阵发性房室结折返性室上性心动过速射频消融临床观察

阵发性房室结折返性室上性心动过速是阵发性室上性心动过速的一种常见类型。多见于无器质性心脏病患者。现报告我们采用射频消融治疗的效果和体会。1对象和方法我院2006年6月～2009年12月经过心内电生理检查确诊为房室结双径路并阵发性室上性心动过速     

阵发性房室或房室结折返性心动过速患者射频消融治疗前后有关心房颤动的研究

心房颤动 (房颤 )是房室旁路参与的房室折返性心动过速 (AVRT )及阵发性房室结折返性心动过速 (AVNRT )患者常见的并发症 ,国外报道发生率为 19%～ 44% ,并因其对显性预激患者具有潜在的导致恶性室性心律失常、血栓栓塞及猝死的危险而倍受重视。射频消融治疗已成为目前治疗AVRT和AVNRT的一线治疗。本研究的目的是总结AVRT和AVNRT患者射频消融治疗前后房颤的发生情况 ,从而分析成功的射频消融慢径及房室旁路对房颤的预防作用。资料和方法对象为 1994年 1月～ 1999年 12月在我院导管室接受射频消融治疗成功的 90例AVRT和AVNRT…     

射频消融房室结折返性心动过速401例临床分析

射频消融术 (RFCA)为治疗室上性心动过速(SVT)的一种最有效方法 ,房室结折返性心动过速(AVNRT)是SVT中最常见的一种。本文总结了 40 1例AVNRT的RFCA资料 ,现报告如下。1 　 对象与方法1 995～ 2 0 0 3年在我院心内科行RFCA治疗的AVNRT患者共 40 1例 ,男 1 32例 ,女 2 69例 ,年龄 9～ 86( 4 6.5± 1 6.7)岁 ,均有频繁的SVT史 ,且药物不能预防发作 ;心动过速时均有心悸、头晕等症状。入院后予体检、X线胸片及超声心动图检查 ,2例Ebstein畸形 ,1例风湿性瓣膜病 ,其余心脏结构和功能基本正常。操作方法 :①先行心内电生理检查 ,…     

射频消融治疗阵发性室上性心动过速110例

目的分析射频消融(RFCA)治疗阵发性室上性心动过速(PSVT)的疗效。方法回顾性分析110例患者临床资料,均采用常规RFCA治疗PSVT患者。结果房室折返性心动过速(AVRT)65例,预激综合征合并房颤3例,计有旁道70条,显性旁道35条,隐匿性旁道35条,其中位于冠状静脉窦憩室颈部心外膜旁道1例,双旁路2例均为左侧。房室结折返性心动过速(AVNRT)42例,均为慢-快型,其中有两例患者术中未能诱发出心动过速,予RFCA阻断慢径治疗。RFCA治疗PSVT总成功率为99.1%,其中房室结双经路介导的PSVT成功率高达100%,复发率为3.6%,均复治成功,并发症发生率5.6%。结论采用常规方法RFCA治疗PSVT成功率高,并发症少。     

低能量射频消融慢径治疗房室结折返性心动过速的评估

目的初步探讨射频改良房室结双径路的能量,房室传导阻滞发生率,初步手术成功率和复发率.方法自1998年1月至2000年6月,对20例(女14例,男6例),平均年龄(43.4±17.1)岁频发房室结折返性心动过速(AVNRT)患者,采用射频消融能量从5W低能量开始,无效则按每5W逐渐递增,限定最大能量为30W进行消融慢径改良房室结功能.结果20例患者全部改良成功,平均释放能量5～30W,平均(17.6±7.2)W,术后平均4～30个月随访,无1例发生房室传导阻滞并发症,其中1例术后2个月复发AVNRT,经再次射频消融慢径改良房室结功能成功.结论采用低能量射频消融改良房室结功能,疗效满意,对减少房室传导阻滞并发症有益.     

