Acute myocardial infarction (AMI) is a serious hazard to human health cardiovascular disease is the leading cause of death worldwide . Nearly 10 years with the continuous improvement of people's living standards and improve the patient of high blood sugar , high blood pressure , high cholesterol is a growing incidence of myocardial infarction growth rate also increased year by year , how to treat AMI, has been more and more people attention, percutaneous transluminal balloon coronary angioplasty (PTCA) and coronary stenting is the most effective method of early opening of the coronary blood vessels , through early reperfusion therapy , you can quickly restore myocardial blood flow , which can effectively save the dying heart, significantly reduced mortality. However, some patients with stenosis of the blood vessel supply areas of acute ischemic myocardial cells , resulting in cardiac structure and metabolic disorders , even restored myocardial reperfusion , infarct size can not be reduced, and thus prognosis of AMI and infarct size , reduced infarct size essential for the treatment of AMI [ 1 ] .

Therefore , therapeutic angiogenesis , namely through the establishment and promotion of angiogenesis in ischemic myocardium artery collateral circulation in the region , has gradually become a hot research . [ 2 ] A number of studies indicate that HMP can promote microvascular endothelial cell proliferation and the formation of the lumen structure , promote angiogenesis microvascular endothelial cells , with obvious pro-angiogenic activity , by promoting new coronary ischemic myocardium after AMI collateral angiogenesis , thereby reducing infarct size , this study investigated the effects of acute myocardial infarction after PCI using different doses of HMP on infarct size , comparing the efficacy , medicine and the application of the guidance MI applied dose.

 

Materials and Methods

 

1.1 The study of Cardiology in our hospital since 2009.6-2010.12 acute anterior myocardial infarction 68 patients were randomly divided into two groups : Group 1 ( low-dose HMP ) 34 cases , 25 males and 9 females . 2 groups ( high dose HMP ) group of 34 patients , 23 males and 11 females . All patients with acute myocardial infarction within 12 hours of admission , this onset to surgery 4 +1.5 h, and no significant differences in age, gender , infarct location areas . 48 males and 20 females . All patients underwent coronary angiography at least a stenosis (≥ 75%), direct PCI treatment, diagnostic criteria for acute myocardial infarction based on 2007 European Society of Cardiology (ESC), Society of the United States heart disease (ACC) jointly develop " global uniform definition of myocardial infarction . " Exclusion criteria: restrictive cardiomyopathy ; valvular heart disease , congenital heart disease ; right bundle branch block ; cardiogenic shock ; receiving thrombolytic therapy .#p#分頁標題#e#
 

1.2 Methods
 

1.2.1 Determination of plasma BNP immediately hospitalized , four weeks , group 1 and 2 resting venous blood 2 ml of EDTA anticoagulated tubes , shake, take 250ul join Triage assay plates , using U.S. BIOSITE ( Bo fitness ) produced the Triage BNP diagnostic testing.
 

1.2.2 OUTCOME MEASURES : QRS scoring in the hospital immediately , four weeks tracings conventional 12 -lead ECG , with W agner and other QRS scoring method [ 3 ] ECG scores for each measure , which means that each lead measurements ( except Ⅲ, aVR ECG ) Q- wave and R -wave width , R / Q and R / S -wave amplitude ratio , calculated scores , the scores will be summed to obtain a copy of ECG score.
 

1.2.3 randomized to group 1, 2 patients were oral perindopril ( Jaster ) 2-4mg, Qd, metoprolol ( metoprolol ) 25-100mg / d, spironolactone 20mg, Qd, 1 groups serving small doses HMP ( Shanghai Hutchison Pharmaceuticals ) , a pill , 2 times / d, 2 groups serving large doses HMP 2 pills, 3 times / d, for taking four weeks to measure the line of plasma BNP and QRS score analysis .
 

1.3 Statistical analysis using SPSS11.5 statistical software to organize , analyze the data , all the measurement data to the " mean + standard deviation ," said the measurement data between groups were compared using t test , P <0.05 was considered statistically significant.

