今日の臨床サポート

wide QRS頻拍

著者: 夛田 浩 福井大学医学部 病態制御医学講座 循環器内科学

監修: 今井靖 自治医科大学 薬理学講座臨床薬理学部門・内科学講座循環器内科学部門

著者校正/監修レビュー済:2020/07/09
患者向け説明資料

概要・推奨   

  1. 心電図上wide QRS頻拍の原因を、体表12誘導心電図から正確に診断することはしばしば困難である(推奨度2)。
  1. 血行動態の安定した規則的な単形性のwide QRS頻拍に対するATPの急速静注は、wide QRS頻拍の原因疾患の鑑別に有用である(推奨度2)。
  1. 血行動態が維持されたwide QRS頻拍は、さまざまな抗不整脈薬を用いて洞調律化を試みることが可能である。しかしながら、抗不整脈薬の使用はQT時間の延長や左室収縮能を抑制することにより血行動態が悪化する危険性があるために、抗不整脈薬の使用経験に乏しい場合や抗不整脈薬の単回投与で頻拍の停止が得られない場合には、鎮静後に同期下カルディオバージョンにより頻拍を停止させることが安全である(推奨度2)。
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薬剤監修について:
オーダー内の薬剤用量は日本医科大学付属病院 薬剤部 部長 伊勢雄也 以下、林太祐、渡邉裕次、井ノ口岳洋、梅田将光による疑義照会のプロセスを実施、疑義照会の対象については著者の方による再確認を実施しております。
※薬剤中分類、用法、同効薬、診療報酬は、エルゼビアが独自に作成した薬剤情報であり、
著者により作成された情報ではありません。
尚、用法は添付文書より、同効薬は、薬剤師監修のもとで作成しております。
※薬剤情報の(適外/適内/⽤量内/⽤量外/㊜)等の表記は、エルゼビアジャパン編集部によって記載日時にレセプトチェックソフトなどで確認し作成しております。ただし、これらの記載は、実際の保険適用の査定において保険適用及び保険適用外と判断されることを保証するものではありません。また、検査薬、輸液、血液製剤、全身麻酔薬、抗癌剤等の薬剤は保険適用の記載の一部を割愛させていただいています。
(詳細はこちらを参照)
著者のCOI(Conflicts of Interest)開示:
夛田 浩 : 講演料(第一三共(株),日本ベーリンガーインゲルハイム(株),ブリストル・マイヤーズスクイブ(株),バイオトロニックジャパン(株)),奨学(奨励)寄付など(第一三共(株),日本ベーリンガーインゲルハイム(株),アボットメディカルジャパン,ノバルティスファーマ(株),ディーセンス(株),小野薬品工業(株))[2021年]
監修:今井靖 : 講演料(第一三共株式会社)[2021年]

改訂のポイント:
  1. 2020年改訂版 不整脈薬物治療ガイドラインに基づき、薬物選択のフローチャートの修正を行った。 

病態・疫学・診察

疾患情報(疫学・病態)  
  1. wide QRS頻拍の原因は、心室頻拍(ventricular tachycardia、VT)であることが多いが、変行伝導を伴う上室頻拍(supraventricular tachycardia、SVT)や右脚ブロックの症例に発作性上室頻拍を合併した場合にも認められる。
  1. 血行動態が不安定であれば、頻拍の原因にとらわれず、速やかな電気的除細動を試みる。
 
心房細動に対してナトリウムチャネル遮断薬を投与中に認められたwide QRS頻拍

心房細動に対してナトリウムチャネル遮断薬を投与した55歳男性。ナトリウムチャネル遮断作用により、心房細動は心房粗動に移行し、かつ房室伝導比が1:1となったため、心房興奮の変行伝導に伴い右脚ブロック型のwide QRSを呈した。

出典

img1:  著者提供
 
 
 
  1. 血行動態が維持される場合は、12誘導心電図を記録し、抗不整脈薬による洞調律化を検討する。
  1. 基礎心疾患に合併したwide QRS頻拍の原因は心室頻拍であることが多く、基礎心疾患の治療、および二次予防目的の植込み型除細動器が必要となる。<図表>
  1. 上室頻拍や特発性心室頻拍がwide QRS頻拍の原因である場合は、抗不整脈薬もしくはカテーテルアブレーションなどの治療が多くの場合有効である。
 
