Coronary flow velocity immediately after primary coronary stenting as a predictor of ventricular wall motion recovery in acute myocardial infarction

OBJECTIVES

The purpose of this study was to examine the relationship between the pattern of coronary blood flow velocity immediately after successful primary stenting and the recovery of left ventricular (LV) wall motion in patients with acute myocardial infarction (AMI).

BACKGROUND

It is difficult to predict the recovery of LV wall motion immediately after direct angioplasty in AMI. Recent reports indicate that dysfunctional coronary microcirculation is an important determinant of prognosis for AMI patients after successful reperfusion.

METHODS

We measured left anterior descending coronary flow velocity variables using a Doppler guide wire immediately after successful primary stenting in 31 patients with their first anterior AMI. The patients were divided into two groups: those with and those without early systolic reverse flow (ESRF). Changes in LV regional wall motion (RWM) and ejection fraction (EF) at admission and at discharge were compared between the two groups. Coronary flow velocity variables immediately after primary stenting were compared with changes in left ventriculographic indexes.

RESULTS

The change in RWM was significantly greater in the non-ESRF group than it was in the ESRF group (0.9 ± 0.7 vs. −0.1 ± 0.3 standard deviation/chord, respectively, p < 0.001). The change in EF was also significantly greater in the non-ESRF group than it was in the ESRF group (10 ± 10 vs. 1 ± 6%, respectively, p < 0.05). In the non-ESRF group (diastolic to systolic velocity ratio [DSVR] <3.0), the DSVR correlated positively with the change in RWM (r = 0.60, p < 0.005, n = 24) and the change in EF (r = 0.52, p < 0.01).

CONCLUSIONS

The coronary flow velocity pattern measured immediately after successful primary stenting is predictive of the recovery of regional and global LV function in patients with AMI.     

急性前壁心肌梗死伴不同下壁导联ST段改变的临床特点

目的探讨ST段抬高急性前壁心肌梗死(简称心梗)伴不同下壁导联ST段改变患者的梗死相关血管以及梗死面积及心功能情况。方法73例急性前壁心梗患者,根据入院时心电图下壁导联ST段改变情况将患者分为3组:A组为Ⅱ、Ⅲ、aVF中至少两个导联ST段抬高;B组为Ⅱ、Ⅲ、aVF中至少两个导联ST段压低,C组为Ⅱ、Ⅲ、aVF中少于两个导联ST段有改变。比较三组CK最大值,左室射血分数以及梗死相关血管(IRCA)。结果CK最大值3组比较A组最低(1280±531IU/Lvs2034±911,1677±630IU/L,P<0.01);左室射血分数A组最高(0.54±0.09vs0.48±0.07,0.47±0.08,P<0.01);三组IRCAA组中85.7%的患者位于“绕过心尖的左前降支(LAD)”的中远段,有14.3%的患者位于右冠状动脉(RCA)的近段;B组的患者中全部为非“绕过心尖的LAD”,其中有70.4%的患者位于非“绕过心尖的LAD”的近段;C组中有96.7%的患者为非“绕过心尖的LAD”,其中有73.3%的患者位于非“绕过心尖的LAD”的近中段,三组比较差异有显著性(P<0.01)。结论IRCA为LAD的急性前壁心梗时下壁ST段改变可能与LAD长度和病变部位有关;前壁合并下壁ST段同时抬高的患者若IRCA为“绕过心尖的LAD”,其梗死面积较小,心功能较好。     

