老年急性心肌梗塞晚发心原性猝死的临床及病理分析

为了分析老年急性心肌梗塞（ＡＭＩ）２周后发生心原性猝死的原因，本文总结了１２例心原性猝死患者，其中６例进行了尸检。认为无论是持续心肌电不稳定所致的原发性室颤，还是梗塞早期的全并症，如休克、心功能不全，梗塞后心绞痛引起的继发性室颤均为晚发心原性猝死的常见原因。尸检结果表明，老年ＡＭＩ晚发心原性猝死多发生于冠脉病变严重者。对于室颤高危患者应采取积极预防措施，如抗心律失常药物的合理应用、改善冠脉循环及改     

64例老年心源性猝死前的临床分析

本文对６４例老年心源性猝死的临床资料，进行回顾性分析，发现老年心源性猝死之前，有以下特点：（１）多患有冠心病等心脏疾患（７５．０％）；（２）有心律失常和（或）心电图异常、心功能不全、心肌梗塞及先兆症状等高危先兆；（３）多数有明确的诱发因素（７１．９％）；（４）猝死的高峰期多在早晨（５９．４％）。     

91例猝死患者尸体解剖病理和临床的回顾性分析

目的探讨猝死的病因、病理基础及防治措施。方法回顾性分析我院91例猝死患者的临床病理资料。结果91例猝死患者中,老年人62例,占681%,非老年人29例,占319%。心源性猝死68例,占747%,其中冠心病43例,患者主要有冠状动脉多支严重病变;非心源性猝死23例,其中以急性出血坏死型胰腺炎所占比例最高,有10例。结论猝死以老年男性多见,有广泛严重冠状动脉病变的冠心病患者猝死发生率高。防治冠心病、改善心肌缺血等综合治疗对预防猝死十分必要。胰源性猝死主要为急性出血坏死型胰腺炎所致,误诊率较高。     

Epidemiology of sudden cardiac death in Spain]

Sudden cardiac death is a remarkable public health problem though its incidence in Spain is lower than in other industrialised countries. Approximately 12% of all natural deaths occur suddenly, and 88% of them are of cardiac origin. This is the form of death in more than 50% of coronary heart disease patients. Moreover, it is the first symptom in 19-26% of cases. This close relationship with coronary heart disease results in cardiovascular risk factors being also risk factors for sudden death. Several factors, such as physical activity or certain drugs may act as sudden death triggers. The more effective strategy addressed to sudden cardiac death prevention includes identification high-risk subgroups of patients (i.e. patients with previous coronary heart disease, heart failure, out-of-hospital sudden death survivors and patients who developed a ventricular fibrillation or tachycardia after a myocardial infarction) and development of efficacious therapeutic interventions. Given that most sudden death are related to coronary heart disease, those primary preventive measures directed to reduce the coronary heart disease incidence rates will also prevent sudden cardiac deaths in population. Finally, community programs directed to reduce the time to reach cardiac emergencies by trained personnel, and to train general population in cardio-respiratory reanimation have shown to be efficacious owing to the fact that most sudden cardiac deaths occur out of hospitals.     

Can the mode of death be predicted in patients with angiographically documented coronary artery disease?

To determine whether sudden versus non-sudden cardiac death could be predicted in high risk patients, 1157 medical patients were followed for an average of 46 months after a diagnostic coronary angiogram and 18 clinical, hemodynamic, and angiographic variables known to be associated with a high risk of mortality were analyzed. The total group of 141 deaths was classified into 3 subgroups: (1) 82 sudden deaths (less than 1 hour after onset of symptoms); (2) 46 deaths due to acute myocardial infarction with or without heart failure, and (3) 13 deaths unrelated to cardiac symptoms. In a subset of 64 patients, the duration of electrical systole (QTc) was calculated before angiography and before death. A comparison was made of QTc measurements at entry with QTc values of subjects with normal coronary arteries and normal left ventricular function. Deaths from cardiac causes could often be predicted from older age, male sex, history of myocardial infarction, unstable angina, congestive heart failure, abnormal cardiothoracic ratio, multivessel disease, abnormal left ventricular contraction, and abnormal ejection fraction. However, these variables did not discriminate between sudden and nonsudden cardiac deaths and both modes of death were characterized by depressed left ventricular function and multivessel coronary disease. During follow-up the incidence of acute myocardial infarction was not different in patients with cardiac and noncardiac deaths and in long-term survivors. However, patients dying from cardiac causes had a higher incidence of heart failure. Patients dying suddenly did not present new infarctions during follow-up whereas patients dying from acute myocardial infarction had a 13% incidence of prior infarction and a higher incidence of heart failure. In addition, QTc at entry was longer in nonsurvivors than in normal subjects (p less than 0.0001) and patients experiencing sudden death exhibited the highest incidence of QTc prolongation (greater than or equal to 440 ms) during follow-up (p less than 0.05). We conclude that: (1) although the severity of coronary disease and left ventricular dysfunction are closely related to cardiac mortality, they do not discriminate between sudden and nonsudden cardiac deaths; (2) patients experiencing sudden death are characterized by a low incidence of new myocardial infarction or congestive heart failure and prolongation of the QTc interval during follow-up.     