  1. 抗不整脈薬の使用はQT時間の延長や左室収縮能を抑制することにより血行動態が悪化する危険性があるために、抗不整脈薬の使用経験に乏しい場合や抗不整脈薬の単回投与で頻拍の停止が得られない場合には、鎮静後に同期下カルディオバージョンにより頻拍を停止させることが安全である(推奨度2OG)。(参考文献:[1]
  1. 血行動態が維持されたwide QRS頻拍に対するさまざまな抗不整脈薬の有効性が検証されている。プロカインアミドは、低血圧やQRS時間の延長(投与前よりQT時間の延長<50%)が認められなければ最大17mg/kgの投与(20-50mg/分)を行い、アミオダロンは初期の10分間で150mg(日本国内では125mg)の静脈内投与およびその後の維持投与を行う。抗不整脈薬で頻拍の停止が得られない場合には、同期下カルディオバージョン(100J)で洞調律化を試みる。いったん、頻拍が不規則な場合や、多形性頻拍へと移行した場合には、電気的除細動(非同期)を速やかに行う。
問診・診察のポイント  
  1. 冷汗や意識レベルの低下を伴い、血行動態の悪化が疑われるwide QRS頻拍の場合、安静臥位としモニターを装着するとともに、急変時の対応に備え、救急カートおよび除細動器、酸素投与などを準備する。

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文献 

著者: Robert W Neumar, Charles W Otto, Mark S Link, Steven L Kronick, Michael Shuster, Clifton W Callaway, Peter J Kudenchuk, Joseph P Ornato, Bryan McNally, Scott M Silvers, Rod S Passman, Roger D White, Erik P Hess, Wanchun Tang, Daniel Davis, Elizabeth Sinz, Laurie J Morrison
雑誌名: Circulation. 2010 Nov 2;122(18 Suppl 3):S729-67. doi: 10.1161/CIRCULATIONAHA.110.970988.
Abstract/Text The goal of therapy for bradycardia or tachycardia is to rapidly identify and treat patients who are hemodynamically unstable or symptomatic due to the arrhythmia. Drugs or, when appropriate, pacing may be used to control unstable or symptomatic bradycardia. Cardioversion or drugs or both may be used to control unstable or symptomatic tachycardia. ACLS providers should closely monitor stable patients pending expert consultation and should be prepared to aggressively treat those with evidence of decompensation.

PMID 20956224  Circulation. 2010 Nov 2;122(18 Suppl 3):S729-67. doi: 1・・・
著者: P Brugada, J Brugada, L Mont, J Smeets, E W Andries
雑誌名: Circulation. 1991 May;83(5):1649-59.
Abstract/Text BACKGROUND: In the differential diagnosis of a tachycardia with a wide QRS complex (greater than or equal to 0.12 second) diagnostic mistakes are frequent. Therefore, we investigated the reasons for failure of presently available criteria, and we identified new, simpler criteria and incorporated them in a stepwise approach that provides better sensitivity and specificity for making a correct diagnosis.
METHODS AND RESULTS: A prospective analysis revealed that current criteria had a poor specificity for the differential diagnosis. The value of four new criteria incorporated in a stepwise approach was prospectively analyzed in a total of 554 tachycardias with a widened QRS complex (384 ventricular and 170 supraventricular). The sensitivity of the four consecutive steps was 0.987, and the specificity was 0.965.
CONCLUSIONS: Current criteria for the differential diagnosis between supraventricular tachycardia with aberrant conduction and ventricular tachycardia are frequently absent or suggest the wrong diagnosis. The absence of an RS complex in all precordial leads is easily recognizable and highly specific for the diagnosis of ventricular tachycardia. When an RS complex is present in one or more precordial leads, an RS interval of more than 100 msec is highly specific for ventricular tachycardia. This new stepwise approach may prevent diagnostic mistakes.

PMID 2022022  Circulation. 1991 May;83(5):1649-59.
著者: J L Isenhour, S Craig, M Gibbs, L Littmann, G Rose, R Risch
雑誌名: Acad Emerg Med. 2000 Jul;7(7):769-73.
Abstract/Text OBJECTIVE: To evaluate the accuracy of the Brugada algorithm for analysis of wide-complex tachycardia (WCT) when applied by board-certified emergency physicians and board-certified cardiologists.
METHODS: A database consisting of 157 electrocardiograms of WCTs were evaluated in a blinded fashion using the Brugada criteria to determine the presence of ventricular tachycardia (VT) or supraventricular tachycardia with aberrancy. These results were then compared with the electrophysiologically proven diagnosis for each tracing. Sensitivity and specificity of the Brugada criteria for diagnosis of VT were calculated. Two board-certified emergency physicians and two board-certified cardiologists analyzed each tracing, and interobserver agreement was determined using the kappa statistic.
RESULTS: Sensitivity and specificity for the determination of VT using the Brugada algorithm were 85% [95% confidence interval (95% CI) = 79% to 91%] and 60% (95% CI = 43% to 78%) for cardiologist 1 (C 1) and 91% (95% CI = 86% to 96%) and 55% (95% CI = 37% to 72%) for C 2. Emergency physician (EP 1) achieved a sensitivity of 83% (95% CI = 78% to 91%) and a specificity of 43% (95% CI = 25% to 59%), while EP 2 attained 79% (95% CI = 73% to 87%) and 70% (95% CI = 51% to 84%), respectively. The original authors achieved a sensitivity of 98.7% and specificity of 96.5% when determining VT in their study population. Interobserver agreement for the emergency physicians and the cardiologists in determining VT was 82% and 81%, respectively.
CONCLUSIONS: Neither the emergency physicians nor the cardiologists were able to achieve a sensitivity or specificity as high as that reported by the original investigators when using the Brugada algorithm to determine the presence of VT.

