動(dòng)脈粥樣硬化性心血管疾病高危患者他汀治療“足劑量”比例堪憂(yōu)

2013美國(guó)心臟病學(xué)會(huì)/美國(guó)心臟學(xué)會(huì)（ACC/ AHA）血脂管理指南自發(fā)布伊始，就引發(fā)了大量的關(guān)注和爭(zhēng)論，其核心焦點(diǎn)就是該指南創(chuàng)新性地提出拋棄沿用已久的血脂管理目標(biāo)水平，而采用他汀治療的強(qiáng)度，即血脂下降的幅度來(lái)評(píng)估他汀治療是否已經(jīng)達(dá)到“足劑量”。有識(shí)之士曾指出，這一舉措可能會(huì)是“疾病預(yù)防史上巨大的模式轉(zhuǎn)換”過(guò)程，但同時(shí)專(zhuān)家也認(rèn)為，如何使得醫(yī)務(wù)人員放棄原本對(duì)于血脂管理目標(biāo)值的認(rèn)知，接受根據(jù)他汀治療強(qiáng)度來(lái)判斷他汀類(lèi)藥物劑量，將會(huì)是一項(xiàng)極富挑戰(zhàn)性的工程。

剛剛結(jié)束的2016歐洲心臟病學(xué)年會(huì)（ESC）上，美國(guó)杜克臨床研究所的Navar博士公布了患者和醫(yī)務(wù)人員血脂管理評(píng)價(jià)（Patient and Provider Assessment of Lipid Management，PALM）注冊(cè)研究的分析結(jié)果，發(fā)現(xiàn)高?；颊咚≈委焺┝坎蛔愕默F(xiàn)象仍普遍存在。

根據(jù)2013班美國(guó)血脂管理指南推薦，年齡＜75歲的動(dòng)脈粥樣硬化性心血管疾?。ˋSCVD）患者、任何低密度脂蛋白膽固醇（LDL-C）水平≥190mg/dl的成人以及發(fā)生ASCVD風(fēng)險(xiǎn)≥7.5%≥10年的40～75歲高危的糖尿病患者須接受高強(qiáng)度他汀治療（每日劑量達(dá)到平均降低LDL-C≥50%）。而作為一級(jí)預(yù)防、75歲以上合并ASCVD的老年患者以及ASCVD風(fēng)險(xiǎn)＜7.5%的糖尿病患者僅需中等強(qiáng)度他汀治療（每日劑量達(dá)到平均降低LDL-C 30%～50%）。

Navar博士的報(bào)告顯示，在分析了5 906例具有他汀治療適應(yīng)證并接受常規(guī)治療的成人中，服用了他汀類(lèi)藥物的患者占74%，但只有45%的患者劑量是合適的。引人注意的是指南推薦需高強(qiáng)度他汀治療的人群中，這組數(shù)據(jù)分別為80%及29%。而相比之下，推薦接受中等強(qiáng)度他汀治療的患者中，這組數(shù)據(jù)為67%及60%。

PALM注冊(cè)研究通過(guò)了入選的140家單位的心內(nèi)科、內(nèi)分泌科以及基礎(chǔ)保健的門(mén)診患者，共納入接受中等強(qiáng)度他汀患者2 532例及高強(qiáng)度他汀患者3 374例。當(dāng)研究人員將患者分為一級(jí)預(yù)防組以及二級(jí)預(yù)防組后發(fā)現(xiàn)，一級(jí)預(yù)防組中他汀劑量不足問(wèn)題更為顯著。在指南推薦應(yīng)接受中等強(qiáng)度他汀治療的人群中，42%一級(jí)預(yù)防患者及19%二級(jí)預(yù)防患者沒(méi)有服用任何他汀類(lèi)藥物。在指南推薦需高強(qiáng)度他汀治療的人群中，僅有36%二級(jí)預(yù)防患者用到了足量，但這仍然比一級(jí)預(yù)防患者（16%）要高得多。在推薦使用高強(qiáng)度他汀類(lèi)藥物治療的人群中，他汀劑量不足患者中女性較多（42.2%比29.6%），非洲裔美國(guó)人多（15.4%比11%），合并糖尿病比例較高（60.9%比53.7%），心血管專(zhuān)科就診次數(shù)達(dá)標(biāo)百分比更少（43.4%比63.2%），差異均有統(tǒng)計(jì)學(xué)意義（P＜0.01）。

