今日の臨床サポート

ST上昇型心筋梗塞

著者: 阿古潤哉 北里大学病院循環器内科

監修: 代田浩之 順天堂大学大学院医学研究科循環器内科学

著者校正/監修レビュー済:2021/09/15
患者向け説明資料

概要・推奨   

  1. 発症12時間以内の患者に対し、できる限り迅速にprimary PCI(ステント留置を含む)を行う(推奨度1)。
  1. ACSが疑われる患者では直ちに(10分以内に)12誘導心電図を記録する(推奨度1)。
  1. ACSを否定できない患者で初回心電図では診断できない場合に、経時的に12誘導心電図を記録する(推奨度1)。
  1. 閲覧にはご契約が必要となります。閲覧にはご契約が必要となります。閲覧にはご契約が必要となり
  1. 閲覧にはご契約が必要となります。閲覧にはご契約が必要となります。閲覧にはご契約が必要とな
  1. 閲覧にはご契約が必要となります。閲覧にはご契約が必要となります。閲覧にはご契約が必要となります。
  1. 閲覧にはご契約が必要となります。閲覧にはご契約が必要
  1. 閲覧にはご契約が必要となります。閲覧にはご契約が必要となります
  1. 閲覧にはご契約が必要となります。閲覧にはご契約
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:
阿古潤哉 : 講演料(日本ベーリンガーインゲルハイム,バイエル薬品,興和,アストラゼネカ,アボットメディカル,ノバルティス,田辺三菱,第一三共),奨学(奨励)寄付など(田辺三菱,第一三共,武田薬品,日本ベーリンガーインゲルハイム)[2021年]
監修:代田浩之 : 未申告[2021年]

改訂のポイント:
  1. 薬剤の位置づけについて見直しを行った。
  1. D2B時間についての記載を削除した。

病態・疫学・診察

疾患情報  
  1. ST上昇型心筋梗塞とは、冠動脈粥腫の破綻(破裂またはびらん)により冠動脈内腔に血栓が形成され、冠動脈が閉塞し心筋壊死を生じた病態である。
  1. ST上昇型心筋梗塞は、速やかに診断し、閉塞した冠動脈を再開通させ、心筋に血流を再灌流することが予後改善に繋がる。
  1. ST上昇型心筋梗塞は、心筋虚血を示唆する症状、心電図でのST上昇、心筋壊死を示す生化学マーカーの一過性上昇により診断される。
  1. 超急性期には、生化学マーカーはいまだ上昇していないことが少なくない。生化学マーカーが上昇していないからといって急性心筋梗塞は否定できず、診断は症状と心電図所見を中心に行う。
 
発症からの経過時間別にみた各心筋傷害マーカーの診断精度

発症早期の診断にはH-FABPが有用であるが特異度に限界があり、発症4時間以降は心筋トロポニンが感度・特異度ともに高く、診断に有用である。

 
  1. 発症12時間以内の患者に対し、できる限り迅速にprimary PCI(ステント留置を含む)を行う(推奨度1)。
  1. ST上昇型心筋梗塞症に対する治療の中心は再灌流療法であり、本邦では現在PCIがSTEMI治療の主体として広く行われている。血栓溶解療法を先行させることなく、再灌流療法としてPCIを選択することをprimary PCIという。
  1. STEMIの治療において、発症から再灌流までの総虚血時間をいかに短くするかが重要である。
  1. STEMIの治療においてはDrug-eluting stent (DES)の使用が推奨される(推奨度1)。
 
 
問診・診察のポイント  
  1. 典型例では、胸部症状が少なくとも20分以上持続するとされている。しかし、実際は典型的な症状を示す例だけでなく、その症状は多様であることを認識しておく。非典型的な症状を訴える例では、むしろ重症が多い。

これより先の閲覧には個人契約のトライアルまたはお申込みが必要です。

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文献 

著者: H Meischke, M P Larsen, M S Eisenberg
雑誌名: Am J Emerg Med. 1998 Jul;16(4):363-6.
Abstract/Text A retrospective observational study using database registry of consecutive patients admitted to 16 King County hospital Coronary Care Units (CCU) was conducted to assess gender differences in symptom presentation for acute myocardial infarction (AMI) and investigate how symptom presentation relates to prehospital delay time interval from acute symptom onset to emergency department (ED) presentation. Between January 1991 and February 1993, 4,497 patients were admitted to the CCUs with diagnosed AMI. Accredited record technicians abstracted age, gender, race, transport method, symptom presentation (chest pain, sweating, nausea, shortness of breath, epigastric pain, and fainting), delay time interval between acute symptom onset and presentation to hospital ED, and discharge diagnosis from the patients' medical records. After adjusting for age and history of diabetes, no gender differences remained for frequencies of chest pain, fainting, or epigastric pain. Women reported more nausea and shortness of breath but less sweating than men as symptoms of AMI. Chest pain, sweating, and fainting were associated with decreasing delay time intervals. Age, gender, histories of AMI and diabetes, and transport choice were also significantly related to delay time interval. These results show that gender differences occur in AMI symptom experience. However, how symptoms relate to the gender gap in delay time interval is not clear. These findings suggest that health care professionals need to tailor information about possible symptoms of AMI to the patient's gender, age, and medical history.

