暴发性病毒性心肌炎1例

1病例资料 患者,男,36岁,因＂突发胸闷痛2d＂于2010-06-20收入广东省人民医院。患者入院前一天的中午12时无明显诱因突然出现胸闷,呈压榨样,持续性,后自行缓解,入院当天早晨6时许再次出现胸闷痛,同时伴全身冷汗,无向它处放射,无气促,无恶心、呕吐,无腹泻。     

二维及脉冲多普勒超声诊断急性下壁心肌梗塞并发室间隔穿孔一例

患者,女,58岁。于1992年1月6日晨4时睡眠中出现胸闷痛,持续3小时后症状减轻,发作时伴烦躁不安不能入睡,症状时有加重。12日大便时胸闷痛加重伴剧烈右上腹痛,气促明显,休息后不能缓解。12小时后入院心电图示急性下壁心肌梗塞(AIMI)ST_I,SVL,V_(1～6)斜形压低,T波倒置,     

妊娠早期冠状动脉痉挛导致急性心肌梗死1例报告

患者女,24岁,孕16周。主因发作性胸痛5d,加重29h人院。患者于5d前在情绪激动后出现胸骨后闷痛,向左肩、背部放射,伴胸闷、乏力、出汗,持续约20min自行缓解,     

干燥综合征患者经皮冠状动脉介入治疗术后支架近端血管严重狭窄1例

正1临床资料患者女,51岁。因"阵发性胸骨后疼痛2 d,加重14 h"于2016年12月22日入住葫芦岛市中心医院心内二科。患者入院前2 d劳累后出现胸骨后闷痛,疼痛可耐受,服用丹参滴丸后症状好转,持续约10 min,后上述症状反复发作,程度及性质同前,14 h前疼痛程度加重,伴大汗,服用速效救心丸     

变异型心绞痛并发室性心动过速及心室颤动1例

患者 ,男 ,73岁。因发作性胸闷痛 6d,再发 1 h于 1 999年 1 2月 1 5日上午 8∶ 40入院。 6d前出现胸闷痛 ,阵发性 ,多于休息时发生 ,疼痛位于胸骨后中下段 ,每次发作持续 5～ 1 0 min,每日发作 1～ 4次 ,无放射痛。 1 999年 1 2月 1 1日曾在门诊做心电图 ( ECG)示窦性心律 ,T波轻度改变 ,拟诊“冠心病、心绞痛”。给予消心痛、速效救心丸等药治疗 ,症状稍有好转。 1 2月 1 5日上午 7∶ 30患者胸痛再发 ,阵发性加剧 ,伴大汗 ,无放射痛及昏厥 ,急诊 ECG示窦性心律 ,前壁损伤电流 ,以“急性心肌梗死”收入院 ,既往无高血压、冠心病、糖尿病…     

鱼刺穿透胃窦形成胃周脓肿1例

病例：患者男，45岁，工人。因“中上腹痛1周，加重伴反复呕吐2d”于2007年7月7日入院。患者入院前一周无明显诱因出现中上腹持续闷痛，阵发性加剧。疼痛与饮食、体位无明显关系。2d前中上腹痛加剧，呈持续性，能忍受，其他部位无放射痛，伴呕吐宿食，呕吐后腹痛无明显缓解，有低热．体温最高38．2℃，无眼黄、尿黄，无呕血、黑便等。     

右胸前导联高R波诊断急性后壁心肌梗死2例

例1,患者女、81岁,因“心前区隐痛20天加重3h”急诊入院。患者每次胸痛发作无明显诱因,持续5-30min,向背部传导,于休息或口服药物后缓解,疼痛发作时不伴晕厥、黑朦等症状。入院前3h患者胸痛发作程度较前加剧,休息及自服药物均不能缓解,遂急诊入院。     

急性下壁心肌梗死顽固性上腹痛心源性休克混合性酸碱失衡

1　病历摘要患者女性 ,73岁。因发作性上腹痛 2年 ,加重 3d于2 0 0 2 - 0 1- 2 3入院。患者 2年前进食后出现上腹痛 ,以右上腹为著 ,并向右肩背部放射 ,曾在我院做腹部B超检查 ,诊断为“胆囊炎” ,给予“消炎利胆片”等治疗后 ,病情好转 ,但易复发 ,且多在进食后发作。 3d前患者进食后又伴有上腹剧痛 ,阵发性发作 ,向背部放射 ,伴有大汗淋漓、恶心、呕吐 ,无寒战、发热 ,门诊以“急性胆囊炎”收入消化内科 ,入院后经查心电图确诊为急性下壁心肌梗死。治疗 30余天 ,病情反复发作而转入心内科。患者有高血压病史 5年 ,有慢性支气管炎病史 30…     

急性心肌梗死致亚急性心室游离壁破裂多器官功能衰竭一例

患男，42岁。因发作性心前区闷痛20天，加重6天于2004年2月25日入院。入院前6天凌晨4时出现心前区闷痛，向左肩部放射，伴出汗，直到上午8时送到当地医院急诊科，心电图示Ⅰ、aVL导联、V1-6导联ST段弓背向上抬高，心肌酶明显升高，提示广泛前壁心肌梗死，当时血压150／85mm Hg(1mm Hg=0．133kPa)，心率90次／min，给予尿激酶150万单位溶栓、     

