急性心筋梗塞(AMI)に伴う合併症のうち,心室中隔穿孔(VSP)はまれであるが高い致死率の疾患である.今回我々は,内科治療の継続中にVSPの自然閉鎖が確認されたAMIの1症例を経験したので報告する.
症例は76歳女性.平成12年7月15日に前壁中隔心筋梗塞を発症.左前下行枝seg7の亜完全閉塞であり,冠動脈内ステントを用いた血行再建術により再灌流に成功した.第11病日に胸骨左縁第4肋間を中心としたLevine III/IVの収縮期心雑音が出現し,経胸壁心エコーにてVSPが認められた.左室造影所見では心室中隔を介しoozing様に右室内への造影剤の漏出を認め,サンプリングによるシャント率は35.8%であった.胸部X線では肺うっ血を呈していたが血行動態はForresterI群であり,内科治療を継続した.心不全は内服加療にてコントロール可能であり,その後の心エコーにてもシャント率の増悪は認めなかった.慢性期に手術を予定していたが,精神疾患の既往があり,家族も内科治療の継続を強く希望したため,手術は行わず第48病日に退院となった.平成13年4月にステント確認造影目的にて再入院となったが,心雑音は消失し,心エコー・左室造影にてもVSPは認められなかった.
本症例は精神疾患の既往等を考慮し内科治療の継続を選択したが,従来の報告では内科治療を選択したVSPの長期予後は不良なことが多い.本症例におけるVSPの自然閉鎖のメカニズムは不明であるが,我々が検索した限りでは同様の報告はいまだなく,貴重な症例と考えられた.

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Although thinning of the ventricular wall due to infarct expansion (septal aneurysm) may contribute to ventricular septal rupture (VSR), spatial factors predisposing to this mechanical complication have not been fully demonstrated. To identify the morphologic predictors of VSR, a retrospective postmortem study was performed on 17 hearts with acute anteroseptal myocardial infarction, comprising 7 with VSR and 10 without rupture. Infarct size and the extent of wall thinning were quantified. Wall thinning was defined as a decrease of less than 50% of thickness of the noninfarcted wall. The total infarct size did not differ among the groups. In the free wall (FW), the infarct was smaller in hearts with VSR than in those with a ruptured FW (p<0.05) or no rupture (p<0.01). The septal involvement was more extensive in patients with VSR than in those with FW rupture (p<0.05). Septal thinning was more extensive in hearts with VSR than in those with FW rupture (p<0.05) or non-rupture (p<0.05). A combination of a small infarct of the FW and a large septal infarct may contribute to the formation of septal aneurysm, which is believed to predispose to VSR. The presence of a small infarct of the anterior septum may be another setting for postinfarction septal rupture. (Jpn Circ J 1999; 63: 485 - 489)

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急性心筋梗塞（AMI）後の左室自由壁破裂（LVFWR）は重篤な合併症であり，特にblow out型は救命が困難である．今回の症例は，64歳男性，ショック状態で当院に搬送され，心電図所見と心エコー検査での心タンポナーデの所見から前壁の急性心筋梗塞による左室破裂と診断し緊急手術を行った．手術では心膜を切開すると血餅が排出され左室前壁の破裂孔から血液が大量に噴出した．Electromechanical dissociation（EMD）となったため経皮的心肺補助装置（PCPS）と大動脈内バルーン・パンピング（IABP）を装着した．フェルト帯をあてモノフィラメント糸でのマットレス縫合で止血しさらにフィブリン糊などで圧迫止血を行った．術後肝不全を併発し血漿交換術・ビリルビン吸着療法を行い，第48病日に独歩退院した．術中にblow out型LVFWRを生じた症例に対しPCPS・IABPにより循環動態を維持しながら縫合止血を行い救命し得たので報告した．

