常规心电图对前壁下壁心肌梗死罪犯血管的预测价值

目的:分析常规心电图对急性前壁下壁心肌梗死罪犯血管的预测价值。方法:选择41例急性前壁合并下壁ST段抬高的心肌梗死者作为研究对象,按冠脉造影资料将梗死罪犯血管分为右冠病变(RCA)组24例和左前降支病变(LAD)组17例,分别测量常规心电图12导联ST段偏移程度及发生的导联数,以计算比较两组间的差异及对不同冠脉之间的预测价值。结果:(1)两组的基线临床资料无显著差异性;(2)RCA组Ⅱ、Ⅲ、aVF导联ST段抬高幅度总和高于LAD组[(2.46±1.24)vs(1.77±0.61)mm,P0.01],ST段抬高III/II1(66%vs 28%,P0.01)或V1/V31(75%vs 12%,P0.05)在RCA组高于LAD组;LAD组V3导联ST段抬高幅度总和高于RCA组[(1.60±0.36)vs(4.44±2.65)mm,P0.01)。结论:Ⅱ、Ⅲ、aVF、V3导联ST段抬高幅度总和及V1/V3比值在诊断急性下壁前壁心肌梗死中对梗死罪犯血管有重要预测价值。     

Concomitant use of intraaortic balloon counterpulsation and streptokinase in acute anterior myocardial infarction.

Using a prospective, nonrandomized design, the authors sought to determine whether concomitant use of intraaortic balloon counterpulsation (IABP) and streptokinase in acute anterior myocardial infarction (MI) would improve the in-hospital mortality rate and angiographic findings. The study included 45 patients with an acute anterior MI. All patients received intravenous streptokinase. Among these, 25 patients had concomitant IABP while the remaining 20 patients had streptokinase alone. All patients underwent cardiac catheterization. Patients treated with concomitant IABP had a significantly higher frequency of thrombolysis in myocardial infarction (TIMI) grade 3 flow (n: 11; 44% vs n: 1; 5%, p<0.05), and there was a trend toward a lower in-hospital mortality rate in the IABP group (n: 0; 0% vs n: 3; 15%, p=0.08). The angiographic presence of thrombus image and grade > or =2 coronary collateral circulation to the infarct-related coronary artery for the IABP and non-IABP groups did not differ significantly. The preliminary results of this study suggest that concomitant use of IABP and streptokinase in acute anterior MI increases the incidence of TIMI grade 3 flow and may have decreased the in-hospital mortality rate without unacceptable rates of vascular or hemorrhagic complications.     

Effects of early high-dose streptokinase intravenously on left ventricular function in acute myocardial infarction

One hundred seven patients who recently had acute myocardial infarction were randomly assigned either to standard heparin therapy or to intravenous streptokinase within 5 hours after the onset of symptoms in 7 hospitals without catheterization facilities. In the third week, the patients were referred to a university hospital, where the patency rate of the infarct-related artery was studied by selective coronary arteriography and left ventricular function by radionuclide angiography. Fifty-five patients received heparin and 52 streptokinase within a mean period of 190 minutes after the onset of symptoms. Seven patients in the heparin group and 4 in the streptokinase group died in hospital. The patency rate of the infarct-related artery was identical in both groups (69% in the heparin group vs 68% in the streptokinase group). Left ventricular ejection fraction was not statistically different (0.44 +/- 0.13 in the heparin group vs 0.45 +/- 0.12 in the streptokinase group). Left ventricular ejection fraction was significantly higher in patients with a patent infarct-related artery than in patients with an obstructed infarct-related artery (0.49 +/- 0.12 vs 0.41 +/- 0.15, p less than 0.01). In patients with inferior wall infarction, left ventricular ejection fraction was identical (0.50 +/- 0.10 in the heparin group vs 0.52 +/- 0.09, in the streptokinase group). In patients with anterior wall infarction, left ventricular ejection fraction was significantly higher in the streptokinase group than in heparin group (0.40 +/- 0.10 vs 0.33 +/- 0.09, p less than 0.05). Analysis of regional wall motion revealed that improvement occurred in the lateral wall of the left ventricle.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effectiveness of intravenous streptokinase on infarct size and left ventricular function in acute myocardial infarction. Prospective and randomized study

