Does chronic ST segment elevation following Q wave myocardial infarction exclude tissue viability?

PURPOSE: Electrocardiographic (ECG) ST segment elevation lasting 2 or more weeks following Q wave myocardial infarction has been associated with 'ventricular aneurysm' and absence of tissue viability. Regional systolic dysfunction may reflect either viable myocardium or scar. Positron emission-tomographic (PET) imaging can distinguish viable from nonviable tissue. We hypothesized that patients with chronic ST segment elevation after Q wave infarction might demonstrate salvageable myocardium in the infarct region. METHODS: The ECGs of 1,229 sequential patients undergoing PET scans for viability assessment were reviewed by an electrocardiographer to identify individuals with chronic anteroseptal Q wave infarctions with persistent ST segment elevation exceeding 1 mV. Patients with QRS duration longer than 0.14 ms or rhythm other than sinus were excluded. Viability was considered present if either a reversible stress-induced perfusion defect (ischemia) or a resting perfusion-metabolism mismatch (hibernation) was identified. RESULTS: Anteroseptal ECG Q wave infarction was identified in 132 subjects (74% male, age 61 +/- 12 years). Chronic ST segment elevation was present in 84 subjects (64%) and absent in 48. Baseline clinical characteristics and left ventricular systolic function were similar in both groups. 63% of those with and 56% of those without chronic ST elevation had viable myocardium. No relationship was noted between chronic ST segment elevation and the presence or absence of myocardial viability. CONCLUSIONS: Chronic ST segment elevation after anteroseptal Q wave myocardial infarction does not exclude myocardial viability in the 'infarct zone'. Evaluation of residual tissue viability is indicated to assess the benefit of revascularization in patients with Q wave infarction and chronic ST segment elevation.     

Correlation between ST Elevation and Q Waves on the Predischarge Electrocardiogram and the Extent and Location of MIBI Perfusion Defects in Anterior Myocardial Infarction

Background: The common electrocardiographic subclassification of anterior acute myocardial infarction (AMI) is not reliable in presenting the exact location of the infarct. We investigated the relationship between predischarge electrocardiographic patterns and the extent and location of perfusion defects in 55 patients with first anterior AMI. Methods: Predischarge electrocardiogram was examined for residual ST elevations and Q waves which were correlated with technetium‐99m‐sestamibi function and perfusion scans. Results: Patients with ST elevations in V2–V4 and Q waves in leads V3–V5 had worse global perfusion scores. Perfusion defects in the apex inferior segment were significantly less frequent in patients with Q waves in leads I and aVL (11% vs 54%, P = 0.027; and 22% vs 60%, P = 0.011, respectively). Patients with Q wave in aVF had more frequently involvement of the apex inferior segment (80% vs 40%; P = 0.035). Patients with Q wave in lead II had significantly more frequent perfusion defects in the inferior wall. ST elevation in V3 and V4 was associated with perfusion abnormalities of the infero‐septal segments. ST elevation in V5 and V6 and Q wave in V5 were associated with regional perfusion defects in apical inferior segment (73% vs 30%, P = 0.002), extending into the mid inferior segment (55% vs 18%, P = 0.005 for Q wave in V5). Q wave in lead aVL is associated with less apical and inferior involvement. Q waves in leads II and aVF are a sign of inferior extension of the infarction. Conclusions: Residual ST elevation in leads V3 and V4 are more frequently associated with involvement of the apical‐inferoseptal segment rather than the anterior wall. Residual ST elevation and Q waves in V5 are related to a more inferior rather than a lateral involvement.     

Myocardial infarction and thrombolysis. Electrocardiographic short term and long term results using precordial mapping.

