预激综合征合并阵发性室上性心动过速家系调查及临床研究

目的探讨预激综合征合并阵发性室上性心动过速（PSVT）的家族性及临床特点。方法对一个预激综合征合并PSVT的家系进行调查,并对其中3例患者进行心内电生理检查和射频消融术,同时观察其临床特点。结果该家系4代30例家系成员中有2代成员4人患病,均为女性,3例为左侧旁道,临床特点及射频消融治疗效果与散发性一致。结论家族性预激综合征合并PSVT为常染色体显性遗传性疾病,可外显不全或延迟外显。临床及心电图表现和治疗效果与散发性相同。     

预激综合征并阵发性室上性心动过速分析（附1例）

患者男，36岁，无器质性心脏病。5年内反复发作阵发性室上速(PSVT)，2003年3月11日上午又因心悸，眼前发黑突然发作就诊。伴有恶心、胸闷。体检：一般情况好，心率188次／min，律匀齐。肺无罗音，肝脾未扪及。     

预激综合征合并室上性心动过速的表现形式及诊断

室上性心动过速(室上速)是预激综合征(预激征)最常见的合并症,指有旁道和正常传导系统共同参加的折返性快速心律。阵发性发     

三磷腺苷治疗阵发性室上性心动过速体会

目的通过对三磷腺苷治疗阵发性室上性心动过速的临床观察,总结及发现其在临床应用过程中所表现的优点与出现的不良反应。方法我院对30例阵发性室上性心动过速患者应用静脉注入三磷腺苷的方法治疗,观察其疗效及不良反应。结果30例患者中28例迅速转为正常窦性心律,转复成功率为93.3%。在转复成功者中均发生一过性窦性停搏及或窦性心动过缓,但时间短暂,患者未因此表现明显不适。另外有2例老年患者出现呼吸困难,有2例冠心病患者出现心绞痛,有5例患者出现轻度头疼和颜面潮红。结论三磷腺苷治疗阵发性室上性心动过速具有作用迅速、转复成功率高、不良反应持续时间短等优点,但也不可忽视其不良反应。     

预激综合征并发阵发性心动过速的临床分析

本文报告预激综合征并发阵发性心动过速25例48次发作的诊断与治疗,认为应将预激综合征并发阵发性心动过速分为:窦性心律并发预激综合征、阵性心动过速并预激综合征两种类型.这有利于预后判断及治疗方法的选择,对房旁路下传型慎用洋地黄类药物,而以乙胺碘呋酮及电复律为佳.对房室结下传型则通常与室上速的治疗方法相同.     

维拉帕米终止阵发性室上性心动过速的观察

目的 总结维拉帕米终止阵发性室上性心动过速（PSVT）的疗效。方法 观察42例22－73岁的PSVT患，其中伴有冠心病3例，高血压性心脏病2例，预激综合征5例。结果 42例PSVT经维拉帕米治疗终止36例，有效率为86％；36例PSVT经维拉帕米终止后出现心律失常6例，短阵房性心动过速（AT）1例，短阵室性心动过速（VT）2例，交接性心律1例，窦性停搏2例，其中3例出现在预激综合征（WPW）合并PSVT。结论 临床工作应对WPW合并PSVT要有足够的认识，从严掌握维拉帕米终止PSVT适应症。     

心律平治疗预激综合征并发室上性心动过速21例疗效分析

目的 观察静脉注射盐酸心律平注射液治疗预激综合征并发阵发性室上性心动过速的疗效。方法 选入的21例心电图诊断为预激综合征并发阵发性室上性心动过速发作时,用心律平注射液70～210mg/次的总量,静注后,观察并记录心电图、血压情况,定期或不定期记录心电图的变化情况,了解对患者血压、心率等的影响。结果本组21例阵发性室上性心动过速注射心律平后全部转复,总有效率达100％,21例均在注射药物后9～53min内转复,平均转复时间(20.6±15.0)min;注射心律平注射液后血压均平稳。结论 心律平治疗预激综合征并发室上性心动过速,起效较快,副作用少,安全,实用。     

ATP治疗阵发性室上性心动过速

观察了ATP不同剂量、ATP加阿托品治疗PSVT的临床情况以及ATP在宽QRS型PSVT诊治中的作用。结果表明:ATP复律疗效高,且有助于明确PSVT的诊断及了解其机制;单用ATP复律以15mg为宜,使用20mg时最好与小剂量阿托品合用;将ATP稀释至5～10ml于5～10秒内静注比稀释至20ml于5秒内静注或不稀释直接静注更恰当;重复给药间期以10分钟左右为宜。     

三磷酸腺苷终止阵发性室上性心动过速的疗效观察

目的探讨三磷酸腺苷治疗阵发性室上性心动过速的有效率。方法对59例经心电图证室正在发作的阵发性室上性心动过速患者快速静脉注射三磷酸腺苷10～20mg,观察其有效率。结果 56例成功复律,总有效率达89.8%。结论三磷酸腺苷终止阵发性室上性心动过速方便、快捷、经济、有效率高。     