Within 3 h after the onset of symptoms of myocardial infarction, 64 patients were randomly assigned to receive either a 1-h intravenous infusion of 1,500,000 IU of streptokinase (SK) or a conventional therapy. Infarct size was estimated in CK gram equivalent (CKg) by measurement of CK-MB every 3 hours during a 48-h period. Enzymatic study revealed that myocardial infarction of the SK group was significantly smaller (61.4 +/- 45 vs. 89.4 +/- 56 CKg, p less than .05). Angiograms were performed at early stage and five weeks after myocardial infarction. At first coronary angiogram, the infarct-related vessel was open in 82% in the SK group versus 12% in controls. The SK group had higher global ejection fraction at second angiogram (57 +/- 11% vs. 49 +/- 11%, p less than .02), but differences in regional wall motion were not significant. By analysis according to patency or occlusion of infarct-related vessel, global and regional ejection fractions were significantly better at first and at second angiograms in all patients and in anterior infarctions with a patent infarct-related coronary artery. There was no significant difference for inferior infarction. We conclude that intravenous streptokinase infusion early after the onset of myocardial infarction reduces infarct size and improves left ventricular function, chiefly in anterior infarction. This benefit appears to be closely correlated to patency of infarct-related vessels.     

C-reactive protein on admission and the success of thrombolytic therapy with streptokinase: is there any relation?

BACKGROUND: Recent evidence has demonstrated that inflammation plays a major role in the initiation and progression of atheroma plaques. C-reactive protein (CRP) is shown to have prognostic significance in acute coronary syndromes. We investigated the influence of CRP levels before thrombolytic therapy on infarct-related artery (IRA) patency and the degree of residual stenosis. METHODS: 45 consecutive patients with a first attack of acute myocardial infarction (MI) who underwent streptokinase therapy and subsequently coronary angiography were enrolled into the study. Patients were divided into 2 groups according to the level of CRP on admission. RESULTS: Serum CRP levels were > or =0.5 mg/dL in 26 patients (Group-I) and <0.5 mg/dL in 19 patients (Group-II). The patency of IRA (TIMI-2 and 3) evaluated at 90th minute after the initiation of thrombolytic therapy was similar between the two groups (62% vs. 68%, p>0.05). However, the presence of TIMI-3 flow was significantly lower and TIMI-2 flow was higher in Group-I as compared to Group-II (12% vs. 53%, p=0.003 and 50% vs. 16%, p=0.018 respectively). Additionally, among patients with patent IRA, the degree of residual stenosis was significantly higher in Group-I (80 +/- 14% vs. 68 +/- 15%, p=0.032). CONCLUSION: High serum CRP levels on admission in patients within 6 hours after the start of acute ST-segment elevation MI are associated with lower TIMI flow grades and higher residual stenosis of IRA after intravenous streptokinase. Our observations imply that patients with higher CRP levels on admission require closer follow-up during and after acute MI.     

The distinction between coronary and myocardial reperfusion after thrombolytic therapy by clinical markers of reperfusion

Objectives. We sought to examine the hypothesis that rapid resolution of ST-segment elevation in acute myocardial infarction (AMI) patients with early peak creatine kinase (CK) after thrombolytic therapy differentiates among patients with early recanalization between those with and those without adequate tissue (myocardial) reperfusion.Background. Early recanalization of the epicardial infarct-related artery (IRA) during AMI does not ensure adequate reperfusion on the myocardial level. While early peak CK after thrombolysis results from early and abrupt restoration of the coronary flow to the infarcted area, rapid ST-segment resolution, which is another clinical marker of successful reperfusion, reflects changes of the myocardial tissue itself.Methods. We compared the clinical and the angiographic results of 162 AMI patients with early peak CK (≤12 h) after thrombolytic therapy with (group A) and without (group B) concomitant rapid resolution of ST-segment elevation.Results. Patients in groups A and B had similar patency rates of the IRA on angiography (anterior infarction: 93% vs. 93%; inferior infarction: 89% vs. 77%). Nevertheless, group A versus B patients had lower peak CK (anterior infarction: 1,083 ± 585 IU/ml vs. 1,950 ± 1,216, p < 0.01; and inferior infarction: 940 ± 750 IU/ml vs. 1,350 ± 820, p = 0.18) and better left ventricular ejection fraction (anterior infarction: 49 ± 8, vs. 44 ± 8, p < 0.01; inferior infarction: 56 ± 12 vs. 51 ± 10, p = 0.1). In a 2-year follow-up, group A as compared with group B patients had a lower rate of congestive heart failure (1% vs. 13%, p < 0.01) and mortality (2% vs. 13%, p < 0.01).Conclusions. Among patients in whom reperfusion appears to have taken place using an early peak CK as a marker, the coexistence of rapid resolution of ST-segment elevation further differentiates among patients with an opened culprit artery between the ones with and without adequate myocardial reperfusion.     

