A pilot study of paramedic-administered,prehospital thrombolysis for acute myocardial infarction

We have implemented a pilot program of supervised paramedic administration of thrombolysis in the field. This program was begun on a small scale by training and equipping one paramedic service of one hospital. Four patients with acute myocardial infarction were rapidly and appropriately treated in the field. We compared these patients with 21 patients who were brought to hospital by ambulance, but treated with thrombolysis conventionally in the emergency department. The patients in the field were treated an average of 86 minutes sooner than the patients treated in the emergency department.     

Noninvasive assessment of reperfusion and reocclusion after thrombolysis in acute myocardial infarction

The clinical significance of ST-segment changes and of the time course of appearance in serum of different cardiac proteins has been reviewed for the diagnosis of coronary reperfusion and reoclusion after thrombolysis. In particular, the value of serial 12-lead electrocardiographic (ECG) studies, of Holter monitoring, and of continuous multilead computer-assisted ECG monitoring is compared. Regarding the serum proteins, the clinical significance of reperfusion indices described so far for serum creatine kinase (CK), its isoenzyme serum creatine kinase MB, the CK isoforms, and myoglobin is reviewed. Emphasis is placed on (1) the calculation method used for deriving the reperfusion indices; (2) the sensitivity and the specificity of the reperfusion indices; (3) the minimum turn-around time needed to produce the reperfusion indices (depending on the practicability of the analytical and calculation methods and their applicability in an emergency laboratory); (4) the ability of the indices to produce reliable estimates of reperfusion efficacy of the thrombolytic agents under study; and (5) the ability of the marker proteins to detect reinfarction as well as the suitability of the markers to detect real-time necrosis.     

Effect of amiodarone on mortality after myocardial infarction: a double-blind, placebo-controlled, pilot study.

OBJECTIVES. The goal of this study was to evaluate the effect of amiodarone on mortality, ventricular arrhythmias and clinical complications in high risk postinfarction patients. BACKGROUND. No therapy has been shown to reduce sudden death in patients ineligible to receive beta-adrenergic blocking agents after myocardial infarction. METHODS. Patients who were not eligible to receive beta-blockers were randomized to receive amiodarone (n = 305) or placebo (n = 308) for 1 year. RESULTS. There were 21 deaths in the amiodarone group compared with 33 in the placebo group (odds ratio 0.62, 95% confidence interval [CI] 0.35 to 1.08, p = 0.095). There were two noncardiac deaths in the amiodarone group and none in the placebo group; thus, the difference in cardiac mortality (19 vs. 33, respectively) was statistically significant (odds ratio 0.55, 95% CI 0.32 to 0.99, p = 0.048). There was a significant decrease in Lown class 4 ventricular arrhythmias (7.5% vs. 19.7%, respectively, p < 0.001). Adverse effects developed in 30% of amiodarone-treated patients and 10% of placebo-treated patients. Pulmonary toxicity, which was mild and reversible, occurred in only one patient in the amiodarone group but in no patient in the placebo group. CONCLUSIONS. This trial demonstrated a significant reduction in cardiac mortality and ventricular arrhythmias with amiodarone treatment. However, given the wide confidence intervals and borderline statistical significance of our trial, larger trials are needed to confirm or refute this view.     

心肌呈色分级评价急性心肌梗死溶栓疗法的疗效

目的以心肌呈色分级(MBG)评估急性心肌梗死溶栓后的心肌灌注状况.方法89例急性心肌梗死患者给予重组组织型纤溶酶原激活剂治疗.各例于给药后90分钟行冠状动脉造影,观察梗死相关动脉前向血流,评估心肌灌注情况,并记录6个月心脏事件发生率.结果溶栓后符合临床再通标准的为87.6%,未再通的为12.4%.冠状动脉造影结果显示,全组梗死相关动脉的再通率(TIMI 2或3级)为82%;心肌再灌注率(MBG 2或3级)为88.8%,完全再通(TIMI 3级)且完全心肌再灌注(MBG 3级)者为40.4%.6个月死亡率为10.1%.多因素分析结果表明,入院时Killip分级和MBG分级是急性心肌梗死死亡的主要独立预测因子(P=0.0001).结论成功的再灌注治疗应该是梗死相关动脉前向血流TIMI 3级且伴良好心肌灌注.     