急性心肌梗死后左心室游离壁破裂患者临床特点分析

目的探讨急性心肌梗死(acute myocardial infarction,AMI)后发生左心室游离壁破裂(free wall rupture,FWR)患者的临床特点及危险因素。方法入选2010年12月至2018年12月南京医科大学附属南京医院明确诊断为AMI的患者4221例,其中发生FWR的患者81例(FWR组),按照1:5匹配原则,随机选取未发生心脏破裂(且未发生室间隔穿孔)的患者405例作为非FWR组,比较两组患者临床基线资料及预后。结果(1)AMI患者中出现FWR的风险为1.9%。(2)与非FWR组相比,FWR组患者年龄偏大,前壁心肌梗死较多,心功能更差,接受手术治疗(包括经皮支架植入和冠状动脉旁路移植术)的患者比例偏低,且所有患者均出现院内死亡。(3)91.4%的患者FWR发生在AMI起病1周之内,其中24 h内发生FWR 37例(45.7%)。(4)COX回归分析发现,年龄(HR=1.055,95%CI:1.032~1.078,P<0.001)、急性前壁心肌梗死(HR=1.907,95%CI:1.211~3.002,P=0.005)和手术治疗(HR=0.126,95%CI:0.072~0.220,P<0.001)是AMI患者出现FWR的独立预测因子。结论AMI患者发生FWR的风险约为1.9%,而且通常发生在心肌梗死1周内,高龄和急性前壁心肌梗死患者容易发生FWR,而手术治疗能明显降低FWR风险。     

心电图诊断急性下壁，前壁心肌梗塞相关动脉的价值

目的：分析急性下壁、前壁心肌梗塞患者心电图表现及梗塞相关动脉的分布特点,评价心电图诊断急性下壁、前壁心肌梗塞相关动脉的价值。方法：对26例急性下壁心肌梗塞、29例急性前壁心肌梗塞患者的心电图和冠状动脉造影资料进行回顾性比较分析。结果：急性下壁心肌梗塞（26例）的梗塞相关动脉为右冠状动脉（RCA）者19例（73％）。回旋支（LCX）6例（23％）;急性前壁心肌梗塞（29例）的梗塞相关动脉为前降支（LAD）者26例（90％）;下壁心肌梗塞相关动脉为RCA的19例中Ⅱ、Ⅲ,aVF导联ST段上移18例（94％）,STⅢ↑／STⅡ↑〉1者16例（84%）。结论：急性下壁、前壁心肌梗塞的心电图表现与梗塞相关动脉有关,有较高的临床诊断价值。     

Relation of late potentials to ejection fraction and wall motion abnormalities in acute myocardial infarction

A prospective study was performed to determine the relation between quantitative signal-averaged parameters and ejection fraction (EF) and wall motion abnormalities determined by radionuclide ventriculography in patients with acute myocardial infarction (AMI). In 50 patients with AMI, signal-averaging of the surface QRS complex (200 beats; filter frequencies of 40 to 250 Hz and 80 to 250 Hz) was performed and radionuclide ventriculograms were recorded 8 +/- 5 days after AMI. Twenty-five of these patients (50%) had anterior wall AMI, 20 (40%) had inferior wall AMI and 5 (10%) had non-Q-wave AMI. The duration of the low-amplitude signals of less than 40 microV, the signal-averaged QRS complex and the root-mean-square voltage of the terminal 40 ms were determined. In addition to EF determinations, wall motion abnormalities were assessed for the presence or absence of dyskinetic, akinetic and hypokinetic segments. A wall motion score was constructed by separating the left and right ventricles into 21 segments in the anterior, left anterior oblique and lateral views. On the basis of the presence or absence of late potentials, the patients were separated into 2 groups: group I comprised 15 patients (30%) with late potentials and group II 35 patients (70%) without late potentials. The low-amplitude signals (49 +/- 12 vs 24 +/- 8 ms) and the signal-averaged QRS complex (122 +/- 20 vs 96 +/- 15 ms) were significantly longer and the root-mean-square voltage (13.8 +/- 4.9 vs 54.3 +/- 27.4 microV) significantly lower in group I than in group II.(ABSTRACT TRUNCATED AT 250 WORDS)     

Serial M-mode echocardiographic mapping in myocardial infarction: A quantitative evaluation of left ventricular wall motion abnormalities