Reciprocal ST-segment depression associated with exercise-induced ST-segment elevation indicates residual viability after myocardial infarction

OBJECTIVES: We evaluated the clinical significance of reciprocal ST-segment depression associated with exercise-induced ST-segment elevation for detecting residual viability within the infarcted area. BACKGROUND: Although the relation between residual viability and exercise-induced ST-segment elevation has been described, there are no reports focusing on the relation between myocardial viability and reciprocal ST-segment depression associated with exercise-induced ST-segment elevation. METHODS: We evaluated regional blood flow and glucose utilization using N-13 ammonia (NH3) and F-18 fluorodeoxyglucose (FDG) positron emission tomography (PET) in 30 patients with a previous Q-wave myocardial infarction (anterior in 15, inferior in 15). All subjects had single-vessel disease and had exercise-induced ST-segment elevations (> or =1 mm) in electrocardiographic leads. RESULTS: Reciprocal ST-segment depression (> or =1 mm) was present in 16 patients (Group A; anterior in 6, inferior in 10) but not in the remaining 14 patients (Group B). The degree of exercise-induced ST-segment elevation (1.8+/-0.2 vs. 2.0+/-0.2 mm) and the time from the onset of infarction to the study (75+/-49 vs. 74+/-52 days) did not differ between groups. There were no significant differences between groups in the severity of left ventricular dysfunction and the residual luminal narrowing in the infarct-related artery (45+/-21 vs. 48+/-25%). The presence and site of infarction were confirmed by NH3-PET in all patients. FDG-PET demonstrated residual tissue viability within infarct-related area in all patients in Group A and in 3 (21%) of 14 patients in Group B (p < 0.01). The sensitivity, specificity and accuracy of reciprocal ST-segment depression associated with exercise-induced ST-segment elevation for detecting residual viability were 84%, 100% and 90%, respectively. CONCLUSIONS: The occurrence of reciprocal ST-segment depression associated with exercise-induced ST segment elevation in patients with a previous Q-wave infarction who had single-vessel disease indicates residual tissue viability within the infarct-related area.     

Diagnosing acute myocardial infarction in patients with left bundle branch block

We compared the clinical features, laboratory and coronary angiographic findings, treatments, and outcomes among patients with ST-segment elevation myocardial infarction (MI) with and without left bundle branch block (LBBB). We examined 5,742 patients with ST-segment elevation MI with and without LBBB treated with primary percutaneous coronary intervention in the Assessment of Pexelizumab in Acute Myocardial Infarction trial. The main outcome measures were obstructive coronary disease, MI, positive cardiac biomarkers, angiographic Thrombolysis In Myocardial Infarction flow, and death, MI, or congestive heart failure at 90 days. LBBB was present in 98 patients (1.7%). According to the protocol, patients with LBBB were eligible only if they had ≥1 mm concordant ST-segment elevation. Obstructive coronary artery disease was present in >87% of the patients with LBBB. Documented MI (elevated biomarkers) with an initially occluded infarct artery was more common in patients with LBBB with concordant ST-segment elevation (71.4%) than in patients without (44.1%; p = 0.027). The use of ST-segment elevation concordance criteria in the presence of LBBB was more often associated with documented MI with an identifiable culprit vessel with an initially occluded infarct-related artery. In conclusion, because a substantial proportion of patients with LBBB have acute MI with a culprit lesion and positive biomarkers, these data support immediate catheterization with the intent for primary percutaneous coronary intervention for all patients presenting with suspected ST-segment elevation myocardial infarction, ischemic symptoms, and presumed new LBBB, particularly if concordant ST-segment elevation is present.     

