急性心梗塞患者的护理体会

急性心梗塞是指冠状动脉急性闭塞,血流中断,使部分心肌因严重的持久性缺血而发生局部坏死,主要表现为持久的胸骨后疼痛、休克、心律失常和心力衰竭,并有血清心肌酶增高以及心电图改变。急性心肌梗塞是内科常见急症,病情复杂,变化快,死亡率高,护理人员如能认真细致观察病情,配合医生进行治疗,做好各方面的护理措施,能有效提高治愈率,减少并发症,降低死亡率。

急性心肌梗塞患者的护理需注意的问题

急性心肌梗塞是冠心病的严重类型，它是由于心肌持久、严重的缺血而引起的部分心肌坏死，在临床上出现一系列的症状、体征和心电图演变，常并发心律失常、心力衰竭、休克、甚至猝死。近年来我国的心肌梗塞的发病率在逐年增高，且中年人所占的比例在大幅度上升。实践证明，急性心肌梗塞发现的早晚、抢救是否及时、护理是否恰当，不仅直接涉及病人生命的安危，而且直接关系到病人的转归及预后，在护理中必须注意以下几个问题。

彩超诊断颈动脉内中膜增厚与2型糖尿病合并心、脑血管梗塞性病变的相关研究

目的：探讨颈动脉内中膜增厚与心、脑梗塞性病变的关系。方法：采用高分辨率彩色多普勒超声仪测量糖尿病性及非糖尿病性心、脑梗塞患者的颈动脉内中膜厚度（IMT），并分析颈动脉IMT与心、脑血管病危险因素间的关系。结果：2型糖尿病合并心、脑梗塞性疾病患者的颈动脉内中膜厚度较非2型糖尿病合并心、脑梗塞患者明显增厚，斑块数量增多。结论：2型糖尿痛合并心、脑梗死患者血糖与颈动脉硬化呈正相关，因此对2型糖尿病患者进行心、脑血管疾病的一级及二级预防具有重要的意义。

急性心肌梗塞心血管内科治疗体会

目的总结急性心肌梗塞心血管的内科治疗方法 ,为临床工作者提供参考。方法回顾分析自2013年1月至2013年12月期间,我院收治的50例急性心肌梗塞患者的临床资料。患者均服用阿司匹林和阿替普酶等溶栓药物,溶栓治疗后注射肝素钠,治疗过程中接受常规护理,出院后随访12个月。结果 50例急性心肌梗塞患者经内科治疗,48例患者治愈,2例患者内科治疗无效中转心脏搭桥手术。随访12个月,48例经内科治愈的患者,心肌梗塞复发的有3例。结论血管内科溶栓治疗急性心肌梗塞具有显著疗效,接受治疗的时间越早,治疗效果和预后的生活质量越佳。

急性心肌梗塞合并心衰患者应用主动脉内球囊反搏的临床疗效观察

目的探讨主动脉内球囊反搏在急性心肌梗塞心衰治疗中的应用效果。方法选取该院2016年6月—2018年6月的80例接受急性心肌梗塞心衰治疗患者作为研究对象,采用硬币法进行分组,数字面为研究组,花面为对照组,两组人数相等。研究组采用经皮冠状动脉介入治疗与主动脉内球囊反搏辅助治疗,对照组采用单纯经皮冠状动脉介入治疗。治疗2周后,比较两组并发症发生率、临床治疗效果。结果治疗后,研究组并发症发生率为7.50%,对照组并发症发生率为40.00%,两组结果差异有统计学意义(χ~2=13.668,P<0.05)。研究组治疗的总有效率为95.00%,高于对照组治疗的总有效率75.00%,差异有统计学意义(χ~2=13.053,P<0.05)。结论使用主动脉内球囊反搏辅助治疗急性心肌梗塞心衰可以降低并发症发生率,减少患者病死率,临床应用效果显著,值得应用与推广。

1000例正常人右胸前单极导联的心电图改变

为探索正常人右胸前导联的心电图改变.对1000例不同性别与年龄组的正清人除做常规导联心电图外.又描记了V_3R、V_4R及V_5R导联的心电图.重点观察了正常人右胸前导联各波形态及正常值范围.以了解正常人右胸前导联心电图的变化.旨从心电图来提高右室梗塞的诊断水平.