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後乳頭筋（PPM）壊死を疑う急性心筋梗塞（AMI）後の左室自由壁破裂（LVFWR）に対し，意図的に外科的修復術を遅延した症例を報告する．症例は胸背部痛を主訴に緊急搬送された67歳女性である．経胸壁心エコー検査（TTE）で心嚢液貯留とPPM頭部の可動性亢進と低輝度所見を認めPPM壊死が疑われた．冠動脈造影検査で回旋枝起始部閉塞を認めた．心臓脱転などの手術操作でのPPM断裂への進展が懸念され，Oozing型で呼吸循環動態破綻がないことからIABP（intra-aortic balloon pumping）管理を含む内科的治療とした．発症から7日目のTTEで心嚢液増加を認め，非縫合術式を行った．術後3日目にIABPを離脱し，12日目に自宅独歩退院となった．

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Background Cardiac rupture after acute myocardial infarction (AMI) is unpredictable and almost always fatal, so the present study reviewed all the clinical characteristics of patients with cardiac rupture to determine if its occurrence can be predicted. Methods and Results The clinical characteristics of 1,296 consecutive AMI patients from January 1992 to February 2002 were retrospectively evaluated using multi-logistic analysis. Cardiac rupture occurred in 45 patients (3.5%), comprising left ventricular free wall rupture (n=23), ventricular septal perforation (n=20) and papillary muscle rupture (n=2). Early-phase rupture (within 72 h after AMI onset) was associated with anterior infarction. Of the 45 patients who experienced ruptures, 24 (53.3%) survived to discharge; 21 (46.6%) of the 45 ruptures occurred after admission. Successful reperfusion therapy was performed within 24 h for 840 patients. The incidence of rupture was significantly lower for reperfused patients than for non-reperfused patients (0.6% vs 3.5%, respectively; p<0.01). Peak C-reactive protein concentration was a reliable predictor of late-phase rupture (p=0.01), but not of early-phase rupture. Conclusions Reperfusion therapy appears to aid in the prevention of cardiac rupture, especially late-phase rupture. (Circ J 2004; 68: 422 - 426)

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症例は40代男性．既往はアトピー性皮膚炎．当院救急外来に発熱，意識障害にて搬送された．来院時の意識レベルはGCS: E3V4M5. 体温40.2°C，感染性心内膜炎（IE）を疑ったが，頻脈であったため心雑音の聴取は困難であり，経胸壁心エコー検査（TTE）の評価も困難であった．採血，髄液検査の結果，菌血症および髄膜炎疑いで入院となり，翌日の血液培養にてMSSAが検出された．入院後もIEを疑い，第2病日にTTEを施行．壁運動異常および大動脈弁逆流（AR）を認めた．左室の壁運動はびまん性に低下し，特に心室中隔から心尖部の壁運動は著明に低下していた．第8病日に経食道心エコーを施行し大動脈弁右冠尖，左冠尖間の弁輪に疣腫を確認した．同部位からもARを確認し，経時的に増加していた．ARの増加に伴い心不全を来したため，準緊急的に外科的治療を行う方針となったが，術前に心室細動となり緊急手術を実施．術後経過は良好でリハビリを進めていた．術後18日目にTTEを施行したところ，術前に高度壁運動低下していた心室中隔の中部は菲薄化し瘤状となり，同部位で左室から右室へ向かう短絡血流を認め，肺体血流比は1.40であった．TTEにより心室中隔穿孔と判断され，翌日緊急に閉鎖術を施行することとなった．今回，我々は非常にまれなIEによる冠動脈塞栓に心室中隔穿孔を合併した1例を経験し，経胸壁心エコー検査が有用であったので報告する．

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Background: Patients with acute myocardial infarction (AMI) whose culprit lesionlies in a branch of the 3 major coronary arteries have well-preserved cardiac function. A first MI with preserved cardiac function is a risk factor for left ventricular free wall rupture (LVFWR), so the aim of this study was to investigate the possible relationship between AMI with branch segment occlusion and LVFWR. Methods and Results: The 439 patients with AMI were retrospectively studied. They were divided into 2 groups: group B (n=70; segments 4 atrioventricular node artery, 4 posterior descending coronary artery, 8, 9, 10, 12, 14, or 15 according to the AHA classification), and group P (n=369; segments 1, 2, 3, 5, 6, 7, 11, or 13). Primary percutaneous coronary intervention (PCI) was more often performed in group P (75% vs 57%; P=0.0018). In-hospital mortality tended to be lower in group B (1.4% vs 6.2%; P=0.105). The incidence of LVFWR was significantly higher in group B (10.0% vs 1.6%; P=0.0002).By multivariate logistic regression analysis, 1-vessel disease, absence of primary PCI, branch segment occlusion, and age were identified as independent predictors of LVFWR. Conclusions: The incidence of LVFWR was higher in group B and branch segment occlusion was identified as an independent predictor of LVFWR. (Circ J 2009; 73: 1473 - 1478)