Clinical and angiographic characteristics of patients with combined anterior and inferior ST-segment elevation on the initial electrocardiogram during acute myocardial infarction

Objective

We evaluated the significance of combined anterior and inferior ST-segment elevation on the initial electrocardiogram (EKG) in patients with acute myocardial infarction (AMI) and correlated it with AMI size and left ventricular (LV) function.

Methods

We analyzed admission EKGs of 2996 patients with AMI from the GUSTO-I angiographic substudy and the GUSTO-IIb angioplasty substudy who underwent immediate angiography. In all, we identified 1046 patients with anterior ST elevation (ST-segment elevation in ≥2 of leads V₁-V₄) and divided them into 3 groups: Group 1, anterior + inferior ST elevation (ST elevation in ≥2 of leads II, III, aVF, n =179); Group 2, anterior ST elevation only (<2 of leads II, III, aVF with ST elevation or depression, n = 447); Group 3, anterior ST elevation + superior ST elevation (ST depression in ≥2 of leads II, III, aVF, n = 420).

Results

Cardiac risk factors, prior AMI, prior percutaneous transluminal coronary angioplasty or coronary artery bypass graft, Killip class, and thrombolytic therapy assignment did not differ among the 3 groups. Group 1 patients had greater number of leads with ST elevation compared to Groups 2 and 3 (ST elevation in ≥6 leads 83% vs 22% vs 49%, P = .001). Despite greater ST-segment elevation, Group 1 patients had a lower peak CK level (median baseline peak CK 1370 vs 1670 vs 2381 IU, P = .0001) and less LV dysfunction (median ejection fraction 0.53 vs 0.49 vs 0.45, P = .0001; median number of abnormal chords 21 vs 32 vs 40, P = .0001). Angiographically, Group 1 had 2 distinct subsets of patients with either right coronary artery (RCA) (59%) or left anterior descending coronary artery (LAD) (36%) occlusion. In contrast, the infarct-related artery (IRA) was almost entirely the LAD in Groups 2 and 3 (97%). Further, the site of IRA occlusion in Group 1 was mostly proximal RCA (67%) in the RCA subgroup and mid or distal LAD (70%) in the LAD subgroup. ST-segment elevation in lead V₁ ≥ V₃ and absence of progression of ST elevation from lead V₁ to V₃ on the EKG differentiated IRA-RCA from IRA-LAD in patients with combined anterior and inferior ST elevation.

Conclusions

The AMI size and LV dysfunction in patients with anterior ST elevation is directly related to the direction of ST segment deviation in the leads II, III, aVF; least with inferior ST elevation, intermediate with no ST deviation, and maximal with superior ST elevation (inferior ST depression). Despite greater ST-segment elevation, patients with combined anterior and inferior ST elevation have limited AMI size and preserved LV function. Angiographically, they comprise 2 distinct subsets with either proximal RCA or mid to distal LAD occlusion. A predominant right ventricular and limited inferior LV AMI from a proximal RCA occlusion, or a smaller anterior AMI from a more distal occlusion of LAD may explain their limited AMI size despite greater ST elevation.     

Bradycardia and hypotension following reperfusion with streptokinase (Bezold-Jarisch reflex): a sign of coronary thrombolysis and myocardial salvage

Acute myocardial infarction, particularly of the inferior wall, is frequently associated with bradycardia and hypotension. This study reports the occurrence of transient bradycardia hypotension (TBH) (Bezold-Jarisch reflex) following thrombolytic therapy with intravenous streptokinase. Of the 52 patients, 42 had successful reperfusion, and 12 of the latter developed reflex TBH. The Bezold-Jarisch reflex occurred in 10 of 24 patients with inferior wall acute myocardial infarction and in 2 of 28 patients with anterior wall infarction (p less than 0.05). The reflex was associated with significantly more non-Q wave infarctions (p less than 0.05) and also with reduction of left ventricular damage, as evidenced by a lower QRS score (4 +/- 3.8 vs 8.9 +/- 5.6, p less than 0.01) and a higher ejection fraction (61 +/- 13% vs 49 +/- 16%, p less than 0.05). Patients with inferior wall acute myocardial infarction were divided into those with TBH (10 patients) and those without TBH (14 patients). TBH was associated with a significantly higher infarct-related regional ejection fraction (60 +/- 19% vs 35 +/- 18%, p less than 0.05). The results of this study confirm previous findings that reperfusion of the inferoposterior myocardium is capable of stimulating reflex TBH. Furthermore, TBH is associated with patency of infarct-related coronary arteries and myocardial salvage.     

