Department of Cardiology, Clinical Center of Serbia and Belgrade University School of Medicine, Koste Todorovića 8, 11000, Belgrade, Serbia.
Heart Fail Rev. 2013 May;18(3):255-66. doi: 10.1007/s10741-012-9335-x.
Despite a myriad of causes, pericardial diseases present in few clinical syndromes. Acute pericarditis should be differentiated from aortic dissection, myocardial infarction, pneumonia/pleuritis, pulmonary embolism, pneumothorax, costochondritis, gastroesophageal reflux/neoplasm, and herpes zoster. High-risk features indicating hospitalization are: fever >38 °C, subacute onset, large effusion/tamponade, failure of non-steroidal anti-inflammatory drugs (NSAIDs), previous immunosuppression, trauma, anticoagulation, neoplasm, and myopericarditis. Treatment comprises 10-14-days NSAID plus 3 months colchicine (2 × 0.5 mg; 1 × 0.5 mg in patients <70 kg). Corticosteroids are avoided, except for autoimmunity, as they facilitate the recurrences. Echo-guided pericardiocentesis (±fluoroscopy) is indicated for tamponade and effusions >2 cm. Smaller effusions are drained if neoplastic, purulent or tuberculous etiology is suspected. In recurrent pericarditis, repeated testing for autoimmune and thyroid disease is appropriate. Pericardioscopy and pericardial/epicardial biopsy may clarify the etiology. Familial clustering was recently associated with tumor necrosis factor receptor-associated periodic syndrome (TNFRSF1A gene mutation). Treatment includes 10-14 days NSAIDs with colchicine 0.5 mg bid for up to 6 months. In non-responders, low-dose steroids, intrapericardial steroids, azathioprine, and cyclophosphamide can be tried. Successful management with interleukin-1 receptor antagonist (anakinra) was recently reported. Pericardiectomy remains the last option in >2 years severely symptomatic patients. In constriction, expansion of the heart is impaired by the rigid, chronically inflamed/thickened pericardium (no thickening ~20 %). Chest radiography, echocardiography, computerized tomography, magnetic resonance imaging, hemodynamics, and endomyocardial biopsy indicate the diagnosis. Pericardiectomy is the only treatment for permanent constriction. Predictors of poor survival are prior radiation, renal dysfunction, high pulmonary artery pressures, poor left ventricular function, hyponatremia, age, and simultaneous HIV and tuberculous infection.
尽管心包疾病有很多病因，但它们只表现为少数几种临床综合征。急性心包炎需要与主动脉夹层、心肌梗死、肺炎/胸膜炎、肺栓塞、气胸、肋软骨炎、胃食管反流/肿瘤和带状疱疹相鉴别。提示需要住院的高危特征包括：体温＞38°C、亚急性起病、大量渗出/填塞、非甾体抗炎药（NSAIDs）治疗无效、既往免疫抑制、创伤、抗凝、肿瘤和心肌心包炎。治疗包括 10-14 天的 NSAIDs 加 3 个月的秋水仙碱（2×0.5mg；体重＜70kg 者用 1×0.5mg）。除了自身免疫病之外，皮质类固醇类药物应避免使用，因为它们会增加复发的风险。对于填塞和渗出量＞2cm 者，建议行超声引导下心包穿刺（可加透视）。对于怀疑肿瘤、化脓或结核性病因的较小渗出液，也需要引流。对于复发性心包炎，应适当重复检查自身免疫和甲状腺疾病。心包镜检查和心包/心外膜活检可能有助于明确病因。最近发现家族聚集性与肿瘤坏死因子受体相关周期性综合征（TNFRSF1A 基因突变）有关。治疗包括 10-14 天的 NSAIDs 和秋水仙碱 0.5mg bid，持续 6 个月。对于无应答者，可以尝试使用低剂量类固醇、心包内类固醇、硫唑嘌呤和环磷酰胺。最近有报道称白细胞介素-1 受体拮抗剂（阿那白滞素）治疗有效。对于＞2 年且症状严重的患者，心包切除术仍然是最后的选择。在心包缩窄中，心脏扩张受到僵硬、慢性炎症/增厚的心包的限制（无增厚约 20%）。胸部 X 线摄影、超声心动图、计算机断层扫描、磁共振成像、血流动力学和心内膜心肌活检有助于诊断。心包切除术是永久性缩窄的唯一治疗方法。预测生存不良的因素包括既往放疗、肾功能不全、肺动脉压高、左心室功能差、低钠血症、年龄以及同时感染 HIV 和结核。
