急性心肌梗死并发室间隔穿孔的临床特点分析

目的分析急性心肌梗死并发室间隔穿孔的临床特点,判断患者预后。方法我院1994年6月～2006年7月共收治2027例急性心肌梗死患者,其中17例患者出现室间隔穿孔,并对其临床和超声心动图资料进行回顾性分析。结果我院急性心肌梗死并发室间隔穿孔的发病率为0.84%。17例室间隔穿孔患者中,9例合并高血压;12例前壁心肌梗死。11例冠状动脉造影检查均为2支以上血管病变;10例患者的梗死相关血管闭塞。超声心动图检查左心室平均直径(54.1±6.2)mm,左心室射血分数(40.4±10.8)%;10例室壁瘤形成,穿孔位置多在室间隔近心段的1/3处,穿孔直径(9.5±3.9)mm。内科保守治疗疗效较差,病死率82.35%。结论急性心肌梗死并发室间隔穿孔多发生在老年前壁心肌梗死患者,内科保守治疗病死率高。     

Cardiac ruptures following myocardial infarction in medicolegal cases]

OBJECTIVE: Characteristics of legal autopsy cases with cardiac rupture following myocardial infarction are investigated in this retrospective observational study and the results are compared with a control group consisting of acute myocardial infarction cases without rupture. METHODS: Legal autopsy reports of 50 cases with heart tamponade resulting from heart muscle rupture following myocardial infarction, autopsied at the Morgue Department of the Council of Forensic Medicine between the years 1998-2005 were retrospectively reviewed. Findings were compared to control group consisting of 30 myocardial infarction cases without rupture. RESULTS: The rupture was located in the left ventricle in 48 of 50 cases. At microscopic examination, infarction date was consistent with first three days, 4-7 days and 1-2 weeks for 30, 12 and 8 cases, respectively. The average volume of fluid leading to tamponade was 467 ml in males and 352.3 ml in females. There were no statistical differences between rupture and control groups for existence of hypertrophy and scar tissue in myocardium and advanced atheromatous lesions in coronaries (p>0.05). Considering the manner of death of the cases died due to heart wall rupture and tamponade formation, 28 of the cases were found dead at home, 6 died suddenly by falling to the ground at home or on the street, and 5 were delivered dead to the hospital. CONCLUSION: The rupture was located in the left ventricle in almost all cases. Ruptures in the left ventricle were found most frequently in the anterior wall. There was no relationship between development of rupture and existence of hypertrophy and scar tissue in myocardium, and advanced atheromatous lesions in coronaries.     

急性ST段抬高心肌梗死中心脏破裂的认识

目的：研究对急性ST段抬高心肌梗死中心脏破裂的认识。方法选择2010年10月-2011年12月,我院收治的急性ST段抬高心肌梗死患者150例,对患者的心脏破裂进行诊断,并根据诊断结果将150例患者分成12例心脏破裂组,138例无心脏破裂组。观察两组患者的性别,年龄,治疗使用的方法。结果在心脏破裂中,年龄、性别,治疗方法的不同对其均有影响（P〈0.05）。结论心脏破裂是急性ST段抬高心肌梗死中最严重的并发症,了解急性ST段抬高心肌梗死中出现心脏破裂的因素,为临床医生在治疗时提供有利依据,延长患者的生命。     

Cardiac rupture complicating acute myocardial infarction in presence of normal electrocardiogram.

Cardiac rupture following acute myocardial infarction occurs most frequently in patients with electrocardiographic evidence of transmural infarction. Unusual presentations of cardiac rupture need immediate recognition to enable successful surgical treatment. An unusual case is presented of cardiac rupture complicating acute myocardial infarction despite a normal electrocardiogram prior to the rupture.     