Reliability of resolution of ST-segment elevation after coronary reperfusion in predicting myocardial salvage in anterior wall acute myocardial infarction

Resolution of ST-segment elevation (ST resolution) after reperfusion therapy has been shown to correlate with improved left ventricular (LV) function in patients with acute myocardial infarction (AMI). However, not all patients with ST resolution have preserved LV function. We evaluated the clinical significance of ST resolution in 129 patients with anterior wall AMI who underwent successful coronary recanalization within 6 hours after symptom onset by studying the relation to myocardial blush grade, another angiographic marker of myocardial reperfusion. A reduction of > or =50% in ST-segment elevation after recanalization was defined as ST resolution. Ninety-eight patients had ST resolution and 31 patients did not. Patients with ST resolution were subdivided into 2 groups according to myocardial blush grade after recanalization: 67 patients with blush grade 2 or 3, and 31 with blush grade 0 or 1. The QRS score after recanalization was higher (5.9 +/- 1.9 vs 3.4 +/- 2.0, p <0.01) and predischarge LV ejection fraction was lower (39 +/- 8% vs 57 +/- 9%, p <0.01) in patients with blush grade 0 or 1 than in those with blush grade 2 or 3. However, the QRS score after recanalization and the predischarge LV ejection fraction were similar in patients who had ST resolution with blush grade 0 or 1 and in those without ST resolution. Our findings suggest that ST resolution after recanalization does not consistently predict myocardial salvage in patients with anterior AMI.     

Stress-induced ST-segment elevation following myocardial infarction and its role in wall motion abnormality, myocardial ischemia and viability: comparison of response to exercise, dobutamine and dipyridamole.

Stress-induced ST-segment elevation following myocardial infarction (MI) has been correlated with myocardial ischemia, viability and wall motion abnormality, but its mechanism is still unclear, so the present study compared ST-segment elevation and wall motion response during exercise, dobutamine and dipyridamole stresses. Twenty-five patients with their first anterior MI underwent exercise, dobutamine and dipyridamole echocardiography on different days 4-6 weeks after MI. Left ventricular wall motion was analyzed using 5-grade/16-segment model and myocardial ischemia was considered as a worsening of the wall motion score index (WMSI) during the stress test; myocardial viability was defined as a reduction of WMSI during low dose dobutamine. Dyskinesis formation was defined by visual analysis as akinesis that became dyskinetic or if the dyskinesis worsened. Both exercise and dobutamine induced ST-segment elevation, but dipyridamole did not. There was no significant difference in the degree of ST-segment elevation between the patients with and without myocardial ischemia or dyskinesis formation. Exercise induced a higher ST-segment elevation in patients with myocardial viability than those without (0.17+/-0.09 mV vs 0.09+/-0.07 mV, p<0.05). Exercise-induced ST-segment elevations correlated with dobutamine-induced ST-segment elevations (p<0.01), changes in heart rate (p<0.05) and systolic blood pressure (p<0.05). In conclusions, stress-induced ST-segment elevation does not correlate with either myocardial ischemia or stress-induced dyskinesis, but may be associated with myocardial viability.     

Angiographic evidence that reciprocal ST-segment depression during acute myocardial infarction does not indicate remote ischemia: Analysis of 23 patients