PMID 9672451  Am J Emerg Med. 1998 Jul;16(4):363-6.
著者: Harshida Patel, Annika Rosengren, Inger Ekman
雑誌名: Am Heart J. 2004 Jul;148(1):27-33. doi: 10.1016/j.ahj.2004.03.005.
Abstract/Text BACKGROUND: Coronary heart disease is a major problem in both men and women, but several studies have shown sex differences in symptoms of acute coronary syndromes (ACS). Some findings, however, have been disparate and inadequate, and thus a comprehensive overview of this literature would be of value.
METHOD: Fifteen studies that identified symptoms of ACS for both women and men were examined through a review of the literature from 1989 to 2002. Terms used for the search included "myocardial infarction," "symptoms," "gender differences," and "acute coronary syndromes."
RESULTS: Although chest pain was the most common symptom in both men and women, several differences were also noted. In all types of ACS, women had significantly more back and jaw pain, nausea and/or vomiting, dyspnea, indigestion, and palpitations. In a number of studies, which solely sampled patients with acute myocardial infarction, women demonstrated more back, jaw, and neck pain and nausea and/or vomiting, dyspnea, palpitations, indigestion, dizziness, fatigue, loss of appetite, and syncope. Men reported more chest pain and diaphoresis in the myocardial infarction sample. The designs and methodologies of the studies varied considerably.
CONCLUSION: In addition to the typical symptom of chest pain in ACS, women experience other atypical symptoms more frequently than men. Thus, there may be sex differences in the symptoms of ACS, differences that have a bearing not only on clinical practice, but also on the interpretation of available clinical studies and the design of future investigations.

PMID 15215788  Am Heart J. 2004 Jul;148(1):27-33. doi: 10.1016/j.ahj.2・・・
著者: Masami Kosuge, Kazuo Kimura, Toshiyuki Ishikawa, Toshiaki Ebina, Kiyoshi Hibi, Kengo Tsukahara, Masahiko Kanna, Noriaki Iwahashi, Jyun Okuda, Naoki Nozawa, Hiroyuki Ozaki, Hideto Yano, Tatsuya Nakati, Ikuyoshi Kusama, Satoshi Umemura
雑誌名: Circ J. 2006 Mar;70(3):222-6.
Abstract/Text BACKGROUND: Many studies have examined sex-related differences in the clinical features of acute myocardial infarction (AMI). However, prospective studies are scant, and sex-related differences in symptoms of AMI remain unclear. We examined differences between men and women in terms of the clinical features of ST-segment elevation AMI.
METHODS AND RESULTS: We studied 457 patients (106 women and 351 men) with ST-segment elevation AMI who were admitted within 24 h after symptom onset. The same cardiologist interviewed all patients within 48 h after admission. Women were older than men (72 vs 62 years, p<0.001) and had higher rates of hypertension (70 vs 56%, p=0.010), diabetes mellitus (36 vs 26%, p=0.047), and hyperlipidemia (51 vs 38%, p=0.019). Women were more likely than men to have non-specific symptoms (45 vs 34%, p=0.033), non-chest pain (pain in the jaw, throat, neck, shoulder, arm, hand, and back), mild pain (20 vs 7%, p<0.001), and nausea (49 vs 36%, p=0.013). On coronary angiography, the severity of coronary-artery lesions was similar in both sexes. In-hospital mortality was significantly higher in women than in men (6.6 vs 1.4%, p=0.003).
CONCLUSIONS: Clinical profiles and presentations differ between women and men with AMI. Women have less typical symptoms of AMI than men.

PMID 16501283  Circ J. 2006 Mar;70(3):222-6.
著者: P B Berger, T J Ryan
雑誌名: Circulation. 1990 Feb;81(2):401-11.
Abstract/Text
PMID 2404629  Circulation. 1990 Feb;81(2):401-11.
著者: H J Wellens
雑誌名: N Engl J Med. 1999 Feb 4;340(5):381-3. doi: 10.1056/NEJM199902043400510.
Abstract/Text
PMID 9929531  N Engl J Med. 1999 Feb 4;340(5):381-3. doi: 10.1056/NEJ・・・
著者: S H Braat, P Brugada, C de Zwaan, J M Coenegracht, H J Wellens
雑誌名: Br Heart J. 1983 Apr;49(4):368-72.
Abstract/Text To study the value of the electrocardiogram in diagnosing right ventricular involvement in acute inferior wall myocardial infarction, the electrocardiographic findings were analysed in 67 patients who had had scintigraphy to pin-point the infarct. All 67 patients were consecutively admitted because of an acute inferior wall infarction. A 12 lead electrocardiogram with four additional right precordial leads (V3R, V4R, V5R, and V6R) was routinely recorded on admission and every eight hours thereafter for three consecutive days. Thirty-six to 72 hours after the onset of chest pain a 99mtechnetium pyrophosphate scintigraphy and a dynamic flow study were performed to detect right ventricular involvement, which was found in 29 of the 67 patients (43%). ST segment elevation greater than or equal to 1 mm in leads V3R, V4R, V5R, and V6R is a reliable sign of right ventricular involvement. ST segment elevation greater than or equal to 1 mm in lead V4R was found to have the greatest sensitivity (93%) and predictive accuracy (93%). The diagnostic value of a QS pattern in lead V3R and V4R or ST elevation greater than or equal to 1 mm in lead V1 was much lower. ST segment elevation in the right precordial leads was short lived, having disappeared within 10 hours after the onset of chest pain in half of our patients with right ventricular involvement. When electrocardiograms are recorded in patients with an acute inferior wall infarction within 10 hours after the onset of chest pain, additional right ventricular infarction can easily be diagnosed by recording lead V4R.