Implantable cardioverter-defibrillators: indications and unresolved issues

Since the implantable cardioverter-defibrillator was first used clinically in 1980, several large randomized controlled trials have shown that therapy with this device can be beneficial in various patient populations. Evidence suggests that this therapy is useful in the secondary prevention of sudden cardiac death among patients who have survived arrhythmic events. Several trials have also shown the usefulness of implantable cardioverter-defibrillator therapy in the primary prevention of sudden cardiac death in patients with coronary artery disease and nonischemic cardiomyopathy. Other data support the use of this device for various infiltrative and inherited conditions. When used with cardiac resynchronization therapy, implantable cardioverter-defibrillators have improved survival rates and quality of life in patients with severe heart failure. Further research is needed to examine the potential benefits of implantable cardioverter-defibrillators in elderly, female, and hemodialysis-dependent patients, and to determine the optimal waiting period for implantation after myocardial infarction, coronary revascularization, and initial heart-failure diagnosis.     

The heart in fatal unstable angina pectoris

Compared to patients with sudden coronary death and acute myocardial infarction, relatively little morphologic data has been reported in patients with unstable angina pectoris. This article reviews necropsy data collected from one laboratory on unstable angina pectoris. From these data, several observations are appropriate: (1) Patients with unstable angina as a group have more coronary narrowing by atherosclerotic plaque than do patients with sudden coronary death or acute or healed myocardial infarction. (2) Patients with unstable angina have a much higher frequency of severe narrowing of the left main coronary artery than do patients in other coronary subsets. (3) The coronary atherosclerotic plaques in unstable angina consist primarily of fibrous tissue, and they are more similar to those found in patients with sudden coronary death than in patients with acute myocardial infarction. (4) The frequency of acute coronary lesions (thrombi, plaque rupture, and plaque hemorrhage) is similar to that observed in patients with sudden coronary death and significantly less than that observed in acute myocardial infarction. (5) The frequency of multiluminal channels throughout the major coronary arteries is significantly higher in unstable angina compared to sudden coronary death or acute myocardial infarction. (6) The major epicardial arteries and the heart are smaller in patients with unstable angina than in patients with sudden coronary death or acute myocardial infarction. (7) The left ventricular cavity is usually of normal size in patients with unstable angina and therefore left ventricular function is usually normal.     

Acute myocardial ischemia and ventricular arrhythmias in the pathogenesis of sudden cardiac death in coronary disease

There is increasing evidence for a fatal interaction of myocardial ischemia, ventricular arrhythmias and sudden cardiac death in some patients with coronary artery disease. Evidence comes from autopsy studies, from the evaluation of patients who survived an episode of sudden cardiac death, from follow-up data of these patients either treated or not by revascularization therapy and/or an implantable cardioverter-defibrillator and indicate that reducing the individual ischemic burden will be beneficial to reduce the incidence of sudden cardiac death. Studies in patients with stable and especially with unstable angina using Holter monitoring could demonstrate that there is a close and causal relationship between myocardial ischemia inducing or aggravating life-threatening ventricular arrhythmias and sudden cardiac death particularly in patients with unstable and postinfarction status. This review summarizes some of our clinical knowledge on this topic and indicates that preventive strategies for myocardial ischemia are the antiarrhythmic treatment of choice in patients with severe coronary artery disease and patients with evidence or at risk for ischemic proarrhythmia.     