研究團(tuán)隊(duì)進(jìn)一步了解了患者的LDL-C水平，進(jìn)而發(fā)現(xiàn)他汀類(lèi)藥物使用不足并非是因?yàn)榛颊週DL-C水平已達(dá)標(biāo)而不需要他汀類(lèi)強(qiáng)化治療。事實(shí)上，其中幾乎半數(shù)推薦需高強(qiáng)度他汀治療的患者存在LDL-C升高（≥100 mg/dl），而在足量他汀治療人群中這一比例僅為22%。這從另一方面也印證了2013版指南所強(qiáng)調(diào)的可能從LDL-C降低獲益最多的高危人群，進(jìn)行高強(qiáng)度他汀治療的必要性。

臨床實(shí)踐中，筆者也深刻感受到對(duì)于高?；颊咚≈委煆?qiáng)度的認(rèn)知存在較大的誤區(qū)。從基層醫(yī)院轉(zhuǎn)診至高級(jí)別醫(yī)院進(jìn)一步診治的高?；颊?，抗血小板的治療通常更容易受到關(guān)注，但他汀劑量是否真的達(dá)到要求卻容易忽視。又或者，門(mén)診隨訪(fǎng)中經(jīng)?？梢?jiàn)經(jīng)皮冠狀動(dòng)脈介入（PCI）術(shù)后復(fù)查的患者，他汀的劑量不斷減少，或從中高強(qiáng)度的他汀減量為低強(qiáng)度的他汀使用，而其依據(jù)往往只是“病好起來(lái)了”或者“費(fèi)用太高了”。從衛(wèi)生經(jīng)濟(jì)學(xué)的角度，患者因體化醫(yī)療的迫切需求。誠(chéng)然，我們認(rèn)同“指南”并非臨床實(shí)踐的“圣經(jīng)”，但是科學(xué)解讀循證醫(yī)學(xué)進(jìn)展，并指導(dǎo)于實(shí)踐，將會(huì)是新時(shí)代賦予醫(yī)務(wù)人員的又一重任。ASCVD導(dǎo)致急性冠狀動(dòng)脈綜合征或是腦卒中的費(fèi)用，只怕比堅(jiān)持他汀類(lèi)藥物治療要多得多。我國(guó)的文化傳統(tǒng)使得我們產(chǎn)生“經(jīng)驗(yàn)醫(yī)學(xué)”的慣性，而現(xiàn)代醫(yī)學(xué)的進(jìn)展則越來(lái)越凸顯出循證醫(yī)學(xué)和個(gè)

（陳涵編譯）

Ventricular tachycardia（VT）may be classsified based on the clinical characteristic（clinical VT, hemodynamically stable or unstable,repetitive, incessant,etc.）,morphology（monomorphic,multiple morphologies,pleomorphic,polymorphic,bidirectional, etc.）ormechanisms（scar-related reentry,automaticity, and triggered activity）.Incessant VT is defined as continuous sustained VT during several hours,which recurs promptly despite repeated intervention for termination.Multiple monomorphic VTs refer to＞1 morphologically distinct monomorphic VT,occurring as different episodes,or induced at different times. Pleomorphic VT has＞1 morphologically distinct QRS complex occurring during the same episode of VT,but the QRS is not continuously changing.Bidirectional VT （BVT）is characterized by beat-to-beat alternation of the QRS axison the ECG and isusually regular.

