Friedman B M, Dunn M I
Department of Internal Medicine, University of Kansas Medical Center, Kansas City 66160-7378, USA.
Clin Cardiol. 1995 Sep;18(9):505-11. doi: 10.1002/clc.4960180905.
Ventricular aneurysms are circumscribed, thin-walled fibrous, noncontractile outpouchings of the ventricle. The majority are apically located, true aneurysms of the left ventricle (LV) that occur as a consequence of transmural myocardial infarction (MI). The precursor of aneurysm formation appears to be infarct expansion early after acute MI and occurrence generally relates to infarct size. The presence of underlying hypertension and the use of steroids and nonsteroidal antiinflammatory agents may promote aneurysm formation. The clinical sequelae include congestive heart failure (CHF), thromboembolism, angina pectoris, and ventricular tachyarrhythmias. Late rupture is a particular complication of false aneurysms in which the pericardium is the aneurysm wall. The diagnosis may be suspected by the clinical finding of a diffuse, pansystolic apical thrust, persistent ST-segment elevation on the electrocardiogram, and distortion of the cardiac silhouette on chest x-ray. This can be confirmed using echocardiography, radionuclide ventriculography, and cardiac catheterization. The latter has the additional advantage of being able to delineate the coronary anatomy. Management involves prevention, specific therapy for the various clinical manifestations, and surgery. Therapeutic interventions with thrombolytic agents, aspirin, heparin, and beta blockers that are applied early in the evolution of an MI may limit infarction size, thereby reducing the tendency toward infarct expansion and aneurysm formation. Patients with mild CHF can usually be controlled with the standard combination of angiotensin-converting enzyme inhibitors, diuretics, and digoxin. Thromboembolism is best prevented by anticoagulation with warfarin for at least 3 months after the acute MI. The choice of pharmacotherapy for ventricular tachyarrhythmias should be guided by electrophysiologic studies. The treatment of patients with angina pectoris utilizes conventional therapeutic modalities.(ABSTRACT TRUNCATED AT 250 WORDS)
室壁瘤是心室的局限性、薄壁纤维性、无收缩功能的向外膨出。大多数位于心尖部，是左心室的真性室壁瘤，由透壁性心肌梗死（MI）引起。瘤形成的先兆似乎是急性心肌梗死后早期的梗死扩展，其发生通常与梗死面积有关。潜在的高血压以及使用类固醇和非甾体类抗炎药可能促进瘤形成。临床后遗症包括充血性心力衰竭（CHF）、血栓栓塞、心绞痛和室性快速心律失常。假性室壁瘤（其瘤壁为心包）的一个特殊并发症是晚期破裂。根据临床发现的弥漫性、全收缩期心尖搏动、心电图上持续的ST段抬高以及胸部X线检查中心脏轮廓的变形，可能怀疑有室壁瘤。这可以通过超声心动图、放射性核素心室造影和心导管检查来确诊。后者的额外优势是能够描绘冠状动脉解剖结构。治疗包括预防、针对各种临床表现的特异性治疗以及手术。在心肌梗死演变早期应用溶栓剂、阿司匹林、肝素和β受体阻滞剂进行治疗干预，可能会限制梗死面积，从而降低梗死扩展和瘤形成的倾向。轻度充血性心力衰竭患者通常可用血管紧张素转换酶抑制剂、利尿剂和地高辛的标准组合来控制。急性心肌梗死后至少3个月用华法林抗凝，可最佳地预防血栓栓塞。室性快速心律失常的药物治疗选择应以电生理研究为指导。心绞痛患者的治疗采用传统治疗方式。（摘要截断于250字）