Magnesium infusion reduces the incidence of arrhythmias in acute myocardial infarction. A double-blind placebo-controlled study

In a double-blind placebo-controlled study, 130 patients with verified acute myocardial infarction were given magnesium or placebo treatment intravenously immediately upon admission to hospital. The incidence of arrhythmias requiring treatment during the initial week of hospitalization was registered. Serum magnesium concentrations were increased from 0.7 mmol/l to 1.3 mmol/l as a result of the magnesium infusions. This pharmacologically induced hypermagnesemia resulted in a reduction in the incidence of arrhythmias from 47% in the placebo group to 21% in the magnesium group (p = 0.003). In the magnesium-treated patients, increments in serum concentrations of magnesium and potassium correlated positively (r = 0.47, p less than 0.001). It is concluded that magnesium infusion in the postinfarct period reduces the incidence of supraventricular tachyarrhythmias, and possible pathophysiological mechanisms involved are discussed.     

Coronary reperfusion by thrombolysis and early beta-adrenergic blockade in acute experimental myocardial infarction

The effects of beta-adrenergic blockade, thrombolysis and their combination on infarct size and left ventricular function were investigated in a canine model of thrombotic occlusion of the left anterior descending coronary artery. Metoprolol was administered intravenously (0.5 mg/kg) over 10 min, starting 15 min after occlusion. Recombinant human tissue-type plasminogen activator (rt-PA) was given intravenously 1 h after occlusion for clot lysis. Anatomic infarct size was measured as a percent of perfusion area and ventricular mass. Left ventricular function was assessed by ejection fraction and the centerline method. Groups 1, 3, 5 and 7 were evaluated after 24 h and received, respectively, metoprolol plus rt-PA, rt-PA, metoprolol and no treatment; groups 2, 4, 6 and 8 were studied after 1 week and treated, respectively, as groups 1, 3, 5 and 7. Metoprolol did not influence infarct size and global or regional ventricular function after 24 h and 1 week. Thrombolysis reduced infarct size from 69.5 +/- 3.4% (24 h) and 76.6 +/- 1.8% (1 week) in the control group to, respectively, 44.1 +/- 11.6% and 39.5 +/- 10.5% (p greater than 0.05), did not influence left ventricular function after 24 h and was accompanied after 1 week by a definite recovery of global and regional left ventricular function when compared with findings in control dogs. Metoprolol plus rt-PA further reduced infarct size (percent perfusion area) to 20.4 +/- 3.7% and 19.9 +/- 8.1% after 24 h and 1 week, respectively (p = NS versus rt-PA).(ABSTRACT TRUNCATED AT 250 WORDS)     

Reciprocal ST change in acute myocardial infarction: assessment by electrocardiography and echocardiography

