急性前壁心肌梗死后T波的动态变化与心肌损害和左心室功能关系

目的 :探讨急性心肌梗死 (AMI)后T波的动态变化与心肌损害和左室功能之间的关系。方法 :6 2例前壁Q波型AMI患者 ,其中T波由倒置转为直立 ,即T波正常化 39例 (<3个月 6例 ,>3～ 6个月 14例 ,6～12个月 19例 ) ;T波持续直立 5例 ;T波持续倒置 18例。AMI后常规记录 12导联心电图。采用二维超声心动图、彩色心室壁动力分析和超声学定量 (AQ)技术检测室壁运动和左心室收缩功能状况。结果 :T波持续倒置组血浆肌酸激酶 (CK)峰值和心室壁运动得分指数 (WMSI)明显高于T波直立组 ,而左心室短轴缩短率 (FS)、峰值排空率 (PER)和射血分数 (EF)显著低于T波持续直立组 ;且T波正常化越早左心功能恢复得越好。T波持续直立组血浆CK峰值、WMSI均高于T波直立各亚组和T波持续倒置组 ,而FS、EF和PER均显著低于各亚组。结论 :AMI后 12个月异常Q波导联的T波动态变化能用于评价左心室的局部和整体收缩功能     

Spontaneous normalization of negative T waves in infarct-related leads reflects improvement in left ventricular wall motion even in patients with persistent abnormal Q waves after anterior wall acute myocardial infarction.

This study aimed to clarify whether spontaneous T-wave normalization (TWN) in infarct-related leads reflects improvement in left ventricular (LV) wall motion even in patients with persistent abnormal Q waves after acute myocardial infarction (AMI). Eighty-five patients were classified into the following 3 groups: patients with Q-wave regression (group A, n = 21), those with persistent abnormal Q waves and TWN (group B, n = 36), and those with persistent abnormal Q waves and absence of TWN (group C, n = 28). Groups A and B had greater improvement in LV ejection fraction and regional wall motion between 1 and 6 months after AMI than group C. In conclusion, spontaneous TWN in the healing stage of anterior AMI reflects functional recovery of viable myocardium in the infarct region even in patients with persistent abnormal Q waves.     

Residual exertional ischemia and unfavorable left ventricular remodeling in patients with systolic dysfunction after anterior myocardial infarction

Objectives. This study investigated whether exercise-induced myocardial ischemia influences left ventricular remodeling after anterior myocardial infarction.

Background. The effects of acute and recurrent ischemia on ventricular function are well established. However, to our knowledge the role of exertional ischemia in the remodeling response after infarction has not been investigated.

Methods. Ninety-one patients with a first anterior Q wave myocardial infarction were studied at 5 weeks by rest echocardiography and exercise scintigraphy. The echocardiographic examination was repeated 6 months later. On the basis of the presence and extent of reversible perfusion defects on exercise scintigraphy, patients were assigned to groups with no exertional ischemia (group 1, n = 20 [22%]), mild to moderate ischemia (group 2, n = 45 [49%]) and severe exertional ischemia (group 3, n = 26 [29%]).

Results. Initial left ventricular volumes were similar, and no differences were found among the three groups in the remodeling response over the 6-month period of the study. However, patients in groups 2 and 3 with an ejection fraction ≤40% showed significant (p < 0.01) ventricular enlargement over time, which was similar between the two groups (end-diastolic volume [mean ± SD] from 74 ± 13 to 80 ± 17 ml/m² in group 2 and from 72 ± 11 to 81 ± 19 ml/m² in group 3; regional dilation from 42 ± 16% to 52 ± 22% in group 2 and from 38 ± 18% to 46 ± 27% in group 3). In contrast, ventricular dimensions did not change in group I patients with an ejection fraction ≤40% as well as in patients in all three groups with an ejection fraction >40%.

Conclusions. Exercise-induced myocardial ischemia may contribute to progressive ventricular enlargement in patients with poor left ventricular function after a large interior myocardial infarction.     