M-mode echocardiographic (echo) mapping was performed in 44 consecutive patients with a first acute transmural myocardial infarction (AMI). Regional left ventricular wall motion, as reflected by mean systolic wall velocity (V?), was analyzed in 16 segments on day 1,2, 10, of hospitalization and after one year. Mean systolic wall velocity was significantly reduced (p < 0.05–0.01) in all segments indicated to be infarcted according to ECG. Anteroseptal and anterolateral AMIs showed similar V? impairment in anterior segments. In one latero-apical segment in anterolateral AMI V? was significantly lower (p < 0.01), while anteroseptal AMI also showed lower values (p < 0.05) for the midsegment of the middle third of septum. Inferior and inferolateral AMI had similar reductions in V? in the inferior segments. In addition depressed wall motion (p < 0.05) was found in one posterior segment in inferior AMI and in two posteroseptal segments in inferolateral AMI. Following the AMI V? successively decreased in the 4 central segments in patients with anterior wall infarction during the first 3 days, followed by a significant (p < 0.001) improvement on day 10. No further significant changes were seen after one year. Centrally infarcted segments in inferior AMI showed a minor (p < 0.05) decrease in V? from day 1 to day 2, with similar V? on day 10. A minor improvement (p < 0.05) was found one year later. Segments adjacent to centrally infarcted segments showed V? values similar to infarcted segments during the first 24 hours, followed by rapid improvement in inferior AMI from day 2, with normalization by day 10. Border segments in anterior AMI showed depressed V? values during the first 3 days, followed by a normalization by day 10. Noninfarcted segments in patients with inferior AMI showed hyperkinetic wall motion during the first 10 days, with normalization at the one year follow-up. The changes were moderate though peak V? values on days 2 or 3 were significantly higher (p < 0.05) than values one year later. Similarly, wall motion in noninfarcted segments in patients with anterior AMI reached hyperkinetic levels days 3 and 10, which was significantly higher (p < 0.01) than values on days 1, 2, or after one year.     

Prediction of wall motion recovery from the left anterior descending coronary artery velocity pattern recorded by transthoracic doppler echocardiography in patients with anterior wall myocardial infarction retrospective and prospective studies

The diastolic deceleration slope of coronary flow velocity is steeper in patients with substantial 'no reflow' phenomenon than in those without it. This study investigated whether functional outcomes in patients with anterior wall acute myocardial infarction (AMI) can be predicted by analyzing the coronary flow velocity pattern recorded with transthoracic Doppler (TTD) echocardiography. Coronary blood flow velocity in the distal left anterior descending coronary artery was recorded with TTD at day-2 after primary percutaneous transluminal coronary angioplasty/Stent in 51 patients with anterior AMI and the diastolic deceleration half time (DHT, ms) was measured. The wall motion score index (WMSI) was measured at day-1 and -21. In the retrospective study, the DHT was much shorter in those with a poor outcome than in those with good outcome (152 +/- 109 vs 395 +/- 128 ms, p<0.05). Receiver-operating characteristic analysis documented that DHT > or = 300 ms is a suitable cut-off point (sensitivity of 83% and specificity of 93%). In the prospective study (n=30), AWMSI(dl-d21) was significantly higher in those with a DHT > or = 300 ms than those without (0.3 > or = 0.5 vs 1.6 > or = 0.7, p<0.001). DHT correlated significantly with AWMSI(dl-d21) (r=0.76, p<0.001). Patients with a shorter DHT of diastolic coronary flow velocity have a poorer functional outcome among patients with anterior AMI. The TTD-determined DHT is a useful predictor of myocardial viability after an anterior AMI.     

Relationship between terminal QRS distortion on the admission electrocardiogram and the time course of left ventricular wall motion in anterior wall acute myocardial infarction

In order to clarify the time course of left ventricular (LV) wall motion in patients with anterior acute myocardial infarction (AMI) showing terminal QRS distortion on the admission electrocardiogram (ECG), the present study examined 106 patients with their first anterior AMI (< or =6 h) who underwent emergency coronary arteriography and cardiac cathetherization at 1 and 6 months after the infarction. The patients were classified into 2 groups according to the presence (group A, n=23) or absence (group B, n=83) of terminal QRS distortion (emergence of the J point at > or =50% of the R-wave amplitude in leads with QR configuration and/or absence of S waves in leads with RS configuration) on the admission ECG. Group A had a lower LV ejection fraction and more reduced regional wall motion (RWM) in the infarct region at both 1 and 6 months after AMI than group B. The degree of improvement in RWM between 1 and 6 months after AMI was less in group A than in group B (-0.1+/-0.5 vs 0.4+/-0.6 SD/chord, p<0.01). This study indicates that patients with anterior AMI showing terminal QRS distortion on the admission ECG have more severely depressed LV wall motion and less improvement in RWM in the infarct region in the healing stage, suggesting that this sign is an indicator of severe myocardial damage.     

