Prospective observational cohort study of time saved by prehospital thrombolysis for ST elevation myocardial infarction delivered by paramedics

Objectives To evaluate a system of prehospital thrombolysis, delivered by paramedics, in meeting the national service framework''s targets for the management of acute myocardial infarction.Design Prospective observational cohort study comparing patients with suspected acute myocardial infarction considered for thrombolysis in the prehospital environment with patients treated in hospital.Setting The catchment area of a large teaching hospital, including urban and rural areas.Participants 201 patients presenting concurrently over a 12 month period who had changes to the electrocardiogram that were diagnostic of acute myocardial infarction or who received thrombolysis for suspected acute myocardial infarction.Main outcome measures Time from first medical contact to initiation of thrombolysis (call to needle time), number of patients given thrombolysis appropriately, and all cause mortality in hospital.Results The median call to needle time for patients treated before arriving in hospital (n=28) was 52 (95% confidence interval 41 to 62) minutes. Patients from similar rural areas who were treated in hospital (n=43) had a median time of 125 (104 to 140) minutes. This represents a median time saved of 73 minutes (P < 0.001). Sixty minutes after medical contact 64% of patients (18/28) treated before arrival in hospital had received thrombolysis; this compares with 4% of patients (2/43) in a cohort from similar areas. Median call to needle time for patients from urban areas (n=107) was 80 (78 to 93) minutes. Myocardial infarction was confirmed in 89% of patients (25/28) who had received prehospital thrombolysis; this compares with 92% (138/150) in the two groups of patients receiving thrombolysis in hospital.Conclusions Thrombolysis delivered by paramedics with support from the base hospital can meet the national targets for early thrombolysis. The system has been shown to work well and can be introduced without delay.     

低分子肝素联合丹参注射液治疗急性心肌梗死的临床研究

目的:观察低分子肝素联合丹参注射液治疗急性ST段抬高型心肌梗死的临床疗效及安全性。方法:按照随机原则将78例急性心肌梗死患者分成两组,在常规溶栓治疗的基础上,其中对照组39人采用低分子肝素治疗,治疗组患者在对照组治疗的基础上给予丹参注射液治疗,对两组临床费用、住院时间和冠脉再通进行评价。结果:治疗组的临床费用、住院时间和冠脉再通与对照组相比,有统计学差异(P0.05)。结论:低分子肝素联合丹参注射液治疗急性心肌梗死的临床疗效确切,值得临床推广。     

Intermittent hypobaric hypoxia applicability in myocardial infarction prevention and recovery

Intermittent hypobaric hypoxia (IHH) has been the focus of important research in cardioprotection, and it has been associated with several mechanisms. Intermittent hypobaric hypoxia inhibits prolyl hydroxylases (PHD) activity, increasing the stabilization of hypoxia-inducible factor-1 (HIF-1) and activating crucial adaptative genes. It has been hence suggested that IHH might be a simple intervention, which may offer a thoughtful benefits to patients with acute myocardial infarction and no complications. Nevertheless, several doubts exist as to whether IHH is a really safe technique, with little to no complications in post-myocardial infarction patients. Intermittent hypobaric hypoxia might produce instead unfavourable changes such as impairment of vascular hemodynamics and hypertensive response, increased risk of hemoconcentration and thrombosis, cardiac rhythm perturbations, coronary artery disease and heart failure, insulin resistance, steatohepatitis and even high-altitude pulmonary oedema in susceptible or nonacclimatized patients. Although intermittent and chronic exposures seem effective in cardioprotection, IHH safety issues have been mostly overlooked, so that assorted concerns should be raised about the opportunity to use IHH in the post-myocardial infarction period. Several IHH protocols used in some studies were also aggressive, which would hamper their widespread introduction within the clinical practice. As such, further research is needed before IHH can be widely advocated in myocardial infarction prevention and recovery.     

Initial Heparin Therapy in Acute Myocardial Infarction

The administration of heparin during the first 48 hours following acute myocardial infarction is widely practised. Heparin treatment is also recommended for acute coronary insufficiency on the grounds that it may prevent development of an impending myocardial infarction. These measures had been accepted without support of a controlled clinical trial. By random selection, 101 patients hospitalized with a provisional diagnosis of acute myocardial infarction received heparin (100 mg. intravenously every eight hours for 48 hours) and 105 patients were assigned to a control group. Both groups of patients received bishydroxycoumarin (Dicumarol). The mortality in the heparin series was 30% and in the control group, 28%. A significantly large number of the heparin-treated patients developed clinical and laboratory proof of recent myocardial infarction. It is concluded that early intermittent intravenous heparin treatment does not lower the mortality in patients with acute myocardial infarction nor does it prevent impending myocardial infarction in patients with acute coronary insufficiency.     

