Recurrent Ischemia After Thrombolysis: Importance of Associated Clinical Findings

Objectives. We sought to assess the incidence and clinical relevance of examination data to recurrent ischemia within an international randomized trial.Background. Ischemic symptoms commonly recur after thrombolysis for acute myocardial infarction.Methods. Patients (n = 40,848) were prospectively evaluated for recurrent angina and transient electrocardiographic (ECG) or hemodynamic changes. Five groups were developed: Group 1, patients with no signs or symptoms of recurrent ischemia; Group 2, patients with angina only; Group 3, patients with angina and ST segment changes; Group 4, patients with angina and hemodynamic abnormalities; and Group 5, patients with angina, ST segment changes and hemodynamic abnormalities. Baseline clinical and outcome variables were compared among the five groups.Results. Group 1 comprised 32,717 patients, and Groups 2 to 5 comprised 20% of patients (4,488 in Group 2; 3,021 in Group 3; 337 in Group 4; and 285 in Group 5). Patients with recurrent ischemia were more often female, had more cardiovascular risk factors and less often received intravenous heparin. Significantly more extensive and more severe coronary disease, antianginal treatment, angioplasty and coronary bypass surgery were observed as a function of ischemic severity. The 30-day reinfarction rate was 1.6% in Group 1, 6.5% in Group 2, 21.7% in Group 3, 13.1% in Group 4 and 36.5% in Group 5 (p < 0.0001); in contrast, the 30-day mortality rate was significantly lower (p < 0.0001) in Groups 1, 2 and 3 (6.6%, 5.4% and 7.7%, respectively) than in Groups 4 and 5 (21.8% and 29.1%).Conclusions. Postinfarction angina greatly increases the risk of reinfarction, especially when accompanied by transient ECG changes. However, mortality is markedly increased only in the presence of concomitant hemodynamic abnormalities.     

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。     

Myocardial infarction with an initially normal electrocardiogram—Angiographic findings

To analyze the paradox of acute myocardial infarction (AMI) with an initially normal electrocardiogram (ECG), we reviewed the records of 732 patients discharged with a final diagnosis of AMI over a 2-year period. Twenty-one patient were identified whose initial ECG was normal and who underwent coronary arteriography during the index hospitalization. According to the ECG evolution, three distinct groups were identified: Group 1: those who subsequently developed ST elevation or Q waves (n = 7), Group 2: those who developed ST depression or T-wave inversion (n = 8), and Group 3: those whose ECG remained normal (n = 6). Peak creatine kinase (CK), timing of the first ECG change, life-threatening complications, and location of the infarct-related coronary lesion were recorded. Infarct-related coronary lesions were also classified into those in a major coronary trunk versus those in secondary branches. The incidence of AMI with a normal ECG was 3.7%. There was no difference in the frequency of coronary artery involvement in the groups studied: left anterior descending (33%), right coronary artery (38%), and circumflex (28%). All ECG changes developed within the first 48 h of hospitalization; 17 ± 15 in Group 1, and 24 ± 12 h in Group 2. All six patients who had a persistently normal ECG (Group 3) had lesions in branch vessels (p < 0.05 when compared with Group 1 plus Group 2). Patients who developed ST elevation or Q waves (Group 1) always had a major artery trunk involved (p < 0.05 when compared with Group 2 plus Group 3). Patients in Group 3 had less myocardial damage and fewer complications compared with the other two groups. Myocardial infarction with an initial normal ECG is uncommon and may result from involvement of any of the three coronary arteries. Electrocardiographic evolution usually occurs within the first 48 h of hospitalization. Patients whose ECGs remain normal appear to have culprit lesions in coronary branches, smaller infarctions, and fewer in-hospital complications.     