Non-Q-wave acute myocardial infarction: Body surface potential map and ventriculographic patterns

Day 5 body surface map and radionuclide angiographic patterns were compared among 56 patients with first non-Q-wave or Q-wave acute myocardial infarction (AMI). Three radionuclide angiographic patterns were recognized in patients with non-Q infarction: no wall motion abnormalities (n = 8), single-segment wall motion abnormalities (n = 10) and multiple-segment wall motion abnormalities (n = 9). In contrast, only 2 radionuclide angiographic patterns were identified in patients with Q-wave infarction: multiple-segment wall motion abnormalities (n = 25) and single-segment wall motion abnormalities (n = 4). The Q-wave distributions of 14 of 18 patients with non-Q infarction with 0 or 1 wall motion abnormalities were normal; 2 patients had “missed” anterior; 1 patient had inferior; and 1 had posterior AMI patterns. Of 9 patients with non-Q infarction who had multiple-segment wall motion abnormalities, 8 had infarct Q waves on the posterior torso. Q-wave patterns in patients with anterior (n = 17) and inferior (n = 12) Q-wave infarctions were typical and homogeneous for each group. Quantitative analysis of minimum Q-zone integral, ΣQ-wave integrals, ST-integral maximum, wall motion abnormality score and ejection fraction revealed no differences between patients with non-Q-wave and those with inferior Q-wave infarction. In contrast, patients with anterior AMI had significantly more abnormal values of all variables than either of the other groups. Overall, the data support the concept of non-Q-wave AMI as a distinct, if heterogeneous, pathophysiologic entity. The variable body surface potential map and radionuclide angiographic patterns of the non-Q-wave AMI subgroups further suggest a variable prognosis. It remains to be determined, however, which patients are at greatest risk and why.     

Relation of QT dispersion to infarct size and left ventricular wall motion in anterior wall acute myocardial infarction.

Previous studies have shown that QT dispersion increases during acute myocardial infarction (AMI). However, the relation of QT dispersion to infarct size and left ventricular (LV) function in AMI has not yet been fully clarified. Accordingly, this study was conducted to elucidate this relation at 1 month after anterior wall AMI. We examined 94 patients with first anterior wall AMI (< or = 6 hours) who underwent coronary arteriography at admission, 1 month, and 6 months after AMI, and left ventriculography at 1 and 6 months after AMI. Mean QT dispersion on the chronic phase (about 1 month after AMI) electrocardiogram was 79 +/- 33 ms. There were no significant correlations between QT dispersion and peak creatine phosphokinase levels, LV ejection fraction, and regional wall motion in the infarct region at 1 month after AMI (r = 0.06, p = 0.57; r = 0.11, p = 0.29; r = -0.05, p = 0.63, respectively). In conclusion, the findings of this study suggest that QT dispersion on the resting electrocardiogram at 1 month after anterior wall AMI is unrelated to infarct size estimated by the peak creatine phosphokinase level and the degree of LV dysfunction.     

Acute anterior wall myocardial infarction entailing st-segment elevation in lead v1: Electrocardiographic and angiographic correlations

Background: The correlation between ST elevation in lead V₁ during anterior wall acute myocardial infaction (AMI) and the culprit lesion site in the left anterior descending (LAD) coronary artery is poor. Hypothesis: The study was undertaken to assess the electrocardiographic (ECG) characteristics and angiographic significance of ST-segment elevation in lead V¹ during anterior wall acute myocardial infarction (AMI). Methods: Data from 115 patients with anterior wall AMI, who underwent coronary angiography within 14 days of hospitalization, were studied. The admission 12-lead ECG was examined and the coronary angiogram was evaluated for the nature of the conal branch of the right coronary artery (RCA) and for the culprit lesion site in the left anterior descending (LAD) coronary artery. Results: Mean ST-segment deviation and the frequency of patients with ST-segment elevation > 0.1 mV were significantly lower in lead V i than in lead V2 (0.136 $$ 0.111 mV vs. 0.421 $$ 0.260 mV, and 37 vs. 96%, for leads Vi and Vi, respectively). A small conal branch not reaching the interventricular septum (IVS) was more prevalent among patients with ST-segnicni elevation >0.1 mV in lead Vi (67%), whereas a large conal branch was more prevalent in patients with ST-segment deviation (1 mV in that lead (83%, p<0.001). No relation was found between ST-segment deviation in lead V i during anterior wall AMI and the culprit lesion site in the LAD. Conclusion: ST-segment elevation in lead V₁ during first anterior wall AMI was found in one third of the patients, and its magnitude was lower than that in the other precordial leads. ST-segment elevation in lead V₁ favors the presence of a small conal branch of the RCA that does not reach the IVS.     