Clinical and angiographic observations on resuscitated victims of exercise-related sudden ischemic death

The clinical and angiographic findings of 17 resuscitated victims of exercise-related sudden ischemic death are reported in an attempt to elucidate the mechanism(s) of these deaths. Ten survivors developed cardiac arrest during or after sporting activities (group A) and 7 others during or after an exercise stress test (group B). There were 15 men and 2 women. The mean age of group A was 46 years and of group B 55 years. Coronary risk factors, as well as previous angina and myocardial infarction, were more frequent in group B. Only 3 of the 17 survivors had anginal symptoms before sudden death. Sudden death in group A was associated with acute myocardial infarction in 8 and unstable angina in 2 and was associated in group B with acute myocardial infarction in 2, unstable angina in 3 and silent ischemia in 2. Coronary angiography was acutely performed in 15 patients. In most patients the ischemia-related coronary artery was totally or subtotally occluded. Clinical and angiographic findings indicate that exercise-related sudden ischemic death was due to an acute coronary event--in most cases unexpected and unpredictable. It is suggested that exercise-induced intracoronary changes were probably responsible for the development of acute coronary (sub)occlusion and sudden death.     

106例心脏性猝死的病理和相关因素分析

目的探讨心脏性猝死(SCD)的病理基础及相关因素,为SCD的诊断和防治提供线索。方法回顾性分析我院106例SCD的临床病理资料,分析SCD的病因及年龄,SCD的诱因,各种导致SCD病因的病理改变。结果106例SCD中,冠心病49例,心肌炎15例,心肌病20例,主动脉夹层动脉瘤破裂7例,先天畸形6例,克山病2例,心肌萎缩1例,心脏轻微病变6例。106例SCD中85例具有诱因。冠心病是中老年人SCD的最主要原因。冠心病SCD49例中,冠状动脉粥样硬化血管Ⅳ级狭窄40例,27例呈多支Ⅳ级狭窄;发生急性心肌梗死(简称心梗)10例,其中2例合并陈旧性心梗,单纯陈旧性心梗21例,18例无心梗,仅有心肌缺血。心肌炎和心肌病是中、青年人SCD的主要病因。有6例心脏无明显器质性改变,称之为阴性解剖或青壮年不明原因猝死。结论尽早防治冠心病、监测粥样硬化斑块成分、改善心肌供血是预防中老年SCD的根本措施,减少不良刺激和情感应激对预防SCD有一定意义。在解剖阴性者中进行分子基因筛查,对解释病因和SCD危险分层有重要作用。     

La mort par infarctus du myocarde chez le sujet jeune : étude de 312 cas de mort subite

Sudden cardiac death in young is seen as a dramatic phenomenon requiring knowledge of its impact. We aim to study the epidemiological characteristics of sudden cardiac ischemic death in young, and to discuss his involvement in the occurrence of death. We performed a retrospective cohort study using autopsy data from the department of forensic medicine of the University Hospital of Fattouma Bourguiba, Monastir-Tunisia. A review of all autopsies performed during 23 years was done. In each case, clinical information and circumstances of death were obtained. We have included all sudden death in persons aged between 1 year and 35 years for the male and from one year to 45 years for female. We collected 312 cases of sudden death during the studied period. The collected data were processed using SPSS 20. The significance level was set at 0.05. Thirty-two cases of cardiac ischemic sudden death have been collected. Myocardial infarction was the second cause of sudden death in young patients. There was a male predominance. The most affected subjects were aged between 25–45 years. The death occurred more frequently at rest. Coronary artery disease has been discovered in twenty-four cases (75%). The myocardial infarction occurred on healthy coronary arteries in eight cases. An anomalous course of coronary arteries, in particular myocardial bridging, was found in eight cases (25%). Toxicological screening was negative in all cases. Identifying epidemiological characteristics of sudden cardiac ischemic death in this population is important for guiding approaches to prevention that must be based on dietary hygienic measures and the control of cardiovascular risk factors.     

