PROGRESSIVE LEFT-VENTRICULAR DYSFUNCTION AND REMODELING AFTER MYOCARDIAL-INFARCTION - POTENTIAL MECHANISMS AND EARLY PREDICTORS
PROGRESSIVE LEFT-VENTRICULAR DYSFUNCTION AND REMODELING AFTER MYOCARDIAL-INFARCTION - POTENTIAL MECHANISMS AND EARLY PREDICTORS
复制标题
DOI：
10.1161/01.cir.87.3.755
复制
发表时间：
1993-03-01
期刊：
影响因子：
37.8
通讯作者：
ERTL, G
中科院分区：
文献类型：
--
作者：
GAUDRON, P;EILLES, C;ERTL, G
背景左心室扩大和慢性心力衰竭的发展是心肌梗死后患者生存的有效预测因素。目前尚没有关于个体患者进行性心室扩大与整体和局部心功能不全以及晚期慢性心力衰竭发作相关的前瞻性研究。本研究的目的是确定左心室扩张与整体和局部心功能不全之间的关系，并确定心肌梗死后患者扩大和慢性心力衰竭的早期预测因素。在首次心肌梗死后4天、4周、6个月、1.5年和3年前瞻性评估左心室容积、18个预定扇区的局部面积收缩分数（门控单光子发射计算机断层扫描）、整体射血分数和静息和运动时的血流动力学（仰卧自行车，50 W，4分钟，Swan-Ganz导管）。70例患者被分配到进行性、有限或无扩张组。未扩张的患者（n=38）保持正常的容量和血流动力学，直到3年。有限扩张（n=18），左心室容积增加至梗死后4周，此后稳定;降低的每搏输出量在梗死后4周恢复，然后在静息时保持稳定。然而，运动过程中的楔压逐渐增加。随着进行性扩张（n=14），降低的心脏和中风指数也恢复了4周，但此后进行性恶化。面积收缩分数作为估计区域左心室功能在正常的部门在4天逐渐恶化，在3年内，但运动功能减退和运动障碍的部门保持不变。射血分数在1.5年后下降，而右房压，楔压。全身血管阻力增加。通过多变量分析，第4天的射血分数和卒中指数、心室造影梗死面积、梗死部位和心肌梗死溶栓试验梗死动脉灌注分级是进行性心室扩大和慢性功能障碍的重要预测因素。几乎26%的患者可能在首次梗死后4周内发生有限的左心室扩张，这有助于恢复静息时的心脏指数和卒中指数，并保持运动能力，因此保持代偿性。较小的一组（20%）发展为进行性结构性左心室扩张，首先是代偿性的，然后发展为非代偿性扩张，最后导致严重的整体左心室功能障碍。在这些患者中，总体射血分数的降低可能是由于最初正常收缩的心肌功能受损所致。多变量分析的早期预测因子可以识别急性梗死后4周内进行性左心室扩张和慢性心室功能不全的高危患者。
Background. Left ventricular enlargement and the development of chronic heart failure are potent predictors of survival in patients after myocardial infarction. Prospective studies relating progressive ventricular enlargement in individual patients to global and regional cardiac dysfunction and the onset of late chronic heart failure are not available. It was the aim of this study to define the relation between left ventricular dilatation and global and regional cardiac dysfunction and to identify early predictors of enlargement and chronic heart failure in patients after myocardial infarction.Methods and Results. Left ventricular volumes, regional area shrinkage fraction in 18 predefined sectors (gated single photon emission computed tomography), global ejection fraction, and hemodynamics at rest and during exercise (supine bicycle, 50 W, 4 minutes, Swan-Ganz catheter) were assessed prospectively 4 days, 4 weeks, 6 months, and 1.5 and 3 years after first myocardial infarction. Seventy patients were assigned to groups with progressive, limited, or no dilatation. Patients without dilatation (n=38) maintained normal volumes and hemodynamics until 3 years. With limited dilatation (n=18), left ventricular volume increased up to 4 weeks after infarction and stabilized thereafter; depressed stroke volume was restored 4 weeks after infarction and then remained stable at rest. Wedge pressure during exercise, however, progressively increased. With progressive dilatation (n=14), depressed cardiac and stroke indexes were also restored by 4 weeks but progressively deteriorated thereafter. Area shrinkage fraction as an estimate of regional left ventricular function in normokinetic sectors at 4 days gradually deteriorated during 3 years, but hypokinetic and dyskinetic sectors remained unchanged. Global ejection fraction fell after 1.5 years, whereas right atrial pressure, wedge pressure. and systemic vascular resistance increased. By multivariate analysis, ejection fraction and stroke index at 4 days, ventriculographic infarct size, infarct location, and Thrombolysis in Myocardial Infarction trial grade of infarct artery perfusion were significant predictors of progressive ventricular enlargement and chronic dysfunction.Conclusions. Almost 26% of patients may develop limited left ventricular dilatation within 4 weeks after first infarction, which helps to restore cardiac index and stroke index at rest and to preserve exercise performance and therefore remains compensatory. A somewhat smaller group (20%) develops progressive structural left ventricular dilatation, which is compensatory at first, then progresses to noncompensatory dilatation, and finally results in severe global left ventricular dysfunction. In these patients, depression of global ejection fraction probably results from impairment of function of initially normally contracting myocardium. Early predictors from multivariate analysis allow identification of patients at high risk for progressive left ventricular dilatation and chronic ventricular dysfunction within 4 weeks after acute infarction.