我们对31例具有适宜于二尖瓣球囊扩张（PBMV）的瓣膜条件但又合并左心房血栓的患者进行了小剂量华法令（2mgöd）抗凝治疗观察。所有左心房血栓均由经食道超声心动图证实和随访，体积最大者3cm×4cm×6cm，最小者1cm×1cm×0.5cm，随访期间定期复查超声心动图、凝血酶原时间（PT）和凝血酶原活动度（PTA）。结果显示：除了3 例患者失访外，其余28例均随访到血栓消失，血栓消失的时间在2～12个月之间，8517%（24ö28）的患者血栓消失的时间是6个月以内；PT较服药前部分延长，PTA轻度下降，无出血并发症和过度抗凝征象；对这些患者在血栓消失后成功地进行了PBMV。结果表明对于二尖瓣狭窄合并左心房血栓患者，小剂量华法令的抗凝溶栓作用安全可靠，药物服用时间以6个月为宜。

Background: The efficacy of angiotensin converting enzyme (ACE) inhibitors in treatment of renovascular disease has been controversial. It is possible that some patients with incidental atherosclerotic renal artery stenosis (ARAS) are treated with ACE inhibitors before being considered for renal revascularization. It has been reported that patients with incidental atherosclerotic renal artery stenosis (ARAS) are sometimes treated with ACE inhibitors before being considered for renal revascularization. This study was designed to describe the frequency and the characteristics of patients with incidental ARAS, and to examine the frequency of ACE inhibitor usage in such patients. Methods: We studied a cohort of consecutive patients undergoing abdominal aortography at the time of cardiac catheterization. Patients were stratified and compared based on the presence and severity of ARAS. Results: ARAS (≥50%) was present in 146 (17.0%) of 859 evaluable patients. Factors independently related to the presence of ARAS were age (OR = 1.07, P<0.001), severity of coronary artery disease (OR=2.13, P<0.001) and peripheral vascular disease (OR=1.79, P=0.021). Among all patients with ARAS, the percentage of ACE inhibitor usage was 74.7% (109/146). Among patients with severe ARAS, moderate ARAS, mild ARAS, insignificant ARAS and normal renal arteries, the percentage of ACE inhibitor usage was 85.7% (95% CI: 69%-100%), 82.9% (95% CI: 71%-95%), 68.5% (95% CI: 59%-78%), 68.6% (95% CI: 55%-82%) and 53.9% (95% CI: 50%-58%), respectively (contingency coefficient=0.17, P<0.001). In patients with severe ARAS, ACE inhibitor use, calcium channel blocker use and diuretic use were shown to correlate significantly with serum creatinine levels after controlling for potential confounding factors. Conclusion: In this study, ACE inhibitors were used commonly in patients with incidental ARAS; the frequency of ACE inhibitor use correlated with the severity of ARAS.

目的 评价高血压病人药物治疗期间24h动态血压变化。方法 26例住院的高血压病人经药物治疗4周连续3d随测血压，血压正常后进入本研究。治疗前后进行24h动态血压监测。结果 患者随测血压（8～9AM，3～4PM）血压恢复到正常水平，但动态血压显示在一段时间内（6～8AM，6～11PM）平均收缩和舒张压仍明显高于正常人平均水平（P< 0.01），而该时间段易被临床医生忽视。结论 随测血压不能实际全面反映高血压病人药物治疗的疗效，24h动态血压的监测可以正确评价高血压病人药物治疗的效果并根据高血压分布的时间来调整降压药的种类和剂量。

The long QT syndrome (LQTS) is a cardiac disorder characterized by prolongation of the QT interval on electrocardiograms (ECGs), syncope and sudden death caused by a specific ventricular tachyarrhythmia known as torsade de pointes. LQTS is caused by mutations in ion channel genes including the cardiac sodium channel gene SCN5A, and potassium channel subunit genes KCNQ1, KCNH2, KCNE1, and KCNE2. Little information is available about LQTS mutations in the Chinese population. In this study, we characterized 42 Chinese LQTS families for mutations in the two most common LQTS genes, KCNQ1 and KCNH2. We report here the identification of four novel KCNQ1 mutations and three novel KCNH2 mutations. The KCNQ1 mutations include L191P in the S2-S3 cytoplasmic loop, F275S and S277L in the S5 transmembrane domain, and G306V in the channel pore. The KCNH2 mutations include L413P in transmembrane domain S1, E444D in the extracellular loop between S1 and S2, and L559H in domain S5. The location and character of these mutations expand the spectrum of KCNQ1 and KCNH2 mutations causing LQTS. Excitement, exercises, and stress appear to be the triggers for developing cardiac events (syncope, sudden death) for LQTS patients with KCNQ1 mutations F275S, S277L, and G306V, and all three KCNH2 mutations L413P, E444D and L559H. In contrast, cardiac events for an LQTS patient with KCNQ1 mutation L191P occurred during sleep or awakening from sleep. KCNH2 mutations L413P and L559H are associated with the bifid T waves on ECGs. Inderal or propanolol (a beta blocker) appears to be effective in preventing arrhythmias and syncope for an LQTS patient with the KCNQ1 L191P mutation.

目的 研究高血压病（EH）合并动脉粥样硬化患者大动脉缓冲功能的改变。方法 选择313例EH患者，其中男性230 例，女性83例，平均年龄（58.5±10.1）岁。应用脉搏波速度（pulsewave velocity， PWV）自动测量系统测定颈动脉-股动脉PWV作为反映大动脉节段扩张性的参数；B型超声对颈动脉进行扫查，动脉粥样硬化的定义为内膜-中层厚度≥1.3mm。颈动脉横断面顺应性和容积扩张性作为评价大动脉缓冲功能的指标。结果 313例EH患者合并颈动脉粥样斑块者120例。与未合并颈动脉粥样硬化患者相比，EH合并颈动脉粥样硬化患者收缩压[（149.76±20.20）mm Hg比（141.62±18.94）mm Hg] 、脉压[（61.72±18.94）mm Hg 比（52.84±14.58）mm Hg]和PWV[（12.91±2. 93）m/s比（10.78±2.02）m/s]显著升高（P均<0.001）；颈动脉横断面顺应性[（64.68±40.52）10-3-mm2/mm Hg 比（81.55±63.45）10-3-mm2/mm Hg]和容积扩张性[（1.71±1.40）10-3-mm Hg 比（2.39±2.01）10-3-mm Hg]显著降低（P均<0.05）。结论 EH合并颈动脉粥样硬化者大动脉弹性减退，缓冲功能显著降低。