Cardiac Ruptures in Northern Norway

Abstract. In 4649 autopsies performed, in 1972–1985, 824 cases of acute myocardial infarction were found. Of these, 104 (12.6%) had cardiac rupture. Ten cases had rupture of the interventricular septum. The clinical and pathological records were reviewed, and the rupture group was compared with a control group of 100 patients who died from acute myocardial infarction without rupture. Of the patients with rupture, 85% died during the first week after the onset of myocardial infarction; three patients with rupture died suddenly without previous clinical evidence of myocardial infarction. Rupture occurred only in hearts with transmural infarcts, and predominantly in the anteroseptal wall. Patients with rupture had significantly higher blood pressure, fewer previous infarcts, higher frequency of coronary thrombi, less myocardial scar tissue and lower heart weight compared to the control group. There were no significant differences regarding age and sex distribution, physical effort at the symptom debut or death, medication, previous and present diseases other than infarcts, complications or the degree of atherosclerosis in the coronary arteries or aorta.     

Factors in myocardial rupture An analysis of two hundred and four cases at Los Angeles County Hospital between 1924 and 1959

The total analysis of 204 cases of myocardial rupture which occurred in the Los Angeles County Hospital was reported. Myocardial rupture rarely occurs under the age of 50 years. Although the incidence of myocardial infarction invariably is reported to be higher among men than women our material indicates that cardiac rupture is somewhat more likely to develop in women [110 women (53.9 per cent), ninety-four men (46.1 per cent)]. Myocardial rupture is relatively rare in Negro patients.

In our material reasonably good correlation was obtained between electrocardiographic indication of acute myocardial infarction and necropsy incidence of myocardial necrosis. As was anticipated, myocardial rupture occurred at or immediately adjacent to the site of necrosis. Ordinarily, myocardial ruptures occur in the left ventricle. In our series the most frequent site of rupture was in the anterior wall, especially at the junction of the anterior wall and the septum.

Average survival time for twenty-one patients admitted to the hospital within 6 hours of the clinical onset of myocardial infarction was 9 days, whereas average survival time for twentyone patients hospitalized 7 hours or longer after the myocardial infarction was only 2.6 days. The longer survival time for patients hospitalized within the first 6 hours may be due to greater restriction of their activity in the immediate postinfarction period. Death usually is immediate in ventricular rupture, whereas in the interventricular septal rupture most of the patients survive a few days.

In the final 8 years and 3 months of our survey, the incidence of rupture following myocardial infarction has undergone a sharp decrease at the Los Angeles County Hospital. This decrease is presumably due to better management of the acute episode of myocardial infarction and more particularly to the use of vasopressor drugs and anticoagulants. Anticoagulants did not increase the incidence of the rupture but cardiac tamponade is relatively frequent in patients with myocardial rupture maintained on anticoagulants. The physician must be alert for signs of tamponade (i.e., pulsating neck veins, increase in cardiac dullness) because tamponade can be managed surgically. Except for the reduced incidence of myocardial rupture in the period of survey, the findings are in agreement with earlier reports from the same hospital.     

Risk factors and effect of reperfusion therapy on left ventricular free wall rupture following acute myocardial infarction

Reperfusion therapy is one of the most effective treatments for acute myocardial infarction, but the effect on left ventricular free wall rupture remains to be determined. This study tried to clarify the risk factors and effect of reperfusion therapy on the risk of free wall rupture following acute myocardial infarction. 2,671 consecutive patients with acute myocardial infarction admitted to our hospital were examined. Incidence of free wall rupture showed no degenerative change(0 to 5.8%; mean 2.1%). The 1,269 consecutive patients from 1985 to 1995 were examined closely to evaluate risk factors and the effect of reperfusion therapy on the risk of free wall rupture. Fourteen patients who underwent emergent coronary artery bypass surgery were excluded. Free wall rupture was found in 25 patients (2.0%). Multivariate analysis confirmed that high age(> or = 70 years) and first acute myocardial infarction were independent risk factors of free wall rupture (odds ratio 3.62, p = 0.003; odds ratio 7.69, p = 0.046, respectively). The incidence of free wall rupture in the conservative therapy group(n = 799) was 2.1%, successful reperfusion group(n = 373) was 0.5%, and unsuccessful reperfusion group(n = 83) was 7.2% with significant statistical differences(p < 0.01). There was no statistical difference between the direct percutaneous transluminal coronary angioplasty group(n = 84, 3.6%) and the thrombolysis group(n = 372, 1.3%). Successful reperfusion was the only independent factor in the reperfusion therapy group that reduced the incidence of free wall rupture(odds ratio = 0.07, p = 0.001). We conclude that reperfusion of the infarct-related artery and more intensive management of unsuccessful reperfusion is important to prevent free wall rupture following acute myocardial infarction.     