Case Report

A 33-year-old male,nondiabetic,nonhypertensive,presented with history of palpitation,chest discom fort,and fatigueof6 hoursduration.He had been otherwise healthy,not on any medications with no history of tobacco,alcohol,or drug use.At presentation, pulse rate was 144 beats per minute,irregular,blood pressure 96/60 mm Hg,and the rest of physical examination was unremarkable.Twelve-lead ECG revealed a wide complex regularly irregular tachycardia at a rate of 144 beats per minute,right bundle morphology,QRS duration of 200 to 220 ms,QRS axis alternating between+160°and-40°,QRS transition alternating from V3to V6,and evidence of atrioventricular dissociation to intravenous lignocaine, esmolol,amiodarone（300 mg during 1 hour）,and 2 attempts of biphasic direct current（DC）cardioversion of 200 J.Because the tachycardiawas incessant,patient was sedated,intubated,ventilated,and continued on intravenous amiodarone（900 mg/24 hours）with further 4 unsuccessful attempts at DC cardioversion. Tachycardia converted to monomorphic VT with occasional VT complexesof the 2ndmorphology（Figure 2）,which terminated 6 hours later while on infusion of amiodarone and lignocaine,and while he was being considered for radiofrequency catheter ablation.ECG in sinus rhythm was essentially normal,chest X-ray revealed superior mediastinal widening,and echocardiogram showed normal left ventricular function. Cardiac MRI revealed focal areas of thickening and increased signal intensity on T2-weighted images.Early gadolinium enhancement was seen in the mid interventricular septum,anterolateral and anteroinferior walls,with the lesions having a target appearance with peripheral slightly hyperintense rim and central hypo intensity（Figure 3A）.Delayed gadolinium enhancement was found predominantly in the midmyocardium and epicardial in basal and lateral segments of the left ventricle.18F-fluoro-2-deoxy-d-glucose（FDG）positron emission tomography scan revealed basal andmid anteroseptal perfusion defect with intense FDG uptake in these regions suggestive of myocardial inflammation along with evidence of inflammation in the paratracheal lymph nodes（Figure 3B）.Serum biochemistry was normal including serum calcium, serum angiotensin-converting enzyme（ACE）,digoxin, blood aconite levels（report received 2 weeks later）, and IgG and IgM assays were negative for tuberculosis bacilli.Transbronchial lymph node biopsy revealed noncaseating granulomas suggestive of sarcoidosis. Patient was initiated on 1 g of methylprednisolone per day for 3 days intravenously and amiodarone infusion of 1 g/d was continued for 3 days after which it was switched to oral therapy and patient was extubated after 36 hours.Later,oral predinsolone was initiated at 60 mg/d for 2 months and was tapered to a maintenancedose of 10 mg/d for 2 years and stopped after a normal repeatpositron emission tomography FDG scan.A single chamber implantable defibrillator was implanted after 5 days of VT-free interval.Amiodarone was tapered and stopped after 6 months.Genetic testing for possible catecholaminergic polymorphic ventricular tachycardia with analysis for 4 genes:RYR2,CASQ2,ANK2,and KCNJ2 were negative.Four years later,patient has not had any device activation and hasnormal leftventricular function.

Figure 1 Tachycardiawasunresponsive.Twelve-lead ECG showingbidirectional ventricular tachycardia.

Figure 2 Twelve-lead ECG showing partial suppression of suppression of focus A resulting in occasional ectopic beats during sustainedmonomorphic ventricular tachycardia（VT）becauseof focusB.

Figure 3 A:T2-weighted cardiac MRI:showing gadolinium enhancement in mid interventricular septum（arrow）.B: 18F-fluoro-2-deoxy-d-glucose（FDG）positron emission tomography scan:showing basal and midanteroseptal perfusion defectwith intense FDG uptake.

Discussion

This case describes an unusual presentation of isolated cardiac sarcoidosis with incessant regularly irregular BVT,normal LV function,and no conduction system involvement as the initial manifestation.Clinical manifestations of cardiac sarcoidosis are dependent on the location,extent,and activity of the disease.The 3 principal sequelae of cardiac sarcoidosis are（1）conduction abnormalities（2）ventricular arrhythmias, and（3）heart failure.Cardiac sarcoidosis usually presents with monomorphic VT or conduction system disturbances.Macroreentry around areas of granulomatous scar is the commonest mechanism of VT in sarcoidosis.