PMID 6299315  Br Heart J. 1983 Apr;49(4):368-72.
著者:
雑誌名: Lancet. 1994 Feb 5;343(8893):311-22.
Abstract/Text Large randomised trials have demonstrated that fibrinolytic therapy can reduce mortality in patients with suspected acute myocardial infarction (AMI). The indications for, and contraindications to, this treatment in some categories of patient are disputed, examples being late presentation, elderly patients, and those in cardiogenic shock. This overview aims to help resolve some of the remaining uncertainties. From all trials of fibrinolytic therapy versus control that randomised more than 1000 patients with suspected AMI, information was sought and checked on deaths during the first 5 weeks and on major adverse events occurring during hospitalisation. The nine trials included 58,600 patients, among whom 6177 (10.5%) deaths, 564 (1.0%) strokes, and 436 (0.7%) major non-cerebral bleeds were reported. Fibrinolytic therapy was associated with an excess of deaths during days 0-1 (especially among patients presenting more than 12 h after symptom onset, and in the elderly) but this was outweighed by a much larger benefit during days 2-35. This "early hazard" should not obscure the very clear overall survival advantage that is produced by fibrinolytic therapy. Benefit was observed among patients presenting with ST elevation or bundle-branch block (BBB)--irrespective of age, sex, blood pressure, heart rate, or previous history of myocardial infarction or diabetes--and was greater the earlier treatment began. Among the 45,000 patients presenting with ST elevation or BBB the relation between benefit and delay from symptom onset indicated highly significant absolute mortality reductions of about 30 per 1000 for those presenting within 0-6 h and of about 20 per 1000 for those presenting 7-12 h from onset, and a statistically uncertain benefit of about 10 per 1000 for those presenting at 13-18 h (with more randomised evidence needed in this latter group to assess reliably the net effects of treatment). Fibrinolytic therapy was associated with about 4 extra strokes per 1000 during days 0-1: of these, 2 were associated with early death and so were already accounted for in the overall mortality reduction, 1 was moderately or severely disabling, and 1 was not. This overview indicates that fibrinolytic therapy is beneficial in a much wider range of patients than is currently given such treatment routinely.

PMID 7905143  Lancet. 1994 Feb 5;343(8893):311-22.
著者:
雑誌名: Circulation. 1994 Apr;89(4):1545-56.
Abstract/Text BACKGROUND: Although coronary thrombosis plays a critical role in the pathogenesis of unstable angina and non-Q-wave myocardial infarction (NQMI), the effects of thrombolytic therapy in these disorders is not clear. Also, the role of routine early coronary arteriography followed by revascularization has not been established.
METHODS AND RESULTS: Patients (n = 1473) seen within 24 hours of ischemic chest discomfort at rest, considered to represent unstable angina or NQMI, were randomized using a 2 x 2 factorial design to compare (1) TPA versus placebo as initial therapy and (2) an early invasive strategy (early coronary arteriography followed by revascularization when the anatomy was suitable) versus an early conservative strategy (coronary arteriography followed by revascularization if initial medical therapy failed). All patients were treated with bed rest, anti-ischemic medications, aspirin, and heparin. The primary end point for the TPA-placebo comparison (death, myocardial infarction, or failure of initial therapy at 6 weeks) occurred in 54.2% of the TPA-treated patients and 55.5% of the placebo-treated patients (P = NS). Fatal and nonfatal myocardial infarction after randomization (reinfarction in NQMI patients) occurred more frequently in TPA-treated patients (7.4%) than in placebo-treated patients (4.9%, P = .04, Kaplan-Meier estimate). Four intracranial hemorrhages occurred in the TPA-treated group versus none in the placebo-treated group (P = .06). The end point for the comparison of the two strategies (death, myocardial infarction, or an unsatisfactory symptom-limited exercise stress test at 6 weeks) occurred in 18.1% of patients assigned to the early conservative strategy and 16.2% of patients assigned to the early invasive strategy (P = NS). In the latter, the average length of initial hospitalization, incidence of rehospitalization within 6 weeks, and days of rehospitalization all were significantly lower.
CONCLUSIONS: In the overall trial, patients with unstable angina and NQMI were managed with low rates of mortality (2.4%) and myocardial infarction or reinfarction (6.3%) at the time of the 6-week visit. These results can be achieved using either an early conservative or early invasive strategy, the latter resulting in a reduced incidence of days of hospitalization and of rehospitalization and in the use of antianginal drugs. The addition of a thrombolytic agent is not beneficial and may be harmful.

PMID 8149520  Circulation. 1994 Apr;89(4):1545-56.
著者: S Matetzky, D Freimark, M S Feinberg, I Novikov, S Rath, B Rabinowitz, E Kaplinsky, H Hod
雑誌名: J Am Coll Cardiol. 1999 Sep;34(3):748-53.
Abstract/Text OBJECTIVES: This study was done to determine whether electrocardiographic (ECG) isolated ST-segment elevation (ST) in posterior chest leads can establish the diagnosis of acute posterior infarction in patients with ischemic chest pain and to describe the clinical and echocardiographic characteristics of these patients.
BACKGROUND: The absence of ST on the standard 12-lead ECG in many patients with acute posterior infarction hampers the early diagnosis of these infarcts and thus may result in inadequate triage and treatment. Although 4% of all acute myocardial infarction (AMI) patients reveal the presence of isolated ST in posterior chest leads, the significance of this finding has not yet been determined.
METHODS: We studied 33 consecutive patients with ischemic chest pain suggestive of AMI without ST in the standard ECG who had isolated ST in posterior chest leads V7 through V9. All patients had echocardiographic imaging within 48 h of admission, and 20 patients underwent coronary angiography.
RESULTS: Acute myocardial infarction was confirmed enzymatically in all patients and on discharge ECG pathologic Q-waves appeared in leads V7 through V9 in 75% of the patients. On echocardiography, posterior wall-motion abnormality was visible in 97% of the patients, and 69% had evidence of mitral regurgitation (MR), which was moderate or severe in one-third of the patients. Four patients (12%), all with significant MR, had heart failure, and one died from free-wall rupture. The circumflex coronary artery was the infarct related artery in all catheterized patients.
CONCLUSIONS: Isolated ST in leads V7 through V9 identify patients with acute posterior wall myocardial infarction. Early identification of those patients is important for adequate triage and treatment of patients with ischemic chest pain without ST on standard 12-lead ECG.

