风湿性主动脉瓣疾病术后再发主动脉病变的外科治疗

目的探讨风湿性主动脉瓣疾病术后再发主动脉疾病的外科治疗,提高对主动脉瓣术后继发主动脉病变防治的认识。方法回顾性分析2003年8月至2012年5月阜外心血管病医院收治的风湿性主动脉瓣疾病术后再发主动脉病变患者27例的临床资料,男20例、女7例,年龄28~69(50±10)岁。继发主动脉病变包括Standford A型主动脉夹层13例(急性夹层4例,慢性夹层9例),升主动脉瘤6例,主动脉根部瘤8例。所有患者均行手术治疗,主动脉根部置换7例,升主动脉+全主动脉弓置换+象鼻支架植入术6例,主动脉根部置换+全主动脉弓置换+支架象鼻手术6例,升主动脉置换8例。对所有出院患者进行门诊复查和电话随访。结果再次手术间隔时间6~110(57±32)个月,术后早期无死亡,再次手术体外循环时间50~274(143±65)min,住院时间13~27(19±11)d。术后早期并发症包括肾功能不全4例,神经功能障碍3例(无轻瘫或截瘫发生),肺部并发症4例,肠道并发症2例。术后随访率81.5%,随访时间4~118(43.5±32.2)个月,随访期间4例死亡,3年生存率为85.1%。结论对因风湿性主动脉瓣疾病行主动脉瓣手术的患者,若同期合并主动脉病变,需积极处理;即使未合并主动脉病变,也应严格随访,定期复查,减少术后主动脉不良事件的发生。     

Optimized Fluoroscopy Setting and Appropriate Project Position Can Reduce X-ray Radiation Doses Rates during Electrophysiology Procedures

Background:

Nonfluoroscopic three-dimensional electroanatomical system is widely used nowadays, but X-ray remains indispensable for complex electrophysiology procedures. This study aimed to evaluate the value of optimized parameter setting and different projection position to reduce X-ray radiation dose rates.

Methods:

From June 2013 to October 2013, 105 consecutive patients who underwent complex ablation were enrolled in the study. After the ablation, the radiation dose rates were measured by two different settings (default setting and optimized setting) with three projection positions (posteroanterior [PA] projection; left anterior oblique [LAO] 30° projection; and LAO 45° projection). The parameter of preset voltage, pulse width, critical voltage, peak voltage, noise reduction, edge enhancement, pulse rate, and dose per frame was modified in the optimized setting.

Results:

The optimized setting reduced radiation dose rates by 87.5% (1.7 Gy/min vs. 13.6 Gy/min, P < 0.001) in PA, 87.3% (2.5 Gy/min vs. 19.7 Gy/min, P < 0.001) in LAO 30°, 85.9% (3.1 Gy/min vs. 22.1 Gy/min, P < 0.001) in LAO 45°. Increase the angle of projection position will increase the radiation dose rate.

Conclusions:

We can reduce X-ray radiation dose rates by adjusting the parameter setting of X-ray system. Avoiding oblique projection of large angle is another way to reduce X-ray radiation dose rates.     

永久起搏器和埋藏式心脏复律除颤器（ICD）在遗传性长QT综合征患者中的应用

目的总结合并窦性心动过缓的遗传性长QT综合征（以下简称遗传性LQTS）患者植入永久起搏器和埋藏式心脏复律除颤器（以下简称ICD）的治疗效果,对比分析这两种治疗在预防患者猝死中的差异。方法对我院从2003年6月到2013年6月出院诊断为遗传性LQTS合并窦性心动过缓、植入了永久起搏器或ICD的全部21例患者,结合门诊、电话和程控随访了解患者的生存状况、手术并发症以及晕厥、室性恶性心律失常的发作情况。结果起搏器组男性2例,女性9例,年龄39.3±14.3岁,随访时间50.6±26.3个月,1例患者猝死,2例患者再发晕厥前兆,其中1例最终更换为ICD。ICD组男性2例,女性8例,年龄34.5±11.9岁,随访时间61.4±43.5个月,3例患者接受了ICD的适当治疗,另2例患者接受了ICD的不适当治疗,1例患者术后出现囊袋感染,1例患者更换为永久起搏器。治疗有效率在起搏器组及ICD组分别为72.7%（8/11）和100.0%（10/10）,未达到统计学差异（p=0.21）。不良事件发生率在起搏器组及ICD组分别为27.3%（3/11）和30.0%（3/10）,也未达到统计学差异（p=0.63）。结论对于不能植入ICD的合并窦性心动过缓的遗传性LQTS患者,植入永久起搏器可能是一个较好的替代方法,但对于QTc≥539ms的患者,只有植入ICD才能预防猝死。植入ICD后长期无心脏事件发生的患者,根据患者意愿,可考虑更换为永久起搏器。     

心脏手术中抗纤溶药物的临床应用进展

心脏手术中过度失血仍是心脏手术面临的的主要挑战之一,抗纤溶药物的临床应用为解决这一难题带来希望。由于抑肽酶可增加肾损伤、增加术后死亡率,赖氨酸类似物成为心脏手术中主要抗纤溶用药,其中氨甲环酸的应用最为广泛。无论是在体外循环心脏手术还是在非体外循环冠状动脉搭桥手术中,氨甲环酸的有效性经多项研究证实。而如今,不同出血风险的心脏手术中氨甲环酸的应用剂量仍未明确。在氨甲环酸广泛应用的同时,其安全性也引起大家质疑,其与术后谵妄的关系也引起大家高度注意,而有专家呼吁抑肽酶有必要再次进入临床。将来,抑肽酶是否会成为高危出血心脏手术中的主要抗纤溶用药,氨甲环酸的合理应用剂量最终怎样界定,对这些问题我们拭目以待。     

Serum–Glucocorticoid Regulated Kinase 1 Regulates Macrophage Recruitment and Activation Contributing to Monocrotaline-Induced Pulmonary Arterial Hypertension

Sustained inflammation is associated with pulmonary vascular remodeling and arterial hypertension (PAH). Serum–glucocorticoid regulated kinase 1 (SGK1) has been shown to participate in vascular remodeling, but its role in inflammation-associated PAH remains unknown. In this study, the importance of SGK1 expression and activation was investigated on monocrotaline (MCT)-induced PAH, an inflammation-associated experimental model of PAH used in mice and rats. The expression of SGK1 in the lungs of rats with MCT-induced PAH was significantly increased. Furthermore, SGK1 knockout mice were resistant to MCT-induced PAH and showed less elevation of right ventricular systolic pressure and right ventricular hypertrophy and showed reduced pulmonary vascular remodeling in response to MCT injection. Administering the SGK1 inhibitor, EMD638683, to rats also prevented the development of MCT-induced PAH. The expression of SGK1 was shown to take place primarily in alveolar macrophages. EMD638683 treatment suppressed macrophage infiltration and inhibited the proliferation of pulmonary arterial smooth muscle cells (PASMCs) in the lungs of rats with MCT-induced PAH. Co-culture of bone marrow-derived macrophages (BMDMs) from wild-type (WT) mice promoted proliferation of PASMC in vitro, whereas BMDMs from either SGK1 knockout mice or WT mice with EMD638683 treatment failed to induce this response. Collectively, the present results demonstrated that SGK1 is important to the regulation of macrophage activation that contributes to the development of PAH; thus, SGK1 may be a potential therapeutic target for the treatment of PAH.