Research of transmyocardial stent to treat acute myocardial infarction

Objectives To explore the feasibility, safety and efficacy of transmyocardial stent to treat acute myocardial infarction. Methods 24 Chinese mini swines have been divided into 2 groups randomly：group myocardial infarction （group MI n1 = 14） and group transmyocardial stent（group ST n2 = 10）. In group MI, acute myocardial infarction animal model has been established by the ligation of the left descending coronary artery. In group ST, after the establishment of the model, 3 transmyocardial stents were implanted. 4 weeks later, echocardiography and pathological analysis have been done. Results The density of blood vessel in group ST is 6.47 ± 0.60/HP which is significandy higher than the group MI. At the same time, left ventricular ejection fraction and regional wall motion score index （WMSI） in group ST are ameliorated significandy compared with group MI. Conclusion It is feasible and safe to implant transmyocardial stents in acute myocardial infarction model. Although the channel can＇ t remain patent in long term, the prolonged stimulation can cause moderate-serious inflammatory reaction and proficient angiogenesis.     

Successful cardiopulmonary resuscitation of a patient developed a 52-minute cardiopulmonary arrest secondary to acute myocardial infarction.

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Thrombolytic intervention of acute myocardial infarction in the 1990s.

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Small bowel obstruction secondary to a giant enterolith complicating Crohn’s disease

Background  

Enterolith formation associated with Crohn’s disease is a very uncommon clinical entity.     

Hydrogen peroxide preconditioning enhances the therapeutic efficacy of Wharton’s Jelly mesenchymal stem cells after myocardial infarction

Background  Exposure of cells to sublethal concentrations of hydrogen peroxide (H₂O₂) can alleviate subsequent oxidative stress-induced apoptosis. We assessed the effects of H₂O₂ preconditioning on the therapeutic potential of human umbilical cord Wharton’s Jelly mesenchymal stem cells (WJ-MSCs) in a murine model of myocardial infarction.

Methods  WJ-MSCs were incubated in the media for 2 hours with or without 200 µmol/L H₂O₂. Mice underwent left anterior descending coronary artery ligation, and received injection of phosphate buffered saline, 1×10⁶ WJ-MSCs, or 1×10⁶ H₂O₂ preconditioned WJ-MSCs 3 hours later via tail vein. Echocardiography was performed 0, 7, 14 and 28 days after surgery, and the mice were euthanized on day 28 for histological analysis. In vitro cytokine concentrations in the WJ-MSC cell supernatant were measured by enzyme-linked immunosorbent assay (ELISA). The effect of WJ-MSC cell supernatant on the migration and proliferation of endothelial cells were observed by transwell migration and 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyl tetrazoliumbromide (MTT) assays.

Results  Echocardiographic measurements revealed a significant improvement in the left ventricular contractility of the WJ-MSCs-H₂O₂ group compared to the WJ-MSCs group. Histological analysis revealed increased neovascularization and reduced myocardial fibrosis in the WJ-MSCs-H₂O₂ group compared to the WJ-MSCs group. Pretreatment of WJ-MSCs with H₂O₂ increased the secretion of interleukin-6 (IL-6) into the cell culture supernatant by approximately 25-fold. The culture supernatant from WJ-MSCs-H₂O₂ significantly increased the migration and proliferation of endothelial cells; these effects could be blocked using an anti-IL-6 antibody.

Conclusions  This study demonstrates that H₂O₂ preconditioning significantly enhanced the therapeutic potential of WJ-MSCs, possibly by stimulating the production of IL-6 by WJ-MSCs, which may cause migration and proliferation of endothelial cells and increase neovascularization.

     

Reperfusion arrhythmias in acute myocardial infarction.

In 27 patients with acute myocardial infarction (MI) and their infarct-related coronary artery being completely occluded who received thrombolytic therapy or percutaneous transluminal coronary angioplasty, reperfusion was confirmed by immediate coronary angiography in 24. Reperfusion arrhythmias (RA) occurred in 19 (79.2%) of the patients, including ventricular arrhythmias in 13 (54.2%). Ventricular fibrillation and sustained ventricular tachycardia developed in 2 (8.4%) and accelerated idioventricular rhythm in 5 (20.8%), the latter was a reliable indicator of coronary recanalization. Transient sinus bradycardia or AV block occurred in 10 (66.7%) of the 15 patients with inferoposterior MI. The occurrence of RA was not related to the duration of ischemia; ventricular RA was also not related to the location of MI and the occurrence and severity of ischemic arrhythmias before reperfusion.