PMID 10483956  J Am Coll Cardiol. 1999 Sep;34(3):748-53.
著者: J B Agarwal, K Khaw, F Aurignac, A LoCurto
雑誌名: Am J Cardiol. 1999 Feb 1;83(3):323-6.
Abstract/Text Criteria for reperfusion therapy in acute myocardial infarction require the presence of ST elevation in 2 contiguous leads. However, many patients with myocardial infarction do not show these changes on a routine 12-lead electrocardiogram and hence are denied reperfusion therapy. Posterior chest leads (V7 to V9) were recorded in 58 patients with clinically suspected myocardial infarction, but nondiagnostic routine electrocardiogram. ST elevation >0.1 mV or Q waves in > or =2 posterior chest leads were considered to be diagnostic of posterior myocardial infarction. Eighteen patients had these changes of posterior myocardial infarction. All 18 patients were confirmed to have myocardial infarction by creatine phosphokinase criteria or cardiac catheterization. Of the 17 patients who had cardiac catheterization, 16 had left circumflex as the culprit vessel. We conclude that posterior chest leads should be routinely recorded in patients with suspected myocardial infarction and nondiagnostic, routine electrocardiogram. This simple bedside technique may help proper treatment of some of these patients now classified as having unstable angina or non-Q-wave myocardial infarction.

PMID 10072216  Am J Cardiol. 1999 Feb 1;83(3):323-6.
著者: Kristian Thygesen, Joseph S Alpert, Harvey D White, Joint ESC/ACCF/AHA/WHF Task Force for the Redefinition of Myocardial Infarction
雑誌名: Eur Heart J. 2007 Oct;28(20):2525-38. doi: 10.1093/eurheartj/ehm355.
Abstract/Text
PMID 17951287  Eur Heart J. 2007 Oct;28(20):2525-38. doi: 10.1093/eurh・・・
著者: Tobias Reichlin, Willibald Hochholzer, Stefano Bassetti, Stephan Steuer, Claudia Stelzig, Sabine Hartwiger, Stefan Biedert, Nora Schaub, Christine Buerge, Mihael Potocki, Markus Noveanu, Tobias Breidthardt, Raphael Twerenbold, Katrin Winkler, Roland Bingisser, Christian Mueller
雑誌名: N Engl J Med. 2009 Aug 27;361(9):858-67. doi: 10.1056/NEJMoa0900428.
Abstract/Text BACKGROUND: The rapid and reliable diagnosis of acute myocardial infarction is a major unmet clinical need.
METHODS: We conducted a multicenter study to examine the diagnostic accuracy of new, sensitive cardiac troponin assays performed on blood samples obtained in the emergency department from 718 consecutive patients who presented with symptoms suggestive of acute myocardial infarction. Cardiac troponin levels were determined in a blinded fashion with the use of four sensitive assays (Abbott-Architect Troponin I, Roche High-Sensitive Troponin T, Roche Troponin I, and Siemens Troponin I Ultra) and a standard assay (Roche Troponin T). The final diagnosis was adjudicated by two independent cardiologists.
RESULTS: Acute myocardial infarction was the adjudicated final diagnosis in 123 patients (17%). The diagnostic accuracy of measurements obtained at presentation, as quantified by the area under the receiver-operating-characteristic curve (AUC), was significantly higher with the four sensitive cardiac troponin assays than with the standard assay (AUC for Abbott-Architect Troponin I, 0.96; 95% confidence interval [CI], 0.94 to 0.98; for Roche High-Sensitive Troponin T, 0.96; 95% CI, 0.94 to 0.98; for Roche Troponin I, 0.95; 95% CI, 0.92 to 0.97; and for Siemens Troponin I Ultra, 0.96; 95% CI, 0.94 to 0.98; vs. AUC for the standard assay, 0.90; 95% CI, 0.86 to 0.94). Among patients who presented within 3 hours after the onset of chest pain, the AUCs were 0.93 (95% CI, 0.88 to 0.99), 0.92 (95% CI, 0.87 to 0.97), 0.92 (95% CI, 0.86 to 0.99), and 0.94 (95% CI, 0.90 to 0.98) for the sensitive assays, respectively, and 0.76 (95% CI, 0.64 to 0.88) for the standard assay. We did not assess the effect of the sensitive troponin assays on clinical management.
CONCLUSIONS: The diagnostic performance of sensitive cardiac troponin assays is excellent, and these assays can substantially improve the early diagnosis of acute myocardial infarction, particularly in patients with a recent onset of chest pain. (ClinicalTrials.gov number, NCT00470587.)