Result
 

2.1 HMP small dose group compared with large doses of HMP group baseline data . One group and two groups of gender, age , heart rate , blood pressure , blood lipids , blood glucose was no significant difference (P> 0.05 Table 1 ) , comparable.
 

2.2 low-dose pill Shexiangbaoxin after high-dose group and HMP PCI group and medication four weeks immediately after BNP testing shows : After taking the 2 groups were decreased significantly decreased high-dose group , the difference was statistically significant (P <0.01 ) , Table 2.
 

2.3 After Pill group and high-dose groups PCI HMP small doses Shexiangbaoxin instantly , four weeks after the QRS score shows : After taking the 2 groups were decreased significantly decreased high-dose group , the difference was statistically significant (P <0.01) Table 3 .

 

Cardiovascular disease has become in the 21st century the number one killer of human health , the most dangerous of acute myocardial infarction. [ 4 ] Statistics show that 17 million people worldwide die of cardiovascular disease each year , more than half died of acute myocardial infarction. Over the past decade , the incidence of acute myocardial infarction has been a clear upward trend . Sudden onset of acute myocardial infarction , acute mortality of about 30 %.
 

The basic cause of acute myocardial infarction is based on coronary atherosclerosis plaque rupture followed on thrombosis , resulting in one or more vascular stenosis and myocardial blood supply shortage , and collateral circulation has not been fully established, Based on this, once the blood supply drastically reduced or interrupted, the corresponding myocardial ischemia and acute severe and lasting more than one hour , resulting in the occurrence of myocardial necrosis . According to the American Heart Association atherosclerotic lesion development process to be broken down into six types: Ⅰ type , lipid -point ; type Ⅱ, fatty streaks ; Ⅲ type , plaque early ; IV type , plaque ; V-shaped , fibrous plaque ; VI , complex lesions. Were seen in the majority of patients with myocardial infarction, coronary plaque on the basis of thrombosis occlusion of the lumen , in addition, infarction occurs between the original and the degree of stenosis of coronary atherosclerotic lesions caused by not showed a parallel relationship , at any stage of atherosclerotic lesions may occur plaque rupture , bleeding and ( or ) thrombosis, resulting in acute myocardial infarction. Pathophysiology of acute myocardial infarction as follows : 1 , pathological inflammation of basic research with the gradual deepening of atherosclerosis , a large number of studies have shown that the incidence of arterial wall inflammation in atherosclerosis is one of the most important risk factors, not just a simple lipid deposition , but an inflammatory disease , is a response to various body tissues damage , both in atherosclerosis development, or both play an important role in the occurrence of myocardial infarction . Vessel wall inflammation can lead to inflammatory cells into foam cells and the formation of atherosclerotic plaque necrotic lipid core, so that the arterial wall thickening , stenosis, while the role of inflammation in plaque rupture , hemorrhage, followed by thrombosis , causing arterial occlusion, acute coronary syndrome. Conversely , endothelial dysfunction, atherosclerotic plaque progress and rupture and thrombosis , in turn leading to further inflammation and the release of inflammatory mediators , allowing patients to a vicious cycle. These inflammatory mediators , including CRP, fibrinogen and serum amyloid A substance , IL-6, Leptin, resistin and Adiponectin, VCAM-1, ICAM-1, selectin and endothelin , LPPLAZ, Ah interferon , tumor necrosis factor a, IL-1, IL-6, IL-8, IL-12, IL-18, matrix metalloproteinase , MIC-I, IL-10 and myeloperoxidase , CD40, tumor growth factor , PDGF and throm -b. spondin and so on. 2 , plaque rupture is well known atherosclerotic vascular wall in essence , a complex pathophysiological process visible blood and blood components interact , the basic lesion is the formation of plaque on the intima uplift . This is usually caused by plaque necrotic lipid core and a layer of fibrous cap components. Recently observed that there is a big difference between plaque composition between different people, or even the same individual or the same composition of vascular atherosclerotic plaque , there are significant differences in the stability of the same plaque there is a big difference in the probability of plaque rupture are not the same [ 5 ] . In recent years, people have certain triggers plaque understanding that plaque rupture is caused by multiple factors , and hemodynamic stability speculated relationship with plaque , and plaque material change within is a major factor causing rupture. In addition, plaque rupture but also with many internal and external factors predisposing factors related to stimulus intensity plaque rupture vulnerability and synergy with predisposing factors related to the degree of effect [ 6 ] . Internal factors include the size and density of the lipid pool , inflammatory infiltration of the fibrous cap thickness , and the repair of the fibrous cap , and plaque morphology by shear force conditions and the like; external factors including smoking , hypercholesterolemia, , hypertension, diabetes , physical load and strong mental load , these factors can increase sympathetic tone , plaque shear stress and inflammatory response. Clinically, the evolution of the process of plaque often expressed as "stable " process, plaque rupture and thrombosis in patients with coronary heart disease often leads to the "stable" development as "unstable ." The extent of coronary blood flow and reduce the duration of the original decision to "stable" coronary heart disease due to plaque rupture and thrombosis and the development of unstable angina , non- ST segment elevation myocardial infarction or ST segment elevation myocardial infarction. 3 , thrombosis, coronary artery lumen decreases sharply in a short time , the occurrence of acute coronary syndrome that occurs when a sharp myocardial oxygen supply or oxygen demand mismatch . Thrombosis, vasospasm , or accompanied by contraction is caused by a sharp narrowing of the lumen in a short time the main reason for the inflammation and plaque rupture is a major factor in the formation of blood clots. In the absence of significant vascular plaque can form blood clots, thrombosis above process is mainly initiated by endothelial dysfunction or endothelial damage. After thrombosis, stenosis of the original extent , the degree of luminal occlusion and the extent and duration of sharp decision occurs clinically unstable angina , non- ST segment elevation myocardial infarction , or ST segment elevation myocardial infarction. Myocardial oxygen supply or aerobic disorders if the degree of luminal occlusion , the extent and duration of sharp caused , to the extent of myocardial ischemia and necrosis occurs in acute myocardial infarction , in short , inflammation and plaque rupture reinforce each other, started a vicious cycle of the pathophysiology of acute coronary syndrome, on the basis of secondary thrombosis , resulting in acute myocardial infarction clinical .#p#分頁標題#e#
 