Rupture of the myocardium. Occurrence and risk factors

The occurrence of myocardial rupture was studied in a well defined unselected population of patients with acute myocardial infarction, and the group of patients who died of rupture of the heart were compared with two control groups. Of a total of 3960 patients, 1746 (44%) fulfilled the diagnostic criteria for acute myocardial infarction. Rupture was defined solely on the basis of the presence of a pathological passage through part of the myocardium, either the free wall of the left ventricle or the septum, found at necropsy or during operation. Two controls were selected for each patient and matched for age and sex, one (control group A) with acute myocardial infarction having died in hospital but not of rupture (non-rupture cardiac death) and one (control group B) with acute myocardial infarction having survived the hospital stay. Necropsy was performed in 75% of all fatal cases with acute myocardial infarction. The total hospital mortality was 19%, the highest mortality being among women over 70 years (29%). Ruptures (n = 56) were found in 17% of the hospital deaths, or 3.2% of all cases of acute myocardial infarction. Women aged less than 70 had the highest incidence of rupture, 42% of deaths being due to rupture. The mean age for patients with rupture and controls was 70.5 years. The median time after admission to death was approximately 50 hours for patients and control group A. Thirty per cent of the patients with rupture occurred within 24 hours of the initial symptoms occurring. Angina and previous acute myocardial infarction were more common among control group A. Patients with rupture and control group B were mostly relatively free of previous cardiovascular or other diseases (chronic angina pectoris ( > 2 months) and previous myocardial infarction). Sustained hypertension during admission to the coronary care unit was more common in patients than in control group A. Hypotension and shock were more common among control group A. Most (79%) of the patients who subsequently ruptured did not receive any corticosteroids at all during the hospital stay. Severe heart failure and antiarrhythmic treatment were more uncommon among patients than among control group A. Patients with rupture received analgesics approximately three times a day throughout their stay. Control group B received analgesics mostly during the first 24 hours. Thus female patients, patients with first infarcts, and patients with sustained chest pain should be investigated for the possibility of rupture. As many as one third (32%) of ruptures may be subacute, and therefore time is available for diagnosis and surgery.     

Case report: An unusual complication of clopidogrel

In an era of early and invasive therapeutic approaches, myocardial rupture has become an uncommon complication of myocardial infarction. While septal wall rupture most often leads to devastating haemodynamic consequences, free wall rupture is usually fatal. We report a case of a 48-year-old man in whom an incomplete myocardial rupture located in the inferior part of the interventricular septum was promptly detected during the acute phase of an inferior myocardial infarction treated by early percutaneous coronary angioplasty. A conservative rather than a surgical approach was decided with a favourable short-term outcome.     

Rupture of the myocardium. Occurrence and risk factors.

