ensive subjects and in patients with end-stage renal disease, but there have been few studies on PWV in Chinese patients with essential hypertension. In this cross-sectional study, we investigated 3,156 consecutive patients (mean age: 53.7±11.58 years) of the Hypertension Division of Ruijin Hospital in Shanghai. Together with sphygmomanometric blood pressure measurements, aortic PWV was measured using a validated automatic device. PWV in patients with pulse pressure (PP) 60 mmHg was significantly greater than that in patients with PP＜60 mmHg ( p＜0.01). PP and PWV were positively related to age (PP: r＝0.396, p＝0.001; PWV: r＝0.531, p＝0.001). After adjustment by age and heart rate, PWV was still closely related to PP (r＝0.249, p＝0.001). At any given systolic blood pressure (SBP), PWV significantly decreased with the increase of diastolic blood pressure (DBP), whereas at any given DBP there was a significant increase of PWV with the increase of SBP. In conclusion, PWV was the major determinant of PP, and was highest in Chinese patients with isolated systolic hypertension, followed by those with systolic and diastolic hypertension, isolated diastolic hypertension, and normal blood pressure.

To assess the clinical features and the management of congenital long QT syndrome (LQTS) in China, we collected the clinical data of 54 LQTS patients (40 females) from our newly established national registry. All patients were symptomatic, with syncope being the most common symptom. The average age of first symptoms was 17.9±15.6 (rang, 0.5-62) years; 55.6% of them had the first symptoms before the age of 20. The most common triggers of the symptoms were physical exercises or emotional stress. The average corrected QT interval was 0.55±0.08s. Using ECG criteria, there were 14 (25.9%) LQT1 patients, 28 (51.9%) LQT2 and 2 (3.7%) LQT3. Thirty (55.6%) patients were treated with β-blockers at the time of enrollment, with propranolol being the most commonly used drug on an average daily dose of 57.5+39.1 mg. Four patients underwent left cardiac sympathectomy. After an average of follow-up of 24.9+13.2 months, 3.1% (1/32) of patients with antiadrenergic therapy, and 9.1% (2/22) without antiadrengergic therapy, died of sudden cardiac death (p<0.05). We concluded that LQT2 might be the most common subtype inthese patients. Antiadrengergic treatment were underused, raising the urgent need for educating both physicians and patients on the nature of the disease and its optimal antiadrenergic therapy.

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.

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.

对561例快速心律失常患者进行射频导管消蚀治疗，其中房室旁路折返性心动过速（AvRT）413例（429条旁路），房室结折返性心动过速（AVNRT）142例，房性心动过速3例，心房扑动2例，心脏正常的室性心动过速1例。显性旁路消蚀成功靶点心电图特征为：AV<40ms，V波较体表心电图最早的delta波提前>20ms，A/V<1。隐匿旁路成功的靶点心电图特征为：心室起搏时VA<40ms，A/v<1。对左前旁路患者、合并主动脉瓣狭窄者、动脉迂曲的老年人或需同时行二尖瓣球囊扩张术者，导管经股动脉逆行放入左室不易到位，可采用房间隔穿刺法，本组6例均获成功。房室结改良患者采用下位法较后位法消蚀的平均放电次数、时间及操作时间均少（P值<0.05）。本组2例（0.4%）发生三度房室传导阻滞，置入永久性心脏起搏器。平均随访6.1±4.9个月，14例（2.6%）复发，均再次消蚀成功。