心肌酶和红细胞形态学参数与心肌梗死的相关性研究

目的:研究红细胞形态学参数对心肌梗死患者诊断作用及其与心肌酶谱的相关性。方法:选取40例心肌梗死患者,40例稳定型心绞痛组患者,40例健康对照组人群。对比分析稳定性心绞痛、急性心肌梗死(入院1h内)和对照组红细胞形态学参数(MCV、MCH、MCHC、RDW)、及心肌酶谱(CK-MB、c Tn I)。分析心肌梗死不同时间MCV、MCH、MCHC、RDW变化趋势。结果:稳定性心绞痛、心肌梗死组1 h内MCV、RDW明显高于正常对照组,差异有统计学意义(P0.05);稳定性心绞痛、心肌梗死组1 h内MCHC、MCH低于对照组,差异有统计学意义(P0.05)。心肌梗死组MCV、RDW在发病后1 h、24 h、48 h、7 d水平逐渐升高,各时间点间差异有统计学意义(P0.05)。心肌梗死组发病后1 h、24 h、48 h、7 d、14 d MCHC、MCH水平逐渐降低,各时间点间差异有统计学意义(P0.05)。RDW和CK-MB、c Tn I呈正相关性(P0.05)。RDW对心肌梗死诊断的灵敏度最高达到93.4%,特异度为69.7%,RDW对急性心肌梗塞的诊断临界值为14.04%。结论:RDW对心肌梗死的诊断具有较高的敏感性,可用于临床早期诊断心肌梗死,为临床诊断提供一新的诊断标准。     

Evaluating chest pain in the emergency department.

Chest pain is one of the most difficult diagnostic problems for physicians working in an emergency department. In this setting, more malpractice dollars are awarded for missed myocardial infarction than for any other physician error. This problem usually occurs when the patient has atypical symptoms, the physician is inexperienced, or the diagnosis is not considered. The clinical manifestations of myocardial infarction vary greatly, and patients with "atypical" presentations have a poorer prognosis than those with classic symptoms. Although no feature of a patient''s history excludes infarction with certainty, pain that is sharp, positional, pleuritic, or reproduced by palpation indicates a lower probability of acute ischemic heart disease. New immunochemical methods and serial sampling strategies have increased the sensitivity of creatine kinase-MB as an indicator for the disorder. Recent investigations have also established the prognostic value of the initial electrocardiogram. These methods allow emergency physicians to assess the risk of complications and to perform triage when there is a shortage of beds in the coronary care unit. Emergency physicians must also consider other diseases for which coronary care might be beneficial.     

Predictive value of circulating miR-328 and miR-134 for acute myocardial infarction

MicroRNA (miRNAs) is demonstrated to be present in the blood of humans and has been increasingly suggested as a novel biomarker for various pathological processes in the heart, including myocardial infarction, myocardial remodeling and progression to heart failure. In this study, we aim to evaluate the diagnostic and prognostic value of circulating miR-328 and miR-134 in patients with acute myocardial infarction (AMI). Circulating levels of miR-328 and miR-134 were detected by quantitative real-time PCR in plasma samples from 359 AMI patients and 30 healthy volunteers. Concentrations of high-sensitivity cardiac troponin T (hs-cTnT) were measured using electrochemiluminescence-based methods. MiRNAs were assessed for discrimination of a clinical diagnosis of AMI and for association with primary clinical endpoint defined as a composite of cardiogenic death and development of heart failure within 6 months after infarction. Results showed that levels of plasma miR-328 and miR-134 were significantly higher in AMI patients than in healthy controls. Receiver operating characteristic curve analyses showed significant diagnostic value of miR-328 and miR-134 for AMI. However, neither of them was superior to hs-cTnT for the diagnosis. Additionally, increased miRNA levels were strongly associated with increased risk of mortality or heart failure within 6 months for miR-328 (OR 7.35, 95 % confidence interval 1.07–17.83, P < 0.001) and miR-134 (OR 2.28, 95 % confidence interval 1.03–11.32 P < 0.001). In conclusion, circulating miR-328 and miR-134 could be potential indicators for AMI, and the miRNA levels are associated with increased risk of mortality or development of heart failure.     