2009 Massachusetts Medical Society
PMID 19710484  N Engl J Med. 2009 Aug 27;361(9):858-67. doi: 10.1056/N・・・
著者: Till Keller, Tanja Zeller, Dirk Peetz, Stergios Tzikas, Alexander Roth, Ewa Czyz, Christoph Bickel, Stephan Baldus, Ascan Warnholtz, Meike Fröhlich, Christoph R Sinning, Medea S Eleftheriadis, Philipp S Wild, Renate B Schnabel, Edith Lubos, Nicole Jachmann, Sabine Genth-Zotz, Felix Post, Viviane Nicaud, Laurence Tiret, Karl J Lackner, Thomas F Münzel, Stefan Blankenberg
雑誌名: N Engl J Med. 2009 Aug 27;361(9):868-77. doi: 10.1056/NEJMoa0903515.
Abstract/Text BACKGROUND: Cardiac troponin testing is central to the diagnosis of acute myocardial infarction. We evaluated a sensitive troponin I assay for the early diagnosis and risk stratification of myocardial infarction.
METHODS: In a multicenter study, we determined levels of troponin I as assessed by a sensitive assay, troponin T, and traditional myocardial necrosis markers in 1818 consecutive patients with suspected acute myocardial infarction, on admission and 3 hours and 6 hours after admission.
RESULTS: For samples obtained on admission, the diagnostic accuracy was highest with the sensitive troponin I assay (area under the receiver-operating-characteristic curve [AUC], 0.96), as compared with the troponin T assay (AUC, 0.85) and traditional myocardial necrosis markers. With the use of the sensitive troponin I assay (cutoff value, 0.04 ng per milliliter) on admission, the clinical sensitivity was 90.7%, and the specificity was 90.2%. The diagnostic accuracy was virtually identical in baseline and serial samples, regardless of the time of chest-pain onset. In patients presenting within 3 hours after chest-pain onset, a single sensitive troponin I assay had a negative predictive value of 84.1% and a positive predictive value of 86.7%; these findings predicted a 30% rise in the troponin I level within 6 hours. A troponin I level of more than 0.04 ng per milliliter was independently associated with an increased risk of an adverse outcome at 30 days (hazard ratio, 1.96; 95% confidence interval, 1.27 to 3.05; P=0.003).
CONCLUSIONS: The use of a sensitive assay for troponin I improves early diagnosis of acute myocardial infarction and risk stratification, regardless of the time of chest-pain onset.

2009 Massachusetts Medical Society
PMID 19710485  N Engl J Med. 2009 Aug 27;361(9):868-77. doi: 10.1056/N・・・
著者:
雑誌名: Lancet. 1988 Aug 13;2(8607):349-60.
Abstract/Text 17,187 patients entering 417 hospitals up to 24 hours (median 5 hours) after the onset of suspected acute myocardial infarction were randomised, with placebo control, between: (i) a 1-hour intravenous infusion of 1.5 MU of streptokinase; (ii) one month of 160 mg/day enteric-coated aspirin; (iii) both active treatments; or (iv) neither. Streptokinase alone and aspirin alone each produced a highly significant reduction in 5-week vascular mortality: 791/8592 (9.2%) among patients allocated streptokinase infusion vs 1029/8595 (12.0%) among those allocated placebo infusion (odds reduction: 25% SD 4; 2p less than 0.00001); 804/8587 (9.4%) vascular deaths among patients allocated aspirin tablets vs 1016/8600 (11.8%) among those allocated placebo tablets (odds reduction: 23% SD 4; 2p less than 0.00001). The combination of streptokinase and aspirin was significantly (2p less than 0.0001) better than either agent alone. Their separate effects on vascular deaths appeared to be additive: 343/4292 (8.0%) among patients allocated both active agents vs 568/4300 (13.2%) among those allocated neither (odds reduction: 42% SD 5; 95% confidence limits 34-50%). There was evidence of benefit from each agent even for patients treated late after pain onset (odds reductions at 0-4, 5-12, and 13-24 hours: 35% SD 6, 16% SD 7, and 21% SD 12 for streptokinase alone; 25% SD 7, 21% SD 7, and 21% SD 12 for aspirin alone; and 53% SD 8, 32% SD 9, and 38% SD 15 for the combination of streptokinase and aspirin). Streptokinase was associated with an excess of bleeds requiring transfusion (0.5% vs 0.2%) and of confirmed cerebral haemorrhage (0.1% vs 0.0%), but with fewer other strokes (0.6% vs 0.8%). These "other" strokes may have included a few undiagnosed cerebral haemorrhages, but still there was no increase in total strokes (0.7% streptokinase vs 0.8% placebo infusion). Aspirin significantly reduced non-fatal reinfarction (1.0% vs 2.0%) and non-fatal stroke (0.3% vs 0.6%), and was not associated with any significant increase in cerebral haemorrhage or in bleeds requiring transfusion. An excess of non-fatal reinfarction was reported when streptokinase was used alone, but this appeared to be entirely avoided by the addition of aspirin. Those allocated the combination of streptokinase and aspirin had significantly fewer reinfarctions (1.8% vs 2.9%), strokes (0.6% vs 1.1%), and deaths (8.0% vs 13.2%) than those allocated neither. The differences in vascular and in all-cause mortality produced by streptokinase and by aspirin remain highly significant (2p less than 0.001 for each) after the median of 15 months of follow-up thus far available.