To evaluate the incidence, time course and significance of reciprocal change, 25 consecutive patients admitted with their first acute transmural myocardial infarction were studied with serial electrocardiography and two-dimensional echocardiography. Reciprocal change was noted in all patients with inferior infarction (mean maximal ST segment depression 3.53 +/- 1.97 mm) and 70% of patients with anterior infarction (mean maximal ST depression 1.45 +/- 0.8 mm, p = 0.001). When initially present, reciprocal change had resolved within 24 hours in 59% of patients. The sum of reciprocal ST depression correlated with the sum of ST elevation in anterior (r = 0.92, p less than 0.001) and inferior (r = 0.55, p = 0.035) infarction, and this relation persisted when maximal ST depression and elevation were considered. Echocardiographic evidence of contraction abnormalities in areas of the left ventricle remote from the infarction was seen in 45% of patients. However, its presence did not correlate with the presence of reciprocal change. Although reciprocal change progressively diminished on serial electrocardiograms (maximal ST depression 2.73 +/- 1.77 mm at 19 hours after onset of symptoms; 1.0 +/- 0.92 mm at 2 to 3 days; and 0.22 +/- 0.26 mm at 7 to 10 days; p less than 0.05), the corresponding serial echocardiograms showed no change in the function of the remote wall (remote wall motion index 1.87 +/- 0.65, 1.81 +/- 0.62, 1.86 +/- 0.47, respectively, p = NS). These data, therefore, do not support the hypothesis that reciprocal ST depressions during early acute transmural myocardial infarction reflect remote ischemia. Rather, these changes are influenced by factors determining the degree of acute ST elevation, previously shown to include infarct size, shape, location, transmurality and duration.     

Electrophysiological effects of intravenous sotalol in acute myocardial infarction: a double-blind placebo-controlled study

Controlled studies of the electrophysiological effects of beta-blockade in acute myocardial infarction have not previously been published. In this controlled, double-blind study 20 patients were randomized to treatment with placebo or sotalol administered as a continuous infusion for 12 h. Programmed electrical stimulation was performed from the right atrium. After 60 min of infusion in the sotalol-treated patients (n = 10) there was a significant prolongation of sinus cycle length (+15%) and sinus node recovery time (+28%). The AV nodal effective refractory period was prolonged by 15% after 45 min of infusion. Variables reflecting myocardial repolarization, atrial effective refractory period and QT interval, were increased by 20% and 10%, respectively. In the placebo group, except at 12 h, there was a general pattern of slightly diminishing values for all measured variables. The electrophysiological changes in the sotalol-treated group could be explained by the combined Class II and III activities of this drug. The infusion of sotalol was well tolerated, and the anticipated electrophysiological and Class II and III antiarrhythmic effects were observed, despite the acute myocardial infarction.     

急性心梗溶栓后再灌注性心律失常临床分析

目的分析急性心梗溶栓后再灌注性心律失常的发病机制和临床防治方法。方法选取我院2012年10月-2013年10月间收治的40名急性心梗患者作为研究对象,对患者实施尿激酶溶栓治疗,严密监测患者的心电图及心肌酶谱、心电图变化情况,同时对再次灌注心律失常发生的临床症状、类型以及发生时间进行记录和总结分析。结果本组40名患者中有35例患者溶栓后冠脉再通,占总数的87.5%,发生再灌注性心律失常的有31例,占总数的77.5%,大部分心律失常的患者为单纯室早,另外少部分患者心律失常的类型为房室传导阻滞、短阵室速以及室颤,再通的时间为(52.9±17.3)min。结论对急性心肌梗死患者实施冠脉再通以后可有效的缓解胸痛症状,但是该项治疗手术容易诱发心律失常,因此对心肌梗死患者实施再次灌注后应密切注意观察患者的心电图和血压变化情况。     

Metoprolol in acute myocardial infarction (MIAMI). A randomised placebo-controlled international trial