The occurrence of myocardial rupture was studied in a well defined unselected population of patients with acute myocardial infarction, and the group of patients who died of rupture of the heart were compared with two control groups. Of a total of 3960 patients, 1746 (44%) fulfilled the diagnostic criteria for acute myocardial infarction. Rupture was defined solely on the basis of the presence of a pathological passage through part of the myocardium, either the free wall of the left ventricle or the septum, found at necropsy or during operation. Two controls were selected for each patient and matched for age and sex, one (control group A) with acute myocardial infarction having died in hospital but not of rupture (non-rupture cardiac death) and one (control group B) with acute myocardial infarction having survived the hospital stay. Necropsy was performed in 75% of all fatal cases with acute myocardial infarction. The total hospital mortality was 19%, the highest mortality being among women over 70 years (29%). Ruptures (n = 56) were found in 17% of the hospital deaths, or 3.2% of all cases of acute myocardial infarction. Women aged less than 70 had the highest incidence of rupture, 42% of deaths being due to rupture. The mean age for patients with rupture and controls was 70.5 years. The median time after admission to death was approximately 50 hours for patients and control group A. Thirty per cent of the patients with rupture occurred within 24 hours of the initial symptoms occurring. Angina and previous acute myocardial infarction were more common among control group A. Patients with rupture and control group B were mostly relatively free of previous cardiovascular or other diseases (chronic angina pectoris ( > 2 months) and previous myocardial infarction). Sustained hypertension during admission to the coronary care unit was more common in patients than in control group A. Hypotension and shock were more common among control group A. Most (79%) of the patients who subsequently ruptured did not receive any corticosteroids at all during the hospital stay. Severe heart failure and antiarrhythmic treatment were more uncommon among patients than among control group A. Patients with rupture received analgesics approximately three times a day throughout their stay. Control group B received analgesics mostly during the first 24 hours. Thus female patients, patients with first infarcts, and patients with sustained chest pain should be investigated for the possibility of rupture. As many as one third (32%) of ruptures may be subacute, and therefore time is available for diagnosis and surgery.     

Rupture of a left ventricular papillary muscle during acute myocardial infarction: analysis of 22 necropsy patients

Certain clinical and cardiac morphologic findings are described in 22 patients, aged 45 to 80 years (mean 64) (15 men [68%]), in whom rupture of a papillary muscle occurred during acute myocardial infarction. In most, the acute infarction associated with papillary muscle rupture was a first coronary event (only 18% had a myocardial scar consistent with prior infarction and 29% had angina pectoris). The posteromedial papillary muscle, presumably because of its more tenuous blood supply, ruptured almost three times more frequently than the anterolateral one (73 and 27%, respectively). Quantitative examination of the amounts of narrowing by atherosclerotic plaque in each of the four major epicardial coronary arteries (right, left main, left anterior descending and left circumflex) disclosed less narrowing in the patients with rupture than in the patients with fatal acute myocardial infarction unassociated with rupture. Of the 519 five mm sections of coronary artery examined (11 patients), only 68 sections (13%) were narrowed greater than 75% in cross-sectional area compared with 34% of 1,403 sections from 27 patients with fatal myocardial infarction without rupture.     

Myocardial rupture after myocardial infarction: Detection by multi-gated image-acquisition scintigraphy

Myocardial rupture following infarction usually is an acute and dramatic event. Rarely, it may take a subacute course, allowing surgical treatment. We report herein a case of subacute rupture of the heart in a 54 year old patient with acute myocardial infarction. The rupture was diagnosed by the appearance of a radiopaque halo around the heart during radionuclide ventriculography. The patient subsequently underwent surgical resection of a large anterolateral aneurysm and a 2 inch long rupture of the myocardium and survived. Clinical suspicion, prompt diagnosis, and surgical intervention are important in the management of this relatively unusual complication of infarction.     

Rupture of the free wall of the heart as cause of death in acute myocardial infarct

Twenty four cases with myocardial rupture among 259 patients with autopsy after death due to myocardial infarction, were compared with patients with acute myocardial infarction and death secondary to other causes. Myocardial rupture occured during the first 72 hours in 58% of the patients and all cases within the first five days. Two thirds of the patients were males and 46% were 70 years of age. There were 24 myocardial ruptures (9.5%). Previous history of arterial hypertension and un-remittent anginal pain were predisposing factors for rupture (p=0.05). Other previously reported bad prognostic factors such as persistent hipertension after acute infarction, severe exercise before infarction and history of Diabetes Mellitus were not statistically significant in this study. Ruptured myocardium was not influenced by a previous history of myocardial infarction, hospitalization delay in the C.C.U., administration of anticoagulants, digitalis or pressor amines. There was no significant difference among the groups compared in enzyme curves or magnitude of leucocytosis. Electromechanic dissociation, sinus bradycardia, nodal rhythm followed by idioventricular rhythm and asystole, were observed following myocardial rupture.     