TCM attributed to acute myocardial infarction , " Jue heartache ", " really sad " , "Chest ", " heartache ", " Death heartache ", " heart paralysis " and other disease areas . State Administration of Traditional unified understanding of acute thoracic obstruction by the Medical Administration Group ( A & E group ) to determine their medicine chest stuffiness heart disease called Jue [ 7 ] . Chest stuffiness and nonaggressive first seen in " Classic" , " Classic" reads: "Heart paralysis who blocked veins , veins who also ? ? government astringent blood is heartbreaking ." "Coffin • Jue card" chapter : "true heartache , sibling Green to the festival, heartache and even , once dead hair evening , evening once dead . " explained the true severity of the disease and poor prognosis heartache . Chinese medicine sector is generally believed that the disease is located in the heart of acute myocardial infarction , and its pathogenesis is the vacuity . Based viscera , systolic blood thus promoting the formation of heart qi flow through the body were the driving force of the gas, the Lotus pivot toward the sink , were air agitation . Yin and yang and blood gas attendant , gas for the commander of blood , blood gas line , gas is weak qi qi stagnation inability to promote blood running , will inevitably lead to blood stagnation, not pain . Some physicians with their own clinical experience, proposed the corresponding argument. Xian-Ming Fang et al [ 8 ] that AMI and more from the dirty air deficiency , gasification disorders, poor working fluid and blood , phlegm , blood stasis within the , Blockage of blood from the so-called " positive qi within , phlegm weakness in the . " Professor Zhao Chun pointed out that this disease occurs more with improper diet , emotional disorders , the invasion of pathogenic cold , old and feeble and other factors related to heart disease location of their collaterals , pathogenesis actual situation has two aspects : the imaginary as the heart, spleen , liver and kidney dysfunction , blood yin deficiency ; actually Hanning qi stagnation , phlegm and blood stasis , such as blocking the collaterals heart [ 9 ] .李南夷et al [10 ] proposed in the disease pathogenesis in hyperacute standard solid -based, Hanning blood, phlegm inverse gas is the main feature of this period , followed by lack of appetite and chest yang heart qi ; acute phase standard real pathogenesis phlegm in the first place ranking , followed by stasis , stasis heat , highlights the deficiency syndrome , yin deficiency is characteristic of this period . In overwork, after the meal , agitation, cold stimulation induced by factors such as the next , so that the heart of the closed block context and made ??for the chest stuffiness heart Jue .

