Poulsen S H
Department of Medicine, Haderslev Hospital, Aahus
Dan Med Bull. 2001 Nov;48(4):199-210.
LV systolic function and dilation after Ml have been extensively studied and have been related to heart failure and cardiac mortality. In recent years, it has been increasingly apparent that LV diastolic dysfunction contributes to signs and symptoms of heart failure and LV diastolic dysfunction is associated with increased mortality rates in patients chronic heart failure independent of systolic function. LV diastolic dysfunction is difficult to assess on basis of clinical examination including chest radiography and electrocardiography. LV diastolic filling has traditionally been evaluated by cardiac catherization with direct measurement of filling pressures and relaxation. However, the invasive approach describing LV compliance and relaxation as the major determinants of LV diastolic function, is not feasible and suitable for routine investigations of diastolic function. Two-dimensional and Doppler echocardiography has become a well accented practical and safe non-invasive method for diagnosis of LV diastolic dysfunction. Combined invasive and echocardiographic studies have shown that analysis of mitral and pulmonary venous flow velocities relate to invasively measured filling pressures and relaxation rate in cardiac diseases. Based on Doppler analysis of mitral and pulmonary venous flow three abnormal LV filling patterns are identified: impaired relaxation, "pseudonormalization" and restrictive. These LV filling patterns have been related to symptoms, relaxation rate, filling pressure and prognosis in patients with restrictive and dilated cardiomyopathy. The Doppler flow profiles are influenced by several factors including age, heart rate, load conditions and valve heart diseases which must be taken into consideration during evaluation. During the last decade information about LV diastolic function assessed non-invasively by Doppler echocardiography has gained in patients with CAD. Myocardial ischemia induced by brief coronary artery occlusion or pacing leads to abnormal myocardial relaxation which can be reversed to normal by restoring normal myocardial blood flow. The diastolic abnormality is present within seconds and a characteristic impaired relaxation filling pattern are identified by mitral and pulmonary venous flow analysis. Diastolic dysfunction has been recognized during the early as well during the post-MI phase with or without LV systolic dysfunction. In the acute phase both an abnormal relaxation pattern and restrictive LV filling pattern are present which has been related to in-hospital heart failure. The identification of a pseudonormal or restrictive LV filling pattern are associated with later readmission to hospital with heart failure and cardiac death. Abnormal relaxation filling is the most pronounced filling pattern after one year which might be related to the remodeling process including compensatory hypertrophy, scarring of the infarct zone leading to a non-uniform relaxation of the LV. Remodeling of the LV following a MI is subject to several factors which might involve diastolic function. This is supported by the presence of an impaired relaxation and restrictive filling pattern are associated with progressive LV dilatation following Ml. Furthermore, the LV remodeling process following the very early phase includes the scarring process with collagen deposition in the infarcted and non-infarcted myocardium. The extent and quality of the repair process involving collagen deposition are believed to influence the remodeling process. Increased collagen deposition in the subacute phase of Ml indicated by elevated values of the collagen marker PIIINP is found to be related to LV dilation, depressed systolic function and restrictive LV filling. Development of a restrictive filling in patients with increased collagen deposition might be due to increasing LV volume but also to increased myocardial stiffness. Regarding prognosis diastolic dysfunction seems to be an important marker of outcome as abnormal diastolic properties are related to progressive LV dilatation, development of heart failure and cardiac death following MI. The beneficial effects of BB on morbidity and mortality in post-MI patients are well established. Recently, it has been demonstrated that BB has beneficial effects on progressive CHF and cardiac mortality in patients with chronic heart failure and moderate to severe systolic dysfunction. The mechanisms behind these effects are not fully understood. However, improvement of both systolic and diastolic function during BB therapy are demonstrated in patients with CHF. A few studies in patients with MI indicates that long-term BB therapy improves LV diastolic function which seems to be followed by improvement in systolic function. BB has the potential to lengthening diastole, improving subendocardial myocardial perfusion and affecting symptomatic amd neurohumoral activation following MI which might affect LV systolic and diastolic function and thereby improving outcome. Functional capacity following Ml is a well known predictor for outcome in MI patients. LV diastolic function a closely related to exercise capacity in contrast to measures of systolic function. BB therapy in patients with mild to moderate systolic dysfunction seems to improve exercise capacity which is related to improvement in LV diastolic function. Thus, BB improves exercise capacity and diastolic function by increasing LV compliance which might have prognostic implications. Even though LV systolic and diastolic dysfunction coexist, few two-dimensional and Doppler echocardiographic variables combine measurements of both phases of the cardiac cycle. Recently, the MPI has been suggested as a measure of combined systolic and diastolic myocardial performance which is based on Doppler time intervals of the systolic and diastolic phases. The MPI is easily obtained, reproducible, non-geometric and seems less dependent on heart rate and load conditions compared to traditional Doppler measurements. In patients with MI is has shown to reflect disease severity and contain prognostic information. The assessment of MPI seems therefore to be a relevant attractive alternative to established measurements of LV function following MI.