Left ventricular wall motion with and without Q-wave disappearance after acute myocardial infarction

Since post-acute myocardial infarction (AMI) Q waves may disappear independent of reinfarction or development of left bundle branch block, the relation between the presence of Q waves and segmental asynergy was assessed in 58 patients with initial Q waves after first AMI. Two-dimensional (2-D) echocardiograms and electrocardiograms were recorded 1 year later. By electrocardiography, 28 had anterior and 25 inferior AMI. At 1 year Q waves had disappeared in 12 of 53 patients (23%): 5 with anterior and 7 with inferior AMI. Segmental asynergy, however, was present in 9 of these 12 patients, although dyskinesia was absent. Presence of Q waves at 1 year (41 patients) was always associated with segmental asynergy. Wall motion score, based on degree of segmental asynergy, was higher in the 41 patients with Q waves compared with patients in whom Q waves disappeared (7.8 +/- 4.4 vs 2.7 +/- 1.9, p less than 0.001). In patients with anterior AMI the number of Q waves at 1 year and the grade of asynergy were correlated. Segmental dyskinesia was rare in patients with inferior AMI (1 of 25) but was common in those with anterior AMI (18 of 28), and was consistently present in patients with more than 2 anterior Q waves.     

Pathologic implications of restored positive T waves and persistent negative T waves after Q wave myocardial infarction

Objectives. We sought to study the pathologic implications of restored positive T waves and persistent negative T waves in the chronic stage of Q wave myocardial infarction.Background. Some inverted T waves (coronary T waves) become positive after acute myocardial infarction: others retain their negative T wave component for a long time. The pathologic implications of the difference between restored positive T waves and persistent negative T waves in leads with Q waves has not, until now, been given much careful study.Methods. Of 17 patients with anterior or anteroseptal myocardial infarction confirmed by autopsy, 8 (group P) had positive and 9 (group N) had negative T waves in precordial leads with Q waves ≥ 1 year after the onset of myocardial infarction. The appearance and extent of the infarct area and the degree of coronary artery stenosis were evaluated in both groups.Results. At autopsy, seven of eight patients in group P had nontransmural fibrotic changes in the anteroseptal or anterior wall. However, seven of nine patients in group N had a transmural myocardial infarction consisting of only a thin fibrotic layer in the anteroseptal or anterior wall. The left anterior descending coronary artery showed 75% stenosis in 1 patient in each group but >90% stenosis in the remaining 15 patients.Conclusions. Persistent negative T waves in leads with Q waves in the chronic stage of myocardial infarction indicate the presence of a transmural infarction with a thin fibrotic layer, whereas positive T waves indicate a nontransmural infarct containing viable myocardium within the layer.     

Exercise training without ventricular remodeling in patients with moderate to severe left ventricular dysfunction early after acute myocardial infarction

BACKGROUND: The purpose of this study was to determine whether or not patients with moderate to severe left ventricular (LV) dysfunction benefit from exercise training starting early after acute myocardial infarction (AMI) without deteriorating LV remodeling. METHODS: We investigated changes in exercise capacity and LV end-diastolic dimension (LVDd by two-dimensional echocardiography) before and after exercise training in 126 patients after AMI. Patients were divided into three groups according to LV ejection fraction (EF) at the beginning of exercise training: 74 patients with LVEF>/=45% (Group H), 35 patients with 35%相似文献   

Relation between left ventricular dysfunction and ventricular arrhythmias after myocardial infarction

Ventricular arrhythmias occurring in the coronary care unit are not good predictors of ventricular arrhythmias or death during follow-up. However, arrhythmias detected by 24-hour electrocardiographic recordings at the time of hospital discharge are predictive of mortality over the subsequent 2 years. At discharge, only about 20% of patients have significant ventricular arrhythmias, defined as frequent or repetitive ventricular premature depolarizations. Using programmed ventricular stimulation, which can detect significant ventricular arrhythmias in patients with very little ectopy in 24-hour electrocardiographic recordings, 20% of patients have ventricular tachycardia 2 to 6 weeks after acute myocardial infarction (AMI). Both diastolic left ventricular (LV) dysfunction in the coronary care unit (i.e., rales or pulmonary congestion) and systolic LV dysfunction (i.e., LV ejection fraction) during hospitalization for AMI are potent predictors of mortality. Two large prospective studies examining the relations between LV dysfunction, ventricular arrhythmias and mortality concluded that mechanical dysfunction and ventricular arrhythmias are independently related to mortality. This finding provides a rationale for treating patients with frequent or repetitive ventricular arrhythmias detected near the time of hospital discharge after AMI. However, no study has yet examined whether reducing ventricular arrhythmias with antiarrhythmic drugs after AMI also reduces mortality. Lacking an answer to this question and given the frequency of adverse effects with antiarrhythmic drugs, most physicians are conservative in the treatment of patients with ventricular arrhythmias after AMI.     

