表现为巨大倒置T波的急性心肌梗死1例

患者,男,57岁.因持续胸骨后疼痛18 h于1998年4月29日入院.既往有高血压病史20年.体检:BP 21/14 kPa,P 75 次/min,呼吸平稳,心律齐,心音低纯,无杂音,心电图(附图A)示窦性心律,心率75 次/min.V1～V3呈rS型,STv1～v3呈弓背向上抬高0.2～0.4 mV,Q-T间期达0.6 s ,V2～V6 T波异常增宽而倒置,V4深达2.4 mV.急查血清酶示:谷草转氨酶 54 IU/L,磷酸肌酸激酶 285 IU/L,乳酸脱氢酶 201 IU/L.     

冠状动脉造影正常的急性心肌梗死1例

患者 ,女 ,31岁。因持续性心前区闷痛并向左肩部放射 ,伴恶心、呕吐、大汗淋漓 7h来院 ,急查心电图提示 : 导联呈 q R( q<1 /4R、时限 <0 .0 4 s) , 、a VF导联呈 r S、ST 、 、a VF呈弓背向上抬高 0 .1～0 .1 5m V,ST 、a VL 压低 0 .0 5～ 0 .1 m V,T 、 平坦、a VF倒置。急查心肌酶提示 :肌酸激酶 ( CK) 550IU/L(正常 2 4～ 1 95IU/L)、谷草转氨酶 ( SGOT)2 33IU/L (正常 <40 IU/L)。拟“急性下壁心肌梗死”收入院。入院体检 :体温 37℃ ,脉搏 70次 /min,呼吸 1 6次 /min,血压 1 2 0 /70 mm Hg( 1 mm Hg=0 .1 33k Pa) ,…     

急性心肌梗死应常规加做V7—V9后胸导联

患者男 ,72岁。与人争吵后胸痛 4小时 ,外院拟诊“急性下壁心肌梗死”转入本院。以往有高血压史。入院后 CPK峰值为 192 5 IU/ L(正常值 :2 2～ 2 6 9IU/ L)。临床诊断 :急性心肌梗死。图 1　说明见文内图 2　说明见文内图 1为急诊时记录的心电图。图中见 、 、a VF和 V7～ V9导联的 ST段弓背型上移 , 、a VF和 V7～ V9导联另可作者单位 :2 0 0 0 2 5上海第二医科大学附属瑞金医院心脏科见小 Q波 :V2 ～ V4导联的 ST段下移 ,以 V3导联最为明显。图 2为二天后的心电图。图中 和 a VF导联的 ST段略有上移 ,另可见小 Q波 ;V7～ …     

系统性红斑狼疮致急性心肌梗死1例

患者,女,56岁。因胸闷、胸痛2d入院,既往有系统性红斑狼疮(SLE)史17年(诊断依据美国风湿病协会1982年修订标准),一直服用泼尼松20mg/d维持治疗,发病前3d自行减量至10mg/d。体检:T38.3℃,P110次/min,R24次/min,BP165/98mmHg(1mmHg=0.133kPa)。神志清,唇无发绀,心界向左下扩大,心率110次/min,律齐。两肺可闻及中等量湿音。腹软、肝脾肋下未及,双下肢不肿,双脚趾可见干性坏疽。实验室检查:WBC4.3×109/L、N89.6%,PLT100×109/L,尿蛋白,血沉113mm/h,血清ANF效价≥1∶160,dsDNA( ),AST126IU/L(10～42IU/L)、CK1038IU/L(22～269…     

心绞痛时T波假性正常致急性心肌梗死一例

患者女性,65岁,因反复发作心绞痛1周余,于1997年11月27日住入我院,既往有高血压、心绞痛、糖尿病、慢性胃炎史,体检:180/82mmHg(1mmHg=0.133kPa),双肺呼吸音清,心界向左下扩大,心率80次/min,心律齐,未闻及杂音。腹部无抵抗,肝脾未触及,双下肢无水肿。空腹血糖9.50mmol/L,胆固醇7.40mmol/L,低密度脂蛋白5.56mmol/L,肾功能正常。核素心肌灌注显像示左心室侧壁灌注减低。常规心电图示V1～V6导联T波倒置,V2～V5的T波呈冠状T伴ST段压低0.05～0.1mV,左心室高电压(图1)。心肌酶学检查:谷丙转氨酶24IU/L、谷草转氨酶24IU/图1　常规体检时心…     