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(1) Intramuscular coronary arterial (I.M.C.A.) (80-500μ) sclerosis as a cause of myocardial disease was studied pathologically.
(2) I.M.C.A. sclerosis was found in high incidence in the cases over 40 years of age, and the tendency of stenosis of the vessels with the lesions increased with age.
(3) The lesions was independent of atherosclerosis of the coronary arterial stem or ante-mortem hypertension.
(4) Severe lesions of this type was considered to be a cause of definite myocardial lesions without atherosclerosis in the coronary arterial stem, and its clinical feature seemed to be a cardiac decompensation without anginal pain.
(5) In addition to atherosclerosis of the coronary arterial stem, I.M.C.A. sclerosis could be an important cause of coronary heart disease, especially in people with a low grade of atherosclerosis such as the Japanese.

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Background Few investigators have studied the anatomy of the sinus node artery (SNA) using noninvasive imaging modalities, so the objective of this study was to visualize the in-vivo 3-dimensional anatomical relations of the SNA using dual-source computed tomography (DSCT). Methods and Results In the 101 patients included in this study, the visualization rate, anatomical type and diameter of the SNA, the distance between the orifice and coronary artery, and the terminal type of SNA were recorded. The visualization rate was 95.2% (96/101). Of 96 patients, 106 SNAs were detected among which 51 (48.1%, 51/106) originated from the right coronary artery, 52 (49.1%, 52/106) from the left circumflex artery, and 3 (2.7%, 3/106) from other branches. There were 3 types of SNA: right (n=52), left (n=45), and posterior (n=9). The distance between the orifice of the right SNA and the right coronary sinus was 14.2±15.2 mm, for the left SNA it was 5.5±3.5 mm, and for the posterior SNA, 33.7±12.8 mm. The average diameter was 1.27±0.29 mm. The SNA approached the nodal tissue by 1 of 3 routes: retrocaval (51.5%), precaval (25.2%), or pericaval (22.3%). Conclusion The SNA can be visualized in vivo using DSCT, which is important for preoperative knowledge of its origin, course, termination, and anatomical type. (Circ J 2008; 72: 1615 - 1620)

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Molecular switches between the troponin T and I isoforms are known to occur in various conditions, but the results from studies of failing human hearts with various etiologies are contradictory and it is not certain whether troponin isoform changes occur. Therefore, the molecular switching of troponin isoforms during normal development and heart failure (HF) after myocardial infarction were investigated in Sprague-Dawley rats at the fetal, neonate, and normal adult stages, and in a postinfarction adult HF group. During normal development, switching from the fetal to the adult pattern of the troponin T and I isoforms was observed. Immunoblotting of postinfarction failing hearts revealed a marked increase in the fetal isoform of cardiac TnT (cTnT) (fetal/adult cTnT isoforms: normal adult = 0.61±0.09 vs postinfarction HF = 1.59±0.13, p<0.001). Also, the amount of the adult troponin I (TnI) isoform decreased significantly in the postinfarction failing heart. In the semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR) with glyceraldehyde-3-phosphate-dehydrogenase (GAPDH) as an internal standard, the mRNA of fetal cTnT increased in the postinfarction failing heart (fetal cTnT/GAPDH: control = 0.22 vs HF rat = 0.84, p<0.05). Therefore, molecular switching of the troponin T and I isoforms occurred during the normal development of the rat, and there was re-expression of the fetal pattern of the isoforms in the postinfarction failing heart of the adult rat. (Circ J 2002; 66: 959 - 964)

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