Contrast echocardiography for detection of incomplete rupture of the left ventricle after acute myocardial infarction

Myocardial rupture is a major complication after acute myocardial infarction. With complete rupture of the free left ventricular wall cardiac tamponade occurs with fatal outcome in most cases. With partial rupture, however, hemorrhage is slower, allowing days or weeks for diagnosis. Survival of these patients strongly depends on early recognition of this complication followed by immediate surgical intervention. Echocardiography is the diagnostic tool of choice to detect myocardial rupture with consecutive hemopericardium but diagnosis remains difficult even if suspected.We describe the case of a patient with inferior infarction who presented with cardiogenic shock, echocardiographic signs of pericardial effusion and abnormal motion and myocardial irregularities of the inferior wall. With Doppler echocardiography no flow across the wall was detected. Left heart contrast echocardiography confirmed the diagnosis of suspected myocardial rupture by clear deliniation of the defect. Immediate surgical repair was successfully performed in this patient with favorable long-term outcome. Thus, echocardiography early after acute myocardial infarction is useful in detecting subsequent complications and the use of contrast echocardiography should be considered in suspected myocardial rupture.     

Sutureless patch repair of post-myocardial infarction left ventricular rupture

Ventricular rupture following myocardial infarction is a serious clinical problem with a high mortality. A 60-year-old man with left ventricular rupture and cardiac tamponade following myocardial infarction was managed successfully by emergency surgery. An onlay patch of Teflon held in place by an adhesive without any sutures was used to repair the ruptured myocardium.     

Myocardial healing and repair after experimental infarction in the rabbit

Adequacy of healing after acute myocardial infarction may determine the incidence of postmyocardial infarction rupture and ventricular aneurysm. Accordingly, in 36 rabbits, from 1 to 8 days after coronary ligation, and in 18 shams, we measured collagen formation and mechanical resistance of the infarcted left ventricle to stretch and rupture. Prolyl hydroxylase, an intracellular enzyme of collagen synthesis, increased from control activity of 3970 +/- 431 to 9224 +/- 643 counts/min per mg (cpm/mg) extractable protein (P less than 0.01) at 48 hours and was nearly maximal at 3 days postmyocardial infarction (14,518 +/- 2,030 cpm/mg, P less than 0.01). Lysyl oxidase, an extracellular collagen cross-linkage enzyme, increased from control activity of 29.6 +/- 4.8 to 74.7 +/- 18.8 cpm/mg extractable protein (P less than 0.01) at 72 hours and peaked at 121.5 +/- 7.3 (P less than 0.01) 4-6 days postmyocardial infarction. Hydroxyproline, a measure of collagen content, increased from control of 2.8 +/- 0.2 to 5.3 +/- 0.6 mg/g dry weight (P less than 0.05) at 72 hours and continued to increase at 8 days postmyocardial infarction (14.5 +/- 1.7 mg/g dry weight; P less than 0.01). When enzyme activities and hydroxyproline content were expressed relative to other reference bases, including DNA, tissue protein, dry weight, and total left ventricle, similar results were obtained. The mechanical properties of the infarcted left ventricle were determined by filling a balloon in the excised left ventricle until rupture. The rupture threshold in the normal left ventricle, [664 +/- 43 mm Hg (n = 16)], was not significantly different from that of the infarcted left ventricle on days 1-8 postmyocardial infarction. However, left ventricular rupture occurred more often through the myocardial infarction on days 1-4 postmyocardial infarction (59%) than on days 6 and 8 (18%; P = 0.03) when collagen content had significantly increased. Wall stress at the point of rupture in left ventricles from shams and normals was 30 +/- 2 g/mm2; tensile strength in isolated left ventricle muscle strips was 25 +/- 4 g/mm2 and in isolated scar strips at 7 days postmyocardial infarction was 59 +/- 7 g/mm2. The passive stiffness of the infarcted left ventricle increased from control of 61 +/- 5 to 94 +/- 6 mm Hg/100 microliters (P less than 0.05) at 4 days and 100 +/- 7 mm Hg/100 microliters (P less than 0.01) at 6 days postmyocardial infarction. Stiffness correlated with hydroxyproline content over the 8 days postmyocardial infarction (r = 0.599; P less than 0.001). Thus, the acutely infarcted ventricle was highly resistant to rupture during the initial 48 hours postmyocardial infarction, before any increase in collagen occurred. This result suggests that the preinfarction collagen content has an important role in preventing rupture. After 72 hours postmyocardial infarction, collagen synthesis appeared to be a determinant of infarct stiffness and resistance of the infarcted ventricle to rupture.     

