左心室流出道不同部位室性早搏的心电图特征及射频消融治疗_林加锋
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左室射血分数与心脏大小的相关性分析
温州医学院附属第二医院 心血管内科 施凤梅 杨鹏麟 郑如莲
目的 探讨左室射血分数(LVEF)与心脏大小的关系。方法 选取2009-2011年温州医学院附属第二医院641例基础病因为扩张型心肌病、高血压性心脏病、冠状动脉粥样硬化性心脏病、老年退行性心脏病等心血管疾病患者,根据其心脏超声多普勒分为2组: LVEF正常组(≥50%)和下降组(<50%)。应用多普勒超声心动图检测LVEF、左室舒张末期内径(LVEDV)、左室收缩末期内径(LVESV)、左房内径(LAD)、右室内径(RVD)等多项指标,对比分析不同LVEF值患者心脏大小的情况。结果 LVEF下降组LVEDV、LVESV、LAD及RVD明显大于LVEF正常组,差异均具有统计学意义(P<0.01)。LVEF与LVEDV、LVESV呈显著负相关关系(r=-0.726,P<0.01;r=-0.828,P<0.01)。结论 LVEF与LVEDV、LVESV呈显著负相关,随着LVEDV、LVESV的增大,LVEF不断减少。
【关键词】左室射血分数;左室舒张末期内径;左室收缩末期内径;心力衰竭
左心室流出道不同部位室性早搏/室性心动过速的
心电图特征及射频消融治疗
温州医学院附属第二医院 心内科
林加锋 林佳选 季亢挺 李 嘉 殷日鹏 李岳春 李 进 张文武
目的 探讨左心室流出道(LVOT)不同起源室性早搏(PVCs)/室性心动过速(VT)的心电图特征及射频消融治疗结果。方法 52例LVOT PVCs/VT均采用常规标测技术经股动脉逆行途径在LVOT主动脉瓣上或瓣下进行标测与消融;随机选取同期住院并经导管射频消融治疗的104例右心室流出道(RVOT) PVCs/ VT进行对照分析,比较RVOT、LVOT及其不同部位PVCs/VT的心电图特征并提出鉴别流程。结果 52例起源于LVOT PVCs/VT射频消融成功47例,成功率90.38%。失败5例,其中4例在冠状动脉左主干标测到最领先心室电位放弃消融,另1例在左冠窦前下方(距左冠窦约0.5cm)标测到心室电位领先PVCs体表心电图QRS波起始点达34ms,反复消融无效。所有患者无严重并发症。经随访12.9±10.4(3~34)个月,复发2例。根据常规标测及消融结果将LVOT PVCs/VT分为以下3组①左冠窦组:32例,男9例,女23例,年龄60.08±13.82 (33~79)岁;②右冠窦组:11例,男4例,女7例,年龄 62.09±14.27 (30~76)岁;③左冠窦下(左纤维三角)组: 9例,男3例,女6例,年龄60.52±17.72(19~76)岁。3组患者激动顺序标测有效靶点心室电位领先程度、手术时间、X线曝光时间、放电时间均无明显差异。但RVOT及LVOT不同部位体表12导联心电图特征有一些差异:⑴若以胸导联移行<V3+胸导联移行指数>0作为诊断LVOT起源PVCs/ VT的指标,其敏感性94.12%、特异性93.00%,阳性预测值为87.27%,阴性预测值为96.88%;⑵LVOT 不同亚组分析显示,①右冠窦组多数患者Ⅰ导联以正向波为主呈r或m型(72.73%)明显多以左冠窦组的12.50%及左冠窦下组的0(均p<0.01),而另2组多数呈rs或rS型,分别占81.25%及66.67%,明显高于前者的9.09%(均p<0.01);②虽然3组患者在Ⅱ、Ⅲ、aVF及V4~V6导联均呈R型,在aVR、aVL导联均呈QS
·71·
型,但其R波高度及QS波深度的分布特征有所不同,右冠窦组100.00%RⅡ>RⅢ、QSaVR>QSaVL,而另2组则相反,多数表现为RⅢ>RⅡ、QSaVL>QSaVR(均p<0.01);③3组胸前导联QRS波群形态亦有区别,左冠窦下组多数患者在V1导联以正相波为主呈R型(77.78%),而右冠窦组(81.82%)及左冠窦组(62.50%)多数以负相波为主呈rS型;④左冠窦下组所有患者胸前导联移行在V1之前,而左冠窦组、右冠窦组多数在V2~V3;⑤左冠窦下组多数患者下壁导联R波降支有切迹(88.89%),而另2组下壁导联R波降支均无切迹。结论 LVOT PVCs并非罕见,多数患者经主动脉逆行途径采用常规标测技术普通温控消融导管进行标测与消融安全有效,LVOT不同起源的体表12导联心电图亦有些不同,认识这些特点,对术前初步判断可能的有效靶点,缩短手术时间及X线曝光时间均有一定的意义。
【关键词】电生理学;室性心律失常;左心室流出道;导管消融;射频电流
The effect of rosuvastatin on the AKT/P-AKT expression of LDLR-/- mouse with atherosclerosis induced by insulin resistance
Department of Cardiology, Shaoxing Peoples Hospital, Shaoxing 312000,China
Hangyuan Guo
Wenzhou Medical College, Wenzhou 325000,China
Haitao Lv
【Objectives】 To investigate the effect of rosuvastatin on the AKT/P-AKT expression of LDLR-/- mouse with atherosclerosis induced by insulin resistance. Method forty-five LDLR-deficient mouse were obtained at 6 wk of age and randomized into five groups (n=8 in each group): control group (NC group), high fat diet group (HF group), high fat and high fructose diet group (HFF group), rosuvastatin intervened groups(HFFR group),rosuvastatin and mevalonic acid intervened group (HFFRMA group) . High fat and high fructose diet were given to establish the mouse model with atherosclerosis induced by insulin resistance. After 12 weeks respective diet,we examined the levels of the TC, TG, LDL-C, HDL-C, FBS and FINS; the morphological of the aorta artery and aorta sinus ; the expression of AKT and P-AKT in liver, cardiac muscle, aorta arch. Result 1.The levels of FBS, FINS, HOMA-IR, TC, TG and LDL-C in HFF group were markedly higher than that of other group (P < 0. 05), and HDL-C level was significantly decreased( P < 0. 05); Contrast to HFF group, in HFFR group all above-mentioned indexes were significantly improved(P < 0. 05). TC and LDL-C level showed no significant difference between HFF and HFFRMA group( P >0. 05). 2. The area of atherosclerotic plaque in HFF are significantly increased than that of other group ( P < 0. 05); The area of atherosclerotic plaque in HFFR and HFFRMA group obvious remarkably, and showed no significant difference between the two groups ( P < 0.
05). 3. The AKT, P-AKT expressions level in HFF group were significantly lower than that of other group( P < 0.
05). In HFFR and HFFRMA group, as compared with HFF group, the corresponding results were improved,and have no significant difference. Conclusion 1、High fat and high fructose diet for 12 weeks can induce insulin resistance in LDLR-/- mice. 2、Insulin resistance can accelerates the development of atherosclerosis. 3、In insulin resistance group, the expression of AKT and P-AKT of liver, cardiac muscle and aorta arch were ·72·