Acute myocardial infarction in a patient with Wolff-Parkinson-White syndrome

It is known that the Wolff-Parkinson-White syndrome （WPW） may either mimic myocardial infarction （MI） or mask the ECG changes of MI. Thus, the diagnosis of MI coexisting with WPW is frequently difficult. Furthermore, patients with WPW occurring acute MI may be life threat- ening. Therefore, early recognition and correct treatment allows rapid restoration of normal sinus rhythm and may decrease morbidity and mortality.

Left ventricular noncompaction associated with hypertrophic cardiomyopathy and Wolff-Parkinson-White syndrome

We report a 35-year-old female patient with hypertrophic cardiomyopathy, left ventricular noncompaction, and Wolff-Parkinson-White EKG pattern. Several other family members present the same clinical condition. We speculate that this phenotype is related to the genotypes PRKAG2 and LAMP2 represented by mutations of the genes encoding AMP-activated protein kinase (PRKAG2) and lysosome associated membrane protein 2 (LAMP2).

STUDY OF OCCURING MECHANISM OF ATRIAL FIBRILLATION IN WOLFF-PARKINSON-WHITE SYNDROME

We selected 231 petients with WPW syndrome that was concomitant withhistory of tachycardia and 200 patients with history of AVNRT.The inci-dence of atrial fibrillation in WPW group was 46.3 % That in AVNRTgroup was 2.5%.Comparison of two groups showed significantly different.Af(+)patients in WPW group were significantly shorter than Af(-)in sameGroup and atrial refractory stage in AVNRT group.Relative smaller wave-length of atrial impulse(FRPA/PA)also showed significantly decreased.The maximal value DI/D2 of prolonsed degrce of persistant time by righttrial wave in high siie was obtained by early stimulating in right atrial highsite.D2/D1 was sited above 1.5 in non-contimal strial active area that con-duced delay ares below 20 ms of persistant time prolonged of atrial waveand area of fast atrial fibrillation.The incidence of these indexes in Af(+)group and RAF(+)was significantlyInased.The results suggested that atrial fibrillation in WPW syndromehas an important relation with pathway existed end atrial characters.

Effect of Accessory Pathway Conduction on PJ Interval in Wolff-Parkinson-White Syndrome

Objective To observe the effect of accessory pathway (AP) conduction on PJ interval in patients with Wolff-Parkinson-White syndrome. Methods 129 patients with a single manifestation of AP who underwent successful radiofrequency ablation (RFCA) were included. Patients were divided into 10 groups according to AP location. The PR intervals, QRS durations and the PJ intervals were measured using simultaneous 12-lead ECG before and after ablation. The PJ intervals before ablation were compared with that after ablation. The atrioventricular (AV) conduction time via atrioventricular node-His conduction system before ablation were compared with the PR intervals after ablation. The ventricular depolarization time via atrioventricular node-His conduction system before ablation were compared with the QRS durations after ablation. Delta waves were compared between each two groups. Results (1) The PJ intervals of right posterior (RP) group and right posteroseptal (RPS) group before ablation were shorter than that after ablation (RP group 226±18 ms vs 236±19 ms, P<0.01, RPS group 221±18 ms vs 238±31 ms, P<0.05, respectively). (2) There were no significant differences between the atrioventricular (AV) conduction time via atrioventricular node-His conduction system before ablation and the PR intervals after ablation. (3)The ventricular depolarization time via atrioventricular node-His conduction system of RP group and RPS group before ablation were shorter than the PR intervals after ablation(RP group 79±12 ms vs 87±9 ms, P=0.01; RPS group 70±13 ms vs 86±9 ms, P<0.05, respectively). (4)The delta waves of RP group and RPS group were longer than that of left posterior group and left posteroseptal group(P<0.05). Conclusion PJ interval is shortened by AP conduction which pre-excites the general last excited part of left ventricle. It is determined by AP location and the extent of preexcitation.