房室折返性心动过速合并阵发性心房颤动的射频导管消融策略

目的探讨房室折返性心动过速（AVRT）合并阵发性心房颤动的射频导管消融（下称消融）策略。方法对经电生理检查证实的AVRT患者15例行旁道消融术,其中男性9例,女性6例,并对术后心房颤动的转归进行12～36个月的随访,观察心房颤动发生、持续时间、有无心律失常等情况。结果13例未再发生心房颤动,2例有严重器质性心脏病的患者仍有阵发性心房颤动复发,但发作次数明显减少,口服胺碘酮可控制症状。1例动态心电图示频发房性期前收缩。结论AVRT与阵发性心房颤动发生率增高密切相关,AVRT是心房颤动的触发因素。旁道消融后,阵发性心房颤动可明显改善,未改善者与心房扩大等心房基质未改善有关。     

房室结折返性心动过速的发作方式及射频消融终点研究

房室结折返性心动过速（AVNRT）是阵发性室上性心动过速（简称室上速）最常见的类型，约占阵发性室上速的50％。而房室结双径路（DAVNP）被认为是发生房室结折返性心动过速的基础。典型房室结折返性心动过速患者的房室结传导曲线（AVNFC）呈“跳跃”状态，然而，近年发现在AVNFC呈非跳跃性的患者也可发生AVNRT。可见房室结结构及其电生理特性极其复杂，本文对房室结折返性心动过速不同的发作方式及房室结传导曲线本质特点、射频消融治疗终点进行综述。     

长期心肌缺血对急性心肌梗塞预后的影响

目的 :探讨长期心肌缺血对急性心肌梗塞 (AMI)临床表现与近期预后的影响。方法 :　回顾性分析了 5 96例心绞痛 (AP)病程≥ 2周的 AMI的临床资料 ,并与无 AP史或 AP<2周的患者比较。结果 :　 AP组合并休克、心衰者少于对照组 (分别为 10 .9%比 15 .8%和 19.8%比 2 5 .0 % ,均 P<0 .0 5 ) ,住院病死率也较低 (11.4%比 15 .7% ,P<0 .0 5 ) ,AP组梗塞前正规治疗者多于对照组 (5 8.4%比 2 9.1% ,P<0 .0 0 1) ,患高血压者也较多(5 3.1%比 41.2 % ,P<0 .0 0 1) ,但大面积梗塞较少 ,肌酸激酶峰值较低。结论 :　长期心肌缺血可能也有缺血预适应作用 ,有益于 AMI的近期预后     

缺血预适应对糖尿病大鼠再灌注心肌的保护作用

目的　通过建立大鼠缺血预适应 (IP)模型 ,探讨IP对缺血 再灌注 (I/P)糖尿病大鼠心肌的保护作用。方法　在SD大鼠腹腔内注射链佐星 (6 0mg/kg)制造糖尿病大鼠模型。 2d后 ,随机时刻测定血糖 ,将血糖≥ 11.1mmol/L定为糖尿病大鼠 2 2只 ,另外 2 2只血糖正常鼠为非糖尿病鼠。 2周后 ,麻醉大鼠 ,结扎和放松冠状动脉左前降支(LAD)复制IP和I/P模型。将 44只大鼠分为IP糖尿病大鼠组 (DIP组 )、IP非糖尿病大鼠组 (NDIP组 )、非IP糖尿病大鼠组 (DNIP组 )和非IP非糖尿病大鼠组 (NDNIP组 )各 11只。记录II导联心电图。取心脏切片染色 ,计算心肌缺血范围和心肌坏死范围。结果　各组间心肌缺血范围无显著差异 (P >0 .0 5 )。DIP组心肌坏死范围较DNIP组明显减小 (P <0 .0 1)。DNIP组室性心律失常增多 ,尤其心室颤动较其他各组显著增多 (P <0 .0 1)。结论　缺血预适应可以减轻糖尿病大鼠随后较长时间缺血 再灌注对心肌的严重损害 ,能减少心肌坏死范围和降低心室颤动的发生率。     

Preconditioning the human myocardium: Recent advances and aspirations for the development of a new means of cardioprotection in clinical practice