Clinical observations and echocardiographic features of mural thrombi in the left ventricle during myocardial infarction]

The incidence and changes in the mural thrombi in left ventricle in ECHO-2D in the acute myocardial infarction as well as relationship between clinical parameters and echocardiographic indices of the left cardiac ventricle contractability asynergy and dynamics of changes in mural thrombi have been investigated. The studies included 137 consecutive patients (98 males and 39 females) treated for the acute myocardial infarction. Patients' age ranged from 35 to 87 years (mean 62 years). Infarction of the anterior and/or lateral wall was diagnosed in 67 patients, and infarction of the inferior and/or posterior wall in 70 patients. Mural thrombi were diagnosed in 42 (31%) patients. Eighteen thrombi (43%) were liquefied during hospitalization. Comparative analysis of patients in whom mural thrombi underwent liquefaction in the hospital and a group of patients with myocardial infarction and persisting mural thrombi showed that return of left ventricle movements with subsequent contractability facilitate liquefaction of mural thrombi. Higher mortality rate in the group of patients with myocardial infarction with mural thrombi is due to extension of the infarction accompanied by marked asynergy of left ventricular contractions which does not decrease in sequential examinations, and increasing congestive heart failure.     

白细胞与心肌缺血的关系

炎症是引发心血管疾病的一个重要的危险因子.白细胞数量增多的患者更容易患上急性心肌梗塞、急性冠状动脉等疾病.对临床上白细胞数量高的数据与疾病预测之间的关系,这其中可能有几种机制.测量白细胞的数量和亚群可能是区分急性血管疾病患者危险程度的一种更好的方法.     

CK-MBmass, hs-cTnT及CK-MB与急性心肌梗死的相关性及其联合诊断价值

摘要 目的：研究肌酸激酶同工酶质量（CK-MBmass)、肌酸激酶同工酶（CK-MB）和高敏心肌肌钙蛋白T（hs-cTnT）在急性心肌梗死患者（AMI）血清中的含量,并探讨三者联合对AMIDE诊断价值。方法：选择2018年1月到2021年10月我院收治的AMI患者90例作为研究组,并选择同期在我院体检健康志愿者40例作为对照组,比较两组AMI患者血清CK-MBmass,hs-cTnT和CK-MB。根据Killp分级法将不同心力衰竭将AMI患者分为II、III和IV级,并根据心肌梗死范围将AMI患者分为轻度、中度和重度心肌梗死组。比较不同AMI患者血清CK-MBmass,hs-cTnT和CK-MB。通过受试者工作曲线计算血清CK-MBmass,hs-cTnT和CK-MB联合诊断AMI的阳性预测值、阴性预测值、敏感度和特异度。结果：（1）AMI患者血清CK-MBmass,hs-cTnT和CK-MB均显著高于健康志愿者（P<0.05）;（2）AMI患者血清CK-MBmass,hs-cTnT和CK-MB随Killp分级或心肌梗死范围升高而升高（P<0.05）;（3）AMI患者血清CK-MBmass,hs-cTnT,CK-MB与急性心肌梗死患者左室射血分数（LVEF）呈负相关（P<0.05）,与左室舒张末期容积（LVEDd）和梗死范围呈正相关（P<0.05）;（4）血清CK-MBmass,hs-cTnT和CK-MB联合检测急性心肌梗死的阳性预测值、阴性预测值、敏感度和特异度均高于单独诊断。结论：血清CK-MBmass,hs-cTnT和CK-MB在AMI患者含量升高,并且与患者心功能和心肌梗死范围有关,适用于AMI的联合诊断。     

Predictive values of sST2 and IL-33 for heart failure in patients with acute myocardial infarction

Timely prediction of the risk of heart failure in acute myocardial infarction patients is critical for better prognosis. This article aims to evaluate the predictive value of serum soluble growth stimulation expressed gene 2 (sST2) and interleukin-33 in patients with acute myocardial infarction complicated by heart failure. A total of 42 healthy controls and 144 acute myocardial infarction patients were recruited in the study. According to Killip cardiac function classification as the basis for concurrent heart failure, they were distributed into non-heart failure group (n = 76) and heart failure group (n = 68). ELISA was utilized to determine the serum sST2 and interleukin-33 levels, and the diagnostic efficiency was evaluated by receiver operating characteristics curve. sST2 and interleukin-33 levels in patients with acute myocardial infarction were significantly increased when compared with normal healthy controls, and were further enhanced in the heart failure group. With the increased Killip cardiac function classification, interleukin-33 and sST2 levels were gradually elevated. Multivariate analysis indicated that interleukin-33 and sST2 could be used as independent predictors for heart failure combined with acute myocardial infarction.     