PMID 10917326  Acad Emerg Med. 2000 Jul;7(7):769-73.
著者: Ernest W Lau, G André Ng
雑誌名: Pacing Clin Electrophysiol. 2002 May;25(5):822-7.
Abstract/Text The authors previously proposed a Bayesian approach to the electrocardiographic diagnosis of regular broad complex tachycardia (BCT), which can be due to VT or supraventricular tachycardia with aberrant conduction (SVTAC). They also published an account comparing the theoretical merits in the design of two of the most commonly used diagnostic algorithms for the same purpose, those of Brugada et al. and Griffith et al. In this study, a direct head-to-head comparison was performed on the practical performances of the three algorithms in this study. A set of 111 ECGs showing regular BCT (77 VT, 34 SVTAC) whose diagnoses were confirmed by electrophysiological study was shown to five internists in general medicine at a district general hospital. The observers were asked to comment on whether the ECG criteria in the three algorithms tested were fulfilled or not, and a computer program then derived the corresponding diagnoses. The sensitivity and specificity for VT achieved by the Brugada algorithm were 92% and 44%, 92% and 44% by the Griffith algorithm, and 97% and 56% by the Bayesian algorithm. The Bayesian algorithm achieved a higher sensitivity and specificity than the other two algorithms, but the differences are not statistically significant (P = 0.6583 and P = 0.5334, respectively). The Brugada, Griffith, and Bayesian algorithms show comparable performances in terms of overall sensitivity and specificity when tested in practice. Of the three algorithms, the Griffith algorithm excels in simplicity and is the easiest to implement in practice. The Bayesian algorithm achieved slightly higher values for sensitivity and specificity than the Brugada and Griffith algorithms but may be more suitable for automated computer-aided diagnosis of ECG due to its complexity.

PMID 12049375  Pacing Clin Electrophysiol. 2002 May;25(5):822-7.
著者: A E Buxton, H L Waxman, F E Marchlinski, M B Simson, D Cassidy, M E Josephson
雑誌名: Circulation. 1983 Nov;68(5):917-27.
Abstract/Text This report describes the clinical and electrophysiologic characteristics of 30 patients without myocardial disease who had ventricular tachycardia with the morphologic characteristics of left bundle branch block and inferior axis. The tachycardias were nonsustained in 24 patients, sustained (greater than 30 sec) in six patients, and provocable by exercise in 14 of 23 patients undergoing a standard Bruce protocol. Ventricular tachycardia was induced during electrophysiologic study in 22 of 30 patients. Programmed stimulation induced tachycardia in 10 of 30 patients, most frequently by rapid atrial or ventricular pacing. Isoproterenol infusion facilitated tachycardia induction in 13 of 23 patients. Endocardial activation mapping, performed in 10 patients, confirmed that earliest ventricular activation during tachycardia occurred at the right ventricular outflow tract on the interventricular septum. These tachycardias were unique in their responsiveness to a wide variety of antiarrhythmic drugs, including type I drugs and propranolol. During a mean follow-up of 30 months, no patient has died or experienced cardiac arrest. Two patients appear to be in spontaneous remission, and no patient has developed additional signs of cardiac disease.

PMID 6137291  Circulation. 1983 Nov;68(5):917-27.
著者: J S Gill, K Blaszyk, D E Ward, A J Camm
雑誌名: Am Heart J. 1993 Nov;126(5):1126-33.
Abstract/Text This study examines the efficacy of verapamil for the suppression of idiopathic ventricular tachycardia (VT) of left bundle branch block LBBB-like morphology. Forty-two patients (mean age 36.2 +/- 12.1 years; 20 men and 22 women) with VT and without any underlying cardiac abnormality on clinical examination and noninvasive investigation were studied. The inducibility of clinical VT was examined by treadmill exercise testing and programmed ventricular stimulation (PVS). In 29 patients VT was inducible by exercise testing, in 24 by PVS, and in 23 there was evidence of VT on Holter monitoring. After baseline testing, patients were treated with verapamil 120 mg thrice daily for at least 5 half-lives for the drug to load before evaluation. With Holter monitoring, 74% of patients with evidence of VT at baseline testing demonstrated a change of status from nonsustained VT to no VT or from sustained VT to nonsustained VT. Four patients had nonsustained VT during verapamil treatment but no VT at baseline. There was a significant reduction in the number of ventricular ectopic beats over 24 hours (baseline: 15,541 +/- 17,599 vs verapamil treatment: 8892 +/- 15,582, p < 0.01). Exercise-induced VT was suppressed in 56% of patients with VT during baseline testing, but no effect of verapamil on the tachycardia was observed in 26%. The remaining patients demonstrated a partial response to verapamil; the rate of VT was unchanged, although the duration of the runs was reduced. Sustained monomorphic VT was inducible in only 5 patients, of whom 4 were rendered noninducible; 1 patient remained inducible.(ABSTRACT TRUNCATED AT 250 WORDS)