Implications of inferior ST-segment elevation accompanying anterior wall acute myocardial infarction for the angiographic morphology of the left anterior descending coronary artery morphology and site of occlusion.

Inferior ST-segment elevation during anterior wall acute myocardial infarction (AMI) due to left anterior descending (LAD) coronary artery occlusion is unusual and was not previously investigated. This study tested the hypothesis that inferior ST-segment elevation during anterior AMI predicts a specific angiographic morphology that satisfies 2 necessary conditions: (1) mass of ischemic anterior wall myocardium is relatively small, resulting in a weaker anterior injury current and less reciprocal inferior ST-segment depression; and (2) there is concomitant inferior wall transmural ischemia that further shifts the inferior ST segments upward. The study group consisted of 42 consecutive patients with anterior AMI undergoing angiography at 4.1 days (range 0 to 14). Coronary angiograms were examined for 3 features: (1) site of LAD artery occlusion (a distal obstruction implying a smaller mass of ischemic anterior wall myocardium), (2) LAD artery extension onto inferior wall of left ventricle (termed a "wrap around" vessel), and (3) collateral flow from LAD artery to inferior wall. The latter 2 features would be expected to contribute to inferior wall transmural ischemia. Acute inferior ST-segment elevation (sum of ST-segment deviation in leads II, III and aVF greater than or equal to 3.0 mm) was seen in 7 patients (16%). A greater number of LAD artery branches proximal to the site of occlusion was significantly correlated with less inferior ST-segment depression (r = 0.59, p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)     

Isolated inferior wall ST segment depression as an early sign of acute anterior wall myocardial infarction

Abstract

Background: Reciprocal changes may accompany ST segment elevation in the ischemic territory during acute myocardial infarction (AMI). We examined the hypothesis that isolated inferior ST segment depression on admission is an early sign of anterior wall infarction. Methods: 49 patients admitted to the coronary care unit between January 1996 and June 2008 who presented with inferior ST segment depression in the absence of ST segment elevation. Electrocardiograms (ECGs) obtained on admission and at 24–48 h were reviewed. Culprit artery was determined based on angiographic and echocardiographic data. Results: All patients had ST segment depression in the inferior leads on admission. A subgroup (55%) presented with concomitant ST segment depression in V5–V6. Follow-up ECG showed that 35% developed ST segment elevations and/or T wave inversions in anterior wall leads over 24–48 h. The left anterior descending (LAD) artery or one of its branches was the culprit in 60% of the patients. Sum of ST segment depression, V5–V6 involvement or presence of ‘hyperacute’ T waves did not predict LAD involvement. Conclusion: Isolated ST segment depression in the inferior wall leads during ACS is usually an early sign of anterior wall AMI, in which the LAD or one of its branches is the culprit artery.     

Left ventricular remodeling after anterior wall acute myocardial infarction in modern clinical practice (from the REmodelage VEntriculaire [REVE] study group)