In a consecutive series of 56 patients with acute myocardial infarction, ST segment depression and elevation in the electrocardiographic limb leads I, II, and III were summated for each patient before and immediately after intracoronary streptokinase infusion and the results compared with the angiographic findings. Forty three patients had angiographically confirmed reperfusion of an initially occluded vessel and showed a significant decrease in summated ST shift. The ST segment changes in the limb leads virtually returned to normal in all 43 patients, and in most, inverted T waves developed. Thrombolysis was unsuccessful in 10 patients, and the infarct related coronary artery was already patent in three. When these two groups are combined, all 13 patients without reperfusion showed no significant change in summated ST segment shift. During percutaneous transluminal angioplasty inflation of the balloon in the vessel that was previously occluded simulated reocclusion and was followed by new ST elevation if the artery supplied viable myocardium. In a further consecutive study of 54 patients with anterior myocardial infarction, the precordial R waves and Q waves were studied over the four to six months following infarction using a standardised 48 electrode mapping system. All patients underwent a repeat angiogram after four to six months. In 36 patients the infarct related vessel was patent. They showed a significant mean increase in summated precordial R wave amplitude and a reduction in the mean number of precordial leads without R waves. In 18 patients with unsuccessful thrombolysis or reocclusion there was a further reduction in mean summated R wave amplitude and an increased number of precordial leads not showing R waves. Precordial R wave mapping seems to be a valuable non-invasive method of assessing the salvage of myocardium after reperfusion and the damage caused by reocclusion. Loss of R waves in the acute phase of myocardial infarction does not necessarily mean an irreversibly damaged myocardium.     

Myocardial infarction and thrombolysis. Electrocardiographic short term and long term results using precordial mapping

In a consecutive series of 56 patients with acute myocardial infarction, ST segment depression and elevation in the electrocardiographic limb leads I, II, and III were summated for each patient before and immediately after intracoronary streptokinase infusion and the results compared with the angiographic findings. Forty three patients had angiographically confirmed reperfusion of an initially occluded vessel and showed a significant decrease in summated ST shift. The ST segment changes in the limb leads virtually returned to normal in all 43 patients, and in most, inverted T waves developed. Thrombolysis was unsuccessful in 10 patients, and the infarct related coronary artery was already patent in three. When these two groups are combined, all 13 patients without reperfusion showed no significant change in summated ST segment shift. During percutaneous transluminal angioplasty inflation of the balloon in the vessel that was previously occluded simulated reocclusion and was followed by new ST elevation if the artery supplied viable myocardium. In a further consecutive study of 54 patients with anterior myocardial infarction, the precordial R waves and Q waves were studied over the four to six months following infarction using a standardised 48 electrode mapping system. All patients underwent a repeat angiogram after four to six months. In 36 patients the infarct related vessel was patent. They showed a significant mean increase in summated precordial R wave amplitude and a reduction in the mean number of precordial leads without R waves. In 18 patients with unsuccessful thrombolysis or reocclusion there was a further reduction in mean summated R wave amplitude and an increased number of precordial leads not showing R waves. Precordial R wave mapping seems to be a valuable non-invasive method of assessing the salvage of myocardium after reperfusion and the damage caused by reocclusion. Loss of R waves in the acute phase of myocardial infarction does not necessarily mean an irreversibly damaged myocardium.     

Brief repetitive balloon occlusions enhance reperfusion during percutaneous coronary intervention for acute myocardial infarction: a pilot study.

The objective of this study was to determine whether acutely ischemic myocardium may be conditioned during percutaneous coronary intervention for acute myocardial infarction. Ischemic preconditioning is a powerful cardioprotective mechanism that limits infarct size in animal investigations and ischemic sequelae during percutaneous coronary intervention in man. However, the conditioning stimulus in all these studies has been applied prior to the defining episode of ischemia. Seventeen patients undergoing percutaneous coronary intervention for acute myocardial infarction were randomly assigned to a standard ischemic preconditioning protocol (n = 10) or a usual-care control group (n =7). ST segment shift response and Doppler-derived distal coronary velocity data were compared. Despite similar degrees of baseline ST segment elevation, the magnitude of final ST segment elevation in the conditioning group was less than that in controls at the protocol conclusion (conditioning, 1.60 +/- 0.8 mV; control, 4.0 +/- 0.5 mV; P < 0.001). The rate of ST segment resolution was greater in the conditioning group (conditioning, 0.28 +/- 0.1 mV/min; control, 0.12 +/- 0.1 mV/min; P = 0.02). Distal coronary velocimetry indicated significant improvement in coronary flow velocity reserve in the conditioning group at the protocol conclusion (conditioning, 1.8 +/- 0.2; control, 1.4 +/- 0.1; P < 0.008). Brief periods of occlusion and reperfusion during percutaneous intervention for acute myocardial infarction mitigate the extent of ischemic injury and improve distal myocardial perfusion. Such ischemic conditioning represents a potentially useful adjunct to strategies for enhancing reperfusion during acute myocardial infarction.     