心室晚电位的频谱分析

用体表叠加平均心电图(SAECG)记录分析系统对115例正常人和116例冠心病心肌梗塞(MI)患者作SAECG记录并进行心室晚电位(VLP)及频谱分析,发现MI患者VLP阳性率为37.30％;正常人SAECG频谱的高频成份(20～150Hz)明显低于MI患者(P<0.01),低频成份(0～20Hz)明显高于MI患者(P<0.01)。提示MI患者可能发生VLP,其频率结构中高频成份明显增多。

Electrophysiologic-electropharmacologic Method for Evaluating the Effects of Antagonizing Ventricular Tachyarrhythmic Drugs

Objective To establish a canine model of electrophysiologic - electropharmacology as assessed by programmed electrical stimulation (PES),and to observe the electrophysiologic effects of Procainamide(PA) on normal and ischemic myocardium in case of ischemic ventricular tachyarrhythmia in this model. Methods A ishemic ventricular tachyarrhythmias canine model was established in open-chest dogs subjected to programmed electrical stimulation(PES)for 5-8 days after acute myocardial infarction. The electrophysiologic effects of procainamide were observed in this model. With routine methods of PES,ventricular tachycardia(VT) and ventricular fibrillation (VF) could be reproducibly initiated. Results Procainamide distinctly lengthened the QTc interval (P【0.01) and effective refractory period(ERP) of normal and ischemic ventricular myocardium(NERP and IERP) respectively (P【0.01), decreased the dispersion of ERP in ischemic myocardium and the dispersion of ERP in left ventricle (P【0.01), and increased the diastolic excitability threshold of normal and ischemic ventricular myocardium remarkably (P【0.01). Procainamide effectively prevented the PES-induced VT or VF (P【0.05) and ischemia-induced VF (P【0.05). Conclusion The results indicated that PES-induced VT/VF were highly reproducible and reliable, this canine model is a worthy and reliable one, procainamide may be effective in preventing the onset of VT and VF after myocardial ischemic damage, and deserves further attention as an antifibrillatory agent.

Antiarrhythmic Efficacy of Neferine Assessed by Programmed Electrical Stimulation in a Canine Model of Electropharmacology

An ishemic ventricular tachyarrhythmias canine model was established in open-chest dogs subjected to programmed electrical stimulation (PES)for 5-8 days after acute myocardial infarction. The electrophysiologic effects of neferine (Nef) and procainamide (PA) were observed in this model. With routine methods of PES,ventricular tachycardia (VT)and ventricular fibrillation (VF) could be reproducibly initiated. Both drugs lengthened the QTc interval (P【0.01) and effective refractory period(ERP)of normal and ischemic ventricular myocardia (NERP and IERP) respectively (P【0.01), decreased the dispersion of ERP in ischemic myocardium and the dispersion of ERP in left ventricle (P【0.01), and increased the diastolic excitability threshold of normal and ischemic ventricular myocardia (P【0.01). The two compounds prevented the PES-induced VT or VF (Nef group P【0.01, PA group P【0.05) and ischemia-induced VF (P【0.05). The results indicated that neferine and procainamide may be effective in preventing the onset of reentrant ventricular tachyarrhythmias after myocardial ischemic damage in dogs.