Although reciprocal ST-segment depression from the remote noninfarcting ventricular wall during acute myocardial infarction (Ml) is a common clinical finding, the significance of this electrocardiographic pattern is unclear. Previous retrospective studies have suggested that these findings may reflect either remote wall ischemia, multivessel coronary artery disease (CAD), extensive MI or a benign electrical phenomenon. Prior studies have lacked angiographic data obtained at the time of these acute electrocardiographic changes. In this study we prospectively evaluated 23 patients with acute MI. Left ventricular wall motion, coronary anatomy and the ECG were all assessed over a short period during the acute phase of the MI. Segmental wall motion was used as a sensitive indicator of ischemia.Seventeen patients had acute anterior MI, of whom 47 % had reciprocal ST-segment depression; 6 patients had inferior MI, with 3 showing reciprocal ST depression. The mean degree of ST-segment elevation from the infarcting wall tended to be greater in patients with reciprocal ST-segment depression than in those without such reciprocal ST depression (2.8 ± 0.4 vs 1.9 ± 0.3 mm, p = 0.06). Patients with and without reciprocal ST-segment depression had similar degrees of segmental dysfunction in the infarct wall. However, no abnormalities in segmental wall motion in the remote wall were seen regardless of the presence or absence of remote wall ST-segment depression. In addition, the presence or absence of ST-segment depression did not predict the extent or degree of CAD. Finally, the magnitude of ST-segment elevation from the acutely infarcting wall correlated significantly with the degree of remote wall reciprocal ST-segment depression (r = 0.83, p < 0.01).Thus, the presence of remote wall reciprocal ST-segment depression on the ECG during the acute phase of an MI does not predict ischemia or the extent of CAD in the arteries supplying the remote noninfarcting wall. Because the reciprocal electrocardiographic changes correlate with the degree of ST-segment elevation, they probably represent a benign electrical phenomenon.     

Changes in contractile function of the left ventricle under the effect of thrombolytic reperfusion of the coronary arteries in acute myocardial infarct

A total of 73 patients with myocardial infarction (MI) were included into a prospective study involving intravenous and/or intracoronary streptokinase administration. The total ejection fraction (EF) and the extent of left ventricular dys- and akinetic areas were measured by contrast ventriculography in the first 3-9 hours and 4 weeks after the onset of MI symptoms. Coronary reperfusion performed in the first 3 hours after the onset of symptoms in patients with anterior MI (n = 8) and following 3-9 hours (mean 6.6 +/- 0.89 hours) in patients with inferior MI (n = 17) significantly (p less than 0.05) reduced the extent of dys- and akinetic areas from 20.5 +/- 4.16 to 6.0 +/- 3.99 and 10.0 +/- 1.56 to 5.0 +/- 1.74%, respectively) following 4 weeks. EF significantly (p less than 0.01) increased in the former and tended to show an increase from 51.0 +/- 2.44 to 64.0 +/- 2.26% (p less than 0.1) in the latter. In patients with anterior MI (n = 19) there was a tendency to a decrease in the extent of dys- and akinetic areas from 26.0 +/- 2.85 to 17.0 +/- 3.9 (p less than 0.1) following 3-9 hours. No substantial changes were observed in the values of left ventricular dys- and akinesis and EF in patients with anterior (n = 13) and inferior (n = 16) MI without coronary reperfusion.     

Limitation of myocardial infarct size and preservation of left ventricular function by early administration of APSAC in myocardial infarction

In cases of acute myocardial infarction (MI), it has been shown that preserving left ventricular function and limiting infarct size with early reperfusion of the occluded artery by means of a thrombolytic agent could eventually result in a reduced mortality rate. The aim of the APSIM study (anisoylated plasminogen streptokinase activator complex [APSAC] dans l'infarctus du Myocarde) was to demonstrate that early administration of APSAC in patients with recent acute MI could limit the infarct size and preserve left ventricular systolic function. In all, 231 patients with a first acute MI were randomly allocated to either APSAC (30 U over 5 minutes) or to conventional heparin therapy (5,000 IU in bolus injection) within 5 hours of the onset of symptoms. Of these patients, 112 received APSAC and 119 received heparin within a mean period of 188 +/- 62 minutes after the onset of symptoms. The patency rate of the infarct-related artery was 77% in the APSAC group and 36% in the heparin group (p less than 0.001). Left ventricular ejection fraction determined from contrast angiography was significantly higher in the APSAC than in the heparin group. This was true for the entire population (0.53 +/- 0.13 vs 0.47 +/- 0.13, p = 0.002) as well as for the subgroups of anterior and inferior wall infarctions (0.47 +/- 0.13 vs 0.4 +/- 0.16, p = 0.004 and 0.56 +/- 0.11 vs 0.51 +/- 0.09, p = 0.02). At 3 weeks, the difference remained significant for patients with anterior MI.(ABSTRACT TRUNCATED AT 250 WORDS)     

Persistent ST-segment elevation after primary stenting for acute myocardial infarction: its relation to left ventricular recovery