The relationship between myocardial ischaemia and cell death during acute myocardial infarction.

Praecordial mapping of the electrocardiogram (ECG) demonstrated the natural history of ST segment elevation, loss of R and appearance of Q waves in 50 patients suffering uncomplicated anterior myocardial infarction. The results showed that ST segment elevation has a complicated natural history. The loss of R wave electromotive force and development of Q waves were complete by 12 h following the onset of chest pain. This evidence for the loss of viable myocardium was complete before the MB-isoenzyme of creatine kinase (MBCK) was detected in the plasma. Regression analysis of these results showed a direct relationship between the praecordial area of ST segment elevation at 2 h (myocardial ischaemia) and the praecordial area of Q waves at 24 h after the onset of symptoms (cell death). The efficacy of interventions on the natural history of myocardial infarction might be assessed by their effects on the relationship between myocardial ischaemia and cell death.     

Assessment of residual tissue viability by exercise testing in recent myocardial infarction: comparison of the electrocardiogram and myocardial perfusion scintigraphy.

The assessment of residual myocardial viability in infarcted areas is relevant for subsequent management and prognosis but requires expensive technology. To evaluate the possibility that simple, easily obtainable clinical markers may detect the presence of within-infarct viable tissue, the significance of exercise-induced ST elevation occurring in leads exploring the area of a recent Q wave myocardial infarction was assessed. Twenty-five patients with recent (less than 6 months) myocardial infarction were studied. All had angiographically documented coronary artery disease, diagnostic Q waves (n = 24) or negative T waves (n = 25) on the rest 12-lead electrocardiogram and exhibited during exercise greater than or equal to 1.5 mm ST segment elevation (n = 17) or isolated T wave pseudonormalization (n = 8) in the infarct-related leads. ST-T wave changes were reproduced in all patients during thallium-201 exercise myocardial scintigraphy. A fixed perfusion defect was observed in 24 of the 25 patients. A reversible defect was seen in 16 (94%) of 17 patients who exhibited transient ST elevation during exercise but in only 4 (50%) of the 8 patients who had only T wave pseudonormalization. In conclusion, in patients with recent myocardial infarction, analysis of simple ST segment variables obtained during exercise testing may allow a first-line discrimination of those who may potentially benefit from a revascularization procedure.     

Variability of electrocardiographic and enzyme evolution of myocardial infarction in man.

We have studied the time course of development of ST segment elevation, R wave loss, and Q wave development in 41 patients using 35 lead praecordial mapping or 12 lead electrocardiograms in those with anterior and inferior infarcts, respectively. The first recording was at a mean time of six hours after the onset of pain; subsequent records were taken every eight hours for 24 hours, every 12 hours for the second day, and every day thereafter. Serial CK MB estimates were obtained at every four hours for the first 72 hours. There was good agreement in the time course between the electrocardiogram and enzyme evolution. Forty-one per cent of patients showed rapid infarction with R wave and Q wave evolution complete within 12 hours of pain and accompanied by a short duration of enzyme release (mean = 19.30 hours). Fifty-nine per cent of patients showed more prolonged infarction with longer R wave and Q wave evolution and enzyme release (mean = 30 hours). Four patients also showed delayed reinfarction. ST segment elevation was maximal at six hours in the whole group and was significantly lower thereafter. Patients with rapid infarction showed high initial ST segment elevation which decreased promptly compared with those with prolonged infarction, who showed moderate but more persistent ST segment elevation. This study shows the variability in the time course of the electrocardiogram and enzyme evolution after myocardial infarction in man.     

Diagnostic Value of Exercise‐Induced ST‐Segment Elevation in Q‐Wave Leads. After Recent Myocardial Infarction

