Myocardial Infarction in Diabetics

The hospital mortality of acute myocardial infarction amongst285 known diabetics treated in the last decade was 39.7 percent at one month and had increased to 51 per cent at 12 months.Treatment in a coronary care unit during the acute stage hadlittle effect on the mortality amongst patients on insulin,but was beneficial for patients whose diabetes had been controlledby oral hypoglycaemic drugs. Female patients on oral hypoglycaemicdrugs had the highest mortality. When considering age, durationof diabetes and presence of retinopathy, acute myocardial infarctionin diabetics controlled on oral therapy appeared to have a worseoutcome than in patients on insulin. Independently of whetherpatients were on insulin or on oral hypoglycaemic drugs 12 monthsafter the acute episode, only about half of them were stillalive.     

ARBs and Myocardial Infarction

A recent editorial in the British Journal suggested that ARBs used for treatment of hypertension may increase the risk of myocardial infarction.     

Treatment After Myocardial Infarction

Persons after myocardial infarction (MI) should have their modifiable coronary artery risk factors intensively treated. Hypertension should be treated with beta blockers and angiotensin-converting enzyme (ACE) inhibitors. The blood pressure should be reduced to <140/90 mmHg and to <130/80 mmHg in persons with diabetes or renal insufficiency. The serum low-density lipoprotein cholesterol should be reduced to <70 mg/dl with statins if necessary. Diabetics should have their hemoglobin A_1c reduced to <7.0%. Aspirin or clopidogrel, beta blockers, and ACE inhibitors should be given indefinitely unless contraindications exist to the use of these drugs. Long-acting nitrates are effective antianginal and antiischemic drugs. Postinfarction patients at very high risk for sudden cardiac death should have an implantable cardioverter-defibrillator. The two indications for coronary revascularization are prolongation of life and relief of unacceptable symptoms despite optimal medical management. Dr. Aronow has no real or apparent conflicts of interest relating to the subject under discussion.     

Complications of Myocardial Infarction

This department offers the latest, proved methods for the treatment and management of commonly encountered conditions based on the extensive experience of the physicians who prepare these summaries for POSTGRADUATE MEDICINE.     

家兔实验性心肌梗塞时心肌细胞凋亡研究

目的：探讨急性心肌梗塞时心肌细胞凋亡情况。方法：采用ＤＮＡ缺口末端标记法（ＮＥＬＭ）、透射电镜和琼脂糖凝胶电泳对家兔实验性心肌梗塞时不同损伤区心肌细胞凋亡情况进行研究。结果：在梗塞交界区心肌组织中可见散在大量ＭＥＬＭ染色阳性细胞；电镜检查细胞呈凋亡特征。在坏死区和正常心肌组织中均未发现ＮＥＬＭ染色阳性细胞。梗塞交界区ＤＮＡ电泳呈梯状，符合细胞凋亡图谱。坏死区心肌ＤＮＡ电泳图谱呈均匀弥散状态，正常心     

Treatment of Acute Myocardial Infarction

Premature ventricular beats are very common in acute myocardial infarction. This arrhythmia requires immediate and aggressive treatment because it is the forerunner of ventricular tachycardia and fibrillation. The treatment of choice is lidocaine, usually in an initial dose of 50 to 100 mg intravenously. Atrial and ventricular transvenous pacing have been effective in overdriving and preventing cases of drug-resistant ventricular arrhythmias.     

Psychiatric Morbidity after Myocardial Infarction

Using a standardized interview, psychiatric morbidity was diagnosedin 35 out of 100 consecutive male patients one week after admissionto hospital following a first acute myocardial infarction. Sixteenof these patients had been psychiatrically ill before the infarctionand their psychiatric symptoms and social difficulties persistedthroughout the 12 month period of observation. In contrast,patients whose psychiatric morbidity had been precipitated bythe infarction tended to have transient symptoms and fewer problemsof social adjustment. Measures of psychiatric morbidity oneweek after the attack did not predict subsequent mortality ordifficulty in returning to work. Only a history of heavy smokingwas significantly associated with mortality during the ensuing12 months. Patients who regarded their illness as a loss ora threat had greater psychiatric morbidity than those who regardedit as an insignificant event.     