PMID 8237755  Am Heart J. 1993 Nov;126(5):1126-33.
著者: Yasuaki Tanaka, Hiroshi Tada, Sachiko Ito, Shigeto Naito, Koji Higuchi, Koji Kumagai, Hitoshi Hachiya, Kenzo Hirao, Shigeru Oshima, Koichi Taniguchi, Kazutaka Aonuma, Mitsuaki Isobe
雑誌名: Circ J. 2011;75(7):1585-91. Epub 2011 May 12.
Abstract/Text BACKGROUND: The prevalence, gender- and age-related differences, ablation success rate and inter-relationship between the origins of the idiopathic ventricular arrhythmias (I-VA) have not been clarified.
METHODS AND RESULTS: A total of 625 consecutive patients with symptomatic, drug resistant I-VA (315 males and 310 females; mean age, 54 ± 17 years; 218 ventricular tachycardias, 407 premature ventricular contractions) who underwent catheter ablation were studied. The patients were divided into 5 groups based on the VA origin: (1) outflow tract (OT)-VA, consisting of right ventricular (RV) OT-VA and left ventricular (LV) OT-VA; (2) inflow tract (IT)-VA, consisting of tricuspid annulus (TA)-free wall (FW)-VA, IT-septum-VA, and mitral (MA)-FW-VA; (3) LV-inferoseptum-VA; (4) LV-other-VA; and (5) RV-other-VA. RVOT-VA in women were 1.5 times more frequent than in men, while LVOT-VA were more frequent in men. The prevalence of LVOT origin I-VA increased with age compared to that for the RVOT. The mean age of MA-FW-VA patients (62 ± 14 years) was higher than that of TA-FW-VA patients (51 ± 18 years; P = 0.03). The ablation success rate for RVOT-VA (88%) was higher than that for LVOT-VA (58%; P<0.0001). A multivariate analysis revealed that the patient age was one of the valuable predictors of a successful ablation (odds ratio=0.97; 95% confidence interval: 0.95-0.99; P=0.007).
CONCLUSIONS: Distinct gender and age differences were found in the incidence of I-VA according to their site of origin.

PMID 21566341  Circ J. 2011;75(7):1585-91. Epub 2011 May 12.
著者: T Ohe, K Shimomura, N Aihara, S Kamakura, M Matsuhisa, I Sato, H Nakagawa, A Shimizu
雑誌名: Circulation. 1988 Mar;77(3):560-8.
Abstract/Text Electrophysiologic studies were performed in 16 patients 11 to 45 years old (mean 33 years) with idiopathic sustained (lasting more than 5 min) ventricular tachycardia (VT) originating from the left ventricle. Endocardial mapping during VT showed that the earliest site of activation was at the apical inferior portion of the left ventricle in 14 patients whose QRS morphology during VT showed a right bundle branch block pattern and left-axis deviation, but at the apical anterosuperior portion of the left ventricle in two patients whose QRS morphology during VT showed a right bundle branch block and right-axis deviation. Single programmed ventricular stimulation induced VT in 13 patients, and rapid ventricular pacing induced VT in the remaining three patients. Rapid ventricular pacing terminated VT in all patients. The relationship between the coupling interval and the echo interval was inverse in all eight patients with a wide VT inducible zone. Entrainment was recognized in three of six patients. The initiation of VT by constant pacing depended on the number of pacing beats but not the duration of pacing in all four patients tested. Intravenous verapamil terminated the VT in 13 of 14 patients. Long-term oral verapamil was also effective in all five patients who required long-term oral therapy for their symptoms associated with VT. In conclusion (1) idiopathic left ventricular tachycardia has unique electrocardiographic, electrophysiologic, and electropharmacological properties, (2) the electrophysiologic characteristics suggest that the mechanism is reentry, and (3) verapamil is effective in both the short- and long-term treatment of VT.