Background: Exercise‐induced ST‐segment elevation in an infarct territory with abnormal Q waves is a known marker for more severe left ventricular wall‐motion abnormalities. However, it is reported, that exercise‐induced ST‐segment elevation in infarct leads may indicate residual viability in the intarctregion. The aim of the study was to test whether exercise‐induced ST‐segment elevation is related to left ventricular (LV) dysfunction or to persistent viability in patients with previous myocardial infarction (MI). Methods: 145 consecutive patients (119 men, 26 women, age 58 ± 11 years) 2–3 weeks after Q‐wave Ml but without ST elevation at rest ECG were enrolled in the study. All patients underwent a target heart rate or symptom‐limited exercise testing (ET) with Bruce protocol. Exercise‐induced ST‐segment elevation < 1 mm above the baseline ST segment level (80 ms after J point) in more than 1 ECG lead with Q wave was considered to be significant. Patients were divided in two groups according to ET results: group I, 25 patients with significant exercise‐induced ST‐segment elevation and group II, 120 patients without exercise‐induced ST‐segment elevation. All patients underwent rest ECHO and low dose dobutamine stress echo (LOSE) within 7 days after ET. LV function was estimated using ejection fraction (EF). Results: More severe LV dysfunction was observed in patients from group 1 (EF 31 ± 8.16% vs EF 45 ± 10.3%). Myocardial viability (defined as an improvement of regional systolic wall thickening in the regions with resting regional wall‐motion abnormalities during LOSE 5 to 15 g/kg/min was recognized in 8 patients (32%) in group I and 31 patients (25.8%) in group II. There was no relation between exercise‐induced ST‐segment elevation and myocardial viability (chi‐square test: 2,809; NS). Conclusions: Exercise‐induced ST‐segment elevation in most cases is associated with left ventricular dysfunction. Patients with exercise‐induced ST‐segment elevation have a lower EF than those without and greater severity of resting wall‐motion abnormalities. Our results suggest that exercise‐induced ST‐segment elevation is not related to residual myocardial viability.     

Electrocardiographic localization of the occlusion site in left anterior descending coronary artery in acute anterior myocardial infarction

BACKGROUND: The site of occlusion of left anterior descending coronary artery is important in acute anterior myocardial infarction because, proximal occlusion is associated with less favorable outcome and prognosis. The present study attempted to evaluate the electrocardiographic correlate of the location of the site of the left anterior descending coronary artery occlusion with respect to first septal perforator and/or the first diagonal branch. METHODS AND RESULTS: The study included 50 patients with a first acute anterior myocardial infarction. The electrocardiogram with the most pronounced ST segment deviation before the start of reperfusion therapy was evaluated and correlated with the left anterior descending occlusion site as determined by coronary angiography. ST segment elevation in lead aVR, ST segment depression in lead V5 and ST segment elevation in V1>2.5 mm strongly predicted left anterior descending occlusion proximal to first septal, whereas abnormal Q wave in V4-6 was associated with occlusion distal to first septal. Abnormal Q wave in lead aVL was associated with occlusion proximal to first diagonal, whereas ST depression in lead aVL was suggestive of occlusion distal to first diagonal branch. For both first septal and first diagonal, ST segment depression > or =1 mm in inferior leads strongly predicted proximal left anterior descending artery occlusion, whereas absence of ST segment depression in inferior leads predicted occlusion distal to first septal and first diagonal. All the patients were followed during their in-hospital stay (median of 7 days), during which four patients in the proximal to first septal and first diagonal group and one patient in the distal to first septal and first diagonal group died (p < or = 0.001). CONCLUSIONS: In acute myocardial infarction electrocardiogram is useful to predict the left anterior descending occlusion site in relation to its major side branches and such localization has prognostic significance.     

Clinical significance of stress-induced ST segment elevation in patients with previous anterior myocardial infarction. Analysis of lactate metabolism with atrial pacing

To clarify the mechanism of stress-induced ST segment elevation in patients with previous anterior myocardial infarction, we examined myocardial lactate metabolism during atrial pacing in 32 patients with previous anterior myocardial infarction (MI group) and 11 control subjects (control group). In the MI group, atrial pacing resulted in new or additional ST segment elevation in leads with Q waves in 15 patients (ST elevation group), ST segment depression in 7 (ST depression group), but induced no appreciable ST segment changes in the remaining 10 patients (ST unchanged group). In all patients, the ST segment changes were identical to the results of exercise stress testing which was carried out prior to the atrial pacing. Lactate extraction ratio increased moderately during the atrial pacing in the control group (p less than 0.01). Although marked reduction of the myocardial lactate extraction ratio was noted in the ST depression group (p less than 0.05), no significant change in the ratio was evoked in the ST elevation group or the ST unchanged group during atrial pacing. Left ventricular end-diastolic pressure (LVEDP) increased markedly in the ST depression group during atrial pacing, but the elevation was less evident in the other groups. The ST elevation group demonstrated the lowest left ventricular ejection fraction and the severest degree of left ventricular asynergy. Thus, the present study indicates that aggravated left ventricular asynergy in the infarcted area and associated left ventricular dysfunction, rather than peri-infarction zone ischemia is a possible mechanism of stress-induced ST segment elevation in leads with Q waves following previous anterior myocardial infarction.     