First electrocardiogram in recent myocardial infarction.

The admission electrocardiogram (ECG) was studied in 898 patients admitted to a coronary care unit over two years. The diagnosis made from this tracing was compared with that made at the end of the patient''s stay. About half the cases of recent myocardial infarct were diagnosed from the admission ECG, but accuracy rose to 83% with serial ECG''s in the unit. The ECG is important but not entirely reliable in the early detection of acute myocardial infarction, which should be largely a clinical diagnosis.     

H-FABP、cTnI及copeptin在老年急性非ST段抬高型心肌梗死患者早期诊断中的应用价值

目的:研究心肌型脂肪酸结合蛋白(H-FABP)、肌钙蛋白I(cTnI)及和肽素(copeptin)在老年急性非ST段抬高型心肌梗死患者早期诊断中的应用价值。方法:选取2016年2月-2018年2月我院收治的老年急性非ST段抬高型心肌梗死患者60例为研究对象,记为观察组。另取同期于我院接受治疗的心绞痛患者50例记为对照组。分别比较患者H-FABP与cTnI阳性、阴性分布情况以及copeptin表达水平。绘制受试者工作特征曲线(ROC),分析H-FABP、cTnI、copeptin以及三项联合检测老年急性非ST段抬高型心肌梗死的早期诊断价值。结果:观察组患者H-FABP与cTnI阳性人数占比均高于对照组(P0.05)。观察组患者copeptin表达水平高于对照组(P0.05)。H-FABP、cTnI及copeptin等3个指标均具有一定的早期诊断价值,H-FABP+cTnI+copeptin联合检测的敏感度和特异度更高,分别为86.46%和87.15%。结论:老年急性非ST段抬高型心肌梗死患者H-FABP、cTnI、copeptin表达较高,联合检查上述三项指标水平可提高临床诊断价值。     

Value and Limitations of Electrocardiogram in Diagnosis of Slight and Subacute Coronary Attacks

The electrocardiogram recorded at the initial consultation was compared with the final diagnosis in 211 consecutive suspected slight or sub-acute coronary attacks in 206 patients.In 77 (36%) of the 211 episodes, acute (or subacute) myocardial infarction was finally diagnosed. The initial E.C.G. showed a diagnostic pattern in only 19 (25%) of these 77 episodes; in 39 (50%) it was abnormal but not diagnostic of recent infarction; while in 19 (25%) the E.C.G. showed no abnormality classified under the Minnesota Code, though in 16 of these there were definite minor changes.In 61 (29%) of the 211 episodes acute myocardial infarction was excluded and an alternative diagnosis was made. The E.C.G. was strictly normal in only 23 (38%) of these 61 episodes; in 15 (25%) it showed minor abnormalities, and in 23 (38%) it was grossly abnormal.     

Increased Sensitivity to Heparin Following Acute Myocardial Infarction

In vivo increased sensitivity to heparin has been demonstrated in patients following an acute myocardial infarction. An intravenous injection of 10,000 units of heparin was given to each of 18 patients with recent myocardial infarction in order to compare them with 17 patients who were not suffering from any acute illness. The changes in whole blood clotting time, recalcified plasma clotting time and prothrombin time were greater and more prolonged in the patients with recent myocardial infarction. Of the three tests, the one-stage prothrombin time provided the simplest and the most precise measurement of heparin sensitivity. The reason for this was not clear: it is possible that it is related to shock and congestive heart failure which were complications of the clinical course following myocardial infarction.     

Is it possible to exclude a diagnosis of myocardial damage within six hours of admission to an emergency department? Diagnostic cohort study

ObjectiveTo assess the clinical efficacy and accuracy of an emergency department based six hour rule-out protocol for myocardial damage.DesignDiagnostic cohort study.SettingEmergency department of an inner city university hospital.Participants383 consecutive patients aged over 25 years with chest pain of less than 12 hours'' duration who were at low to moderate risk of acute myocardial infarction.InterventionSerial measurements of creatine kinase MB mass and continuous ST segment monitoring for six hours with 12 leads.ResultsOutcome of the gold standard test was available for 292 patients. On the diagnostic test for the protocol, 53 patients had positive results and 239 patients had negative results. There were 18 false positive results and one false negative result. Sensitivity was 97.2% (95% confidence interval 95.0% to 99.0%), specificity 93.0% (90.0% to 96.0%), the negative predictive value 99.6%, and the positive predictive value 66.0%. The positive likelihood ratio was 13.9 and the negative likelihood ratio 0.03.ConclusionsThe six hour rule-out protocol for myocardial infarction is accurate and efficacious. It can be used in patients presenting to emergency departments with chest pain indicating a low to moderate risk of myocardial infarction.