Transient severe mitral regurgitation after paroxysmal supraventricular tachycardia in patient with WPW syndrome

A 65-year-old woman was presented with acute ab- dominal pain. The initial heart rate was 170 beats/min and the ECG showed supraventricular tachycardia （Figure IA）. After intra-venous adenosine administered, it recovered to sinus rhythm and the follow-up ECG showed WPW pattern （Figure 1B）. The echocardiography revealed mitral valve prolapse of mid portion of anteromedial valve leaflet （A2） with severe mitral regurgitation （MR） （Figure 2）.

The Use of Trans-Esophageal Electrophysiology Study to Identify a High Risk Asymptomatic Wolff Parkinson White Syndrome Patient

Patients with a Wolff-Parkinson-White (WPW) pattern on their ECG can experience symptoms such as syncope, palpitations, supraventricular tachycardia, and atrial fibrillation, or they can be asymptomatic (aWPW). All patients with WPW, regardless of the presence or absence of symptoms, are at risk of sudden death. Therefore, it is recommended that younger patients with WPW undergo studies to determine their risk. We report a previously asymptomatic WPW patient identified as high risk for sudden death due to?rapid conduction down her accessory pathway during atrial fibrillation induced during a trans-esophageal electrophysiology study.

Inherited Wolff–Parkinson–White Syndrome

Wolff-Parkinson-White(WPW)syndrome is a congenital disorder of cardiac conduction system characterized by electrocardiographic preexcitation and episodes of paroxysmal supraventricular tachycardia.It is caused by a cardiac developmental defect in the electrical insulation between the atria and the ventricles due to the presence of an accessory pathway.WPW syndrome is a common cause of supraventricular tachycardia with benign prognosis.However,this clinical entity also predisposes patients to an increased risk of sudden cardiac death,especially in the setting of preexcited atrial fibrillation.WPW syndrome is usually sporadic and of unknown etiology in most cases.During the past10years,a signifi cant heritable factor is increasingly recognized.Identifi cation of the genetic basis among patients with WPW syndrome has important implications for understanding the molecular mechanism of ventricular preexcitation and the development of therapeutic strategies for risk stratifi cation and management.The goal of this review is to examine the previous studies on hereditary variants,as well as to outline potential future avenues toward defi ning the heritability of WPW syndrome.

Familial Wolff-Parkinson-White syndrome is linked to the loci on chromosome 7q3

OBJECTIVE: Wolff-Parkinson-White syndrome (WPW) is considered to be an autosomal dominant hereditary disease, but the gene is not identified. The objective of this study was to localize the genetic loci of Wolff-Parkinson-White syndrome. METHODS: Linkage analysis between the disease of Wolff-Parkinson-White syndrome and 3 STR (short tandem repeats) markers on 7q3 (D7S505, D7S688, and D7S483) was tested in 3 kindreds of the Wolff-Parkinson-White syndrome (101 numbers in total) by genotyping. RESULTS: Wolff-Parkinson-White syndrome was linked to the loci above. The maximum two-point Lod score detected at D7S505 was 6.4 at a recombination fraction (theta) of 0.1; the Lod score of D7S688, D7S483 was 5.3 vs 2.5. CONCLUSION: The gene of Wolff-Parkinson-White syndrome is located at 7q3.

WPW综合征人群发病率的分析及临床特点

目的:探讨WPW综合征在人群中的发病率,为WPW综合征的早期诊断、病情监测及治疗提供临床依据。方法:应用心电图检查4093例受检者。结果:检出WPW综合征9例,符合泊松分布,检出率为2.2‰。但无统计学意义(P=0.153>0.05)。男女检出率无统计学意义(P> 0.05)。不同职业两组间差异无统计学意义(P>0.05)。结论:WPW综合征是人群中发病率较低的心脏疾病,但对患者危害性大。其诊断主要靠心电图。通过射频消融治疗患者可痊愈。