急性心肌梗死伴与不伴心脏破裂临床病理分析

目的探讨急性心肌梗死(AMI)心脏破裂的原因、好发部位及与冠状动脉狭窄的关系。方法AMI死亡并行尸体解剖检查63例,其中AMI伴心脏破裂18例,不伴心脏破裂45例。结果AMI伴心脏破裂组高血压、溶栓治疗及首次心肌梗死发生率明显升高(P<0．05),而性别、梗死后心绞痛、心源性休克、心肌酶谱峰值、梗死面积与心脏破裂无明显关系(P>0．05)。心脏破裂多发生在AMI后3d内,第1天占33．3％,多见于前壁、心尖部及下壁。尸体解剖示破裂处心肌变薄伴出血,梗死相关血管多为高度狭窄。结论高血压、溶栓治疗及首次心肌梗死均为心脏破裂的危险因素。AMI的超急性期是心脏破裂的高发期。前降支及右冠状动脉高度狭窄导致心脏破裂增加。     

Successful surgical repair of left ventricular rupture after acute myocardial infarction

A 61-year-old man with impending myocardial infarction was admitted and treated by percutaneous transluminal coronary recanalization (PTCR) therapy using Urokinase. Patient's symptoms subsided and his general condition maintained stable until the fifth hospital day, when he developed the signs of cardiac rupture. He was operated upon immediately, and the left ventricular rupture was confirmed and repaired successfully. Patient recovered from the surgery well. This report describes the rare successful surgical case of cardiac rupture secondary to acute myocardial infarction in Japan.     

老年急性心肌梗死并发室间隔穿孔7例临床分析

目的分析急性心肌梗死（AMI）并发室间隔穿孔的临床病例特点,为该并发症的早期诊断和治疗提供依据。方法对7例室间隔穿孔患者的临床特征、治疗和预后进行回顾性分析。结果AMI并室间隔穿孔患者室间隔破裂穿孔常发生于前壁心肌梗死的患者,穿孔部位多位于室间隔近心尖部。高危因素包括高血压、年龄（60～69岁）、女性、缺乏侧支循环和广泛前壁透壁性心肌梗死和右室梗死（常可导致低血压）、无心绞痛病史。患者多存在房性快速型心律失常,新出现右束支传导阻滞提示预后严重不良。室间隔破裂的预后很差。内科保守治疗的院内死亡率高。结论注重体征及尽早行超声心动检查是早期诊断该并发症的关键,进行积极的内科治疗并力争外科手术的机会能降低死亡率。     

Papillary Muscle Rupture Following Non‐ST‐Elevation Myocardial Infarction: A Case Report

Papillary muscle rupture is a serious mechanical complication of acute myocardial infarction typically seen within 5–7 days following transmural ST‐elevation myocardial infarction. The incidence of papillary muscle rupture has markedly decreased in the modern era due to improved diagnosis and early coronary revascularization of ST‐elevation myocardial infarction. As a result, papillary muscle rupture is increasingly seen following non‐ST‐elevation myocardial infarction where both diagnosis and revascularization can be delayed. In this report, we describe two cases of papillary muscle rupture following delayed presentation of non‐ST‐elevation myocardial infarction and delayed recognition of papillary muscle rupture.