What is already known on this topic

Many patients with chest pain in emergency departments indicating a low to moderate risk of myocardial infarction are admitted to rule out myocardial damageSome 6% of those discharged have undiagnosed myocardial damage

What this study adds

An emergency department based chest pain assessment unit protocol to rule out myocardial damage is sensitive enough to allow safe discharge of patients at low to moderate risk of myocardial infarction within six hoursSuch units can also reduce the number of patients admitted unnecessarily     

Diagnostic re-classification and prognostic risk stratification of patients with acute chest pain

Unstable angina and myocardial infarction are prevalent manifestations of acute coronary artery disease, combined in the term ‘acute coronary syndromes’. The introduction of sensitive markers for myocardial necrosis has led to confusion regarding the distinction between small myocardial infarctions and ‘true’ unstable angina, and the application of ever more sensitive markers has accelerated the pace at which patients with unstable angina are being re-classified to non-ST-segment elevation myocardial infarction. But in how many patients with acute chest pain is myocardial ischaemia really the cause of their symptoms? Numerous studies have shown that most have <5 ng/l high-sensitivity cardiac troponin, and that their prognosis is excellent (event rate <0.5% per year), incompatible with ‘impending infarction’. This marginalisation of patients with unstable angina pectoris should lead to the demise of this diagnosis. Without unstable angina, the usefulness of the term acute coronary syndromes may be questioned next. It is better to abandon the term altogether and revert to the original diagnosis of thrombus-related acute coronary artery disease, myocardial infarction. A national register should be the next logical step to monitor and guide the application of effective therapeutic measures and clinical outcomes in patients with myocardial infarction.

     

Implications of troponin testing in clinical medicine

During the past decade considerable research has been conducted into the use of cardiac troponins, their diagnostic capability and their potential to allow risk stratification in patients with acute chest pain. Determination of risk in patients with suspected myocardial ischaemia is known to be as important as retrospective confirmation of a diagnosis of myocardial infarction (MI). Therefore, creatine kinase (CK)-MB - the former 'gold standard' in detecting myocardial necrosis - has been supplanted by new, more accurate biomarkers.Measurement of cardiac troponin levels constitute a substantial determinant in assessment of ischaemic heart disease, the presentations of which range from silent ischaemia to acute MI. Under these conditions, troponin release is regarded as surrogate marker of thrombus formation and peripheral embolization, and therefore new therapeutic strategies are focusing on potent antithrombotic regimens to improve long-term outcomes. Although elevated troponin levels are highly sensitive and specific indicators of myocardial damage, they are not always reflective of acute ischaemic coronary artery disease; other processes have been identified that cause elevations in these biomarkers. However, because prognosis appears to be related to the presence of troponins regardless of the mechanism of myocardial damage, clinicians increasingly rely on troponin assays when formulating individual therapeutic plans.     

Prolactin is involved in the systemic inflammatory response in myocardial infarction

Prolactin may contribute to an atherogenic phenotype. Furthermore, previous studies have shown that prolactin levels increase in situations of acute stress and inflammation. We therefore aimed to investigate the relationship between prolactin, acute stress and inflammation in patients with myocardial infarction. We performed a case-control study in 40 patients with myocardial infarction and 39 controls, aged 41-84 years. Blood for assessment of prolactin and high sensitive C-reactive protein (hsCRP) was drawn at inclusion, that is, during the acute phase of the event, and 2-3 weeks later. Unexpectedly, prolactin levels at inclusion did not differ between cases and controls (7.0 ng/ml and 6.0 ng/ml, respectively, p=0.28). 2-3 weeks later prolactin levels in cases had not decreased. However, univariate regression analysis indicated that hsCRP is associated with prolactin levels (regression coefficient β 0.11; [95% CI 0.01; 0.21]; p=0.03) in cases during the acute phase of myocardial infarction. Our findings may suggest that prolactin is involved in the systemic inflammatory response, which takes place during myocardial infarction; however, this association may not be strong enough to induce higher prolactin levels in patients with myocardial infarction.