Left ventricular performance after acute myocardial infarction

Current knowledge concerning the major hemodynamic features of acute myocardial infarction has been reviewed and discussed in relation to present concepts of cardiac pathophysiology. The physical examination provides a great deal of information and new, noninvasive methods promise to supplement the bedside appraisal of left ventricular function. Direct hemodynamic methods of serially monitoring patients with acute myocardial infarction are finding increasing application and recently have added considerably to our understanding of this condition. Certain limitations in the use of the central venous pressure, pulmonary arterial pressure, and cardiac output in appraising left ventricular function have become apparent, but together with direct catheterization of the left ventricle such hemodynamic studies have now provided limited correlations between the clinical picture and various hemodynamic patterns. It is becoming increasingly clear that most of these features, including cardiogenic shock, probably reflect varying degrees of left ventricular failure. These initial findings and interpretations will require confirmation, however, and so far insufficient objective data are available concerning the natural history of acute myocardial infarction and its responses to various forms of therapy. The aims of investigations now being carried in specialized Myocardial Infarction Research Units and other cardiovascular research centers, are to gain such further understanding of the pathophysiology of this disease and to aid in its clinical management by developing accurate indirect monitoring techniques as well as new forms of therapy.     

Left ventricular dysfunction after acute myocardial infarction: results of a prospective multicenter study

In a multicenter prospective study of 866 patients who survived the coronary care unit phase of an acute myocardial infarction, variables reflecting left ventricular function were examined to assess their impact on 2 year survival. Single variables that reflected left ventricular dysfunction before infarction and in the acute and recovery phases were, respectively, history of prior myocardial infarction, rales in the coronary care unit dichotomized at greater than bibasilar and predischarge radionuclide ejection fraction dichotomized at less than 0.40. When combined in a stepwise fashion, patients lacking these three risk characteristics had a 2 year 4.2% mortality rate, whereas patients possessing all three characteristics had a 45% mortality rate. Rales in the coronary care unit and predischarge ejection fraction act independently, and each contributes to mortality. Fifty-two patients with advanced rales but an ejection fraction of 0.40 or greater had a 21% mortality rate. Similarly, 208 patients with few rales but an ejection fraction of less than 0.40 had a 15% mortality rate. These data suggest that the mortality risk imposed by those factors that assess permanent left ventricular damage is independent of and additive to the mortality risk contributed by dynamic, acute phase dysfunction. These data fit the hypothesis that acute phase dysfunction is, in part, due to transient ischemia that, on reversal, can restore function toward normal. The results suggest 1) that assessment of left ventricular function during the acute and recovery phases of myocardial infarction is necessary to define prognostic characteristics of an individual patient, and 2) that of particular importance is the identification of patients whose postinfarction course is consistent with reversible ischemia.     

急性心肌梗死后左室重构的临床危险因素探讨

目的对急性心肌梗死后左室重构的临床危险因素进行评估。方法将进入本观察的５１例病人,按溶栓治疗后,有无Ｑ波形成,分为Ｑ波组和非Ｑ波组,全部病人入住ＣＣＵ,并在入院即刻及入院后８、１６、２４、４８和７２小时分别进行血清心肌酶学检查。对其中３４例病人在心梗后１周和６周行超声心动图检查,并测定左室质量指数。结果Ｑ波组血清ＣＰＫ峰值（１３４７５８±２２０３３）ＩＵ,左室质量指数在心梗后１周和６周分别为（２３４２８±９２３６）ｇ·ｍ－２、（２７１５２±９３１２）ｇ·ｍ－２,均明显高于非Ｑ波组,随访半年表明新近出现心衰亦明显高于非Ｑ波组。结论溶栓后的有Ｑ波出现,血清ＣＰＫ峰值高于５００ＩＵ,左室质量指数＞２２０ｇ·ｍ－２,是急性心肌梗死后左室重构的危险因素。     

Left ventricular free wall rupture after acute myocardial infarction(The 21th case)

患女性，69岁，退休，以胸闷16h入院。患活动后发病，逐渐出现呼吸困难。否认既往冠心病病史，合并高血压。入院时查体体温36．5℃，心率110次／min，呼吸27次／min，血压90／60mmHg。精神差，心律齐，心音低钝，各瓣膜区未闻及杂音。心尖部可闻及舒张期奔马律，双肺可闻及中到大量湿哕音。急诊心电图：窦性心动过速，前壁及高侧壁导联ST段抬高0．1～0．3mV，Q波形成。心肌酶升高。诊断急性广泛前壁心肌梗死。[第一段]     

急性心肌梗死后左心室重构及其防治

本文简述了急性心肌梗死后左心室重构的发生机制、时间、后果、影响因素及防治措施等     

Left ventricular thrombi after short-term high-dose anticoagulants in acute myocardial infarction

To examine the effect of short-term, high-dose anticoagulationon the subsequent occurrence of left ventricular (LV) thrombiafter a first anterior wall acute myocardial infarction (AMI),21 patients received placebo and 21 high-dose anticoagulantsduring the first 10 days of the acute infarction. They werestudied with cross-sectional echocardiography 10 days and 1-3and 6 months post infarction. At 1 month, 6 of 7 thrombi presentin the placebo group at 10 days were still visible. No thrombiwere detected at 10 days in the anticoagulation group, but 6patients had developed a LV thrombus at 1 month. These 12 patientswith LV thrombi were subsequently treated with oral warfarinfor 2 months, after which all thrombi had disappeared. Warfarinwas then discontinued, and a thrombus had recurred in 5 patientsafter 6 months. Apical akinesis at 10 days a predictor for thrombuswith a sensitivity and specificity of 100% and 72.2% respectively. Three of the 13 patients with LV thrombi suffered stroke incontrast to none without thrombi (P=0.025). We conclude that after discontinuation of short-term high-doseanticoagulation therapy in anterior AMI, LV thrombi may developrapidly and lead to embolic complications, particularly in patientswith persisting apical akinesis.     