The effect of metoprolol on mortality and morbidity after 15days, was compared with that of placebo in a double-blind randomisedinternational trial (the MIAMI trial) in patients with definiteor suspected acute myocardial infarction (AMI). Treatment withintravenous metoprolol (15mg) or placebo was started shortlyafter the patient's arrival in hospital within 24 h of the onsetof symptoms, and then oral treatment (200 mg daily) was continuedfor the study period (15 days). Of the 5778 patients included,2901 were allocated to placebo and 2877 to metoprolol. DefiniteAMI was confirmed in 4127 patients. There were 142 deaths inthe placebo group (4.9%) and 123 deaths in the metoprolol group(4.3%), a difference of 13 per cent with 95 per cent confidencelimits of –8 to +33 per cent, not statistically significant(P=0.29). Previously recorded risk indicators of mortality were analysedin retrospect. These indicated that there was a category whichshowed higher risk which contained approximately 30% of allrandomized patients. In these, the mortality rate in the metoprololtreated group was 29% less than in the placebo group. In theremaining lower risk categories there was no difference betweenthe treatment groups. This subset analysis must be interpretedwith caution in view of the findings from other similar studies. Positive effects were observed on the incidence of definiteAMI and on serum enzyme activity in patients treated early (<7h). There was no significant effect on ventricular fibrillationbut the number of episodes tended to be lower in the metoprololtreated patients during the later phase (6–15 days; 24vs 54 episodes). The incidence of supraventricular tachyarrhythmias,the use of cardiac glycosides and other antiarrhythmics, andthe need for pain-relieving treatment were significantly diminishedby metoprolol amongst all randomised patients. Adverse eventsassociated with metoprolol were infrequent, expected, and relativelymild.     

Efficacy and safety of oral l-arginine in acute myocardial infarction. Results of the multicenter, randomized, double-blind, placebo-controlled ARAMI pilot trial

AIMS: L-arginine is a substrate for nitric oxide (NO) synthesis in vascular endothelial cells. NO bioavailability is decreased during myocardial infarction (MI). It might be expected that administration of L-arginine may maintain NO production and alleviate the course of MI. The aim of the study was to assess safety and effects of treatment with L-arginine on the clinical course of MI. METHODS AND RESULTS: 792 patients (mean age 64 years, 551 men) with ST segment elevation MI admitted within 24h after the onset of symptoms were randomized to oral L-arginine (3.0 t.i.d p.o. for 30 days) or placebo on top of routine therapy. The end point which was the composite of 30 day cardiovascular death, reinfarction, successful resuscitation, shock/pulmonary edema or recurrent myocardial ischemia occurred in 24% patients treated with L-arginine and 27% with placebo (OR 0.63, 95% CI 0.39-1.02, p=0.06). The end point was observed less frequently in 226 patients with hyperlipidemia (19 vs 31, p<0.05). No serious adverse effects were observed during L-arginine supplementation. CONCLUSIONS: This study, which is the first attempt to use L-arginine in MI, showed that oral L-arginine supplementation was well tolerated. Beneficial nonsignificant trend was observed towards reduction of major clinical events.     

QT-interval dispersion in acute myocardial infarction is only shortened by thrombolysis in myocardial infarction grade 2/3 reperfusion

BACKGROUND: Increased QT interval dispersion (QTd) has been found in patients with acute myocardial infarction (AMI). In previous studies this has been shown to decrease with thrombolysis. HYPOTHESIS: The aim of this study was to compare the effects of reperfusion by primary percutaneous transluminal coronary angioplasty (PTCA) and by thrombolysis on QTd and correlate these results with the degree of reperfusion. METHODS: We studied 60 patients with a first AMI. The study cohort included 40 consecutive patients who had received thrombolysis (streptokinase or rt-PA); 20 additional consecutive patients with successful primary PTCA, all with preselected Thrombolysis in Myocardial Infarction (TIMI) grade 3 flow by predefined selection criteria (12 stents); and 20 controls. A 12-lead ECG for QTd calculation was recorded before thrombolysis or PTCA and immediately after the procedure. All values were corrected according to Bazett's formula (QTcd). QTd and QTcd values before and after each procedure in three groups and the respective percent changes of deltaQTd and deltaQTcd were compared separately. RESULTS: QTd and QTcd were significantly increased before thrombolysis/PTCA versus normals. An angiogram performed after thrombolysis showed adequate reperfusion (TIMI grade 2/3) in 20 patients, while in the other 20 only TIMI 0/1 reperfusion was achieved. Thrombolysis-TIMI flow 2/3 and PTCA significantly reduced QTd (from 68 +/- 10 to 35 +/- 8 ms, p < 0.001, deltaQTd = 48 +/- 11%, in the Thr-TIMI flow 2/3 group,and from 79 +/- 11 to 38 +/- 9 ms, p < 0.001, deltaQTd = 52 +/- 9%, in the PTCA group), while in the Thr-TIMI flow 0/1 group no significant changes were recorded. A percent QTd decrease > 30 s had 96% sensitivity, 85% specificity, and 93% positive and 94% negative predictive value, respectively, for TIMI 2/3 flow. CONCLUSIONS: A significant decrease in QT dispersion may provide an additional electrocardiographic index for successful (TIMI 2/3) reperfusion.     