PMID 3342487  Circulation. 1988 Mar;77(3):560-8.
著者: A Nogami, S Naito, H Tada, K Taniguchi, Y Okamoto, S Nishimura, Y Yamauchi, K Aonuma, M Goya, Y Iesaka, M Hiroe
雑誌名: J Am Coll Cardiol. 2000 Sep;36(3):811-23.
Abstract/Text OBJECTIVES: The purpose of this study was to determine the relation of diastolic and presystolic potentials recorded during verapamil-sensitive idiopathic left ventricular tachycardia (ILVT) to reentry circuit.
BACKGROUND: Successful ablation of verapamil-sensitive ILVT at the zone of slow conduction from which the diastolic potential is recorded has been reported. However, the relationship between the diastolic potential and the reentrant circuit remains a matter of debate.
METHODS: Radiofrequency (RF) ablation was performed in 20 patients with verapamil-sensitive ILVT. After identifying the ventricular tachycardia (VT) exit site, we searched for the mid-diastolic potential (P1) during VT. Entrainment followed by RF current application was performed. If the mid-diastolic potential could not be detected, RF current was applied at the VT exit site showing the earliest ventricular activation with a single fused presystolic Purkinje potential (P2).
RESULTS: In 15 of 20 patients, both P1 and P2 were recorded during VT from midseptal region. Entrainment pacing captured P1 orthodromically and reset the VT. The interval from stimulus to P1 was prolonged as the pacing rate was increased. Radiofrequency ablation was successfully performed at this site in all 15 patients. After successful ablation, P1 appeared after the QRS complex during sinus rhythm with the identical sequence to that during VT. In the remaining five patients, the diastolic potential could not be detected, and a single fused P2 was recorded only at the VT exit site. Successful ablation was performed at this site in all five patients.
CONCLUSIONS: This study demonstrates that P1 and P2 are critical potentials in a circuit of verapamil-sensitive ILVT and suggests the presence of a macroreentry circuit involving the normal Purkinje system and the abnormal Purkinje tissue with decremental property and verapamil-sensitivity.

PMID 10987604  J Am Coll Cardiol. 2000 Sep;36(3):811-23.
著者:
雑誌名: Lancet. 1999 Jun 12;353(9169):2001-7.
Abstract/Text BACKGROUND: Metoprolol can improve haemodynamics in chronic heart failure, but survival benefit has not been proven. We investigated whether metoprolol controlled release/extended release (CR/XL) once daily, in addition to standard therapy, would lower mortality in patients with decreased ejection fraction and symptoms of heart failure.
METHODS: We enrolled 3991 patients with chronic heart failure in New York Heart Association (NYHA) functional class II-IV and with ejection fraction of 0.40 or less, stabilised with optimum standard therapy, in a double-blind randomised controlled study. Randomisation was preceded by a 2-week single-blind placebo run-in period. 1990 patients were randomly assigned metoprolol CR/XL 12.5 mg (NYHA III-IV) or 25.0 mg once daily (NYHA II) and 2001 were assigned placebo. The target dose was 200 mg once daily and doses were up-titrated over 8 weeks. Our primary endpoint was all-cause mortality, analysed by intention to treat.
FINDINGS: The study was stopped early on the recommendation of the independent safety committee. Mean follow-up time was 1 year. All-cause mortality was lower in the metoprolol CR/XL group than in the placebo group (145 [7.2%, per patient-year of follow-up]) vs 217 deaths [11.0%], relative risk 0.66 [95% CI 0.53-0.81]; p=0.00009 or adjusted for interim analyses p=0.0062). There were fewer sudden deaths in the metoprolol CR/XL group than in the placebo group (79 vs 132, 0.59 [0.45-0.78]; p=0.0002) and deaths from worsening heart failure (30 vs 58, 0.51 [0.33-0.79]; p=0.0023).
INTERPRETATION: Metoprolol CR/XL once daily in addition to optimum standard therapy improved survival. The drug was well tolerated.

PMID 10376614  Lancet. 1999 Jun 12;353(9169):2001-7.
著者: N Freemantle, J Cleland, P Young, J Mason, J Harrison
雑誌名: BMJ. 1999 Jun 26;318(7200):1730-7.
Abstract/Text OBJECTIVES: To assess the effectiveness of beta blockers in short term treatment for acute myocardial infarction and in longer term secondary prevention; to examine predictive factors that may influence outcome and therefore choice of drug; and to examine the clinical importance of the results in the light of current treatment.
DESIGN: Systematic review of randomised controlled trials.
SETTING: Randomised controlled trials.
SUBJECTS: Patients with acute or past myocardial infarction.
INTERVENTION: beta Blockers compared with control.
MAIN OUTCOME MEASURES: All cause mortality and non-fatal reinfarction.
RESULTS: Overall, 5477 of 54 234 patients (10.1%) randomised to beta blockers or control died. We identified a 23% reduction in the odds of death in long term trials (95% confidence interval 15% to 31%), but only a 4% reduction in the odds of death in short term trials (-8% to 15%). Meta regression in long term trials did not identify a significant reduction in effectiveness in drugs with cardioselectivity but did identify a near significant trend towards decreased benefit in drugs with intrinsic sympathomimetic activity. Most evidence is available for propranolol, timolol, and metoprolol. In long term trials, the number needed to treat for 2 years to avoid a death is 42, which compares favourably with other treatments for patients with acute or past myocardial infarction.
CONCLUSIONS: beta Blockers are effective in long term secondary prevention after myocardial infarction, but they are underused in such cases and lead to avoidable mortality and morbidity.