BVT is a rare ventricular tachyarrhythmia.It is usually regular,demonstrates a beat-to-beat alternation of the QRS frontal axis varying between-20°to-30° and+110°.Tachycardia rate is typically between 140 and 180 beats per minute and the QRS is relatively narrowwith duration of120 to150ms.

BVT in present case has many unusual features. The QRS duration is broad at 200 to 220 ms,unlike casesof inmostBVT where it is relatively narrow at120 to 150 ms.Wide QRS in this case possibly indicates intramyocardial/epicardial site of origin,unlike the usual BVT where the origin is supposedly more closer to the His purkinje system.

The most intriguing feature is the regularly irregular rhythm as seen in Figure 1.A careful analysis of relationship between the 2 morphologies of QRS complexesnamely A and B reveals that the A-A interval is72 beatsper minute（0.88 s）and B-B interval is72 beats perminute（0.88 s）,resulting in tachycardia rate of 144 beats per minute.The relationship of A to B interval is constant at 0.56 s,and B to A interval is constant at 0.32 s,and this relationship is constant throughout the tachycardia resulting in a regularly irregular rhythm.The broad QRS,with axis alternating between+160°and-40°,transition alternating from V3to V6in chest leads,possibly indicates2 independent foci.The original hypothesis of dual ventricular foci firing alternatively that was suggested as themechanism was discarded because of the constant R-R interval that would presuppose a perfect alteration of the 2 foci. However,in this case,regularly irregular rhythm can be explained by automatic firing of 2 different foci at constant intervals and presence of entrance block in each of the foci akin toa dual parasystole.

Parasystole requires an area of focal impulse formation which is surrounded by an area that protects （shield）the focus from external impulses thus resulting in an entry block but no exit block of the focus. Automaticity and protection are the hallmarks of parasystole.This feature lead to the diagnostic triad of classical parasystole,that is,varying coupling intervals of the ectopic focus,mathematically related interectopic intervals and the presence of fusion beats.The original assumption of total independence（protection）of parasystolic focus from extraneous beats is no longer considered true.It is now evident that any pacemaker connected to the surrounding tissues by an area of depressed excitability producing entrance conductiondisturbances while allowing the impulses to exit is subject to1some degree of modulation by electrotonic depolarizations arising in the surrounding tissues,that is,depolarization of the surrounding field will induce a partial depolarization of the pacemaker cells.This results in the occurrence of modulated parasystole.This means that nonparasystolic beats falling close to the parasystolic beats can cause（1）maximal delay,（2）maximal acceleration,（3）lesser effects,（4）practically no effect,or（5）pacemaker annihilation of the parasystolic focus.Nonparasystolic beats falling during the first half of the parasystolic interval induce a prolongation of this interval,those occurring during the second half of the parasystolic cycle length cause an abbreviation of this interval.Theelectrotonic modulation （causing either prolongation or shortening of the parasystolic cycle length）ismaximal at themiddle point of the parasystolic interval.Thus,the coupling interval of the ectopic focus may not be constant in modulated parasystole and interectopic interval may also show variation.Modulation may also cause coupling intervals to be fixed,and the fixed coupling intervals may suggest a reciprocating bigeminy.It has been shown that if the impedance of the communication between the ectopic focusand the surrounding ventricle is low,locking of the ectopic pacemaker could be nearly fixed to give the appearance of a reciprocating bigeminy.This is substantiated by Figure 2 in our case,wherein after infusion of amiodarone there is partial suppression of focus A resulting in occasional ectopic beats during sustained monomorphic VT because of focus B. Measurement of B-B intervals shows that there is doubling of the rate from 0.88 s during BVT as seen in Figure 1,compared with 0.44 s in Figure 2 suggesting a parasystole as the mechanism of arrhythmia.The interlocking of the beat A to beat B still persists.But measurementof intervalsbetween A-A in this strip does notshow amathematical relation relationship,which can be explained by modulation of parasystole focus A by the preceding beat（from focus B）.In the presentcase, dual parasystole is the most plausible explanation.The occurrence of only occasional beats of focus A（Figure 2）where the focus B is continuing in an accelerated rate excludes the possibility of a BVT because of a pingpong effect as there is no consistency in occurrence of focus A,which should have regularly alternated with focus B, if itwasbecauseofping-pongeffect2.