Importance of early and complete reperfusion to achieve myocardial salvage after thrombolysis in acute myocardial infarction.

The importance of the timing and completeness of coronary artery reperfusion for limitation of acute myocardial infarction (AMI) size after intravenous thrombolytic therapy was studied in 39 patients. All had electrocardiographic epicardial injury and acute coronary angiography performed < 8 hours after symptom onset. Acutely jeopardized myocardium was estimated at baseline, and before and after angiography by quantitative ST-segment analysis. The AMI size was estimated on the final electrocardiogram by the Selvester QRS score. Left ventricular ejection fraction was measured at the time of acute angiography and before discharge in 31 of these patients. In the 21 patients with normal flow (Thrombolysis in Myocardial Infarction [TIMI] trial grade 3) in the infarct-related artery, the amount of jeopardized myocardium decreased from baseline to that before and after angiography (17 to 11 and 11%, respectively; p < 0.00005), and the median final AMI size was reduced (17 to 9%; p = 0.0004). In 6 patients with suboptimal flow (TIMI grade 2), the median amount of jeopardized myocardium decreased slightly from baseline to that before to after angiography (15 to 12%); however, the median final AMI size was not reduced (17%). In 12 patients with no reperfusion (TIMI 0 to 1) flow, the median amount of jeopardized myocardium remained unchanged from baseline to that before angiography (21%), and the final AMI size was not significantly reduced. There was a significant inverse correlation between the change in global left ventricular function and the difference between electrocardiographic estimated jeopardized and final AMI size (rs = -0.53; p = 0.008).(ABSTRACT TRUNCATED AT 250 WORDS)     

Hemodynamic effects of metoprolol in acute myocardial infarction. A randomized, placebo-controlled multicenter study

The central hemodynamic effects of metoprolol in acute myocardial infarction have been studied in a multicenter, double-blind, randomized trial. One hundred and ninety patients with acute myocardial infarction not previously on beta blockers with heart rate greater than 65 beats/min and blood pressure greater than 105 mm Hg and without clinical signs of serious heart failure were included. After insertion of a pulmonary artery catheter, patients were randomized to metoprolol, 15 mg intravenously, and 50 mg 4 times a day orally (n = 95) or placebo (n = 95) with a mean delay of 7.2 hours. Hemodynamic measurements were made at baseline and repeatedly during 24 hours. Heart rate, systolic blood pressure and cardiac index were all immediately reduced by 10 to 20% in the metoprolol group and the difference compared with placebo was maintained throughout the 24 hours (p less than 0.001). Pulmonary capillary wedge pressure (PCWP) in the metoprolol group increased from 13.7 +/- 6.7 to a peak of 15.5 +/- 5.5 mm Hg 30 minutes after injection. The difference compared with placebo was maintained for 8 hours (p less than 0.01). This increase was seen only in the patient group with initial PCWP below the median of 13 mm Hg. In patients with initial PCWP above the median a continuous decrease was observed in both the placebo and metoprolol groups. Thus high initial PCWP was not associated with intolerance to metoprolol. Based on hemodynamic measurements tolerance to metoprolol was good.     