Prognostic significance of the initial electrocardiographic pattern in patients with inferior wall acute myocardial infarction

The purpose of the study was to determine whether the initial electrocardiographic pattern is predictive of in-hospital mortality in inferior wall acute myocardial infarction. It is commonly perceived that patients with acute myocardial infarction presenting with greater ST elevation have a worse prognosis. The initial electrocardiogram of patients (n = 213) with inferior wall myocardial infarction was categorized based on the pattern of ST-segment elevation in inferior leads: (A) ST< 1 mm with tall T waves, (B) ST ≥ 1 mm with normal terminal QRS, and (C) ST≥ 1 mm with distortion of terminal QRS. ST deviation from baseline was calculated for all leads. Patients with maximal precordial ST depression in V₄-V₆ and pattern A had an in-hospital mortality rate of 68.8% compared with 16.9% for the entire study group. By univariate analysis, only pattern A was significantly predictive of in-hospital mortality [odds ratio = 2.91,95% confidence interval (CI) 1.22–6.93], but by multivariate analysis adjusted for (1) age, (2) diabetes mellitus, (3) previous myocardial infarction, (4) thrombolytic therapy, (5) precordial ST-depression pattern, and (6) patterns of ST elevation, maximal ST depression in V₄-V₆ was significantly predictive (odds ratio = 4.93, 95% CI 1.79–13.56), whereas pattern A was not (odds ratio = 1.12, 95% CI 0.36–3.52). Contrary to popular perception, patients with inferior wall myocardial infarction presenting with minimal ST-segment elevation are at highest risk for in-hospital mortality, especially if accompanied by maximal precordial ST depression in V₄-V₆.     

Myocardial damage after successful thrombolysis is associated with the duration of ST re-elevation at reperfusion

The purpose of this study was to investigate the significance of ST re-elevation at reperfusion using strict criteria for patient inclusion and exclusion. Twenty-nine patients who had a first anterior infarction with single-vessel disease, successful recanalization by intracoronary thrombolysis (ICT) with urokinase, and an angiographically confirmed patent infarct-related artery after 4 weeks, were divided into three groups according to the deviation of the ST segment at reperfusion: Group A, 10 patients with sustained ST re-elevation; Group B, 10 patients with transient ST re-elevation; and Group C, 9 patients with ST reduction. Left ventricular (LV) function was evaluated from cineventriculograms performed in the 30° right anterior projection 4 weeks after ICT. LV ejection fraction and regional wall motion of the infarct area, evaluated by the centerline method (SD/chords), were significantly lower in Group A (44 ± 10%, -3.2 ± 0.4) than in Group B (61 ± 9%, -1.9 ± 0.7) and Group C (60 ± 5%, -2.0 ± 0.4) (p < 0.01). Peak creatine kinase (CK) activity was significantly higher in Group A (5848 ± 2112 IU) than in Group B (2485 ± 1254 IU) and Group C (1889 ± 1525 IU) (p < 0.05). These data suggest that a sustained ST re-elevation at reperfusion was strongly associated with marked LV dysfunction and higher peak CK activity. It was concluded that sustained, not transient, ST re-elevation associated with successful reperfusion indicates extensive myocardial damage.     

ST segment shifts are poor predictors of subsequent Q wave evolution in acute myocardial infarction. A natural history study of early non-Q wave infarction

Acute ST segment elevation is regarded generally as the sine qua non of evolving Q wave myocardial infarction (MI) because such electrocardiographic (ECG) injury is believed to be a marker of transmural ischemia and a forerunner of transmural necrosis. Alternatively, ST segment depression with or without T wave inversion is viewed as the dominant ECG feature of non-Q wave MI. However, this hypothesis has not been assessed prospectively in an acute MI population. We analyzed 2,304 serial ECGs at study entry (admission), day 2, day 3, and predischarge (mean, 10.2 +/- 2 days) from 576 patients with creatine kinase MB confirmed acute non-Q wave MI to determine what percentage of patients with early ST segment elevation culminated in subsequent Q wave development. Of this group, 187 patients (32%) exhibited 1 mm or greater ST segment elevation in two or more contiguous entry ECG leads. Of those patients whose non-Q wave MI could be localized on the basis of diagnostic admission ST segment shifts, the prevalence of early ST segment elevation was 43% (187 of 439). The sum total mean (+/- SD) peak ST segment elevation by lead group (anterior, inferior, lateral) was 4.0 +/- 2.4, 4.5 +/- 2.4, and 2.5 +/- 0.6 mm, respectively. Despite this, only 20% of patients with ST segment elevation (37 of 187) developed Q waves. Of 252 patients who exhibited early ST segment depression or T wave inversion or both, 39 (15%) evolved subsequent Q waves. Thus, while the prevalence of early ST segment elevation in acute evolving non-Q wave MI was higher than previously reported, 80% of patients with and 85% of patients without ST segment elevation and absent Q waves on the admission ECG did not develop subsequent Q waves during a 2-week period of observation (p = NS). In addition, when patients with ST segment elevation were compared with patients with ST segment depression or T wave inversions or both, there were no between-group differences in log peak creatine kinase (404 vs. 383 IU), reinfarction (6% vs. 8%), postinfarction angina (50% vs. 42%), or early recurrent ischemia (49% vs. 45%), defined as postinfarction angina with transient ECG changes. Thus, in patients who present with initial acute non-Q wave MI, ST segment shifts on admission are unreliable predictors of subsequent Q wave evolution and do not discriminate significant differences in postinfarction outcome. In particular, ST segment elevation during the early hours of evolving infarction is not an invariable harbinger of subsequent Q wave development.     