心肌梗死后左心室收缩功能和扩张已得到广泛研究,且与心力衰竭和心脏死亡率相关。近年来,越来越明显的是,左心室舒张功能障碍会导致心力衰竭的体征和症状,并且左心室舒张功能障碍与慢性心力衰竭患者的死亡率增加相关,而与收缩功能无关。基于包括胸部X线摄影和心电图在内的临床检查很难评估左心室舒张功能障碍。传统上,左心室舒张期充盈是通过心脏导管检查直接测量充盈压和舒张功能来评估的。然而,将左心室顺应性和舒张功能描述为左心室舒张功能主要决定因素的侵入性方法,并不适用于舒张功能的常规检查。二维和多普勒超声心动图已成为诊断左心室舒张功能障碍的一种公认的实用且安全的非侵入性方法。侵入性和超声心动图联合研究表明,二尖瓣和肺静脉血流速度分析与心脏病中侵入性测量的充盈压和舒张速率相关。基于二尖瓣和肺静脉血流的多普勒分析,可识别出三种异常的左心室充盈模式:舒张功能受损、“假性正常化”和限制性充盈。这些左心室充盈模式与限制性和扩张型心肌病患者的症状、舒张速率、充盈压和预后相关。多普勒血流频谱受多种因素影响,包括年龄、心率、负荷状况和瓣膜性心脏病,在评估过程中必须予以考虑。在过去十年中,通过多普勒超声心动图非侵入性评估左心室舒张功能的信息在冠心病患者中有所增加。短暂冠状动脉闭塞或起搏引起的心肌缺血会导致心肌舒张异常,恢复正常心肌血流可使其恢复正常。舒张异常在数秒内出现,通过二尖瓣和肺静脉血流分析可识别出特征性的舒张功能受损充盈模式。在心肌梗死后早期以及有无左心室收缩功能障碍的阶段均已认识到舒张功能障碍。在急性期,会出现异常舒张模式和限制性左心室充盈模式,这与住院期间的心力衰竭有关。识别出假性正常或限制性左心室充盈模式与随后因心力衰竭和心源性死亡再次入院相关。异常舒张充盈是一年后最明显的充盈模式,这可能与包括代偿性肥大、梗死区瘢痕形成导致左心室舒张不均匀在内的重塑过程有关。心肌梗死后左心室的重塑受多种因素影响,这些因素可能涉及舒张功能。心肌梗死后出现舒张功能受损和限制性充盈模式与左心室逐渐扩张相关,这支持了上述观点。此外,心肌梗死后极早期的左心室重塑过程包括梗死和非梗死心肌中胶原沉积的瘢痕形成过程。据信,涉及胶原沉积的修复过程的程度和质量会影响重塑过程。心肌梗死亚急性期胶原标志物Ⅲ型前胶原氨基端肽(PIIINP)值升高表明胶原沉积增加,这与左心室扩张、收缩功能降低和限制性左心室充盈有关。胶原沉积增加的患者出现限制性充盈可能是由于左心室容积增加,也可能是由于心肌僵硬度增加。关于预后,舒张功能障碍似乎是一个重要的预后指标,因为舒张功能异常与心肌梗死后左心室逐渐扩张、心力衰竭的发生和心源性死亡相关。β受体阻滞剂(BB)对心肌梗死后患者发病率和死亡率的有益作用已得到充分证实。最近,已证明BB对慢性心力衰竭和中度至重度收缩功能障碍患者的进行性心力衰竭和心脏死亡率有有益作用。这些作用背后的机制尚未完全了解。然而,在心力衰竭患者中已证明BB治疗期间收缩和舒张功能均有改善。一些对心肌梗死患者的研究表明,长期BB治疗可改善左心室舒张功能,随后似乎收缩功能也有所改善。BB有可能延长舒张期,改善心内膜下心肌灌注,并影响心肌梗死后的症状和神经体液激活,这可能会影响左心室收缩和舒张功能,从而改善预后。心肌梗死后的功能能力是心肌梗死患者预后的一个众所周知的预测指标。与收缩功能测量不同,左心室舒张功能与运动能力密切相关。轻度至中度收缩功能障碍患者的BB治疗似乎可改善运动能力,这与左心室舒张功能的改善有关。因此,BB通过增加左心室顺应性来改善运动能力和舒张功能,这可能具有预后意义。尽管左心室收缩和舒张功能障碍并存,但很少有二维和多普勒超声心动图变量能结合心动周期两个阶段的测量。最近,心肌表现指数(MPI)已被建议作为一种综合收缩和舒张心肌性能的测量指标,它基于收缩期和舒张期的多普勒时间间隔。MPI易于获得、可重复、非几何学,并且与传统多普勒测量相比,似乎对心率和负荷状况的依赖性较小。在心肌梗死患者中,它已被证明可反映疾病严重程度并包含预后信息。因此,MPI评估似乎是心肌梗死后左心室功能既定测量方法的一种相关且有吸引力的替代方法。