BACKGROUND: Early restoration of coronary artery patency in acute myocardial infarction (AMI) has been linked to improvement in survival. However, early recanalization of an occluded epicardial coronary artery by either thrombolytic agents or percutaneous transluminal coronary angioplasty (PTCA) does not necessarily lead to left ventricular (LV) function recovery. HYPOTHESIS: The aim of this study was to evaluate the relation between persistent ST elevation shortly after primary stenting for acute myocardial infarction (AMI) and LV recovery. METHODS: Thirty-one patients with primary stenting for AMI were prospectively enrolled. To evaluate the extent of microvascular injury, serial ST-segment analysis on a 12-lead electrocardiogram recording just before and at the end of the coronary intervention was performed. Persistent ST-segment elevation (Persistent Group, n = 11) was defined as > or = 50% of peak ST elevation and resolution (Resolution Group, n = 20) was defined as < 50% of peak ST elevation. Echocardiography was performed on Day 1 and 3 months after primary stenting. RESULTS: At 3 months, infarct zone wall-motion score index (WMSI, 2.1 +/- 0.6 vs. 2.7 +/- 0.3, p < 0.05) was smaller in the Resolution Group than in the Persistent Group, whereas wall motion recovery index (RI, 0.4 +/- 0.3 vs. 0.1 +/- 0.2, p < 0.05) and ejection fraction (58 +/- 5 vs. 43 +/- 10%, p < 0.05) were larger in the Resolution Group than in the Persistent Group. The extent of persistent ST elevation (% ST) shortly after successful recanalization of the infarct-related artery was significantly related to RI at 3 months (r = -0.4, p < 0.05). However, time to reperfusion was not related to RI at 3 months. There was also significant correlation between corrected TIMI frame count and %ST (r = 0.4, p < 0.05). CONCLUSIONS: Persistent ST-segment elevation shortly after successful recanalization (> or = 50% of the peak value), as a marker of impaired microvascular reperfusion, predicts poor LV recovery 3 months after primary stenting for AMI.     

Effect of preinfarction angina pectoris on ST-segment resolution after primary coronary angioplasty for acute myocardial infarction

The presence of preinfarction angina has been shown to exert a favorable effect on left ventricular function after acute myocardial infarction (AMI). Whether or not preinfarction angina is beneficial for myocardial tissue reperfusion, however, remains to be determined. We sought to evaluate the influence of preinfarction angina on resolution of ST-segment elevation, which could be affected by microcirculatory damage after recanalization therapy. We studied 96 patients with a first AMI in whom Thrombolysis In Myocardial Infarction (TIMI)-3 flow in the infarct-related artery was established by primary angioplasty. Percent reduction in the sum of ST elevation from baseline to 1 hour after angioplasty (percent delta summation operator ST) was examined. Poor ST resolution, defined as percent delta summation operator ST <50%, was observed in 25 patients, who had a worse clinical outcome, larger infarct size, and poorer left ventricular function. On multivariate analysis, the absence of preinfarction angina, as well as anterior wall infarction, were major independent predictors of poor ST resolution, whereas age, sex, coronary risk factors, ischemic time, Killip class on admission, multivessel disease, initial TIMI flow grade, and extent of collaterals were not significant. Patients with preinfarction angina had a greater degree of ST-segment resolution than those without angina (71 +/- 21% vs 49 +/- 43%, p = 0.02). Additional ST elevation after reperfusion was noted exclusively in patients without preinfarction angina (p = 0.02). Preinfarction angina is associated with a greater degree of ST-segment resolution in patients with TIMI-3 flow after primary angioplasty, suggesting a protective effect of preinfarction angina against microcirculatory damage after reperfusion.     

Dobutamine-induced ST-segment elevation associated with a biphasic response of wall motion in patients with a recent myocardial infarction is caused by myocardial ischaemia and is abolished by revascularization of the infarct-related artery