Electrocardiographic findings in acute right ventricular infarction: sensitivity and specificity of electrocardiographic alterations in right precordial leads V4R, V3R, V1, V2, and V3

To determine the sensitivity, specificity, predictive value and diagnostic efficiency of electrocardiographic alterations in the diagnosis of acute right ventricular infarction, 43 autopsy patients with acute myocardial infarction and an electrocardiogram including 12 leads plus leads V3R and V4R were studied. Group A included 21 patients with right ventricular infarction, of whom 14 (group AI) had posterior and 7 (group AII) had anterior right ventricular infarction. Group B included 22 patients without right ventricular infarction. Excluding group AII patients, the sensitivity of the presence of a Q wave reached 78.6% in lead V4R and decreased in leads V1 to V3; its specificity was low in all the leads. The sensitivity of ST segment elevation reached 100% in lead V4R and decreased in leads V1 to V3; its specificity was highest (68.2%) in leads V4R and V3R, its negative predictive value was 100% and its diagnostic efficiency was 80.6%. The criterion of ST segment elevation in lead V4R being higher than that in leads V1 to V3 was less sensitive (78.6%) than ST segment elevation in lead V4R alone, but its specificity reached 100%, its positive predictive value 100% and its diagnostic efficiency 91.7%. In conclusion, there are no electrocardiographic criteria to identify anterior right ventricular necrosis, but posterior right ventricular necrosis may be identified by the presence of a Q wave or ST segment elevation in the right precordial leads, reaching the highest sensitivity and specificity in lead V4R. The criterion of ST segment elevation in lead V4R being higher than that in leads V1 to V3 offers the highest specificity and efficiency in the diagnosis.     

The significance of stress-induced ST segment depression in patients with inferior Q wave myocardial infarction

OBJECTIVES

This study was conducted to evaluate the relationship between ST segment depression (STD) during dobutamine stress tests in different electrocardiogram (ECG) leads and myocardial ischemia assessed by simultaneous single photon emission computed tomography (SPECT) imaging in patients with inferior Q wave myocardial infarction.

BACKGROUND

STD is a standard electrocardiographic sign of myocardial ischemia. Although STD may represent reciprocal changes in patients with previous myocardial infarction, studies of reciprocal changes during stress tests are scarce.

METHODS

Dobutamine (up to 40 μg/kg/min) stress and rest myocardial perfusion scintigraphy using technetium SPECT imaging was performed in 125 patients >3 months after Q wave inferior myocardial infarction. The location of STD at the ECG was defined as anterior (V_1–4), high lateral (I, aVL) and lateral (V_5,6). Ischemia was defined as reversible perfusion abnormalities.

RESULTS

STD occurred in the high lateral leads in 20 patients, in the anterior leads in 12 patients and in the lateral leads in 2 patients. ST segment elevation occurred in 25 patients in the inferior leads. High lateral STD was associated with inferior ST elevation in 16 patients (80%). There was a significant inverse linear correlation between the magnitude of ST segment shift from rest to peak stress in the inferior and the high lateral leads (r = −0.8, p < 0.0005), whereas no significant correlation was found between ST segment shift in the inferior and the anterior leads (r = −0.1, p = NS) or between the inferior and the lateral leads (r = 0.15, p = NS). Ischemia was detected in 45% of patients with and in 42% of patients without high lateral STD (p = NS). Patients with high lateral STD had a higher prevalence of fixed perfusion defects in the inferior wall (100% vs. 70%) and in the posterolateral wall (55% vs. 29%) compared with other patients (both p < 0.05). Ischemia was more prevalent in patients with anterior STD than without (75% vs. 39%, p < 0.05).