Electrophysiologic Effects of Sophoridine on a Canine Model of Ischemic Ventricular Tachyarrhythmias

A canine model of ischemic ventricular tachyarrhythmias was established in open-chest dogs subjected to programmed electrical stimulation (PES) for 5￣8 days after acute myocardial infarction. The electrophysiologic effects of sophoridine (Sop) and procainamide (PA) were observed in this canine model. With routine methods of PES, ventricular tachycardia (VT) and ventricular fibrilation (VF) could be reproducibly initiated in this model. Both drugs distinctly lengthened the QTc interval ( P <0.01) and the effective refractory period (ERP) in normal and ischemic ventricular myocardium ( P <0.01), decreased the dispersion of ERP in ischemic myocardium and the dispersion of ERP in left ventricle (P <0.05), and increased the diastolic excitability threshold of normal and ischemic ventricular myocardium remarkably ( P <0.01). Both drugs effectively prevented the PES-induced VT or VF and ischemia-induced VF ( P <0.05). The results indicated that this canine model is a good and reliable one, sophoridine and procainamide may be effective in preventing the onset of reentrant ventricular tachyarrhythmias after myocardial ischemic damage.

急诊护理对急性心肌梗塞的治疗和预后的影响分析

目的:研究急诊护理对急性心肌梗塞的治疗及干预后的影响分析。方法:收入治疗的120例患有急性心肌梗塞病人被分派为两组,分别设为对照组与观察组,其中对照组实施单纯抢救技术,后者进行护理急救干涉。由此来比较两组患者在各方面的身体指标以判定急诊护理干预效果如何。结果:观察组抢救效率显著,死亡率低;且两者进行抢救时间无明显差别。结论:由于急救护理的实行可显著缩短手术抢救的反应时间,死亡率比普通抢救低,有助于提升身体素质,病人对此护理更满意,临床推广程度高。

Optimal time for mesenchymal stem cell transplantation in rats with myocardial infarction

Background:Bone marrow mesenchymal stem cell (MSC) transplantation is a promising strategy in the treatment of myocardial infarction (MI). However, the time for transplanting cells remains controversial. The aim of this study was to find an optimal time point for cell transplantation. Methods: MSCs were isolated and cultured from Sprague-Dawley (SD) rats. MI model was set up in SD rats by permanent ligation of left anterior descending coronary artery. MSCs were directly injected into the infarct border zone at 1 h, 1 week and 2 weeks after MI, respectively. Sham-operated and MI control groups received equal volume of phosphate buffered saline (PBS). At 4 weeks after MI, cardiac function was assessed by echocardiography; vessel density was analyzed on hematoxylin-eosin stained slides by light microscopy; the apoptosis of cardiomyocytes was evaluated by terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) assay; the expressions of proteins were analyzed by Western blot. Results: MSC transplantation improved cardiac function, reduced the apoptosis of cardiomyocytes and increased vessel density. These benefits were more obvious in 1-week group than in 1-h and 2-week groups. There are more obvious in-creases in the ratio of bcl-2/bax and the expression of vascular endothelial growth factor (VEGF) and more obvious decreases in the expression of cleaved-caspase-3 in 1-week group than those in other two groups. Conclusion: MSC transplantation was beneficial for the recovery of cardiac function. MSC transplantation at 1 week post-MI exerted the best effects on increases of cardiac function, anti-apoptosis and angiogenesis.

Human bone marrow-derived mesenchymal stem cells transplanted into damaged rabbit heart to improve heart function