OBJECTIVE: ST-segment elevation is frequently induced by dobutamine in patients with a recent myocardial infarction and may represent dyskinesia of the infarcted region or myocardial viability and ischaemia. Revascularization of the infarct-related artery may abolish myocardial ischaemia, and thus represents a useful tool to verify the significance of this finding. The aim of this study was to assess the relation between ST-segment elevation and wall motion response during dobutamine echo stress test and to evaluate the effect of coronary revascularization with percutaneous coronary angioplasty of the infarct-related artery on stress test results. METHODS AND RESULTS: Twenty-two patients (17 men; mean age 58+/-12 years) with a first acute myocardial infarction (5 anterior (23%) and 17 (77%) inferior) who showed ST-segment elevation during a dobutamine echo stress test performed early (7+/-5 days) after the acute event where included in the analysis. All patients underwent coronary arteriography followed by percutaneous revascularization with coronary angioplasty or atherectomy with or without stenting of the culprit lesion and a second dobutamine echo stress test at a mean of 40+/-20 days after revascularization. The minimal lumen diameter increased from 0.63+/-0.36 to 3+/-0.44 mm and % diameter stenosis decreased from 80+/-11 to 12+/-7 after revascularization. At baseline evaluation there were 62 normal moving segments (34%), 57 (32%) akinetic and 62 (34%) hypokinetic segments within the area at risk. Maximal ST-segment shift changed from a basal mean value of 0.41+/-0.6 to a peak value of 2.15+/-0.9 mm; angina developed in 6/22 patients (22%). A biphasic response to dobutamine indicative of myocardial ischaemia within the infarcted area was observed in 20/22 patients (91%) and in 54/74 (73%) segments showing wall motion abnormalities. After revascularization of the infarct-related artery 78 (43%) segments were considered to be normal, 46 (25%) akinetic and 57 (32%) hypokinetic. Dobutamine-induced ST-segment elevation in 6/22 cases (27%), but the amount of ST-segment shift at peak stress was significantly reduced (from 2.15+/-0.9 to 0.30+/-0.5 mm) and angina was present in 1 patient only (5%) despite a significant increase of double product compared to the pre-revascularization test (from 17,348+/-3536 to 21,005+/-4105, p < 0.003). At echocardiographic analysis, ischaemia involved only 4 segments (2%), 3 of them showing the persistence of a biphasic response to dobutamine. CONCLUSIONS: In patients with a recent myocardial infarction and no baseline dyskinesia dobutamine-induced ST-segment elevation in the infarct-related leads is usually associated with a biphasic response of wall motion within the infarcted region and may be considered an ancillary sign of myocardial ischaemia because it is abolished in the great majority of cases by successful revascularization of the infarct-related artery.     

急性前壁心肌梗塞下壁导联ST段压低的临床意义

对44例急性前壁心肌梗塞患者,将冠脉造影结果与体表心电图ST段改变进行比较分析.结果发现急性前壁心肌梗塞患者38.6%有下壁导联ST段压低,这些导联ST段压低与多支血管病变无关,而与前降支近端病变有关,可能反映高侧壁导联心肌缺血时心电图对应性改变.     

An electrocardiographic algorithm for the prediction of the culprit lesion site in acute anterior myocardial infarction

BACKGROUND: Although the 12-lead electrocardiogram (ECG) has been found useful in identifying the left anterior descending (LAD) coronary artery as the infarct-related artery in acute myocardial infarction (MI), it has traditionally been felt to be incapable of localizing the culprit lesion within the LAD itself. Such a capability would be important, because anterior MI due to proximal LAD lesions carry a much worse prognosis than those due to more distal or branch vessel lesions. HYPOTHESIS: This study investigated whether certain ECG variables--especially an ST-segment injury pattern in leads aVL and/or V1--would correlate with culprit lesion site, and an ECG algorithm was developed to predict culprit lesion site. METHODS: The initial ECGs of 55 patients who had undergone cardiac catheterization after an anterior or lateral MI were reviewed to identify the leads with an ST-segment injury pattern; the corresponding catheterization films were then reviewed to identify the location of the culprit lesion; and these separate findings were then compared. RESULTS: The sensitivity and specificity of an ST-injury pattern in aVL in predicting a culprit lesion before the first diagonal branch were 91 and 90%, respectively; the same values in predicting a lesion prior to the first septal branch were 85 and 78%. ST-segment elevation in V1, on the other hand, was a much less sensitive and specific predictor of a preseptal lesion. Overall, our algorithm correctly identified the culprit lesion location in 82% of our patients. CONCLUSION: Based on our findings, we conclude that a ST-segment injury pattern in aVL during an anterior myocardial infarction predominantly reflects a proximal LAD lesion and therefore constitutes a high-risk finding.