     

Acute myopericarditis masquerading as acute myocardial infarction

Patients with abrupt onset of chest pain,ischemic ECG abnormalities and elevated levels of cardiac markers could be given a diagnosis of acute myocardial infarction.However,some other diseases should be taken into consideration in this clinical setting when coronary arteries are proven to be normal.Here we report a case of acute myopericarditis with clinical presentation of myocardial infarction and normal coronary anatomy.The Herpes Simplex Virus II was considered as the organism causing myopericarditis and the patient was recovered by the treatment with valacicloavir.A precise diagnosis is a prerequisite of successful treatment and favorable prognosis.     

Spontaneous coronary dissection associated with myocardial bridge causing acute myocardial infarction

Spontaneous coronary artery dissection （SCAD） is a rare cause of myocardial ischemia, myocardial infarction and sudden-cardiac death.This disease mainly occurs in young women with oral contraceptive or during the peripartum period, without risk factors for coronary artery disease. Although SCAD results in a hemorrhagic separation of the intima and the media, and creates a false lumen, leading to distal myocardial ischemia, infarction and sudden death, the causes and the optimal management for this challenging condition are still controversial.     

Impact of patients’ symptom interpretation on care-seeking behaviors of patients with acute myocardial infarction

Background Delay in seeking medical care in patients with acute myocardial infarction （AMI） is receiving increasing attention. This study aimed to examine the association between expected symptoms and experienced symptoms of AMI and its effects on care-seeking behaviors of patients with AMI. Methods Between November 1, 2005 and December 31, 2006, a cross-sectional and multicenter survey was conducted in 19 hospitals in Beijing and included 799 patients with ST-elevation myocardial infarction （STEMI） admitted within 24 hours after onset of symptoms. Data were collected by structured interviews and medical record review. Results The median （25%, 75%） prehospital delay was 140 （75, 300） minutes. Only 264 （33.0%） arrived at the hospital by ambulance. The most common symptoms expected by patients with STEMI were central or left chest pain （71.4%）, radiating arm or shoulder pain （68.7%）, shortness of breath or dyspnea （65.5%）, and loss of consciousness （52.1%）. The most common symptoms experienced were central or left chest pain （82.1%）, sweats （71.8%）, shortness of breath or dyspnea （43.7%）, nausea or vomiting （32.3%）, and radiating pain （29.4%）. A mismatch between symptoms experienced and those expected occurred in 41.8% of patients. Patients who interpreted their symptoms as noncardiac in origin were more likely to arrive at the hospital by self-transport （86.5% vs. 52.9%, P 〈0.001） and had longer prehospital delays （medians, 180 vs. 120 minutes, P 〈0.001） compared to those who interpreted their symptoms as cardiac in origin. Conclusions Symptom interpretation influenced the care-seeking behaviors of patients with STEMI in Beijing. A mismatch between expectation and actual symptoms was associated with longer prehospital delay and decreased use of emerqency medical service （EMS）.     

Intracoronary stenting in 18 cases of acute myocardial infarction

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Determining the Amount of Anesthetic Medicine to Be Applied by Using Elman’s Recurrent Neural Networks via Resilient Back Propagation

In this study, Elman recurrent neural networks have been defined by using conjugate gradient algorithm in order to determine the depth of anesthesia in the continuation stage of the anesthesia and to estimate the amount of medicine to be applied at that moment. The feed forward neural networks are also used for comparison. The conjugate gradient algorithm is compared with back propagation (BP) for training of the neural Networks. The applied artificial neural network is composed of three layers, namely the input layer, the hidden layer and the output layer. The nonlinear activation function sigmoid (sigmoid function) has been used in the hidden layer and the output layer. EEG data has been recorded with Nihon Kohden 9200 brand 22-channel EEG device. The international 8-channel bipolar 10–20 montage system (8 TB-b system) has been used in assembling the recording electrodes. EEG data have been recorded by being sampled once in every 2 milliseconds. The artificial neural network has been designed so as to have 60 neurons in the input layer, 30 neurons in the hidden layer and 1 neuron in the output layer. The values of the power spectral density (PSD) of 10-second EEG segments which correspond to the 1–50 Hz frequency range; the ratio of the total power of PSD values of the EEG segment at that moment in the same range to the total of PSD values of EEG segment taken prior to the anesthesia.     

Clinical trial of China-made recombinant streptokinase in acute myocardial infarction

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Monocyte chemotactic protein 1 increases homing of mesenchymal stem cell to injured myocardium and neovascularization following myocardial infarction