Treatment of acute myocardial infarction in constant development , the efficacy of different treatment methods are also different. Only western conservative treatment mortality rate was 30%. 1977 Gruentzig conducted a new era of interventional cardiology world's first percutaneous transluminal coronary angioplasty (PTCA), pioneered . From then to the rapid development of PTCA -based percutaneous coronary intervention techniques. Currently, the best treatment of acute myocardial infarction treatment in the international arena is reperfusion therapy , an important part of percutaneous coronary intervention (percutancouscoronaryinterventions, PCI) treatment has obvious advantages , emergency PCI treatment can in a short period of coronary occlusion recanalization , rapid recovery of myocardial reperfusion , thus saving the ischemic myocardium , to reduce infarct size and cardiac function protection purposes , which greatly improved the prognosis of patients with acute myocardial infarction . With the popularity of PCI technology matures and is currently about 250 million people worldwide each year intervention, our country every year there are many patients who received reperfusion therapy , and the annual growth rate of 20% -30 %. However, also found in the clinical treatment , was still occurring after the epicardial coronary recanalization , the scope of myocardial infarction may still continue to expand serious ventricular remodeling and enlargement, heart failure and other complications of malignant arrhythmia in increased, these become the new treatment of reperfusion therapy problems and confusion. [ 11 ] reported in the literature : acute coronary syndrome patients after acute intervention TIMI3 blood level is still about 30% of patients did not reach the level of myocardial tissue perfusion , cardiac function in these patients is poor, more complications after myocardial infarction and the prognosis is poor. How to further reduce complications after myocardial infarction reduces infarct size after primary PCI become cardiovascular research hotspot. Angiogenesis is early in embryonic development by endothelial progenitor cells.#p#分頁標題#e#
 

A number of studies suggest that therapeutic angiogenesis can effectively reduce infarct size , this treatment method is aptly called " the heart of the drug to promote their own bridge" , causing more and more attention in the modern treatment of coronary heart disease . The so-called therapeutic angiogenesis , is through the action of certain drugs , promote the expression and release of ischemic myocardium parts of the vascular endothelial growth factor , or by increases related receptors , eventually forming ability of many small blood vessels , and has appeared narrow or blocked coronary arteries surrounding the formation of a new bypass loop , thereby improving myocardial ischemia , to increase the blood supply to the heart and improve heart function , which may improve the quality of life of patients and prolong life [ 12 ] . Angiogenesis in pathological conditions , including the following two forms , including [ 13 ] , angiogenesis (neovaseularization) including angiogenesis (vaseulogenesis) and neovascularization (angiogenesis), angiogenesis is the development in the early embryo , the progenitor cells ( endothelialprogenitoreell, EpC) or hemangioblastoma (angioblast) the formation of new blood vessels ; angiogenesis is generally believed that the latter is present in the body of the fetus or adult , is already present in the tissue of vascular endothelial cell proliferation and migration of mature , the formation of small blood vessels. Recent studies have found that there may be blood in the presence of endothelial progenitor cells involved in angiogenesis severe ischemic region appeared , and fetal vascular pathogenesis of the same .
 