Continuous vectorcardiography is superior to standard electrocardiography in the prediction of long-term outcome after thrombolysis in patients with acute myocardial infarction

BACKGROUND: Thrombolytic therapy results in reperfusion of the occluded coronary vessel in approximately 75% of treated patients with acute myocardial infarction (AMI). Unsuccessful thrombolysis results in impaired outcome. This study was undertaken to evaluate reperfusion assessments with 12-lead standard static electrocardiography (ECG) and continuous vectorcardiography (VCG) in AMI patients treated with thrombolytic therapy, with particular emphasis on the value of these assessments in relation to long-term outcome. METHODS: ST-recovery analysis 90 and 180 min after the start of thrombolytic therapy was performed by repeated ECG and by VCG in 63 AMI patients. Median follow-up was 255 days. RESULTS: No significant differences in long-term outcome were found between patients with or without obtained reperfusion, as assessed by ECG. For VCG, we found significant elevated relative risks for experiencing death (relative risk = 11.00, confidence interval = 2.70-44.90); P = 0.0008 for the group with ST-vector magnitude recovery of less than 50% at 90 min from start of thrombolytic therapy. CONCLUSION: We demonstrated that early reperfusion assessment with VCG enables the prediction of long-term outcome and is superior to reperfusion assessment with standard static ECG in this regard. We therefore recommend continuous ischemia monitoring of AMI patients treated with thrombolytic therapy as a routine procedure.     

Early flow propagation velocity for assessment of diastolic function in myocardial infarction treated with acute reperfusion.

INTRODUCTION: Acute myocardial infarction (MI) causes left ventricular (LV) diastolic dysfunction, which influences prognosis and clinical evolution. Early flow propagation velocity (FPV), evaluated by color M-mode Doppler, has been demonstrated to be a diastolic function parameter with excellent correlation with relaxation constant tau, and is relatively independent of pre- and afterload. OBJECTIVE: The aim of this study was to evaluate left ventricular relaxation in MI patients treated with acute reperfusion therapy. METHODS: Patients with ST-elevation MI treated with reperfusion therapy were evaluated by echocardiagraphy in the first 48 hours and after one week. The parameters studied were: early peak filling velocity (E), late peak filling velocity (A), E/A ratio, E-wave deceleration time (EDT), isovolumic relaxation time (IVRT) and FPV. The values obtained at the first and second evaluation were compared; we evaluated the relation between pain-to-reperfusion time (PRT; < or =3 hours vs. >3 hours) and the presence of single-vessel or multivessel disease with the parameters previously mentioned. RESULTS: 40 patients were studied and 19 included, 15 (80%) male, mean age 57+/-14 The most prevalent risk factors were: hypertension (11 patients - 58%), smoking (14 - 74%), diabetes (6 - 30%), and dyslipidemia (12 - 63%). MI location was anterior in six patients (31%) and inferior in 13 (69%). Five patients (26%) underwent fibrinolysis and 14 (74%) direct percutaneous coronary intervention. Mean pain-to-reperfusion time was 3.7+/-2.8 hours. Four patients (21%) had single-vessel disease and 14 (74%) had multivessel disease. Near significance was found for the difference in the E/A ratio between the two evaluations and a significant difference in the FPV. A significant correlation was also found between PRT and E/A ratio at the two evaluations (p=0.003, p=0.05), and between PRT and IVRT after one week (p=0.011). E/A ratio, IVRT and FPV were normal at the two evaluations in patients who had undergone earlier reperfusion therapy. No significance was found between the number of diseased vessels and the parameters of diastolic function assessed. DISCUSSION AND CONCLUSIONS: In the early phase of M1 treated with acute reperfusion, a delayed relaxation pattern was observed, which evolved to a normal pattern by the second evaluation, as statistically confirmed by FPV. Earlier reperfusion therapy preserves diastolic function. FPV is a sensitive and independent parameter for assessment of diastolic function in MI patients treated with acute reperfusion therapy.