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。     

Additional ST segment elevation during the first hour of thrombolytic therapy: an electrocardiographic sign predicting a favorable clinical outcome.

OBJECTIVES. The aim of this study was to investigate the significance of further ST elevation that occurs during the 1st h of thrombolytic therapy before the expected resolution. BACKGROUND. Early resolution of ST segment elevation is commonly accepted as a marker of clinical reperfusion during thrombolytic therapy for acute myocardial infarction. Using frequent electrocardiographic recordings, we observed in some patients further ST elevation that occurred during hour 1 of thrombolysis before the expected resolution. METHODS. To investigate the significance of this pattern, we classified 177 consecutive patients with a first acute myocardial infarction into two groups: Group A, 98 patients with ST elevation > or = 1 mm above the initial ST elevation during the 1st h of thrombolytic therapy, and Group B, 79 patients without this finding. RESULTS. Although the presence or absence of additional ST elevation was not associated with a clinical or prognostic difference in patients with a first inferior or posterior acute myocardial infarction, its presence indicated a more favorable clinical outcome and prognosis in patients with anterior infarction. Among the patients with anterior infarction the 65 patients in Group A had a higher ejection fraction (44 +/- 9% vs. 35 +/- 11%, p < 0.01), less heart failure (15% vs. 35%, p = 0.02) and a lower in-hospital mortality rate (0% vs. 8%, p = 0.04) than did the 37 patients from Group B. CONCLUSIONS. Additional ST elevation early during thrombolytic therapy in patients with anterior infarction suggests a favorable clinical outcome and thus may be indicative of successful reperfusion.     

Comparison of the effect of heparin and aspirin versus aspirin alone on transient myocardial ischemia and in-hospital prognosis in patients with unstable angina

Objectives. This study compared the effects of heparin and aspirin versus aspirin alone on transient myocardial ischemia and in-hospital prognosis in patients with unstable angina.Background. Transient myocardial ischemia occurring in patients with unstable angina is associated with an adverse prognosis. Heparin and aspirin are two drugs used frequently in the treatment of this condition, but the effect of combination therapy versus aspirin alone on transient myocardial ischemia is unknown.Methods. Two hundred eighty-five consecutive patients with unstable angina were randomized to receive either intravenous heparin plus oral aspirin (150 mg once daily) (Group H + A) or aspirin alone (Group A). Patients also received a beta-adrenergic blocking agent, diltiazem and intravenous nitrates. ST segment monitoring was performed for the 1st 48 h of treatment. Patients were followed up for the duration of their in-hospital stay.Results. One hundred fifty-four patients (30 women, mean [±SEM] age 58.3 ± 0.8 years) received heparin and aspirin (Group H + A), and 131 patients (26 women, mean age 60.6 ± 0.8 years) received aspirin only (Group A). ST segment monitoring (11,622 h) yielded 244 episodes of transient myocardial ischemia of a total duration of 7,819 min. There were no significant differences between the two treatment arms in the number of patients with transient myocardial ischemia (27 [18%] in Group H + A vs. 31 [24%] in Group A), number of episodes (96 in Group H + A vs. 148 in Group A) or total duration of transient myocardial ischemia (2,911 min in Group H + A vs. 4,908 min in Group A). The incidence of in-hospital myocardial infarction or death was significantly higher in patients with transient myocardial ischemia (53% vs. 22%, p < 0.0001). Five of the six deaths occurred in patients with transient myocardial ischemia. Event-free survival from myocardial infarction or death was similar in both treatment groups. Preadmission therapy with aspirin was associated with a lower in-hospital infarction rate (19% vs. 34%, p = 0.01).Conclusions. The presence of transient myocardial ischemia in patients with unstable angina is associated with a significantly higher incidence of myocardial infarction or death in hospital. Combined therapy with heparin and aspirin compared with aspirin alone makes no difference in the development of these events, nor does it reduce the development of transient myocardial ischemia.     