Electroversion in treatment of arrhythmia in a patient with Wolff-Parkinson-White syndrome and cervical spinal cord injury

We report electroversion in treatment of atrial fibrillation （AF） and atrioventricular nodal reentry ta- chycardia （AVNRT） in a patient with Wolff-Parkinson-White syndrome and cervical spinal cord injury. At first, the pa- tient sustained respiratory failure and weak cough reflex, thereafter repeated bronchoscopy was used to aspirate the sputum as well as control the pneumonia, which resulted in arrhythmia （AF and AVNRT）. Two doses of intravenousamiodarone failed to correct the arrhythmia. After restora- tion of sinus rhythm by electroversion, he was successfully weaned from mechanical ventilation and discharged from the intensive care unit without recurrent arrhythmia.

WPW综合征体表心电图酷似心肌梗死临床研究

目的报告5例酷似心肌梗死的WPW综合征,探讨其体表心电图(EKG)特征。方法回顾性分析了15例诊断为WPW综合征患者的临床资料,其中5例EKG表现酷似心肌梗死,后均行心脏电生理检查(EPS)以明确旁道位置。结果 5例酷似心肌梗死的WPW综合征中:2例为左侧壁房室旁道,2例为左后壁房室旁道,1例为后间隔房室旁道。结论不同房室旁道位置会导致EKG出现类似心肌梗死表现,临床工作中应予以重视。

基于虚拟心脏的心电逆问题求解

心电逆问题研究的目标是要从无损测得的体表电位来找出心脏的对应状态。以往的心电逆问题求解方法有二类，一类是基于等效心电源法，另一类是基于心外膜电位解法。这二类方法都存在病态问题，同时所求出的解并不是真正的心脏状态解，而是一种中间解。本文提出了一种新的心电逆问题求解方法，即从体表电位求出虚拟心脏的模型参数，由所求得的虚拟心脏的模型参数即可确定心脏所处的状态。该法把欠定的逆问题求解问题转化为正问题的参数优化问题，避免了以往心电逆问题求解方法中的病态问题。为了检验该法的有效性，我们做了对ＷＰＷ预激综合征旁道室内预激点进行定位的模型试验，结果表明逆解得出的预激点位置误差一般不超过４．５ｍｍ。

射频消融左侧旁道有效消融点标准探讨

报道３０例预激综合征左侧旁道射频消融（ＲＦＣＡ）有效和无效消融点放电前的电生理特点。结果表明：①显性旁道有效消融点特征为房室传导时间极短（≤３０ｍｓ），房波和室波间无等电位线，室波等于或超前标测电极室波；②隐匿旁道有效消融点特征为逆传房波紧随室波后，室波和房波间无等电位线，逆传房波等于或超前标测电极房波。认为ＲＦＣＡ中正确识别上述特征有助于提高消融疗效和减少放电次数。

B型预激综合征左后间隔旁道的体表心电图特征及射频消融的体会

目的提高体表心电图对显性房室旁道定位的准确性及射频消融术的治疗疗效。方法回顾性分析了53例B型预激综合征经过手术证实为左后间隔房室旁道的体表12导联同步心电图特征,并与162例B型预激综合征经过手术证实为右后间隔房室旁道体表12导联同步心电图进行比较。12导联心电图均采用GE Marquette Cardiosoft V4.11心电图机进行采集。结果B型预激综合征左后间隔与右后间隔房室旁道V1δ波方向、P-R间期、胸导联的移行区、Ⅱ、Ⅲ、avF导联Q/R之比以及V1导联QRS波的形态存在显著差别,而Ⅱ、Ⅲ、avF导联δ波的方向相同。结论在其他条件符合后间隔房室旁道的情况下,预激充分时V1导联QRS波呈Qr型,房室旁道为左后间隔,V1导联QRS波呈QS型时,房室旁道为右后间隔;预激不充分时V1导联呈rs或rS型时,V1导联P-R间期大于或等于110ms为左后间隔旁道,V1导联P-R间期小于或等于80ms右后间隔旁道。