超大剂量尿激酶治疗急性心肌梗塞2例报告

例 1:患者男 ,5 6岁。因突发胸痛、胸闷 40分钟以急性心肌梗塞 (下壁 前壁 )收入院。患者有高血压病史 3月。入院查体 :T36 .1℃ ,P74次 / min,Bp70 / 15 k Pa,颈软 ,双肺 (- ) ,心率74次 /分 ,律齐 ,无杂音 ,腹 (- )。心电图示 、 、av F ST段斜行抬高 0 .1mv,V2 ～ V4ST段抬高 0 .10 5 mv,T波高尖。CK-MB2 9IU/ L。入院后 ,立即给予尿激酶 15 0万 U 5 %GS2 0 m L5～ 8分钟内静注 ,尿激酶 15 0万 / U 5 %GS10 0 ml30 min内静滴 ,肝素 5 0 mg静推。至 2小时 ,患者胸痛消失 ,抬高的 ST段下降 >80 % ,未出现再通性心律失常。…     

外伤致急性心肌梗死二例

例1女性,70岁,因外伤后胸痛3d于2002年7月25日入院。患者于3d前站立时被一快速飞跑的男孩头部撞击前胸后出现持续性胸痛伴胸闷、气短。既往无高血压、糖尿病。查体:血压120/80mm Hg(1mm Hg=0.133kPa),左前胸皮肤有3.0cm×3.0cm淤斑,轻度肿胀,触痛明显,双肺呼吸音清,心界不大,心率80次/min,律齐,各瓣膜听诊区未闻及杂音。胸片示心肺正常。心电图示Ⅰ、Ⅱ、aVL、V2～V6ST段压低1.2mm,T波深倒5～15mm,无病理性Q波。心肌酶谱:肌酸激酶(CK)625U/L,肌酸激酶同工酶(CK-MB)88U/L,乳酸脱氢酶(LDH)400U/L,α-羟丁酸脱氢酶(α-HBDH)650U/L…     

持久性B型间隔支阻滞酷似陈旧性前间壁心肌梗死

患者男,28岁,因心悸,胸闷于97年10月就诊。体检以及血常规、血沉、血糖和胸片等检查均无异常。心电图示窦性心律,心率71次/分,P-R0.14s,心电轴 90°,V1、V2导联呈Qr型,V3、V3R、V4R导联呈QS型,I导联呈rs型,V5、V6导联呈Rs型;V1～V3导联ST段呈正常抬高;V4R～V1导联T波倒置,V2、V3导联T波直立,表现为前间壁心梗图型(图1A)。次日查血脂,总胆固醇及血生化均正常。心肌酶谱:CK-MB:30IU/L、CK:88IU/L、LDH:152IU/L、AST:31IU/L、HBDH:340IU/L。心脏多普勒超声检查未见异常。治疗后心悸、胸闷等症状消失。98年10月28日复查…     

冠状动脉介入治疗术后亚急性血栓1例

患者,男,65岁.因胸痛1 d入院.患者既往有高血压史8年,最高血压180/100 mmHg(1 mmHg=0.133 kPa),未正规服用降压药,入院确诊患有2型糖尿病.入院前1 d出现胸痛,持续时间最长40 min,能自行缓解,但反复出现胸痛发作,伴有汗出.入院体检:T 36.5℃,P 78次/min,R 20次/min,血压140/90 mmHg,神志清楚,两肺未闻及干湿性啰音,心率78次/min,律齐.实验室检查:心电图:Ⅰ、aVL导联ST段下斜性压低最大达0.15 mV, V2~V6 ST段压低最大达0.2 mV;心肌酶谱:AST 110 IU/L,LDH 308 IU/L,CK 201 IU/     