ST-Segment depression on ambulatory electrocardiography in the early in-hospital period after acute myocardial infarction predicts early and late mortality: A short-term and a 3-year follow-up study

A surveillance study was conducted to determine the in-hospital and long-term prognostic value of ST-segment depression assessed by ambulatory electrocardiographic monitoring (AEM) during the early in-hospital period after acute myocardial infarction (AMI). ST-segment depression (STD) was determined by computer analysis of 24-h ECG tapes as a horizontal or downsloping change in ST level by ≥ 0.1 mV from the reference base line. The ST level was measured 80 ms after the J point of all normally conducted complexes for ≥ 1 min. All computer-detected ST events were verified by one trained reader. Tapes corresponding to 74 patients were analyzed. In addition, 23 tapes corresponding to age- and gendermatched controls were also analyzed. Patients were divided into two groups: 22 patients (30%) showed STD (Group A), and 52 patients (70%) had no episode of STD (Group B). Among controls, 1 person (4%) showed STD. During the early follow-up period (14 ± 11 days after hospital admission), cardiac events occurred in 11 patients [7 (32%) in Group A and 4 (8%) in Group B, p < 0.01], including 6 cardiac deaths [5 (23%) in Group A and 1 (2%) in Group B, p < 0.01], 3 acute coronary artery bypass surgeries [2 (9%) in Group A and 1 (2%) in Group B, p = NS], and 2 nonfatal myocardial infarctions (both in Group A, p = NS). During a mean follow-up period of 3 years (36 ± 15 months), 18 patients died [10 (45%) in Group A and 8 (15%) in Group B, p = 0.01]. Eleven deaths were sudden [7 (32%) in group A and 4 (8%) in Group B, p <0.01 ]. Eighteen AMI occurred [11 (50%) in Group A and 7 (13%) in Group B, p < 0.005]. Twenty patients underwent revascularization procedures [7 (32%) in Group A and 13 (25%) in Group B, p=NS]. Thirty-eight patients [18 (82%) in Group A and 20 (38%) in Group B, p<0.001] suffered at least one cardiac event during the follow-up period (death, myocardial infarctions, and revascularization therapy). Survival analysis using Kaplan-Meier curves showed that patients with STD (Group A) had shorter survival times (p < 0.001, Log rank test) than those without STD (Group B). The same analysis showed that patients in Group A had shorter survival times free of cardiac events (myocardial infarction, p < 0.001; sudden death, p < 0.001; revascularization therapy, p < 0.05; all cardiac events, p < 0.001) than those in Group B. No coronary events were reported in control persons. A multivariate stepwise regression analysis (Cox's proportional hazards model) of a number of clinical variables, including STD, showed that its presence was the most important factor predicting mortality (p < 0.001, hazards ratio 5.09), followed by the presence of diabetes (p < 0.01, hazards ratio 4.67) and hypertension (p < 0.01, hazards ratio 3.52). The findings of this survey illustrate both the short- and long-term prognostic value regarding mortality and morbidity of STD recorded on AEM during the early in-hospital period after AMI.     

Is the shortening of the QTc interval in Q-wave leads showing ST segment shift during exercise testing a new ECG marker of myocardial ischemia and viability in patients with previous anterior myocardial infarction?