Triggered activity and abnormal automaticity have been described secondary tomyocardial inflammation in myocarditis.Incessant nature of the tachycardia, unresponsive tomultiple DC cardioversion,antiarrhythmic agentssuch asβ-blockersand lignocaine,suggests that the possible mechanism of VT is enhanced automaticity because arrhythmias either because of reentry or because of delayed after depolarization typically are responsive to these maneuvers.It is possible that local inflammation around the automatic foci could create an entry block in cardiac sarcoidosis, resulting in parasystole.Multiple areas of granulomatous inflammation which is not uncommon in cardiac sarcoidosis could allow 2 parasystolic foci to coexist as in the presentcase.

詞匯

incessant adj.不停的,沒(méi)完沒(méi)了，頑固的，連續(xù)的

pleomorphic adj.多型的,多晶的

hyperintense n.高信號(hào)

paratracheal adj.氣管旁的

aconite n.烏頭，烏頭毒草

granulomatous adj.肉芽腫的

intrigue n.&v.陰謀,情節(jié),私通;耍陰謀,吸引,使...困惑,私通

discard n.&v.丟棄;丟牌,丟棄,打出，放棄，遺棄

extraneous adj.體外的,額外的,非必要的，外來(lái)的

impedance n.阻抗

substantiate v.證實(shí),使...具體化,充實(shí)

注釋

1.be subject to指“易受…的”，如Many physiological measures are continuous variables that are subject to the influence of external stimuli and internal homoeostatic control mechanisms.許多生理測(cè)值是連續(xù)變量，易受外部刺激和內(nèi)在體內(nèi)控制機(jī)制的影響。

2.ping-pong effect“乒乓效應(yīng)”或“乒乓機(jī)制”，指的是在兩個(gè)不同的狀態(tài)之間來(lái)回變化，不同的領(lǐng)域都有此表述。醫(yī)學(xué)上描述雙向性室性心動(dòng)過(guò)速的乒乓機(jī)制常指延遲后除極介導(dǎo)的觸發(fā)活動(dòng)，具有兩種特性：（1）高于某一閾值心率的延遲后除極在前一動(dòng)作電位后觸發(fā)單一的動(dòng)作電位，引起室性二聯(lián)律，（2）與二聯(lián)律相關(guān)的閾值心率因心臟部位而變化。

參考譯文

第73課不常見(jiàn)的頑固性室性心動(dòng)過(guò)速——基礎(chǔ)病因和可能的機(jī)制是什么？

室性心動(dòng)過(guò)速根據(jù)臨床特征（血流動(dòng)力學(xué)穩(wěn)定與否、反復(fù)的、頑固的）、波形（單形性、多種形態(tài)、多形性、雙向性等）或發(fā)病機(jī)制（瘢痕相關(guān)折返、自律性增高、促發(fā)活動(dòng)）進(jìn)行分類(lèi)。頑固性室性心動(dòng)過(guò)速是指持續(xù)數(shù)小時(shí)、即使反復(fù)干預(yù)中止后仍會(huì)迅速?gòu)?fù)發(fā)的室性心動(dòng)過(guò)速。多發(fā)單形性室性心動(dòng)過(guò)速是指不同時(shí)段發(fā)作或誘發(fā)的單形性室性心動(dòng)過(guò)速形態(tài)超過(guò)一種。多形性室性心動(dòng)過(guò)速是指同一發(fā)作時(shí)段出現(xiàn)1種以上的QRS形態(tài)，但QRS形態(tài)不呈連續(xù)性變化。雙向性室性心動(dòng)過(guò)速特征表現(xiàn)為心電圖上QRS心電軸呈每搏交替，通常是規(guī)則的。