非体外循环下冠状动脉旁路移植术后桥血管出血成功救治一例

1临床资料 患者,男性,67岁,因“活动后胸闷痛8年,加重3月”为主诉入院。3个月前发作急性心梗,心前区闷痛,并向左肩部及背部放射,伴大汗,就诊于当地医院。冠脉造影显示：冠脉三支病变。行药物保守治疗,症状缓解后出院。但出院后患者仍间断发作胸闷痛,为进一步诊治,来我院。     

冠心病和心力衰竭

冠心病心力衰竭（简称冠心病心衰）顾名思义是指由于冠心病引起的心力衰竭,据统计大约65％的心力衰竭由冠状动脉疾病引发的。冠心病心衰在临床上分急性和慢性两种,急性心衰主要由急性心肌梗死和急性冠脉缺血诱发的心肌收缩或舒张功能异常所致,慢性心衰主要是心肌梗死后心肌重塑和心肌的血供长期不足,心肌组织发生营养障碍和萎缩,以致纤维组织增生所致。由于冠心病导致心衰的成因不同,因此治疗上的侧重点就会有所不同,下面就对冠心病心衰发病机制及诊治作一浅谈。     

甲状腺功能亢进性心脏病

甲状腺功能亢进(甲亢)性心脏病是由于甲亢时过量的甲状腺激素对心脏的直接毒性作用或间接影响而引起的一系列心血管系统症状和体征的一种内分泌代谢紊乱性心脏病.它的发生与患者的年龄、病程、治疗是否规范、低钾、感染和妊娠等因素有关.甲亢性心脏病目前尚无统一的诊断标准,一般认为,甲亢伴心律失常、心脏扩大、心力衰竭常为其必备症状和体征,但需除外其他原因引起的心脏疾患,以减少误诊和漏诊.而且多数甲亢性心脏病可随甲亢的治愈或有效控制而治愈或好转,但也町继续存在,甚全成为永久性后遗症.     

Chagas' heart disease

Chagas' disease is caused by a protozoan parasite, Trypanosoma cruzi, that is transmitted to humans through the feces of infected bloodsucking insects in endemic areas of Latin America, or occasionally by nonvectorial mechanisms, such as blood transfusion. Cardiac involvement, which typically appears decades after the initial infection, may result in cardiac arrhythmias, ventricular aneurysm, congestive heart failure, thromboembolism, and sudden cardiac death. Between 16 and 18 million persons are infected in Latin America. The migration of infected Latin Americans to the United States or other countries where the disease is uncommon poses two problems: the misdiagnosis or undiagnosis of Chagas' heart disease in these immigrants and the possibility of transmission of Chagas' disease through blood transfusions. Diagnosis is based on positive serologic tests and the clinical features. The antiparasitic drug, benznidazole, is effective when given for the initial infection and may also be beneficial for the chronic phase. The use of amiodarone, angiotensin-converting enzyme inhibitors, and pacemaker implantation may contribute to a better survival in selected patients with cardiac involvement of chronic Chagas' disease.     

Carcinoid heart disease

The carcinoid syndrome is usually evident when enterochromaffin (EC) cell-derived neuroendocrine tumors (carcinoids) metastasize to the liver. In addition to carcinoid symptomatology, about 40% of patients exhibit carcinoid heart disease (CHD) with fibrotic endocardial plaques and associated heart valve dysfunction. The mechanism behind CHD development is not fully understood, but serotonin (5-HT) is considered to be a major initiator of the fibrotic process. Most patients present with right-sided heart valve dysfunction since pulmonary and tricuspid valves lesions are the most common (>95%) cardiac pathology. Left-sided valvular involvement, and angina associated with coronary vasospasm occur in ~10% of subjects with CHD. Pathognomonic echocardiograpic features include immobility of valve leaflets and thickening and retraction of the cusps most commonly resulting in tricuspid valve regurgitation and pulmonary stenosis. Therapeutic options include cardioactive pharmacotherapy for heart failure and, in selected individuals, cardiac valve replacement. Previously valve replacement was reserved for advanced disease due to a perioperative mortality of >20% however in the last decade, technical advances as well as an earlier diagnosis have decreased surgical mortality to <10% and valve replacements are undertaken more frequently. A recent analysis of 200 cases demonstrated an increase in median survival from 1.5 years to 4.4 years in the last two decades. Although the improved prognosis might also reflect the increased use of surgical cytoreduction, hepatic metastatic ablative therapies and somatostatin analogs a robust correlation between diminution of circulating tumor products and an increased long-term survival in CHD has not been rigorously demonstrated.     

Diabetic heart disease

Diabetes mellitus is responsible for a spectrum of cardiovascular disease. The best known complications arise from endothelial dysfunction, oxidation, inflammation, and vascular remodelling and contribute to atherogenesis. However, the effects on the heart also relate to concurrent hypertensive heart disease, as well as direct effects of diabetes on the myocardium. Diabetic heart disease, defined as myocardial disease in patients with diabetes that cannot be ascribed to hypertension, coronary artery disease, or other known cardiac disease, is reviewed.