PURPOSE: To evaluate whether the shortening of the QTc-interval, measured in Q-wave leads showing ST segment elevation during exercise testing may be a marker of stress-induced transmural ischemia (and indirectly of myocardial viability) in the infarct zone in patients with prior Q-wave anterior myocardial infarction. METHODS: We evaluated 15 consecutive patients (Group A) with previous anterior myocardial infarction presenting these peculiarities: 1) ST segment elevation over Q waves during exercise testing; 2) critical (> 75%) stenosis of LAD; 3) evidence by echocardiography and stress-redistribution-reinjection 201thallium myocardial scintigraphy (SRR201TIMS) of viable myocardium in the infarct zone (akinetic segments with normal echo-reflectivity plus > 7 mm end-diastolic wall thickness and significant 201thallium redistribution after reinjection). The study control group (Group B) consisted of 15 patients with previous myocardial infarction, critical stenosis of LAD and evidence of scarring by imaging techniques (increased echo-reflectivity associated with an end-diastolic wall thickness < 6 mm and no 201thallium redistribution in infarcted areas). The QTc interval was measured at rest and at peak stress in all leads, and particularly in infarct-related leads showing ST-T changes, and the lead-by-lead fractional difference percentage between the QTc intervals (delta QTc) was calculated. The delta QTc was measured again during exercise testing in 11 patients from Group A (Group A1) who showed significant contractility recovery three months after complete myocardial revascularization. A delta QTc shortening < -10% was considered "significant". RESULTS: In 14/15 patients from Group A, a significant delta QTc shortening was measured, while in 14/15 patients from Group B no significant delta QTc shortening was detected (sensitivity = 93.3%; specificity = 93.3%) (p < 0.0001). The mean delta QTc in Group A was -18.1 +/- 8.5%; the mean delta QTc in Group B was -4.2 +/- 7.8% (p < 0.0001). No patient from Group A1 showed a significant delta QTc shortening in Q-wave leads (mean delta QTc group A1 = +6.9 +/- 14.8%). CONCLUSIONS: delta QTc shortening in infarct-related leads during exercise testing is a simple ECG marker of transmural ischemia and, indirectly, of myocardial-viability. This sign is no more evident after myocardial revascularization and may be useful in identifying "hibernating-myocardium".     

Abnormal Q waves on the admission electrocardiogram of patients with first acute myocardial infarction: Prognostic implications

Background: Q waves developed in the subacute and persisting into the chronic phase of myocardial infarction (MI) usually signify myocardial necrosis. However, the mechanism and significance of Q waves that appear very early in the course of acute MI (<6 h from onset of symptoms), especially if accompanied by ST elevation, are probably different. Hypothesis: This study assesses the prognostic implications of abnormal Q waves on admission in 2,370 patients with first acute MI treated with thrombolytic therapy <6 h of onset of symptoms. Results: Patients with abnormal Q waves in ≥2 leads with ST-segment elevation (n = 923) were older than patients without early Q waves (n = 1,447) (60.6 ±11.9 vs. 58.8 ±11.9 years, respectively; p = 0.0003), and had a greater incidence of hypertension (34.3 vs. 30.5% p = 0.05) and anterior MI (60.6 vs. 41.1 % p<0.0001). Time from onset of symptoms to therapy was longer in patients with Q waves upon admission (208 ± 196 vs. 183 ± 230 min; p = 0.01). Peak serum creatine kinase (2235 ± 1544 vs. 1622 ± 1536 IU; p<0.0001), prevalence of heart failure during hospitalization (13.8 vs. 7.0%, p<0.0002), hospital mortality (8.0 vs. 4.6% p = 0.02), and cardiac mortality (6.6 vs. 4.5%, p = 0.11) were higher in patients with anterior MI and with abnormal Q waves than in those without abnormal Q waves upon admission. There was no difference in peak creatine kinase, prevalence of heart failure, in-hospital mortality, and cardiac mortality between patients with and without abnormal Q waves in inferior MI. Multivariate regression analysis confirmed that mortality is independently associated with presence of Q waves on admission (odds ratio 1.61; 95% CI 1.04–2.49; p = 0.04 for all patients; odds ratio 1.65; 95% CI 0.97–2.83; p=0.09 for anterior wall MI. Conclusion: Abnormal Q waves on the admission electrocardiogram (ECG) are associated with higher peak creatine kinase, higher prevalence of heart failure, and increased mortality in patients with anterior MI. Abnormal Q waves on the admission ECG of patients with inferior MI are not associated with adverse prognosis.     