Summary Ischemic preconditioning has been shown to be one of the most powerful means of protecting the myocardium from ischemic injury in experimental animal models, although the mechanism is incompletely understood. In this review we discuss the evidence for preconditioning occurring in ischemic syndromes in humans, whether the human myocardium can be preconditioned, and whether preconditioning would have a place as a therapeutic tool in clinical practice. Some studies evaluating patients after acute myocardial infarction have shown a better outcome in patients reporting angina before the onset of the infarction, but this is not a universal finding, and it is difficult to exclude other confounding factors, such as collateral flow, from influencing the results. More controlled prospective studies have evaluated patients undergoing percutaneous transluminal coronary angioplasty and have found less ST-segment change and less reported angina during the second balloon inflation when compared with the first. Again, it is impossible to completely exclude other causes for this effect, but the dependence on mechanisms that are known to be important for preconditioning in animal models does suggest the phenomena are the same. Further experiments using isolated human atrial muscle have shown that human myocardium can be preconditioned and that the mechanisms involved are similar to those elucidated in animal models (adenosine, protein kinase C, and ATP-dependent potassium channels). In clinical medicine preconditioning is most likely to benefit patients when it is used to protect against the ischemia induced by cardiac surgery. In this respect, a study has shown that in patients undergoing coronary artery bypass grafts, the reduction in ATP occurring during the first ischemic period is attenuated in those given an ischemic preconditioning protocol beforehand. Despite these advances, it is likely that the full potential of preconditioning in clinical practice will not be realized until the whole mechanism of protection is understood and a safe pharmacological preconditioning agent becomes available.     

Insulin addition after ischemia improves recovery of function equal to ischemic preconditioning in rat heart

Background Ischemic preconditioning (IPC) is considered the most potent mechanism to improve ischemia tolerance. We have demonstrated that insulin addition during reperfusion improves recovery of function in the isolated working rat heart. We herein compare the relative importance of these two mechanisms in improving recovery of postischemic function.Methods Isolated working rat hearts were perfused with Krebs-Henseleit buffer containing glucose (5 mmol/l) plus oleate (0.4 mmol/l) for 20 min and were then subjected to 15 min of ischemia followed by 35 min of reperfusion. IPC was achieved by an ischemic period of ve minutes followed by 10 minutes of reperfusion before ischemia. Insulin (1 mU/ml) was or was not added at the beginning of reperfusion. Wortmannin (WM, 3 µmol/l), an inhibitor of phosphatidylinositol 3-kinase, was or was not present in the perfusate from the beginning of the experiments. We measured glucose uptake with [2-³H]glucose, cardiac power and tissue metabolite content at the end of the experiments.Results Cardiac power before ischemia ranged from 7.17 to 10.4 mW. After ischemia, cardiac power recovered to 65.7 ± 3.8% (Control). Insulin signicantly improved recovery (96.3 ± 10.8%, p < 0.05 vs. Control). This effect was also achieved by IPC (recovery 86.2 ± 6.2%, p < 0.05). The effects of insulin and IPC were not additive (recovery 83.4 ± 6.2%, p < 0.05). WM fully inihibited the effects of both insulin and IPC (69.5 ± 3.3, 72.0 ± 6.9, respectively). Basal glucose uptake ranged from 2.53 to 3.46 µmol/gdry, and was signicantly lower after ischemia in the presence of WM.Conclusions Insulin is a potent tool to improve postischemic contractile function. The improvement of recovery afforded by insulin added after ischemia may be mediated through a similar mechanism as ischemic preconditioning.     

Effect of remote ischemic preconditioning on hepatic microcirculation and function in a rat model of hepatic ischemia reperfusion injury

Background:

Liver transplantation involves a period of ischemia and reperfusion to the graft which leads to primary non-function and dysfunction of the liver in 5–10% of cases. Remote ischemic preconditioning (RIPC) has been shown to reduce ischemia reperfusion injury (IRI) injury to the liver and increase hepatic blood flow. We hypothesized that RIPC may directly modulate hepatic microcirculation and have investigated this using intravital microscopy.

Methods:

A rat model of liver IRI was used with 45 min of partial hepatic ischemia (70%) followed by 3 h of reperfusion. Four groups of animals (Sham, IRI, RIPC+IRI, RIPC+Sham) were studied (n= 6, each group). Intravital microscopy was used to measure red blood cell (RBC) velocity, sinusoidal perfusion, sinusoidal flow and sinusoidal diameter. Neutrophil adhesion was assessed by rhodamine labeling of neutrophils and cell death using propidium iodide.

Results:

RIPC reduced the effects of IRI by significantly increasing red blood cell velocity, sinusoidal flow and sinusoidal perfusion along with decreased neutrophil adhesion and cell death.

Conclusions:

Using intravital microscopy, this study demonstrates that RIPC modulates hepatic microcirculation to reduce the effects of IRI. HO-1 may have a key role in the modulation of hepatic microcirculation and endothelial function.     