PMID 2899772  Lancet. 1988 Aug 13;2(8607):349-60.
著者:
雑誌名: J Am Coll Cardiol. 1988 Dec;12(6 Suppl A):3A-13A.
Abstract/Text 17,187 patients entering 417 hospitals up to 24 h (median 5 h) after the onset of suspected acute myocardial infarction were randomized, with placebo control, between i) a 1 h intravenous infusion of 1.5 million units of streptokinase; ii) 1 month of 160 mg/day enteric-coated aspirin; iii) both active treatments; or iv) neither. Streptokinase alone and aspirin alone each produced a highly significant reduction in 5 week vascular mortality: 791/8592 (9.2%) vascular deaths among patients allocated streptokinase infusion versus 1029/8595 (12.0%) among those allocated placebo infusion (odds reduction: 25% +/- 4; 2p less than 0.00001); 804/8587 (9.4%) vascular deaths among patients allocated aspirin tablets versus 1016/8600 (11.8%) among those allocated placebo tablets (odds reduction: 23% +/- 4; 2p less than 0.00001). The combination of streptokinase and aspirin was significantly (2p less than 0.0001) better than either agent alone. Their separate effects on vascular death appeared to be additive: 343/4292 (8.0%) among patients allocated both active agents versus 568/4300 (13.2%) among those allocated neither (odds reduction: 42% +/- 5; 95% confidence limits 34% to 50%). There was evidence of benefit rom each agent even for patients treated late after pain onset (odds reduction at 0-4, 5-12, and 13-24 h: 35% +/- 6, 16% +/- 7 and 21% +/- 12 for streptokinase alone; 25% +/- 7,21% +/- 7 and 21% +/- 12 for aspirin alone; and 53% +/- 8,32% +/- 9 and 38% +/- 15 for the combination of streptokinase and aspirin). Streptokinase was associated with an excess of bleeds requiring transfusion (0.5% versus 0.2%) and of confirmed cerebral hemorrhage (0.1% versus 0.0%), but with fewer other strokes (0.6% versus 0.8%). These "other" strokes may have included a few undiagnosed cerebral hemorrhages, but still there was no increase in total strokes (0.7% streptokinase versus 0.8% placebo infusion). Aspirin significantly reduced nonfatal reinfarction (1.0% versus 2.0%) and nonfatal stroke (0.3% versus 0.6%), and was not associated with any significant increase in cerebral hemorrhage or in bleeds requiring transfusion. An excess of nonfatal reinfarction was reported when streptokinase was used alone, but this appeared to be entirely avoided by the addition of aspirin. Those allocated the combination of streptokinase and aspirin had significantly fewer reinfarctions (1.8% versus 2.9%), strokes (0.6% versus 1.1%), and deaths (8.0% versus 13.2%) than those allocated neither.(ABSTRACT TRUNCATED AT 250 WORDS)

PMID 2903874  J Am Coll Cardiol. 1988 Dec;12(6 Suppl A):3A-13A.
著者: H Yasue, H Ogawa, H Tanaka, S Miyazaki, R Hattori, M Saito, K Ishikawa, Y Masuda, T Yamaguchi, T Motomiya, Y Tamura
雑誌名: Am J Cardiol. 1999 May 1;83(9):1308-13.
Abstract/Text Aspirin therapy confers conclusive net benefits in the acute phase of evolving myocardial infarction, but no clear evidence of benefit from the long-term use of aspirin after acute myocardial infarction (AMI) has been shown in any single study. This multicenter study, the Japanese Antiplatelets Myocardial Infarction Study, was performed to find out whether aspirin or trapidil would improve clinical outcome compared with no antiplatelets in postinfarction patients. The study was a multicenter, open-label, randomized controlled trial of aspirin 81 mg/day, trapidil 300 mg/day, and no antiplatelets in patients with AMI admitted within 1 month from the onset of symptoms. Seven hundred twenty-three patients were enrolled at 70 hospitals in 18 prefectures of Japan; 250 were randomly assigned to treatment with 81 mg aspirin (aspirin group), 243 to that with trapidil (trapidil group), and 230 were not given antiplatelet agents. The mean follow-up period was 475 days. This study demonstrated that long-term use of aspirin at the dose of 81 mg/day reduced the incidence of recurrent AMI compared with the group receiving no antiplatelets after AMI (p = 0.0045) and that trapidil also reduced the occurrence of reinfarction compared with the group receiving no antiplatelets, but the difference was not significant (p = 0.0810). The incidence of cardiovascular events including cardiovascular death, reinfarction, uncontrolled unstable angina requiring admission to hospital, and nonfatal ischemic stroke was reduced in the group receiving 300 mg trapidil daily compared with the group receiving no antiplatelets (p = 0.0039). The use of aspirin 81 mg/day provided almost no benefit over no antiplatelets therapy in the incidence of cardiovascular events. In conclusion, low-dose aspirin (81 mg) effectively prevented recurrent AMI in postinfarction patients after thrombolysis or coronary angioplasty when used over a long term. Furthermore, the long-term use of trapidil resulted in a significant reduction in the incidence of cardiovascular events.