Chinese herbal medicine angiogenic therapy , with our distinctive national characteristics . HMP is a traditional Chinese medicine treatment of coronary heart disease most influential representatives of medicine , HMP is the main component of : musk, storax , borneol , ginseng , toads , bezoar . Which contains ginseng extract 27% , 6% of musk , Toad 4% storax 8% , borneol 19% , 12% of the bezoar , cinnamon 24%. Prescription monarch followed the principles , features are: cold temperature and used to warm -based ; through supplementation and to complement the supplement ; either treat the aroma of warming , and righting Qi cardiac solidify this . Musk , storax , the main effect toad is making life easier , qi stasis , promoting blood circulation ; ginseng was righting Qi , Pei-Yuan consolidate . [ 14 ] Modern pharmacological studies have shown that HMP ingredients Styrax , borneol with increasing myocardial hypoxia tolerance , and heart rate , increase coronary blood flow , reducing myocardial oxygen consumption effect. Ginseng is a strong heart, lowering blood pressure, free radical scavenging, inhibition of vascular smooth muscle proliferation , reversing cardiac remodeling [ 15 ] , heart rate ; bezoar , Toad has increased inotropic effect , help relieve heart failure . [ 16 ] In recent years, many Chinese scholars use different methods , from the molecular level , organizational level , anatomical level in vitro and in animal models confirmed the HMP promote therapeutic angiogenesis effect. Also, clinical studies have corroborated from different aspects of this role HMP 's . HMP has obvious pro-angiogenic activity , can promote the proliferation of capillary endothelial cells and the formation of the lumen structure, increasing the areal density of myocardial blood vessels , which promote angiogenesis and its mechanism can express and release of pro- related vascular endothelial growth factor . ① HMP promote ventricular infarct region [ 5,17 ] vascular endothelial growth factor expression and angiogenesis. Myocardial infarction in rats demonstrated that HMP infarct region can promote the expression of vascular endothelial growth factor and angiogenesis , and promote microvascular endothelial cells to form tubular structure , the chick embryo chorioallantoic membrane (chorioallantoicmembrane, CAM) model [ 18 ] also proved to be promote the growth of new blood vessels , through the establishment of rat model of myocardial infarction and were given HMP and control drug intervention , from the perspective of the body confirmed the catalytic role HMP ischemic cardiac angiogenesis. ② HMP promote [ 19 ] microvascular endothelial cells to form tubular structure . ③ promote chick chorioallantoic membrane (CAM) model on the growth of new blood vessels . HMP angiogenic , promote angiogenesis in vivo chorioallantoic membrane in vitro can promote microvascular endothelial cell proliferation and the formation of the lumen structure. Its pro-angiogenic mechanism may be related to endothelial cells can express human umbilical vein endothelial cells of vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) increased the mRNA and the release of VEGF and bFGF increase related. By promoting the new AMI coronary collateral angiogenesis , and reduce infarct size .#p#分頁標題#e#

Drug therapy after acute myocardial infarction , we measured plasma BNP by QRS scoring on infarct size predicted.
 