Objective: The present study was designed to test whether transplantation of human bone marrow-derived mesen- chymal stem cells (hMSCs) in New Zealand rabbits with myocardial infarction can improve heart function; and whether engrafted donor cells can survive and transdifferentiated into cardiomyocytes. Methods: Twenty milliliters bone marrow was obtained from healthy men by bone biopsy. A gradient centrifugation method was used to separate bone marrow cells (BMCs) and red blood cells. BMCs were incubated for 48 h and then washed with phosphate-buffered saline (PBS). The culture medium was changed twice a week for 28 d. Finally, hematopoietic cells were washed away to leave only MSCs. Human MSCs (hMSCs) were premarked by BrdU 72 h before the transplantation. Thirty-four New Zealand rabbits were randomly divided into myocardial infarction (MI) control group and cell treated group, which received hMSCs (MI+MSCs) through intramyocardial injection, while the control group received the same volume of PBS. Myocardial infarction was induced by ligation of the left coronary artery. Cell treated rabbits were treated with 5×106 MSCs transplanted into the infarcted region after ligation of the coronary artery for 1 h, and the control group received the same volume of PBS. Cyclosporin A (oral solution; 10 mg/kg) was provided alone, 24 h before surgery and once a day after MI for 4 weeks. Echocardiography was measured in each group before the surgery and 4 weeks after the surgery to test heart function change. The hearts were harvested for HE staining and immunohistochemical studies after MI and cell transplantation for 4 weeks. Results: Our data showed that cardiac function was significantly improved by hMSC transplan- tation in rabbit infarcted hearts 4 weeks after MI (ejection fraction: 0.695±0.038 in the cell treated group (n=12) versus 0.554±0.065 in the control group (n=13) (P<0.05). Surviving hMSCs were identified by BrdU positive spots in infarcted region and transdifferentiated into cardiomyocytes characterized with a positive cardiac phenotype: troponin I. Conclusion: Transplan- tation of hMSCs could transdifferentiate into cardiomyocytes and regenerate vascular structures, contributing to functional im- provement.

Bone marrow mesenchymal stem cell transplantation combined with perindopril treatment attenuates infarction remodelling in a rat model of acute myocardial infarction

Objective: This study was performed to evaluate whether implantation of mesenchymal stem cell (MSC) would reduce left ventricular remodelling from the molecular mechanisms compared with angiotensin-converting enzyme inhibitors (ACEIs) perindopril into ischemic myocardium after acute myocardial infarction. Methods: Forty rats were divided into four groups: control, MSC, ACEI, MSC+ACEI groups. Bone marrow stem cell derived rat was injected immediately into a zone made ischemic by coronary artery ligation in MSC group and MSC+ACEI group. Phosphate-buffered saline (PBS) was injected into control group. Perindopril was administered p.o. to ACEI group and MSC+ACEI group. Six weeks after implantation, the rats were killed and heart sample was collected. Fibrillar collagen was observed by meliorative Masson’s trichome stain. Western Blotting was employed to evaluate the protein expression of matrix metalloproteinase (MMP)-2, matrix metalloproteinase (MMP)-9 in infarction zone. The transcriptional level of MMP2, MMP9 and tissue inhibitor of matrix metalloproteinase (TIMP)-1 in infarction area was detected by reverse transcriptase PCR (RT-PCR) analysis. Results: The fibrillar collagen area, the protein expression of MMP2, MMP9 and the transcriptional level of MMP2, MMP9 mRNA in infarction zone reduced in MSC group, ACEI group, and MSC+ACEI group. No significant difference was detected in the expression of TIMP1 mRNA among the 4 groups. Conclusion: Both MSC and ACEI could reduce infarction remodelling by altering collagen metabolism.

Early association of electrocardiogram alteration with infarct size and cardiac function after myocardial infarction

Objective: Myocardial infarction (MI) is the main cause of heart failure, but the relationship between the extent of MI and cardiac function has not been clearly determined. The present study was undertaken to investigate early changes in the electrocardiogram associated with infarct size and cardiac function after MI. Methods: MI was induced by ligating the left anterior descending coronary artery in rats. Electrocardiograms, echocardiographs and hemodynamic parameters were assessed and myocardial infarct size was measured from mid-transverse sections stained with Masson抯 trichrome. Results: The sum of pathological Q wave amplitudes was strongly correlated with myocardial infarct size (r = 0.920, P < 0.0001), left ventricular ejection fraction (r = -0.868, P < 0.0001) and left ventricular end diastolic pressure (r = 0.835, P < 0.0004). Furthermore, there was close relationship between MI size and cardiac function as assessed by left ventricular ejection fraction (r = -0.913, P < 0.0001) and left ventricular end diastolic pressure (r = 0.893, P < 0.0001). Conclusion: The sum of pathological Q wave amplitudes after MI can be used to estimate the extent of MI as well as cardiac function.