PMID 10381708  BMJ. 1999 Jun 26;318(7200):1730-7.
著者: J M Brophy, L Joseph, J L Rouleau
雑誌名: Ann Intern Med. 2001 Apr 3;134(7):550-60.
Abstract/Text PURPOSE: Congestive heart failure is an important cause of patient morbidity and mortality. Although several randomized clinical trials have compared beta-blockers with placebo for treatment of congestive heart failure, a meta-analysis quantifying the effect on mortality and morbidity has not been performed recently.
DATA SOURCES: The MEDLINE, Cochrane, and Web of Science electronic databases were searched from 1966 to July 2000. References were also identified from bibliographies of pertinent articles.
STUDY SELECTION: All randomized clinical trials of beta-blockers versus placebo in chronic stable congestive heart failure were included.
DATA EXTRACTION: A specified protocol was followed to extract data on patient characteristics, beta-blocker used, overall mortality, hospitalizations for congestive heart failure, and study quality.
DATA SYNTHESIS: A hierarchical random-effects model was used to synthesize the results. A total of 22 trials involving 10 135 patients were identified. There were 624 deaths among 4862 patients randomly assigned to placebo and 444 deaths among 5273 patients assigned to beta-blocker therapy. In these groups, 754 and 540 patients, respectively, required hospitalization for congestive heart failure. The probability that beta-blocker therapy reduced total mortality and hospitalizations for congestive heart failure was almost 100%. The best estimates of these advantages are 3.8 lives saved and 4 fewer hospitalizations per 100 patients treated in the first year after therapy. The probability that these benefits are clinically significant (>2 lives saved or >2 fewer hospitalizations per 100 patients treated) is 99%. Both selective and nonselective agents produced these salutary effects. The results are robust to any reasonable publication bias.
CONCLUSIONS: beta-Blocker therapy is associated with clinically meaningful reductions in mortality and morbidity in patients with stable congestive heart failure and should be routinely offered to all patients similar to those included in trials.

PMID 11281737  Ann Intern Med. 2001 Apr 3;134(7):550-60.
著者: F Burkart, M Pfisterer, W Kiowski, F Follath, D Burckhardt
雑誌名: J Am Coll Cardiol. 1990 Dec;16(7):1711-8.
Abstract/Text In view of the high risk of sudden cardiac death and the prognostic importance of complex ventricular ectopic activity, the effects of prophylactic antiarrhythmic treatment were investigated prospectively in patients with persisting asymptomatic complex arrhythmias after myocardial infarction. End points were total mortality and arrhythmic events (sudden death, sustained ventricular tachycardia and ventricular fibrillation). Of 1,220 consecutively screened survivors of myocardial infarction, 312 had Lown class 3 or 4b arrhythmia on 24 h electrocardiographic recordings before hospital discharge and consented to the study. They were randomized to individualized antiarrhythmic treatment (Group 1, n = 100), treatment with low dose amiodarone, 200 mg/day (Group 2, n = 98) or no antiarrhythmic therapy (Group 3 [control group], n = 114). During the 1 year follow-up period, 10 patients in Group 1 died, as did 5 in Group 2 and 15 in Group 3. On the basis of an intention to treat analysis, the probability of survival of patients given amiodarone was significantly greater than that of control patients (p less than 0.05). In addition, arrhythmic events were significantly reduced by amiodarone (p less than 0.01). These effects were less marked and not significant for individually treated patients (Group 1). These findings suggest that low dose amiodarone decreases mortality in the 1st year after myocardial infarction in patients at high risk of sudden death.