Significance of inferior ST segment changes in acute anterior myocardial infarction--relationship between the distribution of left anterior descending artery and concomitant ischemia of the inferior wall

The significance of inferior ST segment changes was studied in 23 patients with acute anterior myocardial infarction by the distribution of the left anterior descending artery (LAD) after percutaneous transluminal coronary recanalization. In 9 patients (Group A) LAD supplied the anterior wall of the left ventricle up to or including the apex but did not reach the inferior wall; in 8 patients (Group B) it continued beyond the apex onto the inferior wall of the left ventricle with well developed collateral circulation; in 6 patients (Group C) it continued beyond the apex onto the inferior wall of the left ventricle with less-developed or no collateral circulation. Thallium-201 scintigraphy and contrast left ventriculography showed that inferior myocardial ischemia was significantly more prominent in Group C than Group A. These results were consistent with coronary anatomy. Inferior ST segment was significantly more depressed in Group A with no concomitant inferior wall ischemia, than in Group C with concomitant inferior wall ischemia (maximal inferior ST segment change: -1.7 +/- 1.1; 0.8 +/- 1.7 mm, respectively; p less than 0.02). In Group A inferior ST segment was depressed in all 6 patients with lateral ST segment elevation, but it was depressed in only one of 3 patients with no lateral ST segment change. Lateral ST segment elevation tended to cause inferior ST segment depression. This study indicates that the inferior ST segment changes in patients with acute anterior myocardial infarction depend on concomitant ischemia of the inferior wall of the left ventricle by the distribution of LAD and the lateral ST segment changes.     

溶栓后早期转运PCI与保守治疗/补救转运PCI治疗STEMI患者的比较

目的：本研究回顾分析比较急性心肌梗塞（AMI）患者在基层医院行溶栓治疗后,早期转运到上级医院行经皮冠状动脉介入治疗（PCI）和继续在当地予保守治疗然后作转运PCI的优劣。方法：315例AMI患者在发病12h内,于基层医院接受溶栓治疗,其后183例直接转诊行PCI（A组）,132例在当地继续保守治疗,67例因再次出现心肌缺血症状行补救性转运PCI（B组）。比较两组1年内全因死亡、再梗死、难治性心肌缺血发生率及30d内严重出血和脑卒中发生率,以及治疗前后左室射血分数（LVEF）改变情况。结果：与B组比较,A组1年内全因死亡率（6.8%比1.6%）、再梗死发生率（17.4%比3.3%）、难治性心肌缺血发生率（22.7%比4.4%）均明显降低（P均〈0.05）,而LVEF改善情况A组明显优于B组[（58.7±12.4）%比（47.6±11.9）%,P〈0.05]。结论：溶栓后的ST段抬高性心肌梗死患者应尽早转运到上级医院接受PCI治疗,以取得更好疗效。     

Are Reciprocal Changes a Consequence of “Ischemia at a Distance” or Merely a Benign Electrical Phenomenon? A Pulsed‐Wave Tissue Doppler Echocardiographic Study

Objectives: The aim of the present study was to investigate whether ST segment depression in precordial leads at the time of acute inferior myocardial infarction represents a reciprocal change rather than concurrent anterior wall ischemia on the surface electrocardiography. Background: The mechanism of reciprocal ST segment depression during acute myocardial infarction is controversial. “Ischemia at a distance” or a benign electrical phenomenon has been implicated in numerous reports. Pulsed‐wave tissue Doppler (PWTD) echocardiography can be used to examine the regional diastolic motion of the left ventricular myocardial wall and may allow the detection of ischemic segments. Methods: We evaluated regional myocardial ischemia using PWTD echocardiography in 48 patients with a first inferior wall myocardial infarction. The left ventricle was divided into 16 segments. PWTD echocardiographic velocities were obtained from each left ventricular segments. Results: Reciprocal ST segment depression was present in 35 patients (Group 1) but not in the remaining 13 patients (Group 2). There were no significant differences between groups 1 and 2 with respect to systolic (S) (7.4 ± 1.1 vs 6.8 ± 0.9 cm/s; P > 0.05), early (E) (10.5 ± 2 vs 9.4 ± 1.2 cm/s; P > 0.05), and late (A) (9.5 ± 3.2 vs 8.5 ± 2.3 cm/s; P > 0.05) diastolic waves peak velocities, E/A ratio 1.1 ± 0.2 vs 1.1 ± 0.1; P > 0.05), Ewave deceleration time (DT) (92 ± 17 vs 101 ± 16 ms; P > 0.05) and regional relaxation time (RT) (82 ± 19 vs 93 ± 21 ms; P > 0.05) in anterior wall (basal levels), which correspond to reciprocal ST segment depression on electrocardiography. According to E/A ratio detected by PWTD echocardiography in anterior wall and anterior septum, patients with reciprocal ST segment depression were also divided into two groups: Group A, with E/A ratio > 1; Group B, with E/A ratio < 1. Among the 35 patients with reciprocal ST segment depression, anterior wall ischemia was present in 10 patients and absent in 25 patients, whereas anterior septal ischemia was present 12 patients and absent in 23 patients. Conclusions: Reciprocal ST segment depression during the early phases of inferior infarction is an electrical reflection of primary ST segment elevation in the area of infarction.     