Since Selvester [20] and Wagner [21] and other scholars will be made public after the QRS scoring method , QRS score has been shown to better reflect the positive correlation between infarct size and infarct size was . 1972 Selvester proposed 57 / 32 minute standard , every minute is equal to 3% of the left ventricular area . Later, Wagner et al introduced a simplified 37 / 29 points system QRS scoring criteria . Wagner Act autopsy confirmed left ventricular anterior wall of the scoring method , the sidewalls M IA estimate effective [22] Hirdman and other items on the basis of Wagner37 / standard 29 -point QRS scoring system adds 20 to form a generally accepted 54 Debt / 32 points scoring system . Sevilla , etc. In contrast through autopsy studies [ 23-25 ??] , an increase of one condition to improve blood supply to the area for the circumflex artery infarct size estimation skills. [26] Freye found as to myocardial infarction left ventricular hypertrophy is not suitable for 54 / 32 minutes standard , modified into suitable myocardial infarction with left ventricular hypertrophy case 49 /31 points system standard score exceeds 3:00 , a specificity of 95% . [ 27 ] determined that M IA ECG method is simple, fast , economical , compared with biochemical markers early, but not suited to non- ST -segment elevation myocardial infarction. Initially last M IA MIA and QRS scoring method used to calculate the ST segment showed a linear correlation between sensitivity and specificity similar. Initial decision anterior infarction M IA factor is the number of ST-segment elevation , and the next wall M IA predictors mainly numerical ST -segment elevation . Changes in Q -wave or QRS complex is often the outcome of infarction , and ultimately to Selverster54 term projections MIA / 32 -point QRS scoring system is superior. QRS scoring proceeds will generally score a point considered as 3% M IA. According to Wagner et QRS scores can range area will be divided into small groups MIA (≤ 5 points ) , medium size group ( 6-9 points ) , large group (≥ 10 points ) .
 

BNP is an increase in blood volume and pressure overload case mainly by a neurohormone secreted by the ventricles , as an important indicator of heart failure diagnosis. Under physiological conditions, the atrial and ventricular amount of synthesis and secretion of BNP, the normal blood circulation in only low concentrations of BNP. Ventricular muscle subjected to stretch or ventricular pressure increases , BNP mainly in the left ventricle was a lot of explosive synthesis and secretion . BNP biological half-life of 20 min, it is clear there are two ways : The first is through receptor-mediated phagocytosis , intracellular lysosomal finally dissolving the enzyme deactivation ; the second is by the neutral endopeptidase is degraded cleared. [ 28 ] Studies suggest that BNP measurement can effectively help determine the acute coronary syndrome (ACS) patient's prognosis , when the AMI occurred BNP secreted primarily from the infarcted area is located at the junction with the non- infarct zone myocardial ischemic injury AMI patients with early onset of plasma BNP levels that were significantly increased , reaching a peak within 24 h , and the peak concentration was positively correlated with infarct size ; cells, and the survival of infarct zone myocardial ischemic injury .#p#分頁標題#e#
 

This research study in acute myocardial infarction after oral administration of different doses of PCI HMP right, through the BNP, QRS detection index integral concept of efficacy. HMP between high-dose group and low dose group sex , age , heart rate , blood pressure , blood lipids , blood glucose was not statistically significant (P> 0.05), comparable. Two groups immediately after PCI and 4 weeks after taking blood BNP testing shows : After taking two groups decreased , high-dose group decreased significantly , and the difference was statistically significant (P <0.01), before taking a small dose / high dose group : 340.8 +82.5 / 395.6 +64.8, P> 0.05; after 4 weeks , 2 set of values ??decreased , P <0.05, high-dose group decreased more significantly : 102.6 +12.4 / 55.8 +14.2, P <0.01. HMP small doses of high-dose group HMP group and immediately after PCI , four weeks after the QRS score shows : After taking the 2 groups were decreased significantly decreased high-dose group , the difference was statistically significant. Before taking a small dose / high dose group : 6.43 +0.36 / 6.39 +0.25, P> 0.05; After 4 weeks , 2 set of values ??decreased , P <0.05, high-dose group decreased more significantly : 4.84 +0.41 / 3.76 + 0.33, P <0.01, the same conclusion with the detection of BNP conclusion , indicating that HMP study in acute myocardial infarction patients after PCI reduced infarct size effect on the clear, acute myocardial infarction has a good effect , can effectively inhibit atherosclerosis , protect endothelial ; promote therapeutic angiogenesis , establishment of collateral circulation ; reduce infarct size , prevention of ventricular remodeling, thus effectively reducing the risk of cardiovascular events . Integrative treatment of acute myocardial infarction with high clinical value.

 

 

Conclusions

 

HMP can reduce acute myocardial infarction after PCI infarct size .

 

References

 

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