Non-invasive diagnosis of concealed Wolff-Parkinson-White syndrome by detection of concealed anterograde pre-excitation

Electrophysiological findings suggest that concealed anterograde conduction through accessory pathways may exist even during sinus rhythm in patients with so-called concealed Wolff-Parkinson-White (WPW) syndrome. To evaluate the pre-excitation characteristics in various types of WPW syndrome, high-resolution electrocardiograms were analyzed in 81 consecutive WPW syndrome patients and 50 age-matched normal subjects. The WPW group consisted of 30 cases of concealed WPW diagnosed by electrophysiological study, 38 cases of manifest WPW in which apparent delta waves were constant, and 13 cases of intermittent WPW in which the delta waves appeared periodically. The duration of the low-amplitude, high-frequency components of the signal-averaged filtered QRS complex that preceded the earliest upstroke of the surface QRS, including any delta waves (preceding potential duration, PPD), and the duration of low amplitude signals less than 10 microV (I-LAS10) or 20 microV (I-LAS20) were measured as parameters of pre-excitation. The PPDs in concealed and intermittent WPW were both significantly longer than in manifest WPW or in control subjects (6.8+/-2.7 ms, 7.9+/-3.5 ms vs 2.3+/-3.2 ms, 1.0+/-1.6 ms, both p<0.0001). Abnormally prolonged PPDs (>4 ms) were observed in 90% of concealed WPW cases and 76.9% of intermittent WPW, but in only 4% of normal subjects and 31.6% of manifest WPW. Both I-LAS10 and I-LAS20 in the 3 types of WPW syndrome were significantly longer than in normal subjects. The initial portion of the filtered QRS in concealed WPW closely resembled that of intermittent WPW. These results strongly suggest that in concealed WPW anterograde conduction through accessory pathways does occur and produces small amounts of pre-excitation even during sinus rhythm. The study concluded that, despite its name, concealed WPW is not completely concealed, and that non-invasive diagnosis during sinus rhythm is possible by using high-resolution electrocardiography to detect the concealed anterograde pre-excitation.     

Acute treatment of paroxysmal tachycardia by adenosine

Background: Adenosine has proven efficacy in clinical trials and in the electrophysiological laboratory for the treatment of paroxysmal tachycardia.
Aims: To evaluate the efficacy and safety of adenosine administered in a clinical setting by non-consultant staff.
Methods: Incremental doses of adenosine were administered intravenously to five children and 32 adults during 39 episodes of paroxysmal tachycardia in a clinical setting. Structural heart disease was present in 43% of patients.
Results: Of 35 episodes of narrow complex tachycardia, adenosine terminated 26 of 28 episodes of supraventricular re-entrant tachycardia (SVRT), one episode of ectopic atrial tachycardia, and induced transient atrioventricular block to reveal atrial arrhythmias in four. Termination of SVRT occurred at a mean (SD) dose of 9.2 (4.0) mg in adults and 0.09 (0.04) mg/kg in children, but two patients had later spontaneous reinitiation of SVRT. Two patients with narrow complex tachycardia who failed to respond to adenosine were subsequently found to have ventricular tachycardia. Adenosine was therapeutic or diagnostic in three of four episodes of broad complex tachycardia. Overall, by intention to treat by the clinician, adenosine was therapeutic or diagnostic in 34 of 39 episodes (87%). Breathlessness (26%), chest tightness (18%) and flushing (18%) occurred transiently. There were no episodes of hypotension. Adenosine was given safely to 15 patients in whom verapamil was considered contraindicated.
Conclusions: Adenosine is a safe treatment for both narrow and broad complex tachycardias; usually effective for the former and diagnostic for the latter.     

Effects of acebutolol on paroxysmal atrioventricular reentrant tachycardia in patients with manifest or concealed accessory pathways

Electrophysiologic studies before and after administration of 50 mg of intravenous (IV) acebutolol were performed in 20 patients. Four of the 20 had persistent preexcitation, two had intermittent preexcitation, and 14 had a concealed retrogradely conducting accessory pathway (AP). Acebutolol depressed anterograde AP conduction with loss of preexcitation in one patient and increased the effective refractory period of AP in the remaining three; in most, it depressed anterograde normal pathway conduction. The longest atrial paced cycle length producing atrioventricular (AV) nodal block increased from 290 +/- 7 to 39 +/- 6 msec (mean +/- SEM) after acebutolol (p less than 0.01). Acebutolol had no significant effect on retrograde AP conduction. Sustained AV reentrant tachycardia was inducible in all 20 patients before acebutolol and in 19 after acebutolol. The cycle length of tachycardia increased from 323 +/- 8 to 352 +/- 8 msec after acebutolol (p less than 0.01), reflecting an increment of A-H interval from 148 +/- 8 to 174 +/- 9 msec (p less than 0.01). Electrophysiologic studies were reported after 800 mg of oral acebutolol given in four divided doses at six-hour intervals in eight patients. The results were comparable to those of IV acebutolol. Thus, acebutolol depresses AV nodal conduction and slows the rate of AV reentrant tachycardia, but is generally ineffective in inhibiting the induction of sustained tachycardia. It occasionally depresses anterograde AP conduction.     