The giant R wave of acute myocardial infarction

The common clinical electrocardiographic criteria for diagnosis of acute transmural myocardial infarction include ST segment elevation and tall, upright T waves, but do not include changes in QRS morphology. The purpose of this study was to show that development of a 50% or greater increase in R wave amplitude, the giant R wave, in patients with acute transmural myocardial infarction occurs, and also to characterize changes in QRS morphology which may aid the ECG diagnosis of acute transmural myocardial infarction. Over the past 6 years, 36 patients with an increase in R wave amplitude during acute transmural myocardial infarction were identified at the Strong Memorial Hospital Coronary Care Unit. A significant increase in R wave height (0.33 +/- 0.10 to 0.97 +/- 0.08 mV, p less than 0.05), width (0.03 +/- 0.00 to 0.08 +/- 0.01, p less than 0.05) and area (0.01 +/- 0.00 to 0.05 +/- 0.01 mV-msec, p less than 0.05) appeared in the same ECG lead demonstrating ST segment elevation and tall T waves during the acute phase of transmural myocardial infarction. Patients with diaphragmatic myocardial infarction showed a significant (p less than 0.05) rightward QRS frontal plane axis shift and patients with anterior wall myocardial infarctions developed an anterior QRS axis shift in the horizontal plane during occurrence of the giant R wave. We conclude from this preliminary study that the giant R wave may be observed during acute transmural myocardial infarction and may in part be caused by local intramyocardial conduction delay in acutely ischemic tissue as supported by an increase in the R wave width along with shifts in the frontal and horizontal plane QRS axis toward the area of acute ischemia. The giant R wave occurs in conjunction with ST segment elevation and tall T waves and may aid the ECG diagnosis of acute transmural myocardial infarction.     

Intracoronary ST segment evolution during primary coronary stenting predicts infarct zone recovery

In patients with acute myocardial infarction (AMI), early ST segment elevation resolution on ECG predicts myocardial reperfusion and LV recovery. Intracoronary ECG is more sensitive than surface ECG to detect regional ischemia. In patients undergoing primary percutaneous coronary intervention (PCI), we investigated if failed myocardial reperfusion, despite successful infarct vessel recanalization, could be rapidly and easily identified by intracoronary ST segment monitoring from guidewire recording. We recorded intracoronary and standard ECG during primary coronary stenting (PCI) in 50 patients with AMI (59 ± 11 years; anterior AMI in 66%). All patients had a successful PCI and underwent 2D echocardiography soon after PCI and 6 months later. Following PCI, intracoronary ST resolution ≥ 50% from baseline was documented in 39 patients (78%; group A; from 11 ± 8 to 1 ± 2 mm) but not in 11 (22%; group B; from 11 ± 8 to 8 ± 5 mm). Group A had slightly shorter ischemic time (202 ± 94 vs. 238 ± 112 min in B; P = 0.2) and smaller peak CK values (2,752 ± 2,038 vs. 4,802 ± 3,671 U/L in B; P = 0.02). After PCI, ST resolution was found on standard ECG in 34 (87%) group A and in 3 (27%) group B patients. At 6‐month follow‐up, left ventricular ejection fraction was greater in group A (47% ± 8% vs. 39% ± 8% in B; P < 0.001) with improved wall motion score index (from 2.2 ± 0.3 to 1.7 ± 0.3 in A; from 2.3 ± 0.4 to 2.1 ± 0.4 in B; P < 0.001). There were no significant differences between intracoronary and standard ECG for sensitivity (92% vs. 86%) and specificity (62% vs. 57%) to predict improved infarct zone recovery after 6 months. ST elevation resolution on intracoronary recording during PCI predicts infarct zone recovery. Monitoring ST segment evolution by intracoronary ECG allows prompt and inexpensive identification in the catheterization laboratory of those patients without myocardial reperfusion, who may require adjunctive therapeutic interventions after successful infarct vessel recanalization. Catheter Cardiovasc Interv 2005;64:53–60. © 2004 Wiley‐Liss, Inc.     