Left ventricular (LV) remodeling after acute myocardial infarction (AMI) has been well described in previous studies. However, there is a paucity of data on the incidence of and risk factors for LV remodeling in modern clinical practice that incorporates widespread use of acute reperfusion strategies and almost systematic use of "antiremodeling" medications, such as angiotensin-converting enzyme inhibitors and beta blockers. We enrolled 266 patients with anterior wall Q-wave AMI who had >or=3 segments of the infarct zone that were akinetic on echocardiography before discharge. Echocardiographic follow-up was performed 3 months and 1 year after AMI. LV volumes, ejection fraction, wall motion score index, and mitral flow velocities were determined in a blinded analysis at a core echocardiographic laboratory. Acute reperfusion was attempted in 220 patients (83%; primary angioplasty in 29% and thrombolysis in 54%). During hospitalization, 99% of patients underwent coronary angiography and 87% underwent coronary stenting of the infarct-related lesion. At 1 year, 95% of patients received an antiplatelet agent, 89% a beta blocker, 93% an angiotensin-converting enzyme inhibitor or angiotensin II receptor blocker, and 93% a statin. Echocardiographic follow-up was obtained in 215 patients. There was recovery in LV systolic function as shown by a decrease in wall motion score index and an increase in ejection fraction. There was a significant increase in end-diastolic volume (EDV; 56.4 +/- 14.7 ml/m2 at baseline, 59.3 +/- 15.7 ml/m2 at 3 months, 62.8 +/- 18.7 ml/m2 at 1 year, p <0.0001). LV remodeling (>20% increase in EDV) was observed in 67 patients (31%). Peak creatine kinase level, systolic blood pressure, and wall motion score index were independently associated with changes in EDV. In conclusion, recent improvements in AMI management do not abolish LV remodeling, which remains a relatively frequent event after an initial anterior wall AMI.     

ST-segment re-elevation unrelated to left ventricular ejection fraction or volume after anterior wall acute myocardial infarction treated with successful reperfusion

Ventricular remodeling is a major determinant of the long-term prognosis of patients with acute myocardial infarction (AMI). No previous study examined the relation of ST-segment re-elevation to left ventricular (LV) volume and function in patients with successful reperfusion. We examined the relation of ST-segment re-elevation to LV function and volume indices in 51 patients with anterior wall AMI who underwent successful reperfusion by direct coronary angioplasty. A 12-lead electrocardiogram was recorded once a day until 7 days after the onset of AMI. ST-segment shift was measured and Sigma ST was defined as the sum of ST-segment elevation obtained from leads V2, V3, and V4. ST-segment re-elevation was defined as present when the difference between maximal and minimal Sigma ST (Delta ST) was >0.3mV. LV indices were obtained from left ventriculography performed approximately 1 month after the onset of AMI. ST-segment re-elevation was observed in 15 patients (29%). No significant differences were observed between the ST- re-elevation group and non-ST-re-elevation group in LV ejection fraction (49.4+/-14.0 vs. 51.2+/-11.5%), LV end-systolic volume index (35.8+/-13.1 vs. 33.8+/-12.5 mL/m(2)) or LV end-diastolic volume index (69.7+/-12.8 vs. 68.3+/-14.4 mL/m(2)). The difference between maximal and minimal Sigma ST (Delta ST) was not significantly correlated with any LV index examined. In conclusion, the present study revealed that ST-segment re-elevation after successful reperfusion in anterior wall AMI patients was not related to LV volume or function, indicating that ST-re-elevation is not a clinically meaningful indicator of LV remodeling.     

Angiographic and clinical significance of 'transient' ST-segment depression in the lateral chest leads in anterior wall acute myocardial infarction

This study aimed to clarify the significance of ST-segment depression in the lateral chest leads in anterior wall acute myocardial infarction (AMI) with ST-segment elevation. A total of 196 patients with their first anterior wall AMI (< or =6h) were divided into 2 groups according to the presence (group A, n=39) or absence (group B, n=157) of ST-segment depression > or =0.1 mV in V5 and/or V6 on the admission electrocardiogram. Patients with electrocardiographic confounding factors were excluded. No patients had persistent ST-segment depression in the lateral chest leads. Emergency coronary angiography revealed that group A had higher incidences of occlusion of the left anterior descending coronary artery (LAD) proximal to its first septal branch (77% vs 51%, p<0.01) and good collateral circulation than group B (46% vs 25%, p<0.05). Peak creatine kinase levels were significantly lower in group A than in group B (2060+/-1099 vs 2873+/-2077 IU/L, p<0.01). Left ventricular ejection fraction in the chronic phase was significantly greater in group A than in group B. Regional wall motion in the infarct region in the chronic phase was better in group A than in group B. These results indicate that patients with 'transient' ST-segment depression in the lateral chest leads in anterior wall AMI had a relatively smaller infarct size, despite their higher incidence of occlusion of the LAD proximal to its first septal branch, because of their higher incidence of good collateral circulation.     