急性心肌梗塞的治疗

截至2002年7月,急性心肌梗塞(acute myocardial infarction,AMI)治疗的临床证据如下:(1)改善AMI预后的证据:①血管紧张素转换酶抑制剂(ACEI):1篇概述和1个(AMI 36 h到14 d内接受治疗的患者)系统评价发现,血管紧张素转换酶抑制剂和安慰剂相比,患者30 d后的死亡率明显减少;血管紧张素转换酶抑制剂和安慰剂相比,显著增加了持续低血压和肾功能不全.血管紧张素转换酶抑制剂是提供给每一位存在AMI的患者,还是仅提供给有心衰征象的患者,目前尚无定论.②阿司匹林:1个系统评价发现,阿司匹林与安慰剂相比,能明显减少1个月时的死亡率、非致死性再梗塞以及非致死性中风.③β受体阻滞剂:2个系统评价和1个后来的RCT发现,在AMI数小时内给予β受体阻滞剂与对照比较,显著减少死亡率和再梗塞率.溶栓治疗的RCT发现,美托洛尔的及时使用与延后使用相比,明显减少患者6 d后再梗塞率以及复发的胸痛,但使用该药6 d和1年间的死亡率没有显著差异.1个研究比较了在近期有心肌梗塞并且左室射血分数小于40%,或者基本没有接受溶栓治疗的患者中使用卡维地洛与安慰剂的RCT发现,尽管单独的死亡率和复发性非致死性AMI在卡维地洛组中明显较低,但1.3年后各种原因的死亡率以及由于心血管事件住院的联合终点并没有差异.④钙离子拮抗剂:9个RCT发现,在AMI头几天范围内,二氢吡啶和维拉帕米与安慰剂相比并不降低死亡率.1个左心衰的RCT发现有限的证据表明,在AMI的头几天给予硝苯地平与安慰剂比较可能会增加死亡率.⑤糖蛋白Ⅱb/Ⅲ a拮抗剂:2个大型的RCT发现,在AMI患者中联合使用半剂溶栓剂和阿昔单抗与使用全剂量的溶栓剂相比,并没有减少1个月时的死亡率,但可预防非致死性的心血管事件;用阿昔单抗联合治疗增加了出血并发症,特别是颅外的出血.3个RCT发现,尽管加用阿昔单抗增加了出血的危险,但将阿昔单抗加到AMI患者最初的冠脉成型术或者支架中的益处仍有争议.⑥溶栓之外的硝酸盐制剂:2个溶栓时期使用硝酸盐与安慰剂的RCT发现,死亡率没有显著差异.⑦没有溶栓时的硝酸盐制剂:1个在溶栓时代前所做试验的系统评价发现,硝酸盐较安慰剂显著降低AMI患者的死亡率.⑧早期的经皮腔内冠状动脉成形术与溶栓比较(在专业中心完成):2个系统评价发现,早期的经皮腔内冠状动脉成形术与早期的溶栓相比明显降低了急性心肌梗塞患者的死亡率以及30 d的再梗塞率.在非专业中心开展的有关比较经皮腔内冠状动脉成形术与溶栓的试验结果尚不清楚.⑨溶栓:1篇研究对象为AMI患者以及最初的心电图上存在ST段上抬或者束支传导阻滞的患者的试验的概述发现,及时的溶栓治疗(症状发作后的6 h内或许到12 h或者更长)与安慰剂比较显著降低短期内的死亡率;溶栓与对照相比明显增加了中风和大出血的危险.不同类型的溶栓剂之间相互比较的RCT的Meta分析发现,死亡率没有显著差异.(2)AMI继发心源性休克的预后证据:①早期侵入性的心脏血管重建:1个以AMI 48 h内发生心源性休克患者为研究对象的RCT发现,早期侵入性的心脏血管重建与最初的单独药物治疗相比显著降低了6～12 d后的死亡率.1个样本含量较小的RCT也得出了相似的结果,但差异并不显著.②主动脉内的球囊反搏术:1个在AMI后的心源性休克患者中将主动脉内的球囊反搏术加溶栓与单用溶栓作比较的RCT摘要发现,6个月后的死亡率没有显著差异.③1个来自比较溶栓与不溶栓的RCT的AMI后心源性休克患者的亚组分析发现,21 d后的死亡率没有显著差异.④在心脏移植、早期心脏手术、正性肌力药和血管扩张剂、肺动脉插管及左心室支持系统方面,尚未发现有关这些干预措施效果的RCT证据.     

Vasospasm-lnduced Myocardial Infarction With Sumatriptan

Sumatriptan, a 5-hydroxytryptamine¹ (5-HT₁) receptor agonist is an effective abortive agent for migraine headaches. A common side effect in 3% to 7.9% of patients is chest pain. Although most cases of chest pain are not thought to be of cardiac origin, its mechanism is not entirely understood. Rare examples of electrocardiogram changes consistent with transient ischemia have been reported. Isolated instances of angina, arrhythmia, myocardial infarction, and death have been temporally associated with sumatriptan administration. In most cases, it is unclear whether underlying cardiovascular disease existed or contributed to this adverse event. We report the history of a 56-year-old female patient with migraine who experienced myocardial infarction shortly after using sumatriptan, despite having had a normal cardiovascular evaluation. As she had a normal cardiac catheterization after the event, we find it probable that sumatriptan induced coronary vasospasm and myocardial infarction.     