Correlation between growth differentiation factor-15 and collagen metabolism indicators in patients with myocardial infarction and heart failure

BackgroundGrowth differentiation factor （GDF）-15, a divergent member of the transforming growth factor beta super-family does appear to be up-regulated in response to experimental pressure overload and progression of heart failure （HF）. HF frequently develops after myocardial infarction （MI）, contributing to worse outcome. The aim of this study is to assess the correlation between GDF-15 levels and markers related to collagen turnover in different stages of HF.MethodsThe study consists of a cohort of 179 patients, including stable angina pectoris patients （AP group,n= 50）, old MI patients without HF （OMI group,n = 56）, old MI patients with HF （OMI-HF group,n= 38） and normal Control group （n = 35）. Both indicators reflecting the synthesis and degradation rates of collagen including precollagen I N-terminal peptide （PINP）, type I collagen carboxy-terminal peptide （ICTP）, precollagen III N-terminal peptide （PIIINP） and GDF-15 were measured using an enzyme-linked inmunosorbent assay.ResultsThe plasma GDF-15 level was higher in OMI-HF group （1373.4 ± 275.4 ng/L） than OMI group （1036.1 ± 248.6 ng/L）, AP group （784.6 ± 222.4 ng/L） and Control group （483.8 ± 186.4 ng/L） （P〈 0.001）. The indi-cators of collagen turnover （ICTP, PINP, PIIINP） all increased in the OMI-HF group compared with Control group （3.03 ± 1.02μg/Lvs. 2.08 ± 0.95μg/L, 22.2 ± 6.6μg/Lvs. 16.7 ± 5.1μg/L and 13.2 ± 7.9μg/Lvs. 6.4 ± 2.1μg/L, respectively;P〈 0.01）. GDF-15 positively cor-related with ICTP and PIIINP （r = 0.302,P〈 0.001 andr= 0.206,P= 0.006, respectively）. GDF-15 positively correlated to the echocardio-graphic diastolic indicators E/Em and left atrial pressure （r= 0.349 and r= 0.358, respectively;P〈 0.01）, and inversely correlated to the systolic indicators left ventricular ejection fraction and the average of peak systolic myocardial velocities （Sm） （r=-0.623 and r=-0.365, respectively;P〈 0.01）.ConclusionPlasma GDF-15 is associated with the indicators of type I and III collagen turnover.

Epidemiology and genetics of ventricular fibrillation during acute myocardial infarction

Sudden cardiac death （SCD） from ventricular fibrillation （VF） during coronary artery disease （CAD） is a leading cause of total and cardiovascular mortality, and in more than half of SCD cases VF occurs as the first symptom of CAD. Several epidemiological studies have shown that sudden death of a family member is a risk factor for SCD and VF during acute myocardial infarction （MI）, independent of traditional risk factors including family history of MI, suggesting a genetic component in the susceptibility to VF. To prevent SCD and VF due to MI, we need a better understanding of the genetic and molecular mechanisms causing VF in this apparently healthy population. Even though new insights and technologies have become available, the genetic predisposition to VF during MI remains poorly understood. Findings from a variety of different genetic studies have failed to reach reproducibility, although several genetic variants, both common and rare variants, have been associated to either VF or SCD. For this review, we searched PubMed for potentially relevant articles, using the following MeSH-terms： ＂sudden cardiac death＂, ＂ventricular fibrillation＂, ＂out-of-hospital cardiac arrest＂, ＂myocardial infarction, myocardial ische- mia＂, ＂coronary artery disease＂, and ＂genetics＂. This review describes the epidemiology and evidence for genetic susceptibility to VF due to MI.