病例報(bào)告

患者男性，33歲，無(wú)糖尿病、無(wú)高血壓，因心悸、胸部不適和疲勞6h而就診。既往體健，沒(méi)有服用任何藥物，無(wú)吸煙飲酒及藥癮史。入院體檢：脈率144次/min，不規(guī)則，血壓96/60mmHg，其他無(wú)異常。12導(dǎo)聯(lián)心電圖顯示規(guī)律性不規(guī)律寬QRS波群心動(dòng)過(guò)速，頻率144次/min，呈右束支圖形，間期200～220ms,QRS電軸在+160°與-40°交替，QRS波群移行從V3到V6，存在房室分離（圖1）。心動(dòng)過(guò)速對(duì)靜脈注射利多卡因、艾斯莫、胺碘酮（1h內(nèi)300mg）及2次200J的雙向直流電擊無(wú)反應(yīng)。鑒于心動(dòng)過(guò)速持續(xù)，對(duì)患者進(jìn)行鎮(zhèn)靜、氣管插管和機(jī)械通氣，持續(xù)靜脈給胺碘酮（900mg/24h），進(jìn)一步直流電擊4次無(wú)效。心動(dòng)過(guò)速轉(zhuǎn)為單形性室性心動(dòng)過(guò)速，偶見(jiàn)第2種形態(tài)的室性心動(dòng)過(guò)速（圖2），6h后在滴注胺碘酮和利多卡因期間中止，此時(shí)正準(zhǔn)備行射頻消融治療。竇性心律心電圖基本正常，X線(xiàn)胸片檢查提示上縱隔增寬，超聲心動(dòng)圖顯示左心室功能正常。心臟MRI顯示局灶性增厚和T2WI信號(hào)增強(qiáng)?？梢?jiàn)間隔中部、前側(cè)壁和前下壁早期釓強(qiáng)化，以及周邊輕度強(qiáng)化而中心低強(qiáng)度的靶形病灶（圖3A）。延遲強(qiáng)化主要見(jiàn)于左心室基底和側(cè)壁節(jié)段的心肌中層和外膜。18F-氟脫氧葡萄糖（FDG）正電子發(fā)射掃描顯示支持心肌炎癥的基底部和前間隔中部灌注缺損伴FDG攝取增加，并有氣管旁淋巴結(jié)炎癥的依據(jù)（圖3B）。血清鈣、ACE、地高辛、血烏頭毒草濃度（2周后報(bào)告）正常，結(jié)核桿菌IgG和IgM陰性。經(jīng)氣管淋巴結(jié)活檢顯示非干酪樣肉芽腫，提示類(lèi)肉瘤病?；颊叱跏冀邮苊刻? g的甲基強(qiáng)的松龍靜脈注射3d，胺碘酮每天1g滴注3d，其后改口服，36h后候拔除氣管插管。隨后，口服強(qiáng)的松龍60 mg/d，2個(gè)月，逐漸減量至每天10 mg達(dá)2年，復(fù)查正電子發(fā)射斷層FDG掃描正常后停藥。在室性心動(dòng)過(guò)速中止后5d植入單腔植入型除顫器。胺碘酮逐漸減量并于6個(gè)月后停止?；驒z測(cè)RYR2,CASQ2,ANK2和KCNJ2陰性，排除兒茶酚胺性多形性室性心動(dòng)過(guò)速。隨訪(fǎng)4年，除顫器未發(fā)生除顫工作，左心室功能正常。