Q波型与非Q波型心肌梗死患者的近期预后

为探讨心肌梗死有无Ｑ波对近期预后的影响，随诊７８例无Ｑ波型心肌梗死（ＮＱＭＩ）和２２４例Ｑ波型心肌梗死（ＱＭＩ）患者，随诊以死亡为终点或随诊至患病后６个月。两组相比：１．院内死亡率分别为２．５６％和１３％（Ｐ〈０．０１），２．Ｋａｐｌａｎ－Ｍｅｉｅｒ曲线６个月生存率分别为９４．９％和８１．５％（时距检验Ｐ〈０．０１），６个月无心脏再发缺血事件发生分别为８５．５％和６９．１％（时距检验Ｐ〈０．０１）     

Alcohol consumption and prognosis in patients with left ventricular systolic dysfunction after a myocardial infarction

OBJECTIVES: We assessed the influence of alcohol intake on the development of symptomatic heart failure (HF) in patients with left ventricular (LV) dysfunction after a myocardial infarction (MI). BACKGROUND: In contrast to protection from coronary heart disease, alcohol consumption has been linked to cardiodepressant effects and has been considered contraindicated in patients with HF. METHODS: The Survival And Ventricular Enlargement (SAVE) trial randomized 2231 patients with a LV ejection fraction (EF) <40% following MI to an angiotensin-converting enzyme inhibitor or placebo. Patients were classified as nondrinkers, light-to-moderate drinkers (1 to 10 drinks/week), or heavy drinkers (>10 drinks/week) based on alcohol consumption reported at baseline. The primary outcome was hospitalization for HF or need for an open-label angiotensin-converting enzyme inhibitor. Analyses were repeated using alcohol consumption reported three months after MI. RESULTS: Nondrinkers were older and had more comorbidities than light-to-moderate and heavy drinkers. In univariate analyses, baseline light-to-moderate alcohol intake was associated with a lower incidence of HF compared with nondrinkers (hazard ratio [HR] 0.71; 95% confidence interval [CI] 0.57 to 0.87), whereas heavy drinking was not (HR 0.91; 95% CI 0.67 to 1.23). After adjustment for baseline differences, light-to-moderate baseline alcohol consumption no longer significantly influenced the development of HF (light-to-moderate drinkers HR 0.93; 95% CI 0.75 to 1.17; heavy drinkers HR 1.25; 95% CI 0.91 to 1.72). Alcohol consumption reported three months after the MI similarly did not modify the risk of adverse outcome. CONCLUSIONS: In patients with LV dysfunction after an MI, light-to-moderate alcohol intake either at baseline or following MI did not alter the risk for the development of HF requiring hospitalization or an open-label angiotensin-converting enzyme inhibitor.     

Sudden cardiac death early after ST elevation myocardial infarction with and without severe left ventricular dysfunction

Introduction

There is high incidence of SCD in the early period following STEMI. We compared the temporal patterns and predictors of SCD amongst patients with LVEF ≤35% and LVEF >35%.

Methods

Data from STEMI patients was prospectively collected. SCD cases formed the study cohort and were categorized into 2 groups based on their LV function.

Results

There were 929 patients (mean age 55 ± 17 years) with a follow up of 41 ± 16 months. 154 pts (16.6%) had LVEF ≤35% (Group A, LVEF-29.9% ± 6%) and 775 pts had LVEF >35% (Group B, LVEF – 49% ± 14%). The two groups were similar with respect to sex distribution, age, prevalence of hypertension, and mean period of presentation. They differed in incidence of anterior wall MI (77.2% vs 55%), reperfusion (69% vs. 75%), prevalence of diabetes (50.6% vs 42%), and medication non-compliance (34% vs. 13%). The total SCD was 78 [Gp A, 25 (16.2%); Gp B, 53 (6.8%); p < 0.001]. The temporal cumulative SCD related mortality in the 2 groups was 1st month (8% vs. 4% p = 0.075), 3 months (14% vs. 5%, p < 0.001), 6 months (17% vs. 5%, p < 0.001), 1 year (18% vs. 6%, p < 0.001), at end of follow up (27% vs. 8%, p < 0.001). Multivariate predictors of SCD were medication compliance in the first month, and severe LV dysfunction with medication compliance beyond 1st month.