PMID 10235086  Am J Cardiol. 1999 May 1;83(9):1308-13.
著者: G G Schwartz, A G Olsson, M D Ezekowitz, P Ganz, M F Oliver, D Waters, A Zeiher, B R Chaitman, S Leslie, T Stern, Myocardial Ischemia Reduction with Aggressive Cholesterol Lowering (MIRACL) Study Investigators
雑誌名: JAMA. 2001 Apr 4;285(13):1711-8.
Abstract/Text CONTEXT: Patients experience the highest rate of death and recurrent ischemic events during the early period after an acute coronary syndrome, but it is not known whether early initiation of treatment with a statin can reduce the occurrence of these early events.
OBJECTIVE: To determine whether treatment with atorvastatin, 80 mg/d, initiated 24 to 96 hours after an acute coronary syndrome, reduces death and nonfatal ischemic events.
DESIGN AND SETTING: A randomized, double-blind trial conducted from May 1997 to September 1999, with follow-up through 16 weeks at 122 clinical centers in Europe, North America, South Africa, and Australasia.
PATIENTS: A total of 3086 adults aged 18 years or older with unstable angina or non-Q-wave acute myocardial infarction.
INTERVENTIONS: Patients were stratified by center and randomly assigned to receive treatment with atorvastatin (80 mg/d) or matching placebo between 24 and 96 hours after hospital admission.
MAIN OUTCOME MEASURES: Primary end point event defined as death, nonfatal acute myocardial infarction, cardiac arrest with resuscitation, or recurrent symptomatic myocardial ischemia with objective evidence and requiring emergency rehospitalization.
RESULTS: A primary end point event occurred in 228 patients (14.8%) in the atorvastatin group and 269 patients (17.4%) in the placebo group (relative risk [RR], 0.84; 95% confidence interval [CI], 0.70-1.00; P =.048). There were no significant differences in risk of death, nonfatal myocardial infarction, or cardiac arrest between the atorvastatin group and the placebo group, although the atorvastatin group had a lower risk of symptomatic ischemia with objective evidence and requiring emergency rehospitalization (6.2% vs 8.4%; RR, 0.74; 95% CI, 0.57-0.95; P =.02). Likewise, there were no significant differences between the atorvastatin group and the placebo group in the incidence of secondary outcomes of coronary revascularization procedures, worsening heart failure, or worsening angina, although there were fewer strokes in the atorvastatin group than in the placebo group (12 vs 24 events; P =.045). In the atorvastatin group, mean low-density lipoprotein cholesterol level declined from 124 mg/dL (3.2 mmol/L) to 72 mg/dL (1.9 mmol/L). Abnormal liver transaminases (>3 times upper limit of normal) were more common in the atorvastatin group than in the placebo group (2.5% vs 0.6%; P<.001).
CONCLUSION: For patients with acute coronary syndrome, lipid-lowering therapy with atorvastatin, 80 mg/d, reduces recurrent ischemic events in the first 16 weeks, mostly recurrent symptomatic ischemia requiring rehospitalization.

PMID 11277825  JAMA. 2001 Apr 4;285(13):1711-8.
著者: Christopher P Cannon, Eugene Braunwald, Carolyn H McCabe, Daniel J Rader, Jean L Rouleau, Rene Belder, Steven V Joyal, Karen A Hill, Marc A Pfeffer, Allan M Skene, Pravastatin or Atorvastatin Evaluation and Infection Therapy-Thrombolysis in Myocardial Infarction 22 Investigators
雑誌名: N Engl J Med. 2004 Apr 8;350(15):1495-504. doi: 10.1056/NEJMoa040583. Epub 2004 Mar 8.
Abstract/Text BACKGROUND: Lipid-lowering therapy with statins reduces the risk of cardiovascular events, but the optimal level of low-density lipoprotein (LDL) cholesterol is unclear.
METHODS: We enrolled 4162 patients who had been hospitalized for an acute coronary syndrome within the preceding 10 days and compared 40 mg of pravastatin daily (standard therapy) with 80 mg of atorvastatin daily (intensive therapy). The primary end point was a composite of death from any cause, myocardial infarction, documented unstable angina requiring rehospitalization, revascularization (performed at least 30 days after randomization), and stroke. The study was designed to establish the noninferiority of pravastatin as compared with atorvastatin with respect to the time to an end-point event. Follow-up lasted 18 to 36 months (mean, 24).
RESULTS: The median LDL cholesterol level achieved during treatment was 95 mg per deciliter (2.46 mmol per liter) in the standard-dose pravastatin group and 62 mg per deciliter (1.60 mmol per liter) in the high-dose atorvastatin group (P<0.001). Kaplan-Meier estimates of the rates of the primary end point at two years were 26.3 percent in the pravastatin group and 22.4 percent in the atorvastatin group, reflecting a 16 percent reduction in the hazard ratio in favor of atorvastatin (P=0.005; 95 percent confidence interval, 5 to 26 percent). The study did not meet the prespecified criterion for equivalence but did identify the superiority of the more intensive regimen.
CONCLUSIONS: Among patients who have recently had an acute coronary syndrome, an intensive lipid-lowering statin regimen provides greater protection against death or major cardiovascular events than does a standard regimen. These findings indicate that such patients benefit from early and continued lowering of LDL cholesterol to levels substantially below current target levels.

Copyright 2004 Massachusetts Medical Society
PMID 15007110  N Engl J Med. 2004 Apr 8;350(15):1495-504. doi: 10.1056・・・
著者: Tomohiro Sakamoto, Sunao Kojima, Hisao Ogawa, Hideki Shimomura, Kazuo Kimura, Yasuhiro Ogata, Naritsugu Sakaino, Akira Kitagawa, Multicenter Study for Aggressive Lipid-Lowering Strategy by HMG-CoA Reductase Inhibitors in Patients With Acute Myocardial Infarction Investigators
雑誌名: Am J Cardiol. 2006 Apr 15;97(8):1165-71. doi: 10.1016/j.amjcard.2005.11.031. Epub 2006 Mar 10.
Abstract/Text Statins have been shown to prevent coronary artery disease and to preserve left ventricular function in dilated cardiomyopathy. We hypothesized that early use of statins would decrease cardiovascular events, including heart failure in patients with acute myocardial infarction (AMI). To examine the effect of statins in Japanese patients with AMI, a prospective, randomized, open-label trial was conducted in 486 patients with normal total cholesterol levels. Patients were randomly assigned to receive any available statin (n = 241) within 96 hours of AMI onset or no statin (n = 245) and were followed for up to 24 months. The primary end point was a composite of cardiovascular death, nonfatal AMI, recurrent symptomatic myocardial ischemia, congestive heart failure, and stroke. Event rate for the primary end point was lower in the statin group than in the nonstatin group (6.1% vs 11.4%, p = 0.0433). The statin group had a lower risk of congestive heart failure and symptomatic myocardial ischemia (p = 0.0154 and 0.0264, respectively). In conclusion, early lipid-lowering therapy with statins decreases recurrent cardiovascular events, in particular, congestive heart failure.