Lessons learnt from the autopsies of 445 cases of sudden cardiac death in adults

AIM: To determine the cause of sudden cardiac death in adults who underwent autopsy. METHODS: Four hundred and forty-five sudden cardiac deaths occurred within 1 h of the symptoms onset, and all other cardiac and noncardiac causes having been excluded from autopsy and toxicology screening, were retrospectively identified from among 902 autopsies performed in a 2-year period on the island of Crete. The presence of acute coronary thrombi and myocardial infarction was documented macroscopically and by light microscopy and histology. RESULTS: In all 445 cases, at least one coronary artery had evidence of moderate to advanced atherosclerosis. About two thirds were between 50 and 70 years. Men had a higher incidence than women, but with advancing age (>60 years) this difference was reduced. Myocardial infarction was found in 17 cases (11 acute; 6 acute and healed). Fifty-eight cases (13.0%) had coronary thrombi, mostly involving the left anterior descending and the right coronary arteries (81%); only six of these were associated with acute myocardial infarction. CONCLUSION: In our population, arrhythmia was the most common cause of sudden cardiac death, while acute coronary thrombi and acute myocardial infarction were detected only in some cases. Because of the heterogeneity in the cause of sudden cardiac deaths in adults, a detailed forensic investigation may provide important information on the cause of death and help in the development of primary and secondary prevention.     

Sequelae of Kawasaki disease in adolescents and young adults

Kawasaki disease is an acute vasculitis of unknown etiology that predominantly affects children <5 years of age. Structural damage to the coronary arteries after the acute, self-limited illness is detected by echocardiography in ∼25% of untreated patients. The long-term effects of the acute coronary arteritis are unknown. To define the spectrum of clinical disease in young adults that can be attributed to Kawasaki disease in childhood, we performed a retrospective survey of cases reported in the English and Japanese published data of adult coronary artery disease attributed to antecedent Kawasaki disease. The mean age at presentation with cardiac sequelae was 24.7 ± 8.4 years (range 12 to 39) for the 74 patients identified with presumed late sequelae of Kawasaki disease. Symptoms at the time of presentation with cardiac sequelae included chest pain/myocardial infarction (60.8%), arrhythmia (10.8%) and sudden death (16.2%). These symptoms were precipitated by exercise in 82% of patients. One-third of the patients in whom a chest radiograph was taken had ring calcification. Angiographic findings included coronary artery aneurysm (93.2%) and coronary artery occlusion (66.1%). Extensive development of collateral vessels was reported in 44.1% of patients. Autopsy findings included coronary artery aneurysms (100%0 and coronary artery occlusion (72.2%). The acute vasculitis of Kawasaki disease can results in coronary artery damage and rheologic changes predisposing to thrombus formation or progressive atherosclerotic changes that may remain clinically silent for many years. Coronary artery aneurysms and calcification on chest radiography were unusual features in this group of patients. A history of antecedent Kawasaki disease should be sought in all young adults who present with acute myocardial infarction or sudden death.     

Acute myocardial infarction late after Mustard procedure for dextrotransposition of the great arteries

Systemic right ventricular dysfunction has been closely linked to late mortality and sudden cardiac death in patients with Mustard procedure for dextrotransposition of the great arteries. Two young patients with dextrotransposition of the great arteries late after Mustard procedure who presented with acute transmural myocardial infarction and sudden cardiac death (one patient) without prior exertional angina or causative coronary abnormalities are reported. It is surmised that acute coronary emboli originating from a severely dilated, hypocontractile systemic ventricle were the cause of transmural myocardial infarction. This phenomenon may be an important and as yet unrecognized factor in late morbidity and mortality in such patients.     

How to evaluate sudden cardiac death risk after myocardial infarction?

Sudden cardiac death is the mode of death of more than half of coronary heart disease patients. Preventing sudden cardiac death involves prevention of ventricular arrhythmias occurrence as well as the treatment by an implantable cardioverter defibrillator. The evaluation of sudden cardiac death risk should consider the underlying cardiopathy, the associated coronary risk factors and all pharmacological treatment efficient to reduce ventricular remodeling and myocardial ischemia. Only significant low ejection fraction and positive ventricular testing in some cases are now considered are now considered by the current French recommendations for cardioverter defibrillator implantation in primary prevention. However, other noninvasive markers such as heart rate variability and T wave alternans are of interest in sudden cardiac death risk stratification after myocardial infarction.     