Conclusion

The incidence of SCD is high in first month after STEMI, irrespective of LV function. The number of SCD is higher in Group B patients. Algorithms to assess risk of SCD in early post STEMI period are urgently needed.     

Deep negative T waves associated with reversible left ventricular dysfunction in acute adrenal crisis

We report two cases of reversible left ventricular dysfunction associated with deep negative T waves during acute adrenal crisis due to isolated deficiency of adrenocorticotrophic hormone. There were no symptoms suggestive of heart disease in either case and left ventricular wall motion abnormalities, present mainly around the left ventricular apex, returned to normal in 1–2 weeks. Deep negative T waves normalized 4 weeks after corticosteroid administration. Acute adrenal crisis should be considered when deep negative T waves are associated with left ventricular dysfunction without cardiac symptoms.     

Left ventricular thrombosis after anterior myocardial infarction with and without thrombolytic treatment

Abstract. Objectives. To examine the incidence of left ventricular thrombus in patients with anterior myocardial infarction, with and without streptokinase treatment. To identify predictors of thrombus development. Design. Consecutive patients prospectively studied during the hospitalized period. Echocardiography was performed within 3 days of admission and before discharge. Setting. Umeå University Hospital, a teaching hospital in Northern Sweden. Subjects. Ninety-nine patients with anterior myocardial infarction of whom 74 were treated with streptokinase. Main outcome measures. Left ventricular thrombus and left ventricular segmental myocardial function. Results. During the hospital stay, a thrombus developed in 46% (95% confidence interval [CI], 35–57%) of the patients in the thrombolysis group and in 40% (95% CI, 21–59%) of the patients in the non-thrombolysis group. No difference in left ventricular segmental myocardial function was found between the thrombolysis and non-thrombolysis groups at hospital discharge. No embolic events were observed. The occurrence of a left ventricular thrombus at hospital discharge was significantly associated with previous myocardial infarction, peak enzyme levels, left ventricular global and segmental dysfunction and an increased dose of peroral diuretics or use of parenteral diuretics. In a multiple logistic regression model, left ventricular segmental dysfunction was the most important predictor of left ventricular thrombus. Conclusion. Thrombolytic treatment with streptokinase does not prevent the development of a left ventricular thrombus but the risk of embolic complications is low. The left ventricular segmental myocardial score can be used to assess the risk of thrombus development, also, after thrombolysis.     

Reversible left ventricular dysfunction simulating a myocardial infarction after pericardiectomy

A 39 year old man with postoperative constrictive pericarditis after pericardiectomy developed major left ventricular systolic dysfunction with an anterior wall infarct pattern on ECG but no regional wall motion abnormalities by echocardiography or serum enzymatic evidence of a myocardial infarction. The left ventricular dysfunction resolved over two weeks with supportive treatment. It is postulated that this patient's transient left ventricular dysfunction and ECG changes were caused by myocardial inflammation and oedema induced by operative trauma during pericardiectomy.     

Cell therapy in patients with left ventricular dysfunction due to myocardial infarction

Objectives: The purpose of this study was to determine the impact of autologous transplantation of mononuclear bone marrow cells on myocardial function in patients with left ventricular (LV) dysfunction due to an acute myocardial infarction. Methods: The randomized study included 82 patients with a first acute myocardial infarction treated with a stent implantation. This presentation is a subanalysis of 47 patients with left ventricular dysfunction–EF (ejection fraction) ≤ 40%. Group H patients (n = 17) received higher number (100,000,000) of cells; Group L patients (n = 13) received lower number (10,000,000) of cells. The patients of control Group C (n = 17) were not treated with cells. The Doppler tissue imaging and single photon emission computed tomography were performed before cell transplantation and 3 months later. Results: At 3 months of follow‐up, the baseline EF of 35%, 36%, 35% in Groups H, L, and C increased by 6% (P < 0.01 vs. baseline), 5% (P < 0.01 vs. baseline), and 4% (P = NS vs. baseline), respectively, as assessed by single photon emission computed tomography (P = NS between groups). The baseline number of akinetic segments of 6.9, 7.0, and 6.2 in H, L, and C groups decreased by 1.7 (P < 0.01 vs. baseline), 1.5 (P < 0.01 vs. baseline), and 0.7 (P = NS vs. baseline, P = NS between groups), respectively, as demonstrated by echocardiography. Conclusion: In our study, the statistically important effect of transplantation of mononuclear bone marrow cells on myocardial function was not found. Only an insignificant trend toward the improvement of global LV EF fraction was found at 3‐month follow‐up.     