Left ventricular pseudoaneurysm after myocardial infarction

In this report, a case of a left ventricular (LV) pseudoaneurysm due to a previous myocardial infarction, which was repaired successfully, is described. A 62-year-old man, with a history of acute anterior wall myocardial infarction 6 months previously, was admitted with the complaints of acute dyspnea and palpitation. Echocardiography revealed an LV aneurysm, and ventriculography showed ventricular dysfunction and an LV pseudoaneurysm. Coronary angiography showed total occlusion of the proximal segment of the left anterior descending artery with a very thin lumen and insufficient retrograde filling. Under cardiopulmonary bypass and beating heart, the pseudoaneurysm was resected and the defect on the ventricular free wall was closed by the remodeling ventriculoplasty method of Dor. Histopathologic examination of the resected material confirmed the diagnosis of pseudoaneurysm. The postoperative course of our patient was uneventful. He was discharged on the ninth postoperative day.     

Left ventricular thrombi after short-term high-dose anticoagulants in acute myocardial infarction

To examine the effect of short-term, high-dose anticoagulationon the subsequent occurrence of left ventricular (LV) thrombiafter a first anterior wall acute myocardial infarction (AMI),21 patients received placebo and 21 high-dose anticoagulantsduring the first 10 days of the acute infarction. They werestudied with cross-sectional echocardiography 10 days and 1-3and 6 months post infarction. At 1 month, 6 of 7 thrombi presentin the placebo group at 10 days were still visible. No thrombiwere detected at 10 days in the anticoagulation group, but 6patients had developed a LV thrombus at 1 month. These 12 patientswith LV thrombi were subsequently treated with oral warfarinfor 2 months, after which all thrombi had disappeared. Warfarinwas then discontinued, and a thrombus had recurred in 5 patientsafter 6 months. Apical akinesis at 10 days a predictor for thrombuswith a sensitivity and specificity of 100% and 72.2% respectively. Three of the 13 patients with LV thrombi suffered stroke incontrast to none without thrombi (P=0.025). We conclude that after discontinuation of short-term high-doseanticoagulation therapy in anterior AMI, LV thrombi may developrapidly and lead to embolic complications, particularly in patientswith persisting apical akinesis.     

Left ventricular thrombus formation after first anterior wall acute myocardial infarction

The characteristics of the left ventricle and coronary arteries associated with left ventricular (LV) thrombus in patients with recent anterior acute myocardial infarction were defined. Of 77 patients studied, 35 (46%) had LV thrombi. The presence of LV thrombus was not correlated to the extent of coronary artery disease. The frequency of LV thrombus progressively increased with groups of increasing wall motion abnormality as determined by the extent of akinesia and dyskinesia (%AD) (%AD 0 to 14, thrombus present in 3 of 16 [19%], %AD 15 to 29, thrombus in 8 of 27 [30%]; %AD greater than or equal to 30%, thrombus in 24 of 34 [71%]; p less than 0.001) and with increasingly severe degrees of early ventricular shape change (normal or mildly abnormal contour, 16% with thrombus; moderately abnormal contour, 36% with thrombus; severely abnormal contour, 70% with thrombus; p less than 0.001). Patients with thrombi had higher diastolic (249 +/- 55 vs 225 +/- 48 ml; p less than 0.05) and systolic (158 +/- 48 vs 120 +/- 45 ml; p less than 0.001) volumes than patients without thrombi, respectively. A stepwise discriminant analysis identified ejection fraction, extent of early shape change and LV end-diastolic pressure as independent correlates of LV thrombus after acute myocardial infarction.     

Left ventricular pseudoaneurysm following acute myocardial infarction

We describe a case of 57-year-old man who presented with acute myocardial infarction (AMI) and heart failure with rapid progression of cardiomegaly. Cardiac multislice computed tomography and echocardiography showed the ventricular pseudoaneurysm, probably due to cardiac free wall rupture caused by AMI. Cardiac CT is another useful tool for the non-invasive diagnosis of cardiac rupture.     

急性心肌梗死后左室重构的临床危险因素

目的对急性心肌梗死后左室重构的临床危险因素进行评估。方法将进入本观察的51例患者,按溶栓治疗后有无Q波形成,分为Q波组和非Q波组,全部患者入住CCU,并在入院即刻,入院后8、16、24、48、72h分别进行血清心肌酶学检查。对其中34例患者在心梗后1周、6周行超声心动图检查,并测定左室质量指数。结果Q波组血清CPK峰值(1347.58±220.33)IU,左室质量指数分别为234.82±92.36(1周),271.52±93.12(6周)均明显高于非Q波组,随访半年表明新近出现心衰明显高于非Q波组。结论溶栓后的有Q波出现,血清CPK峰值高于500IU,左室质量指数>220g/m3,是急性心肌梗死后左室重构的危险因素。