Usefulness of ultrasonic strain measurements to predict regional wall motion recovery in patients with acute myocardial infarction after percutaneous coronary intervention

Strain Doppler echocardiography can detect systolic regional myocardial dysfunction. This study assessed whether strain could predict recovery of regional left ventricular function in patients with acute myocardial infarction (AMI) after percutaneous coronary intervention. Forty-three patients with anterior AMI undergoing successful percutaneous coronary intervention of the left anterior descending coronary artery were studied. Longitudinal myocardial strain was measured at the left anterior descending coronary artery territory in the apical long-axis view within 24 hours after percutaneous coronary intervention. Regional wall motion was analyzed by the anterior wall motion score index (A-WMSI). Viable myocardium was defined as a decrease < or = 2.0 in A-WMSI. Patients were categorized as A-WMSI at 4 weeks into a viable group (n = 24) and a nonviable group (n = 19). End-systolic strain and peak strain were significantly lower in the nonviable group than in the viable group (-4.8 +/- 4.8% vs -9.9 +/- 4.7 %, p <0.005; -9.9 +/- 4.6 vs -13.5 +/- 4.1 %, p <0.05). Moreover, corrected time to peak strain (cTPS; time delay from end-systolic to peak strain/RR interval) was significantly longer in the nonviable group than in the viable group (0.19 +/- 0.04 vs 0.13 +/- 0.03, p <0.0001). For prediction of viable myocardium, cTPS <0.15 had a sensitivity of 95% and a specificity of 85%. In conclusion, strain, especially cTPS, is useful for predicting recovery of regional left ventricular function in patients with AMI after percutaneous coronary intervention.     

体表心电图对老年急性前壁心肌梗死左前降支闭塞部位的预测价值

目的探讨体表心电图对老年急性前壁心肌梗死左前降支（LAD）闭塞部位的预测价值。方法对62例老年急性前壁心肌梗死患者的入院心电图和冠状动脉造影资料进行回顾性分析,寻找可以预测LAD闭塞部位的心电图改变。结果62例老年急性前壁心肌梗死患者均为LAD闭塞,其中近段闭塞者45例（72.6%）,远段闭塞者17例（27.4%）。经χ2检验,STⅠ抬高、STaVL抬高、STaVF压低或至少2个下壁导联ST段压低等指标提示LAD近段闭塞（P均〈0.05）。其中,STaVF压低或至少2个下壁导联ST段压低的特异度和阳性预测值最高,为94%左右,灵敏度以STaVL抬高最高,为56%;反之,STaVL压低和STⅢ抬高则在预测LAD远段闭塞上有显著意义（P均〈0.05）,特异度和阳性预测值以STaVL压低为最高,均为100%。结论急性前壁心肌梗死时,体表心电图对预测LAD闭塞部位有重要价值。     

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.     

Two-dimensional echocardiographic demonstration of restoration of normal wall motion after acute myocardial infarction

Left ventricular wall motion was assessed by 2-dimensional (2-D) echocardiography in 17 patients admitted with a first transmural acute myocardial infarction (AMI). The left ventricular myocardium was divided into 17 segments and wall motion was scored from 1 (dyskinesia) to 6 (hyperkinesia) in each segment. Reproducibility of the wall motion scoring system when assessed separately by 2 observers was 89% and when assessed by the same observer at different times, 91%. Seven patients had anterior and 10 inferior wall AMI on the electrocardiogram. Abnormal wall motion was present in 7.3 +/- 2.8 segments (mean +/- standard deviation) on the initial 2-D echocardiogram. On follow-up echocardiograms wall motion was unchanged in 7 patients. In 5 wall motion improved by at least 2 in 2 or more contiguous segments. In 5 other patients wall motion returned to normal in all segments that had shown an abnormality on the initial echocardiogram. These 5 patients (group A), compared with the 12 patients in whom wall motion did not return to normal in all segments (group B), showed fewer involved segments (5.4 +/- 1.7 vs 8 +/- 2.8) and a higher total wall motion score (76 +/- 4 vs 63 +/- 7) (p less than 0.05) on the initial echocardiogram. Duration from the time of the AMI to return of normal wall motion in group A varied from 2 to 8 weeks. Thus, wall motion abnormalities seen on 2-D echocardiography after transmural AMI often improve and wall motion returns to normal in some patients.