PMID 16616020  Am J Cardiol. 2006 Apr 15;97(8):1165-71. doi: 10.1016/j・・・
著者: Shinya Okazaki, Takayuki Yokoyama, Katsumi Miyauchi, Kazunori Shimada, Takeshi Kurata, Hitoshi Sato, Hiroyuki Daida
雑誌名: Circulation. 2004 Aug 31;110(9):1061-8. doi: 10.1161/01.CIR.0000140261.58966.A4. Epub 2004 Aug 23.
Abstract/Text BACKGROUND: Recent clinical trials have demonstrated that aggressive lipid lowering by statins could prevent recurrent events after acute coronary syndrome (ACS). We hypothesized that this efficacy was caused by a significant reduction in plaque volume by aggressive LDL cholesterol (LCL-C) lowering. The present study investigated the effect of early statin treatment on plaque volume of a nonculprit lesion by serial volumetric intravascular ultrasound in patients with ACS.
METHODS AND RESULTS: Seventy patients with ACS were enrolled. All patients underwent emergency coronary angiography and percutaneous coronary intervention (PCI). They were randomized to intensive lipid-lowering therapy (n=35; atorvastatin 20 mg/d) or control (n=35) groups after PCI. Volumetric intravascular ultrasound analyses were performed at baseline and 6-month follow-up for a non-PCI site in 48 patients (atorvastatin, n=24; control, n=24). LDL-C level was significantly decreased by 41.7% in the atorvastatin group compared with the control group, in which LDL-C was increased by 0.7% (P<0.0001). Plaque volume was significantly reduced in the atorvastatin group (13.1+/-12.8% decrease) compared with the control group (8.7+/-14.9% increase; P<0.0001). Percent change in plaque volume showed a significant positive correlation with follow-up LDL-C level (R=0.456, P=0.0011) and percent LDL-C reduction (R=0.612, P<0.0001), even in patients with baseline LDL-C <125 mg/dL.
CONCLUSIONS: Early aggressive lipid-lowering therapy by atorvastatin for 6 months significantly reduced the plaque volume in patients with ACS. Percent change in plaque volume showed a significant positive correlation with percent LDL-C reduction, even in patients with low baseline LDL-C.

PMID 15326073  Circulation. 2004 Aug 31;110(9):1061-8. doi: 10.1161/01・・・
著者: Takafumi Hiro, Takeshi Kimura, Takeshi Morimoto, Katsumi Miyauchi, Yoshihisa Nakagawa, Masakazu Yamagishi, Yukio Ozaki, Kazuo Kimura, Satoshi Saito, Tetsu Yamaguchi, Hiroyuki Daida, Masunori Matsuzaki, JAPAN-ACS Investigators
雑誌名: J Am Coll Cardiol. 2009 Jul 21;54(4):293-302. doi: 10.1016/j.jacc.2009.04.033.
Abstract/Text OBJECTIVES: The objective of this study was to evaluate whether the regressive effects of aggressive lipid-lowering therapy with atorvastatin on coronary plaque volume (PV) in patients with acute coronary syndrome (ACS) are generalized for other statins in multicenter setting.
BACKGROUND: A previous single-center study reported beneficial regressive effects of atorvastatin in patients with ACS on PV of the nonculprit site by intravascular ultrasound (IVUS) evaluation. The effect of statins other than atorvastatin on PV has not been evaluated in the setting of ACS.
METHODS: The JAPAN-ACS (Japan Assessment of Pitavastatin and Atorvastatin in Acute Coronary Syndrome) study was a prospective, randomized, open-label, parallel group study with blind end point evaluation conducted at 33 centers in Japan. A total of 307 patients with ACS undergoing IVUS-guided percutaneous coronary intervention were randomized, and 252 patients had evaluable IVUS examinations at baseline and 8 to 12 months' follow-up. Patients were randomly assigned to receive either 4 mg/day of pitavastatin or 20 mg/day of atorvastatin. The primary end point was the percentage change in nonculprit coronary PV.
RESULTS: The mean percentage change in PV was -16.9 +/- 13.9% and -18.1 +/- 14.2% (p = 0.5) in the pitavastatin and atorvastatin groups, respectively, which was associated with negative vessel remodeling. The upper limit of 95% confidence interval of the mean difference in percentage change in PV between the 2 groups (1.11%, 95% confidence interval: -2.27 to 4.48) did not exceed the pre-defined noninferiority margin of 5%.
CONCLUSIONS: The administration of pitavastatin or atorvastatin in patients with ACS equivalently resulted in significant regression of coronary PV (Japan Assessment of Pitavastatin and Atorvastatin in Acute Coronary Syndrome; NCT00242944).

PMID 19608026  J Am Coll Cardiol. 2009 Jul 21;54(4):293-302. doi: 10.1・・・

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