF／PVT的PVC消融后随访的10～36个月期间,所有6例患者未再发生晕厥、VF及心脏骤停。结论：恶性VF／PVT可能由一些特发性PVC诱发,射频导管消融PVC治疗可作为一项有效的治疗选择。