討論

本病例描述了不常見(jiàn)的孤立性心臟類(lèi)肉瘤病，初始表現(xiàn)為頑固的規(guī)律性不規(guī)律雙向性室性心動(dòng)過(guò)速，左心室功能正常，未累及傳導(dǎo)系統(tǒng)。心臟的類(lèi)肉瘤病表現(xiàn)決定于部位、范圍和疾病的活動(dòng)性。心臟類(lèi)肉瘤病的3個(gè)主要后果是：（1）傳導(dǎo)異常；（2）室性心律失常；（3）心力衰竭。心臟類(lèi)肉瘤病通常表現(xiàn)為單形性室性心動(dòng)過(guò)速或傳導(dǎo)功能障礙。圍繞肉芽腫瘢痕形成的大折返環(huán)是導(dǎo)致類(lèi)肉瘤病室性心動(dòng)過(guò)速的最常見(jiàn)機(jī)制。

雙向性室性心動(dòng)過(guò)速是罕見(jiàn)的室性快速性心律失常。通常是規(guī)則的，QRS波群額面心電軸在-20°到-30°與+110°之間每搏交替。心動(dòng)過(guò)速頻率在140～180次/min，QRS波群相對(duì)較窄，120～150ms。

本例雙向性室性心動(dòng)過(guò)速具有許多不常見(jiàn)的特性。QRS間期寬達(dá)200～220 ms,而多數(shù)雙向性室性心動(dòng)過(guò)速是相對(duì)較窄的，120～150ms。本例的寬QRS波群提示可能起源于心肌內(nèi)或心外膜，不像常見(jiàn)的雙向性室性心動(dòng)過(guò)速，認(rèn)為其起源更接近希浦系統(tǒng)。

最令人感興趣的特征是規(guī)律性不規(guī)律節(jié)律，見(jiàn)圖1。仔細(xì)分析A和B兩種形態(tài)的QRS波群之間的關(guān)系顯示，A-A間期72次/min（0.88s），B-B間期72次/min（0.88s），結(jié)果為144次/min的心動(dòng)過(guò)速。A與B的間期為0.56s，而B(niǎo)與A的間期為0.32s，這種關(guān)系在整個(gè)心動(dòng)過(guò)速中保持不變，形成規(guī)律性不規(guī)律心律。寬QRS波群、電軸在+160°到-40°之間交替，轉(zhuǎn)折位于胸導(dǎo)聯(lián)V3到V6，提示存在兩個(gè)獨(dú)立的起搏點(diǎn)。要保持R-R間期的恒定，需要兩個(gè)起搏點(diǎn)的精準(zhǔn)交替，因此，有關(guān)心室兩個(gè)起搏點(diǎn)交替起搏作為機(jī)制的起始學(xué)說(shuō)遭到遺棄。然而，本病例的規(guī)律性不規(guī)律心律，可由兩個(gè)不同的起搏點(diǎn)依恒定的間期自發(fā)起搏、合并各自的傳入阻滯產(chǎn)生雙重平行心律來(lái)加以解釋。