PMID 2254558  J Am Coll Cardiol. 1990 Dec;16(7):1711-8.
著者: S N Singh, R D Fletcher, S G Fisher, B N Singh, H D Lewis, P C Deedwania, B M Massie, C Colling, D Lazzeri
雑誌名: N Engl J Med. 1995 Jul 13;333(2):77-82. doi: 10.1056/NEJM199507133330201.
Abstract/Text BACKGROUND: Asymptomatic ventricular arrhythmias in patients with congestive heart failure are associated with increased rates of overall mortality and sudden death. Amiodarone is now used widely to prevent ventricular tachycardia and fibrillation. We conducted a trial to determine whether amiodarone can reduce overall mortality in patients with congestive heart failure and asymptomatic ventricular arrhythmias.
METHODS: We used a double-blind, placebo-controlled protocol in which 674 patients with symptoms of congestive heart failure, cardiac enlargement, 10 or more premature ventricular contractions per hour, and a left ventricular ejection fraction of 40 percent or less were randomly assigned to receive amiodarone (336 patients) or placebo (338 patients). The primary end point was overall mortality, and the median follow-up was 45 months (range, 0 to 54).
RESULTS: There was no significant difference in overall mortality between the two treatment groups (P = 0.6). The two-year actuarial survival rate was 69.4 percent (95 percent confidence interval, 64.2 to 74.6) for the patients in the amiodarone group and 70.8 percent (95 percent confidence interval, 65.7 to 75.9) for those in the placebo group. At two years, the rate of sudden death was 15 percent in the amiodarone group and 19 percent in the placebo group (P = 0.43). There was a trend toward a reduction in overall mortality among the patients with nonischemic cardiomyopathy who received amiodarone (P = 0.07). Amiodarone was significantly more effective in suppressing ventricular arrhythmias and increased the left ventricular ejection fraction by 42 percent at two years.
CONCLUSIONS: Although amiodarone was effective in suppressing ventricular arrhythmias and improving ventricular function, it did not reduce the incidence of sudden death or prolong survival among patients with heart failure, except for a trend toward reduced mortality among those with nonischemic cardiomyopathy.

PMID 7539890  N Engl J Med. 1995 Jul 13;333(2):77-82. doi: 10.1056/NE・・・
著者: D G Julian, A J Camm, G Frangin, M J Janse, A Munoz, P J Schwartz, P Simon
雑誌名: Lancet. 1997 Mar 8;349(9053):667-74.
Abstract/Text BACKGROUND: Ventricular arrhythmias are a major cause of death after myocardial infarction, especially in patients with poor left-ventricular function. Previous attempts to identify and suppress arrhythmias with various antiarrhythmic drugs failed to reduce or actually increase mortality. Amiodarone is a powerful antiarrhythmic drug with several potentially beneficial actions, and has shown benefit in several small-scale studies. We postulated that this drug might reduce mortality in patients at high risk of death after myocardial infarction because of impaired ventricular function, irrespective of whether they had ventricular arrhythmias.
METHODS: The European Myocardial Infarct Amiodarone Trial (EMIAT) was a randomised double-blind placebo-controlled trial to assess whether amiodarone reduced all-cause mortality (primary endpoint) and cardiac mortality and arrhythmic death (secondary endpoints) in survivors of myocardial infarction with a left-ventricular ejection fraction (LVEF) of 40% or less. Intention-to-treat and on-treatment analyses were done.
FINDINGS: EMIAT enrolled 1486 patients (743 in the amiodarone group, 743 in the placebo group). Median follow-up was 21 months. All-cause mortality (103 deaths in the amiodarone group, 102 in the placebo group) and cardiac mortality did not differ between the two groups. However, in the amiodarone group, there was a 35% risk reduction (95% CI 0-58, p = 0.05) in arrhythmic deaths.
INTERPRETATION: Our findings do not support the systematic prophylactic use of amiodarone in all patients with depressed left-ventricular function after myocardial infarction. However, the lack of proarrhythmia and the reduction in arrhythmic death support the use of amiodarone in patients for whom antiarrhythmic therapy is indicated.

PMID 9078197  Lancet. 1997 Mar 8;349(9053):667-74.
著者:
雑誌名: Lancet. 1997 Nov 15;350(9089):1417-24.
Abstract/Text BACKGROUND: There have been 13 randomised controlled trials of prophylactic amiodarone in patients with recent myocardial infarction (MI) or congestive heart failure (CHF). None of these was powered to detect a mortality reduction of about 20%. We undertook a meta-analysis, based on data from individual patients, to provide a more sensitive and accurate assessment of the benefits and risks of prophylactic amiodarone.
METHODS: Individual data from the studies were abstracted according to a predefined protocol. The summary odds ratios were calculated according to standard methods.
FINDINGS: There were eight post-MI and five CHF trials; nine trials were double-blind and placebo-controlled, and four compared amiodarone with usual care. 6553 patients were randomly assigned treatment, of which 78% were in post-MI trials and 22% in CHF trials. 89% had had previous MI. The mean left-ventricular ejection fraction was 31%, and median frequency of ventricular premature depolarisation 18 per h. Total mortality was reduced by 13% (odds ratio 0.87 [95% CI 0.78-0.99], p = 0.030) based on classic fixed-effects meta-analysis and by 15% (0.85 [0.71-1.02], p = 0.081) with the more conservative random-effects approach. Arrhythmic/sudden death was reduced by 29% (0.71 [0.59-0.85], p = 0.0003). There was no effect on non-arrhythmic deaths (1.02 [0.87-1.19], p = 0.84). There was no difference in treatment effect between post-MI and CHF studies. The risk of arrhythmic/sudden death in control-group patients was higher in CHF than in post-MI studies (10.7 vs 4.1%), and the best single predictor of risk of arrhythmic/sudden death among all patients was symptomatic CHF. The excess (amiodarone minus control) risk of pulmonary toxicity was 1% per year.
INTERPRETATION: Prophylactic amiodarone reduces the rate of arrhythmic/sudden death in high-risk patients with recent MI or CHF and this effect results in an overall reduction of 13% in total mortality.