Objective：To investigate the effect of MCP-1 on mesenchymal stem cells（MSCs） homing to injured myocardium in a rat myocardial infarction（MI） model. Methods：Rat myocardial infarction model was established by permanent left anterior descending branch ligation. Mesenchymal stem cells from donor rats were cultured in IMDM and labeled with BrdU. The Rats were divided into two groups. Monocyte chemotactic protein I（MCP-1） expression were measured by in situ hybridization and immunohistochemistry in the sham operated or infarcted hearts at 1, 2, 4, 7, 14 and 28 days post operation in MCP-1 detection group. The rats were injected with MCP-1, anti-MCP-1 antibody or saline 4 days after myocardial infarction in intervention group. Then, a total of 5 × 10^6 cells in 2.5 ml of PBS were injected through the tail vein. The number of the labeled MSCs in the infarcted hearts was counted 3 days post injection. Cardiac function and blood vessel density were assessed 28 days post injection. Results：Self-generating MCP-1 expression was increased at the first day, peaked at the 7^th day and decreased thereafter post MI and remained unchanged in sham operated hearts. The MSCs enrichment in the host hearts were more abundant in the MI groups than that in the non-MI group（P= 0.000）, the MSCs enrichment in the host hearts were more abundant in the MCP-1 injected group than that in the anti-MCP-1 antibody and saline injected groups （P = 0.000）. Cardiac function was improved more in MCP-1 injected group than anti-MCP-1 antibody and saline injected groups（P= 0.000）. Neovascularization in MCP-1 injected group significantly increased compared with that of other groups（P = 0.000）. Conclusion： Myocardial MCP-1 expression was increased only in the early phase post MI. MCP-1 may enhance MSCs homing to the injured heart and improve cardiac function by promoting neovascularization.     

Evaluation of serum troponin T measurement in acute myocardial infarction.

The release kinetics of the cardiac specific troponin T (cTnT), measured by an immunosorbent assay, in 32 patients with acute myocardial infarction (AMI) was evaluated. In 8 AMI patients (25%), the release kinetics of serum cTnT showed biphasic serum concentration curves with a large peak at 10 to 18 hours after onset and the serum cTnT concentrations were up to 30 to 120 times of the normal upper limit-detected (0.2 μg / ml), and another samll cTnT peak at 70 to 100 hours after onset of pain. The serum cTnT measurements in the remaining 24 AMI patients (75%) gave only one large peak which was around 32 to 108 hours after onset of pain. cTnT appeared in serum as early as 3 to 4 hours and remained elevated until 240 hours after the infarctions. The results indicated that (1) cTnT was a sensitive and specific marker of AMI; (2) the biphasic curve of cTnT releae in general, the ratio of cTnT at around 14 to 32 (14/32)>1 in particular, may be a useful marker suggesting early reperfusion; (3) the continuous     

Effect of simvastatin on pro-inflammatory cytokines after myocardial infarction in rats

INTRODUCTIONT here was evidence that pro inflammatory cytokinesand their gene expression increased in post MI rat,which related to ventricular remodeling and heart fail ure[1]. Investigators found that reduction of those cy tokines might improve ventricular remodeling and heartfailure[2].　Several clinical trials had demonstrated the benefit ofstatins for the primary and secondary prevention of coro nary heart disease (CHD). Although it is widely accept ed that the majority…     

Phenomenon of high anterior wall T-waves in inferior lateral myocardial infarction

ＰｈｅｎｏｍｅｎｏｎｏｆｈｉｇｈａｎｔｅｒｉｏｒｗａｌＴｗａｖｅｓｉｎｉｎｆｅｒｉｏｒｌａｔｅｒａｌｍｙｏｃａｒｄｉａｌｉｎｆａｒｃｔｉｏｎＺｈａｏＢｏ赵波，ＺｈａｎｇＬｉｊｕａｎ张丽娟ａｎｄＹａｎｇＱｉｎｇｘｉａｎｇ杨庆祥Ｔｈｉｓｐａｐｅｒａｎａ...     

Antithrombotic effects of Andrographis paniculata nees in preventing myocardial infarction.

In 16 dogs the endothelium of the left anterior descending coronary artery was injured mechanically. Then a copper wire was inserted into the lumen as a choke of flow and the vessel was slightly compressed from outside by a constrictor. Eight dogs had been treated beforehand with a preparation of flavone extracted from the root of the Chinese medicinal herb Andrographis paniculata (TFAP). In the control group, saline solution was given, the epicardially recorded ST segment started to elevate within 15 minutes, the platelet aggregation rate and the plasma levels of TXB2 increased rapidly, whereas the level of 6-k-PGF1 alpha remained stable. Platelet cGMP rose continuously; however, platelet cAMP rose only at 60 minutes. Histological findings confirmed the occurrence of arterial thrombus and myocardial necrosis. Contrariwise, in the pretreated group there was no elevation of the ST segment, plasma 6-k-PGF1 alpha and platelet cAMP were increased, the production of TXB2 and aggregation of platelets were inhibited, and no thrombus or myocardial infarction was induced. All data suggest that TFAP might promote the synthesis of PGI2, inhibit the production of TXA2, stimulate the synthesis of cAMP in platelets, impede aggregation of platelets, and thereby prevent the formation of thrombi as well as the development of myocardial infarction.