冠状动脉瘘并发急性心肌梗死2例

1　临床资料病例 1　男 3 2岁 ,以突发心前区疼痛 2天为主诉入院。疼痛呈压榨性 ,向左肩背放射 ,未用药治疗 ,既往健康。查体 :血压 10 0 / 70 m m Hg,心率 92次 / m in,无发绀 ,淋巴结不大 ,甲状腺未扪及 ,双肺呼吸音清晰 ,心界不大 ,心律齐 ,胸骨左缘第四助间可闻及 ～ 级收缩期吹风样杂音 ,无放射传导 ,无震颤 ,腹软 ,肝脾未及。EKG:窦性心律 ,V1 ～ V3呈 QS型 ,S- T段无抬高 ,T波倒置。心肌酶谱 :肌钙蛋白 T(+) ,肌酸磷酸激酶 5 2 6IU/ L,肌酸磷酸激酶同工酶 (CK- MB) 3 2 IU/ L,乳酸脱氢酶 3 2 9IU/ L。UCG:心腔正常 ;射…     

Severe acute pancreatitis in acute hepatitis E.

We report an 18-year-old boy with severe acute pancreatitis developing during acute hepatitis E and complicated by sepsis and acute renal failure. The patient recovered on supportive management.     

Myocarditis associated with acute nasopharyngitis and acute tonsillitis

Thirty-five instances of fatal myocarditis atributable to acute nasopharyngeal and tonsillar infections have been reported. The available evidence indicates that these are samples of a not uncommon type of cardiac disease which fortunately has a relatively good prognosis. Further investigation should be carried on to establish fully the etiological agent and the pathogenesis of the lesion. Although the pathologic observations indicated that all patients died of cardiac failure, heart disease was suspected clinically in only three, and in fifteen patients death was unexpected. Significant clinical observations which would seem to be of importance in the recognition of the process were: disproportion of the temperature and pulse rate, hypotension, thready or feeble pulse, and substernal oppression. Cyanosis, dyspnea, and orthopnea occurred frequently.Autopsy findings included significant enlargement of the heart in many cases. The microscopic changes, similar in both nasopharyngeal and tonsillar infections, have been classified in three overlapping groups. In all of these the inflammatory process was observed to be patchy, frequently showing considerable variation in intensity from one area to another and having no predilection for a particular portion of the myocardium. Significant (moderate or marked) degrees of muscle degeneration observed in the diffuse type of myocardial lesion were not present in the interstitial form. The cellular reaction, which was characteristically more intense than that observed in diphtheritic myocarditis, was predominantly mononuclear, but significant numbers of polymorphonuclear leucocytes accumulated at sites of more severe inflammation.Although the figures are too small to justify conclusions, there appears to be significant correlation between the clinical occurrence of hypotension and the estimated severity of the myocarditis, since it was a feature in every severe case in which the blood pressure was recorded. The only available electrocardiograms (four), abnormal in every case, were from patients whose hearts showed muscle degeneration of moderate or marked degree. Anginal pains were related to the presence of hypotension. Fibrosis of the heart muscle was related both to the muscle degeneration and to duration of illness.In therapy, attention is called to the danger involved in the administration of intravenous fluids.     

Philadelphia chromosome-positive acute lymphoblastic leukemia preceded by acute pleuropericarditis

A 69-year-old woman was admitted with sudden chest pain and high fever. Electrocardiography showed negative T waves in the precordial leads. Subsequently, pleural and pericardial effusion developed, but the symptoms and signs subsided without specific therapy. On day 31, fever, left shoulder pain and pleural effusion reappeared. 67Ga scintigraphy showed abnormal uptake in the chest and left shoulder. Blasts were detected in the peripheral blood on day 44, and in the pleural effusion and bone marrow on day 45. The blasts were positive for Philadelphia chromosome, CD10, CD19, CD33, CD34 and IgH-chain rearrangement and negative for myeloperoxidase. The clinical picture of the preceding pleuropericarditis was that of viral or idiopathic origin, but its relationship with acute lymphoblastic leukemia was unclear. Inflammatory chemokines in the pleural space may have induced invasion of the leukemic cells.     

Fatal idiopathic acute eosinophilic pneumonia with acute lung injury

A fatal case of idiopathic eosinophilic pneumonia with acute lung injury is described. The patient required treatment with mechanical ventilation and intravenous corticosteroids, however, she died on the third hospital day. At autopsy, both exudative and proliferative phases of diffuse alveolar damage were observed bilaterally. Marked eosinophilic infiltrate was noted in the alveolar wall and within the alveolar cavities with occasional abscess-like features. To our knowledge, this is the first report of fatal acute eosinophilic pneumonia, and provides important information for the management of this condition.