平行心律需要局灶起搏點(diǎn)周?chē)M織能阻止外來(lái)激動(dòng)侵入但又不引起傳出阻滯。自律性與受保護(hù)是平行心律的標(biāo)志。這一特性形成經(jīng)典平行心律的診斷三聯(lián)征，即異位起搏點(diǎn)的不固定聯(lián)律間期、異位搏動(dòng)之間存在數(shù)學(xué)上的關(guān)系以及出現(xiàn)融合波。不再認(rèn)為平行起搏點(diǎn)完全獨(dú)立（受保護(hù)）于外來(lái)搏動(dòng)的這一最初學(xué)說(shuō)是正確的?，F(xiàn)已證實(shí)，與興奮性受抑導(dǎo)致傳入紊亂，但允許沖動(dòng)外傳的周邊組織相連的任何起搏點(diǎn)在一定程度上受到周邊組織電張除極的影響，即周邊區(qū)域的除極會(huì)引起起搏細(xì)胞的部分除極。這可導(dǎo)致調(diào)節(jié)性平行心律的發(fā)生。意味著非平行搏動(dòng)落在平行心律附近可以引發(fā)平行搏動(dòng)點(diǎn)的（1）最大的延遲、（2）最大的加速、（3）較小效應(yīng)、（4）實(shí)際無(wú)效應(yīng)或（5）平行節(jié)律點(diǎn)的起搏點(diǎn)湮滅。非平行搏動(dòng)落在平行收縮間期前半時(shí)段的使這一間期延長(zhǎng)，落在平行周期后半部的可使這一間期縮短。在平行收縮間期中點(diǎn)的電張調(diào)節(jié)（引起平行周期延長(zhǎng)或縮短）最大。這樣，異位搏動(dòng)的聯(lián)律間期在調(diào)節(jié)性平行心律中可以不固定，異位搏動(dòng)間期也可變化。調(diào)節(jié)也可引起偶聯(lián)間期的固定。固定偶聯(lián)間期可能提示折返型二聯(lián)律。業(yè)已顯示，當(dāng)異位搏動(dòng)與周?chē)氖抑g傳遞阻抗低時(shí)，異位起搏點(diǎn)的鎖定可以近乎固定，以致呈折返型二聯(lián)律表現(xiàn)。這在本病例的圖2中得以證實(shí)，在起搏點(diǎn)B的持續(xù)性單形性室性心動(dòng)過(guò)速中，滴注胺碘酮后起搏點(diǎn)A的部分抑制導(dǎo)致偶發(fā)異位搏動(dòng)。測(cè)定B-B間期顯示頻率加倍，從圖1雙向性室性心動(dòng)過(guò)速時(shí)0.88s到圖2的0.44s，提示平行心律為心律失常的機(jī)制。A搏對(duì)B搏的鎖定呈持續(xù)狀態(tài)。但測(cè)定此圖片上A-A間期并未顯示數(shù)學(xué)上的關(guān)系，這可由其前B搏動(dòng)對(duì)A搏動(dòng)的調(diào)節(jié)來(lái)解釋。對(duì)于本病例，雙重平行心律是最合理的解釋。僅有偶發(fā)的A激動(dòng)（圖2）和持續(xù)加快節(jié)律的B激動(dòng)排除了乒乓效應(yīng)的雙向性室性心動(dòng)過(guò)速，因?yàn)闆](méi)有持續(xù)的A激動(dòng)發(fā)生，如果是乒乓效應(yīng)，A激動(dòng)應(yīng)與B激動(dòng)呈有規(guī)律的交替。

有報(bào)道觸發(fā)活動(dòng)和異常自律性繼發(fā)于心肌炎炎癥后。對(duì)多次直流電擊、抗心律失常藥如β受體阻滯劑和利多卡因無(wú)反應(yīng)的頑固性特性，提示室性心動(dòng)過(guò)速的機(jī)制是自律性增高，因?yàn)檎鄯祷蜓舆t后除極引起的心律失常這些措施有效。心臟類(lèi)肉瘤病時(shí)自律性起搏點(diǎn)周?chē)木植垦装Y可能產(chǎn)生單向阻滯，導(dǎo)致平行心律。心臟類(lèi)肉瘤病時(shí)不常見(jiàn)的多區(qū)域肉芽腫炎癥，使得本病例中的2個(gè)平行起搏點(diǎn)得以并存。

圖1 12導(dǎo)聯(lián)心電圖顯示雙向性室性心動(dòng)過(guò)速。

圖2 12導(dǎo)聯(lián)顯示在起搏點(diǎn)B的持續(xù)性單形性室性心動(dòng)過(guò)速中，部分抑制起搏點(diǎn)A導(dǎo)致偶發(fā)異位搏動(dòng)。

圖3 A.T2W心臟MRI:顯示室間隔中部釓強(qiáng)化。B.18F-氟脫氧葡萄糖（FDG）正電子發(fā)射掃描顯示基底和前中間隔灌注缺損伴FDG攝取增加。

[1]Shenthar J.Unusual Incessant Ventricular Tachycardia-What Is the Underlying Cause and the Possible Mechanism？[J].Circ Arrhythm Electrophysiol，2015，8∶1507-1511.e112（1-11）.

（童鴻）

Unusual incessant ventricular tachycard ia-What is the underlying cause and the possib le mechanism?

Lesson Seventy-three