Effects of verapamil on supraventricular tachycardia in patients with overt and concealed Wolff-Parkinson-White syndrome

Verapamil (0.15 mg/kg) intravenously, was administered to 19 patients with recurrent supraventricular tachycardia (SVT) undergoing electrophysiological evaluation. Twelve patients had overt Wolff-Parkinson-White (WPW) syndrome and seven patients had concealed accessory pathways conducting in the retrograde direction only. Verapamil had a significant effect in delaying conduction and prolonging refractoriness in the atrioventricular (AV) node, but no significant actions on any of the other cardiac tissues that formed the tachycardia circuit in these patients. In particular, it had no significant effects on anterograde or retrograde bypass conduction or refractoriness. Sustained SVT was initiated in 15 patients, and was terminated within 60 to 105 seconds of a 30-second injection of verapamil in 13 patients. Cycle length alternation during SVT was seen in six patients prior to reversion, and spontaneous ventricular complexes (VPCs) were observed following verapamil administration in five patients. Two patients with apparently normal sinus node function showed prolongation of their sinus node recovery times immediately following reversion of SVT by verapamil. Echo zones were assessed before and after verapamil, and sustained or self-terminating SVT could still be induced after the drug in 13 of the 15 patients who had sustained SVT beforehand. It was concluded that intravenous verapamil was effective in terminating sustained SVT in the majority of patients with overt or concealed WPW and that, despite a potential for sinus node depression and the initiation of VPCs, it had no clinically significant side effects. The ability to reinitiate SVT following its administration suggests the need for immediate follow-up with maintenance drug therapy.     

Study of thyroid function in patients with paroxysmal supraventricular tachycardia

Twenty-nine patients with paroxysmal supraventricular tachycardias of different origins and clinical pattern were investigated to detect latent thyroid disorders; hyperthyroidism was diagnosed in 2 of those, and hypothyroidism, in 4. Functional thyroid disorders were more common in patients with mitral prolapse and supraventricular tachycardias due to additional conductive pathways (the Wolff-Parkinson-White syndrome) and paroxysmal nodal reciprocal tachycardia, particularly if they were resistant to antiarrhythmic treatment and/or had aggravated thyroid history. It is suggested that thyroid dysfunction is just a triggering factor of arrhythmia since thyrostatic and replacement therapy eliminate paroxysms of tachycardia, while organic pathology of the heart and its conductive network remains unaffected.     

Choosing calcium channel blockers for pregnant women with paroxysmal supraventriclar tachycardia and preterm labor: a case report

Preterm labor is a major clinical hazard causing both maternal and neonatal morbidity and mortality. Paroxysmal supraventricular tachycardia (PSVT) complicated by preterm labor is rare. Of the many drugs used to treat PSVT, only calcium channel blockers are tocolytics. Here, we present the case of a 29-year-old female admitted to our ward with previously diagnosed PSVT and preterm labor at 31 weeks' gestation of her fourth pregnancy. Calcium channel blockers were administered and her uterine contractions subsided. Afterwards, no side effects were noted and she suffered no further tachycardic attacks during her pregnancy. She successfully delivered a full-term baby and received subsequent regular follow-up at the outpatient clinic.     

The status anginosus induced by paroxysmal auricular fibrillation and paroxysmal tachycardia

We have reported here four unusual but important cases to illustrate the fact that a status anginosus may occur without coronary thrombosis.A great increase in heart rate due to paroxysmal auricular fibrillation or paroxysmal tachycardia (with accompanying drop in systolic blood pressure or pulse pressure) was evidently responsible for the induction of the angina pectoris that was at other times a characteristic result of effort in all of these four cases. Two of the patients were men, aged sixty-two and sixty-six years, and two were women, aged sixty-eight and seventy-five years. One of the men (the first) and one of the women (the second) died suddenly eighteen months and fifteen months, respectively, after the first attack of angina pectoris induced by the abnormal heart rhythm. The other two patients were alive one year after their first attacks of this nature.     

显性预激综合征患者平板运动试验后预激波情况分析

目的：分析平板运动试验后显性预激综合征患者预激波的变化情况。方法选取160例15～40岁的显性预激综合征患者,观察平板运动试验过程中其预激波的变化,记录并分析预激波消失的比例。结果平板运动试验后显性预激综合征患者预激波消失的总比例为12．5％,继发性 ST-T 改变随预激波消失均恢复正常,A 型预激组预激波消失比例显著高于B 型预激组。结论部分显性预激综合征患者运动试验后心率加快,预激波可以消失。