心脏破裂的预测和预防邯郸市第一医院心内科邯郸市心血管病.ppt

心脏破裂的预测和预防 邯郸市第一医院心内科 邯郸市心血管病研究所 信栓力 博士 河北唐山2010.11.19,分类,室间隔破裂 乳头肌断裂 心室游离壁破裂,在再灌注时代之前，室间隔破裂发生率1-3% 在GUSTO-1研究，应用SK/tPA时代，室间隔穿孔的发生率0.34%，确诊的为0.2% 提示再灌注治疗降低了室间隔破裂的发生率,室间隔破裂的危险因素,前壁心梗比其他部位的心梗更容易发生 溶栓时代之前的常见危险因素：高血压、高龄（60-69）、女性和无心绞痛及心梗病史（首次心梗！） 女性高龄心梗患者溶栓，容易发生！ 大面积心梗、右室心梗也是危险因素！ 心绞痛常意味着预适应和侧枝形成，不利于破裂。,病理学改变,破裂部位的室间隔变薄和坏死 中性粒细胞浸润 凋亡 分解酶的释放解聚心肌组织 病理改变呈现时间依赖性，24为凝固性坏死 早期破裂发生在粘膜内有巨大血肿的梗塞,病理学,游离壁破裂分了三型： 室壁没有变薄而突然撕裂 破裂之前心肌糜烂但有血栓覆盖 心肌明显变薄，继发室壁瘤形成，然后在瘤的中央穿孔 - Becker and van Mantgem,病理学,破裂的大小：数毫米到几个厘米 简单破裂和复杂破裂,Figure 1. Findings at Autopsy in a Patient with a Simple Ventricular Septal Rupture. There is a discrete defect with a direct through-and-through communication across the septum. The perforation is at the same level on both sides of the septum: the left ventricular aspect of the interventricular septum (LVS), and the right ventricular aspect of the interventricular septum (RVS). MV denotes mitral valve.,前壁心梗的简单破裂,好发时段,没有再灌注的第一周内容易破裂 破裂有两个高峰：心梗第一天；3-5天 罕见于两周以后 溶栓的患者好发的中位时间为24小时 溶栓虽然缩小心肌梗塞面积，但加重血肿促发撕裂,造影所见,多支病变患者多发? 但GUSTO-1研究发现，室间隔破裂者中57%为单支病变 侧支降低破裂风险,临床表现,胸疼 心衰表现，恶心，欲呕 粗糙、全收缩期杂音，胸骨左缘 向背部、心尖区或胸骨右缘放射 半数患者可触及胸骨旁震颤 S3奔马律常见,诊断,心梗病人出现泵衰时，可见于好多情况 超声的敏感性和特异性几乎100% 机械通气的患者可能需要经食道超声 肺动脉导管-右心室血氧饱和度增加 左心室造影,治疗和预后,非常的差！,Frequency United States,Myocardial rupture complicates up to 10% of AMIs. Approximately 6-10% of penetrating chest wounds and 15-75% of blunt chest traumas are associated with cardiac injury. Myocardial rupture occurs in 10-15% of fatal motor vehicle accidents. Incidence of cardiac rupture following blunt trauma is 0.5-2% among hospital trauma admissions.,Mortality/Morbidity,Myocardial rupture is responsible for nearly 15% of all in-hospital deaths among patients with AMI. It is the second most common cause, after pump failure, of in-hospital mortality among patients with AMI. History Myocardial rupture after AMI may occur from 1 day to 3 weeks after infarction. Most ruptures occur 3-5 days after infarction.,Causes：Acute myocardial infarction Risk factors for myocardial rupture following AMI include a relatively small first AMI, female sex, age older than 60 years, hypertension, use of nonsteroidal anti-inflammatory drugs (NSAIDs) or steroids during the acute phase of AMI (interference with the healing process), late thrombolysis (11 h), postinfarct angina and elevated peak serum C-reactive protein. Protective factors include LV hypertrophy, history of previous infarcts, congestive heart failure, history of chronic ischemic heart disease, early use of beta-blockers after AMI, and successful (and timely) primary percutaneous coronary intervention.,Causes：Trauma,Trauma may be blunt or penetrating. Trauma also may be iatrogenic in nature, resulting from (1) diagnostic catheterization, including transseptal puncture and endomyocardial biopsy; (2) balloon valvuloplasty; (3) pericardiocentesis; (4) placement of temporary or permanent pacing catheters; and (5) cardiac surgery, especially mitral valve replacement.,Causes：Infection,Rupture of a myocardial abscess or AMI secondary to coronary embolism of the vegetative material may occur in patients with infective endocarditis. Other infections may include tuberculosis, echinococcal cysts, and myocarditis.,causes,Aortic dissection Aortic dissection is also a cause. Malignancy Primary cardiac tumors may be present. Patients may have secondary or metastatic tumors of the heart. Patients may have lymphoma or acute myeloblastic leukemia. Sarcoidosis Sarcoidosis has been noted.,辅助检查,Chest radiograph in posteroanterior projection showing a large pseudoaneurysm manifesting as a bulge in the left cardiac border,Electrocardiogram,Evidence for transmural (ST elevation) AMI is present in most patients with ischemic myocardial rupture prior to the event. Persistent ST segment elevation following AMI is associated with higher incidence of myocardial rupture. In the setting of an anterior AMI, ST elevation or development of Q waves in inferior leads (as a result of occlusion of a large, wrap-around left anterior descending coronary artery) is associated with an increased risk of VSD. Following traumatic cardiac injury, ECG changes usually are nonspecific.,Free wall rupture is often associated with a sudden onset of bradycardia and electromechanical dissociation (pulseless electrical activity).,In pericardial tamponade, the ECG may show low-voltage QRS complexes, especially in the precordial leads. Electrical alternans, commonly seen with large, slowly accumulating effusions, is often absent in the setting of acute hemorrhagic pericardial tamponade.,Right bundle branch block is frequently observed in patients with VSD. Less frequently, patients may have complete heart block. Patients with pseudoaneurysm may demonstrate ST-segment elevation, nonspecific ST changes, or pathologic Q waves on ECG. All patients with significant thoracic blunt trauma should have ECG and cardiac monitoring. The ECG may show ST elevation or nonspecific ST-T changes. Normal ECG findings do not exclude myocardial injury following blunt trauma.,最有意义的提示,69岁患者无明显冠心病危险因素。因胸疼就诊，因心电图和酶学正常而出院。5天后胸疼持续急诊入院，心电图心梗后演变加酶学有意义，诊断亚急性下壁心肌梗塞。因胸疼严重而行急诊手术 右冠状动脉TIMI2血流，成功一枚DES 症状发作7天（PCI后第二天）后，心电图有了新的变化。,于是复查了心肌酶，但和PCI后的比较无增高 但CRP和WBC轻度升高 病人一般情况出奇的好！ 于是床旁TTE:少到中量的心包积液，下壁和后壁稍多。,A canalicular tract from endo to pericardium was seen along the interface between the necrotic and the normal contracting myocardium (Figure 3, Additional file 2, Additional file 3, Additional file 4).,Power-Doppler evaluation add