PMID 9371164  Lancet. 1997 Nov 15;350(9089):1417-24.
著者:
雑誌名: N Engl J Med. 1997 Nov 27;337(22):1576-83. doi: 10.1056/NEJM199711273372202.
Abstract/Text BACKGROUND: Patients who survive life-threatening ventricular arrhythmias are at risk for recurrent arrhythmias. They can be treated with either an implantable cardioverter-defibrillator or antiarrhythmic drugs, but the relative efficacy of these two treatment strategies is unknown.
METHODS: To address this issue, we conducted a randomized comparison of these two treatment strategies in patients who had been resuscitated from near-fatal ventricular fibrillation or who had undergone cardioversion from sustained ventricular tachycardia. Patients with ventricular tachycardia also had either syncope or other serious cardiac symptoms, along with a left ventricular ejection fraction of 0.40 or less. One group of patients was treated with implantation of a cardioverter-defibrillator; the other received class III antiarrhythmic drugs, primarily amiodarone at empirically determined doses. Fifty-six clinical centers screened all patients who presented with ventricular tachycardia or ventricular fibrillation during a period of nearly four years. Of 1016 patients (45 percent of whom had ventricular fibrillation, and 55 percent ventricular tachycardia), 507 were randomly assigned to treatment with implantable cardioverter-defibrillators and 509 to antiarrhythmic-drug therapy. The primary end point was overall mortality.
RESULTS: Follow-up was complete for 1013 patients (99.7 percent). Overall survival was greater with the implantable defibrillator, with unadjusted estimates of 89.3 percent, as compared with 82.3 percent in the antiarrhythmic-drug group at one year, 81.6 percent versus 74.7 percent at two years, and 75.4 percent versus 64.1 percent at three years (P<0.02). The corresponding reductions in mortality (with 95 percent confidence limits) with the implantable defibrillator were 39+/-20 percent, 27+/-21 percent, and 31+/-21 percent
CONCLUSIONS: Among survivors of ventricular fibrillation or sustained ventricular tachycardia causing severe symptoms, the implantable cardioverter-defibrillator is superior to antiarrhythmic drugs for increasing overall survival.

PMID 9411221  N Engl J Med. 1997 Nov 27;337(22):1576-83. doi: 10.1056・・・
著者: Douglas S Lee, Lawrence D Green, Peter P Liu, Paul Dorian, David M Newman, F Curry Grant, Jack V Tu, David A Alter
雑誌名: J Am Coll Cardiol. 2003 May 7;41(9):1573-82.
Abstract/Text OBJECTIVES: The aim of this study was to compare the effectiveness of the implantable cardioverter defibrillator (ICD) and medical strategies for prevention of arrhythmic events and death.
BACKGROUND: The ICD is a potential strategy to reduce mortality in patients at risk of sudden death.
METHODS: The MEDLINE, EMBASE, and Cochrane Library electronic databases were searched from January 1966 to April 2002. All published randomized controlled trials comparing ICD implantation with medical therapy were reviewed. Four independent reviewers extracted data on all-cause mortality, nonarrhythmic death, and arrhythmic death using a standardized protocol.
RESULTS: Nine studies including over 5,000 patients were synthesized using both fixed-effects and random-effects models. The primary and secondary prevention trials showed a significant benefit of the ICD with respect to arrhythmic death, with relative risks (RR) of 0.34 and 0.50, respectively (both p < 0.001). The mortality benefit of the ICD was entirely attributable to a reduction in arrhythmic death (all trials: p < 0.00001). Whereas the secondary prevention trials exhibited a robust decrease in all-cause ICD mortality (RR 0.75; p < 0.001), the pooled primary prevention trials demonstrated decreased all-cause ICD mortality (RR 0.66; p < 0.05) which was dependent on selected individual trials. The disparity in ICD-related mortality reductions in the primary prevention trials was related to variability in the incidence of arrhythmic death between individual studies.
CONCLUSIONS: Although the ICD decreases the risk of arrhythmic death, its impact on all-cause mortality is related to the underlying risk of arrhythmia-related death relative to competing causes. Given the cost of the device strategy, policies of targeted intervention based on the future risk of arrhythmia are warranted.

PMID 12742300  J Am Coll Cardiol. 2003 May 7;41(9):1573-82.

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