CONCLUSIONS

In patients with inferior Q wave myocardial infarction, stress-induced STD in high lateral leads should be recognized as a reciprocal change for ST elevation in the inferior leads, and therefore, should be interpreted with the consideration of the significance of ST elevation if present, rather than being indicative of myocardial ischemia on its own. The STD found in the anterior leads appears to be a sign of myocardial ischemia. These findings should be considered in the definition of a positive ECG stress test and in establishing the criteria for the termination of stress test.     

Giant R wave, convex ST-segment elevation, and negative T wave during exercise treadmill test

The giant R wave syndrome is characterized by giant R wave accompanied by widening of the QRS complex, marked ST segment elevation, QRS axis deviation, and the formation of monophasic QRS-ST complex with obliteration of S wave in leads facing the ischemic zone. This report describes a 65-year-old-man with variant angina who had a transient giant R wave syndrome during an exercise treadmill test. Initially, at peak exercise, there was a convex ST segment elevation ending in a negative T wave in the same (inferior) leads which showed giant R waves. Later, in the recovery period and coinciding with an amelioration of myocardial ischemia, there was a less marked increase of R wave amplitude associated with concave ST segment elevation and positive T wave in the inferolateral leads. Subsequently, a ST segment depression in the inferolateral leads preceded the ECG normalization. The patient had also a concave ST segment elevation and positive T wave in inferolateral leads during a spontaneous episode of variant angina at rest. An emergency coronary arteriography showed a dominant right coronary artery with an 80% and a 75% diameter stenosis of the middle and distal segment, respectively; the other arteries and left ventriculogram were normal. The underlying mechanisms of the different shapes of ST segment elevation and T waveform in the setting of acute transmural myocardial ischemia are discussed.     

头胸导联右胸心电图诊断急性右室梗塞的价值

选择急性下壁合并右室梗塞（依据血液动力学诊断）患者３４例，比较其同部位、同时间右胸Ｗｉｌｓｏｎ导联（Ｖ３Ｒ～Ｖ７Ｒ）和头胸导联（ＨＶ３Ｒ～ＨＶ７Ｒ）的心电图，探讨后者诊断急性右室梗塞的价值。首次记录心电图的时间为发病１０（平均４±２．８）ｈ２４例（Ａ组），超过１０（平均３１±１６．８）ｈ１０例（Ｂ组），两组Ｖ５Ｒ～Ｖ７Ｒ、ＨＶ５Ｒ～ＨＶ７Ｒ导联病理性Ｑ波出现率均为１００％。Ｖ４Ｒ（ＨＶ４Ｒ）或Ｖ７Ｒ（ＨＶ７Ｒ）ＳＴ段抬高≥０．１ｍＶ者，Ａ组为１００％，Ｂ组Ｗｉｌｓｏｎ导联为６０％、头胸导联为１００％。头胸导联ＳＴ段抬高幅度高于Ｗｉｌｓｏｎ导联０．０５～０．１５ｍＶ；头胸导联不仅ＱＲＳ－Ｔ波群呈现急性损伤期向充分发展期的衍变与ａＶＦ导联一致，并且ＳＴ段抬高持续的时间也与ａＶＦ导联一致，此特征有利于急性右室梗塞的诊断。     

首次急性ST段抬高与非ST段抬高心肌梗死患者临床及冠状动脉病变特点比较

目的回顾性分析比较首次发生急性ST段抬高心肌梗死与非ST段抬高心肌梗死的临床及冠状动脉病变的特点。方法选择首次急性ST段抬高心肌梗死患者50例(ST段抬高组)和急性非ST段抬高心肌梗死患者50例(非ST段抬高组),均行冠状动脉造影检查,对其发病特点、临床表现、并发症、心功能以及冠状动脉病变进行回顾性分析。结果 ST段抬高组起病急,主要以剧烈胸痛为主,就诊时间较早,非ST段抬高组首发症状多样。ST段抬高组总并发症、室性心律失常、窦性心动过缓及传导阻滞发生率明显高于非ST段抬高组(P<0.01),左心室射血分数明显低于非ST段抬高组(P<0.05)。与ST段抬高组比较,非ST段抬高组冠状动脉病变血管支数较多,3支病变、侧支循环比例较高(P<0.05,P<0.01)。结论急性ST段抬高心肌梗死起病急,并发症多,影响心功能,应积极尽快实施血运重建,以开通梗死相关血管,但急性非ST段抬高心肌梗死冠状动脉病变往往较重。急性心肌梗死的近期预后与起病急缓、透壁性心肌坏死范围等有关。     