预激综合征合并症的心电图诊断

预激综合征易并发室上速，但绝大多数患者无器质性心脏病，传统上认为是良性心律失常。最近发现，其死亡率占所有心性猝死的0．15％-0．39％，且猝死者也多数无器质性心脏病，主要死于合并心肌梗死或心律失常，故提高对其合并症诊断及危险分层的能力，及时进行干预，具有重要的临床意义。为此，将其有关问题进行综述。

预激方案治疗老年高危骨髓增生异常综合征的临床研究

目的：探讨预激方案治疗老年高危骨髓增生异常综合征（MDS）的临床效果,以期提高临床治疗水平。方法：随机选取2010年1月~2012年12月的90例MDS患者为研究对象,分成两组,每组45例,对照组采用标准方案治疗,观察组予以预激方案治疗,观察两组治疗后在临床效果上的差异性。结果：对照组CR＋PR例数为35例,比率为77.78%,CR＋PR＋SD比率为88.89%,观察组CR＋PR例数为38例,比率为84.44%,CR＋PR＋SD比率为93.33%。两组比较无差异性（P〉0.05）;对照组不良反应发生率46.67%,观察组不良反应发生率6.66%;两组在血红蛋白、血小板、肾功能、胸片上比较有显著差异性（P〈0.05）,具有统计学意义;而在白细胞、肝功能上比较则无明显差异性（P〉0.05）。结论：预激方案治疗老年高危MDS临床效果满意,不良反应发生率低。

心律失常合并急性心肌梗死的心电图诊断

众所周知，急性心肌梗死（AMI）病理性Q波是初始向量改变的结果，故凡改变初始向量的心律失常均可产生掩盖或酷似心肌梗死的心电图改变。另外，有些心律失常虽未影响初始向量改变，也可产生酷似心肌梗死的心电图改变。当出现酷似AMI时，易误诊，给患者造成精神上及经济上的负担；而掩盖时易漏诊，贻误抢救时机，造成严重的后果，

射频消融房室旁路治疗室上性心动过速

对27例WPW综合征(13例显性,14例隐性)患者的29条旁路进行了导管射频消融,其中左侧旁路23条,右侧旁路6条。当时成功率为100％。术后检查7例CPK酶轻度增高,1例有少量心包积液,余未见任何严重并发症。随访1.5～24个月,1例复发,总成功率为96.5％。

心电图酷似心肌梗死的预激综合征——附28例临床分析

目的 旨在分析心电图酷似心肌梗死的预激综合征 ,避免误诊。方法 对 2 8例酷似心肌梗死心电图图形的预激综合征患者进行综合临床分析。结果 2 8例预激综合征患者的心电图均呈现了窦性心律、短P -R间期(0 .10 1± 0 .0 18)s、delta波、病理性Q波 [时限 (0 .0 81± 0 .0 2 9)s,振幅 (0 .78± 0 .5 2 )mV],仅 1例证实为预激综合征并陈旧性心肌梗死。结论 一些预激综合征患者呈现出心肌梗死的心电图表现形式 ,极少数与心肌梗死并存 ,提示在见到病理性Q波而作出心肌梗死诊断前 ,要进行综合临床分析 ,避免误诊 ,尤其二者并存时 ,应慎重诊断 ,避免漏诊心肌梗死。

异丙肾上腺素诱发房室折返性心动过速对预激综合征的临床意义

作者比较分析了20例无药状态下不能诱发出心动过速的旁道患者与20例诱发出心动过速旁道患者的电生理试验资料。研究组中14例使用异丙肾上腺素或阿托品后立即重复电生理试验,其中7例诱发出心动过速,诱发出心动过速的原因是正常房室传导系统顺传功能的改善。对旁道逆传功能不佳的患者仍难以诱发出心动过速。