声学密度定量技术在急性心肌梗塞早期预测再灌注心肌的存活

目的：本试验是利用声学密度定量技术（ＡＤ－ＩＢＳ）预测再灌注心肌存活。方法：在发病当天,发病后第３天,第２１天分别对２０例急性心肌梗塞患者进行ＡＤ－ＩＢＳ检查。结果：标化ＣＶＩＢ在发病后第３天有所恢复（不依赖于室壁运动的恢复）的梗塞区心肌,其在发病后第２１天的室壁增厚率可达到与正常心肌区无明显差异。结论：帮可认为心肌梗塞后标化ＣＶＩＢ可早期预测再灌注心肌的存活。     

Determinants of Myocardial Strain in Experimental Chronic Myocardial Infarction

We evaluated the relationships between regional myocardial strain measured by speckle tracking echocardiography and viability, fibrosis, hypertrophy and oxygen consumption in the infarcted or remote myocardium in a pig model of chronic myocardial infarction (MI). Thirteen farm pigs with surgical occlusion of the left anterior descending coronary artery and five sham-operated pigs were studied 3 mo post-MI. Computed tomography revealed significant left ventricle remodeling. Reduced radial or circumferential strain identified areas of transmural infarction (area under the curve: 0.82 and 0.79, respectively). In the remote non-infarcted area, radial strain correlated inversely with the amount of fibrosis (r?=?–0.66, p?=?0.04) and myocyte hypertrophy (r?=?–0.68, p?=?0.03). Radial strain rate inversely correlated with myocardial resting oxygen consumption assessed with ¹¹C-labeled acetate positron emission tomography (r?=?–0.71, p?=?0.006). In conclusion, myocardial strain and strain rate reflect fibrosis, hypertrophy and oxygen consumption of the remote areas after MI.     

心梗患者的颈动脉粥样硬化与脑梗塞

目的：观察心肌梗塞后患者一年内发生脑梗塞的心源性病因及颈动脉粥样硬化情况。方法：应用超声心动图和颈动脉超声。结果：９２．３％的心梗患者合并有颈动脉粥样硬化。脑梗塞组（５例）患者中３例（６０％）存在颈动脉内膜粗糙（Ｐ＜０．０５）；１例有心腔内附壁血栓；心功能指标二组间无差异。结论：为了防止心梗后并发脑梗塞，心脏和颈动脉病变的情况同样需要充分的了解     

急性心肌梗死后心肌内出血

在急性心肌梗死患者中, 通过经皮冠状动脉介入治疗进行血管重建能够有效降低死亡率。然而, 即使成功开通了心外膜血管, 仍有相当比例的急性心肌梗死患者发展为慢性心力衰竭。研究发现, 冠状动脉微血管阻塞引起的"无复流"现象及随后出现的心肌内出血是参与此过程的重要因素。了解心肌内出血在"无复流"现象和心肌损伤中的作用, 对制定新的急性心肌梗死治疗策略至关重要。本文将对心肌内出血的病理生理学、影像学、临床意义和治疗策略等最新进展进行综述。     

院前静脉溶栓抢救急性心肌梗死

目的　为缩短急性心肌梗死 (AMI)患者发病至溶栓开始的时间 ,提高溶栓疗效 ,探讨院前静脉溶栓的可行性、安全性。方法　接受院前尿激酶静脉溶栓治疗的AMI患者 5 2例为观察组 ,同期住院后行尿激酶静脉溶栓治疗的AMI患者5 8例为对照组 ,两组进行比较。结果　患者从发病至溶栓开始的时间观察组为 3 .12± 1.17小时 ,对照组为 5 .42± 1.92小时 ,P <0 .0 1。冠脉再通率观察组为 71.2 % (3 7/ 5 2 ) ,对照组为 5 1.7% (3 0 / 5 8) ,P <0 .0 5。 5周病死率观察组为 7.7%(4 / 5 2 ) ,对照组为 10 .3 % (6/ 5 8) ,P >0 .0 5。院前AMI诊断准确率达 10 0 % ,院前无 1例死亡。结论　AMI院前静脉溶栓能赢得救治时间 ,提高冠脉再通率 ,院前静脉溶栓安全、可行。