Electrocardiographic alterations in leads V1 to V3 in the diagnosis of right and left ventricular infarction

As Q wave and ST segment elevation in leads V1 to V3 may be due either to right ventricular infarction (RVI) or to anterior left ventricular infarction (ALVI), 72 autopsy patients with acute myocardial infarction who had had conventional 12-lead ECG records were studied to determine the accuracy of these ECG criteria, both for the diagnosis of RVI (29 patients, group A) and of ALVI (43 patients, group B). The accuracy of three ECG criteria (Q wave, ST segment elevation greater than or equal to 0.05 mV, and ST segment elevation greater than or equal to 0.1 mV) in diagnosing group A and group B patients was determined in each precordial lead (V1, V2, and V3) and the three criteria were found to be significantly more accurate in diagnosing group B than group A patients. In conclusion, although Q wave and ST segment elevation in leads V1, V2, and V3 may be present in some cases of RVI, their accuracy is too low to be considered useful diagnostic criteria in these patients.     

急性心肌梗死墓碑形ST段抬高的临床意义

目的探讨急性心肌梗死（acute myocardial infarction，AMI）墓碑形ST段抬高的临床意义。方法将86例AMI患者以ST段抬高的特征分为两组，墓碑形抬高组36例、其他形抬高组50例。观察两组的一般临床资料（年龄、有否合并糖尿病），并比较两组AMI的发生部位、PCI前心梗后心绞痛、并发症及死亡的发生率、首次CK值、各项心电指标及PCI后心肌缺血再灌注损伤的发生率。结果两组各项临床指标及心电图指标差异均有统计学意义；墓碑形ST段抬高组PCI后心肌缺血再灌注损伤的发生率亦明显高于其他形ST段抬高组。结论墓碑形ST段抬高患者梗死部位特殊而广泛、并发症多、死亡率高、易出现心肌缺血再灌注损伤，对此类患者应高度重视并积极预防心肌缺血再灌注损伤的发生。     

ST段早期恢复反映急性心肌梗死溶栓治疗后心肌再灌注

目的 比较溶栓再通后早期ST段恢复与未恢复者住院期间临床结局的差异，探讨ST段早期恢复在心肌再灌注中的作用。方法 108例溶栓经酶学等指标临床判定再通的急性心肌梗死（AMI）患者，按照有无早期（溶栓后2h)ST段恢复分为两组。连续测定血清肌酸激酶（CK）水平，了解心肌酶峰出现时间及峰值；放射性核素评估左心室功能。观察4周住院期间充血性心力衰竭（CHF）、室壁瘤、心肌梗死后心绞痛发生情况及病死率。结果 无论是前壁MI还是下壁MI，ST段早期恢复组左心室射血分数均高于未恢复组（P＜0．05）；CK峰值则低于未恢复组（P＜0．05）。住院期间ST段恢复组核素心肌显像充盈缺损、CHF及室壁瘤发生率低，心肌梗死后心绞痛发生率高（P值均小于0.05)。结论 同ST段未恢复组相比，溶栓再通后ST段早期恢复者临床预后好。心电图模式可以反映再灌注程度。     

梗死性室性异位心搏的临床及心电学特点

探讨梗死性室性异位心搏 (IVEB)的临床及心电学特点。对 2 4例在急性心肌梗死 (AMI)时出现IVEB的患者与同期住院的 71例无IVEB的AMI患者进行回顾性对照分析 ,并比较IVEB和同期与梗死充分进展期窦性心律的QRS ST T波群形态学改变。结果 :①IVEB的QRS波常呈右束支阻滞形态 (RBBBM) ,除Q波型AMI外 ,非Q波型AMI亦可发生IVEB ;②下 (后 )壁伴或不伴右室AMI、大面积AMI、梗死后心功能差、梗死早期 (<6h)及接受溶栓治疗冠状动脉再通者易发生IVEB ;③与同期窦性心律比较 ,IVEB梗死导联Q波出现及ST段抬高提早 ,且更具有AMI的特征 ;④IVEB可发生于心肌酶谱升高及窦性心律典型AMIECG图形出现之前 ,其对AMI的早期诊断及定位优于同期窦性心律。结论 :IVEB并非罕见 ,它有利于AMI的早期诊断与定位