Proximal coronary hemodynamic changes evaluated by intracardiac echocardiography during myocardial ischemia and reperfusion in a canine model

BACKGROUND: The purpose of this study was to assess whether the dynamic changes in coronary flow velocity and coronary flow velocity reserve (CFVR) by intracardiac echocardiography (ICE) within proximal coronary arteries are related to myocardial perfusion status and infarct size in a myocardial ischemia-reperfusion injury model. METHODS: In 14 dogs, left anterior descending coronary artery (LAD) was ligated for 2 hours followed by 2 hours reperfusion. Coronary flow velocity was obtained by ICE within coronary arteries at baseline, and at the end of both occlusion and reperfusion period. The CFVR was calculated as the ratio of hyperemic to resting peak diastolic velocity (PDV). Myocardial perfusion was evaluated by real time myocardial contrast echocardiography (MCE). The infarct area was detected by triphenyltetrazolium chloride (TTC) staining and expressed as the percentage of the whole left ventricular (LV) area. RESULTS: CFVR significantly decreased both in proximal LAD and left circumflex (LCx) artery at the end of occlusion, and did not recover at the end of reperfusion. However, no significant difference in flow parameters was observed between dogs with myocardial perfusion defect and those without. CFVR in LAD at the end of reperfusion did not correlate with the infarct size (r =-0.182, P = NS) either. CONCLUSIONS: Decreased CFVR detected by ICE occurs both in ischemic and in nonischemic proximal arteries during myocardial ischemia and early stage of reperfusion. This change in CFVR has poor correlation with the extent of microvascular impairment and cannot be used to predict infarct size.     

Acute myocardial infarction in a patient with severe aortic stenosis and normal coronary arteries

We report a case of acute myocardial infarction occurring ina patient with severe aortic stenosis and left ventricular hypertrophy.A coronary angiogram performed during the acute phase of evolvingmyocardial infarction excluded coronary obstruction as the causeof acute myocardial infarction in this patient.     

大鼠缺血预处理对心肌保护作用及脂联素表达的影响

目的探讨心肌缺血预处理(IPC)对成年和老年大鼠的心功能及心肌组织和血浆中脂联素表达的影响。方法取成年和老年大鼠各85只,将IPC成功的成年和老年大鼠各50只中,随机各取40只为IPC组,另10只再建心肌梗死(M1)模型为IPC-M1组;只穿线不阻断血流的成年和老年大鼠各30只中,随机各取20只作为假手术组,另10只建MI模型为单纯MI组。假手术组及IPC组又分别于IPC后0、6、12和24h 4个时间点观察。将未结扎冠状动脉的成年和老年大鼠各5只作为对照组。用M型超声检测心功能,Masson's Trichrome染色,测量MI面积,免疫组织化学法和RT-PCR法测心肌组织脂联素蛋白和mRNA的表达,用ELISA法检测血浆脂联素含量。结果老年大鼠IPC-MI组存活率显著低于单纯MI组和对照组(P<0.05),而成年大鼠3组生存率无变化(P>0.05)。成年大鼠IPC-MI组短轴缩短率较单纯MI组明显升高,MI面积显著减小(P<0.05);与假手术组比较,IPC组6和12h心肌组织脂联素mRNA表达明显升高(P<0.05),血浆脂联素在0、6和12h显著升高(P<0.05)。老年大鼠IPC组各时间点心肌组织脂联素mRNA表达与假手术组无显著差异,血浆脂联素24 h明显升高(P<0.05)。结论成年大鼠IPC后心肌组织和血采脂联素表达均升高,心功能改善,老年大鼠脂联素变化不明显,提示脂联素参与成年大鼠IPC发挥的心肌保护作用。     

Multiple coronary thrombosis in a patient with thrombocytosis

A 59-year-old woman was admitted with acute inferior myocardial infarction. Cardiac catheterization revealed total occlusion in the right coronary artery and thrombus-like filling defect in the left anterior descending coronary artery. With simultaneous intracoronary urokinase infusion to the right and left coronary arteries, the right coronary artery became patent and the thrombus in the left anterior descending coronary artery was released to the distal coronary artery. Thrombocytosis was disclosed by laboratory examination. The relationship between myocardial infarction and thrombocytosis is discussed.