Myocardial bridging in adult patients with hypertrophic cardiomyopathy

OBJECTIVES: This investigation examined the risk of sudden cardiac death and other mortality in adult patients with hypertrophic cardiomyopathy (HCM) who have myocardial bridging diagnosed at coronary angiography. BACKGROUND: Several reports have associated myocardial bridging with an adverse prognosis in pediatric HCM patients, but the prognosis of myocardial bridging in adult patients with HCM is unknown. METHODS: The coronary angiograms of 425 patients with HCM (mean age 60 +/- 15 years [range 18 to 89 years]) at the Mayo Clinic were examined for the presence of myocardial bridging. Clinical follow-up was conducted to assess mortality. Survival of patients with bridging was compared with HCM patients who also underwent angiography but who did not have evidence of bridging. RESULTS: A total of 64 patients (15%) had myocardial bridging. The mean follow-up for the entire study was 6.8 +/- 5.4 years. There was no difference in survival free of all-cause mortality (5-year estimate, bridging vs. no bridging, 91% vs. 85%; p = 0.42), all cardiac death (93% vs. 89%; p = 0.60), and sudden cardiac death (95% vs. 97%; p = 0.72). Univariate and multivariate proportional hazards models also did not identify the presence of bridging or specific characteristics of the degree or extent of bridging with a poor outcome. CONCLUSIONS: This study observed no increased risk of death, including sudden cardiac death, among adult patients with HCM who had myocardial bridging diagnosed at coronary angiography.     

Clinical and biochemical factors associated with prognosis after myocardial infarction at a young age

Objectives. This study examined the effect of metabolic disturbances, hemostatic function, coronary artery disease severity and left ventricular function on the long-term prognosis after myocardial infarction in men <45 years old.Background. Heavy smoking; dyslipoproteinemias involving very low density lipoprotein (VLDL), low density lipoprotein (LDL) and high density lipoprotein (HDL); a family history of premature coronary artery disease; hyperinsulinemic responses to oral and intravenous glucose challenges; and defective fibrinolytic function characterize the young postinfarction patient, but the influence of these features on the long-term prognosis is virtually unknown.Methods. Measurements of hemostatic function and metabolic and angiographic indicators of risk were included in a prospective cohort study of variables predictive of reinfarction, cardiac death and major coronary events within 6 to 9 years in 108 unselected nondiabetic men with a first myocardial infarction before age 45 years.Results. During follow-up, 20 patients had sudden cardiac death, and 53 had a major coronary event (reinfarction, sudden cardiac death, bypass surgery or intervention by catheterization). In multivariate analysis, VLDL and global coronary atherosclerosis score predicted reinfarction; plasma plasminogen activator inhibitor-1 (PAI-1) activity and global coronary stenosis score predicted cardiac death; and VLDL triglyceride levels, global coronary atherosclerosis score and age predicted any major coronary event.Conclusions. This prospective cohort study shows that hypertriglyceridemia, impaired fibrinolytic capacity secondary to plasma PAI-1 activity elevation and extensive coronary artery disease increase the risk of recurrences in men with a first myocardial infarction before age 45 and contribute to the relatively poor long-term prognosis in this patient group.     

心源性晕厥或猝死的原因分析

分析 32例在入院时或入院后至少发生 1次或 1次以上心源性晕厥或猝死患者的原因及其发作时与发作前、后的常规 12导联心电图或持续心电监视心电图。结果 :引起心源性晕厥或猝死的基本原因可分为以下几种类型 :①冠心病急性或陈旧性心肌梗死 ;②长QT(U)综合征 ;③Brugada综合征 ;④扩张型和肥厚型心肌病 ;⑤特发性巨大异常J波 ;⑥其他原因。上述各种心源性晕厥或猝死患者有各自不同的心电学特征。结论 :心源性晕厥或猝死是由不同原因、不同心电学特征所致的非单一独立的临床实体     

Angina pectoris, myocardial infarction and sudden cardiac death with normal coronary arteries: a clinicopathologic study of 9 patients with progressive systemic sclerosis

The syndrome of angina pectoris or acute myocardial infarction without obstructive coronary artery disease has been the subject of much interest. We studied nine autopsied patients with progressive systemic sclerosis and evidence of ischemic heart disease but morphologically normal coronary arteries. Three patients had angina pectoris and three others chest pains of unknown etiology, six had ventricular arrhythmias, four had clinically suspected acute myocardial infarction, and eight had sudden cardiac death. At autopsy extensive focal myocardial necrosis was present in seven patients and myocardial scarring in all nine, but all patients had widely patent intramural and extramural coronary arteries. The finding of contraction band myocardial necrosis in seven of the eight patients who experienced sudden death suggests that the myocardial damage was a consequence of reperfusion of focally nonperfused myocardium, and thus due to a myocardial Raynaud's phenomenon. Patients with PSS may provide a model of spasm of intramyocardial vessels causing angina pectoris or myocardial infarction with morphologically normal coronary arteries.