Significance of Q-wave regression after anterior wall acute myocardial infarction

Aims This study was conducted to clarify the significance of abnormalQ-wave regression in anterior wall acute myocardial infarction. Methods A total of 74 patients who presented with a first anterior wallacute myocardial infarction within 6h of onset were dividedinto two groups according to the presence (group A, n=29) orabsence (group B, n=45) of regression of abnormal Q waves. Regressionof abnormal Q waves was defined as the disappearance of theQ wave and the reappearance of the r wave 0·1mV in atleast one of leads I, aVL, and V₁to V₆. Results Emergency coronary arteriography revealed that group A had ahigher incidence of spontaneous recanalization or good collateralcirculation than group B (55% vs 31%,P<0·05). Peakcreatine kinase activity tended to be lower in group A thanin group B (2358±1796 vs 3092±1946IU.L^–1,P=0·09).Group A had a greater left ventricular ejection fraction andbetter regional wall motion at 1 and 6 months after acute myocardialinfarction than group B. The degree of improvement of left ventricularejection fraction and regional wall motion between 1 and 6 monthsafter acute myocardial infarction was significantly greaterin group A than in group B. Conclusion Patients with anterior wall acute myocardial infarction showingQ-wave regression had a trend towards a smaller amount of necroticmyocardium and a significantly larger amount of stunned myocardium.     

Left coronary artery spasm causing severe left ventricular dysfunction without myocardial infarction

This report describes a patient with persistent, recurrent left anterior descending coronary artery spasm, which causes marked left ventricular dysfunction in a clinical course that is typical of acute myocardial infarction with hyperacute electrocardiographic changes. However, after emergency coronary artery bypass surgery, the patient had complete reversal of left ventricular dysfunction, with no residual evidence of acute myocardial infarction by electrocardiograph or gated blood pool imaging and no CPK enzyme rise. The patient therefore demonstrates that coronary spasm in some instances clearly precedes the sequence of pathophysiologic events leading to acute myocardial infarction. Our report also demonstrates for the first time in man that massive left ventricular dysfunction may occur in this intermediate coronary syndrome, presenting clinically as impending myocardial infarction. With aggressive surgical intervention and emergency bypass surgery, left ventricular function was restored to normal. Despite the semantic problems of categorizing such patients as having impending myocardial infarction, the severe left ventricular dysfunction and alarming course of this patient's illness was resolved by emergency surgery, suggesting that, in some instances, aggressive therapy is warranted.     

Stress-induced ST-segment elevation in patients without prior Q-wave myocardial infarction

Background

Stress-induced ST-segment elevation is an uncommon finding that usually occurs in patients with prior myocardial infarction (MI). Our purpose was to assess the angiographic and clinical significance of this finding in patients without prior MI.

Methods

Of the 29 002 consecutive ambulatory patients who underwent stress myocardial perfusion imaging over a 5-year period, 205 (0.7%) developed stress-induced ST-segment elevation, of whom 39 (19%) had no Q-wave MI in leads showing ST-segment elevation during either exercise (n = 31) or dipyridamole (n = 8) stress myocardial perfusion imaging. All 39 patients were hospitalized and underwent coronary angiography.

Results

Significant coronary artery disease was found in all 39 patients: 87% had critical (≥90%) stenosis, and 59% had multiple vessel disease. During hospitalization, 37 patients (95%) underwent revascularization.

Conclusions

In patients without prior Q-wave MI, stress-induced ST-segment elevation is associated with critical coronary artery disease. Therefore, these patients should be considered for early coronary investigation.