Silent ischemia and loss of reversible myocardial dysfunction following myocardial infarction

Sixty-seven asymptomatic patients were enrolled after a first uncomplicated myocardial infarction (MI) so as to study the relevance of reversible myocardial dysfunction in determining left ventricular function soon after the acute episodes and 12 months later. Moreover, the potential role of silent ischemia in conditioning the evolutive aspects of contractile dysfunction has been investigated. Postextrasystolic potentiation during two-dimensional echocardiographic (2-D echo) monitoring has been used to detect the presence of viable myocardium in asynergic myocardial segments. Results of electrocardiographic (ECG) ambulatory monitoring at predischarge determined patient groups: Group A included 49 patients without ST changes during monitoring, while Group B included 18 patients with silent ischemia. Incidence of reversible myocardial dysfunction was similar in the two study groups (82 vs. 86%, p = NS). Group B patients were older (59.6 ± 6.7 vs. 50.6 ± 10.6 years, p < 0.015) and had lower ejection fractions (EFs, 43.4 ± 6.4% vs. 51.2 ± 8.3%, p = 0.026) and higher at-rest wall-motion scores (WMSs, 11.4 ± 5.9 vs. 7.2 ± 3.8, p = 0.019). Left ventricular end-diastolic volume (LVEDV) and potentiated WMS did not differ. At 1-year examination, Group B patients exhibited a greater LVEDV index (96 ± 6.5 vs. 70.7 ± 14 ml/m², p < 0.002) with a worsening both in rest and in potentiated wall-motion score index (12.8 ± 4.6 vs. 5.3 ± 1.8, p < 0.001; 9.2 ± 3.6 vs. 4.8 ± 2.2, p < 0.001, respectively). Left ventricular EF remained significantly depressed in Group B patients (42 ± 8.7% vs. 55.5 ± 8.1%, p < 0.002). Over the first year, spontaneous functional recovery of asynergic segments occurred in 60% of Group A patients with reversible myocardial dysfunction at early study. In Group B patients, only three (20%) showed functional recovery, and a small number (24%) maintained reversible contractile dysfunction. Thus, reversible contractile dysfunction is a common finding in asymptomatic patients without clinical ischemia soon after a first MI. The presence of silent ischemia during ambulatory ECG monitoring identifies a group of patients at high risk of further loss of myocardial viability and progressive left ventricular dilation over the first year.     

Role of myocardial ischemia in the genesis of stress-induced S-T segment elevation in previous anterior myocardial infarction

This study tests the hypothesis that myocardial ischemia is responsible for exercise-induced S-T segment elevation in patients with previous anterior myocardial infarction (MI). Exercise stress testing in conjunction with thallium imaging of the myocardium was performed in 28 patients with previously documented anterior MI. Thallium images were analyzed by computer for the presence of initial uptake defects and evidence of abnormal clearance of the isotope from the myocardium (that is, imaging evidence of ischemia). Total S-T segment elevation (∑ST) in precordial leads V₁ to V₆ at rest was subtracted from ∑ST at peak stress in order to quantitate the extent of S-T elevation induced by stress (ΔST). Two groups of patients were identified; 1 with stress-induced S-T elevation (Group I, ΔST ≥ 4.0 mm) and 1 without this abnormality (Group II, ΔST < 4.0 mm). Evidence of abnormal thallium washout from myocardial scan segments occurred in 12 of 15 Group I patients versus 9 of 13 Group II patients (difference not significant). In addition, abnormal tracer washout from anterolateral or septal scan segments occurred in 5 patients in each group. Likewise, abnormal thallium clearance from inferior or posterior scan segments occurred in 8 of 15 Group I patients versus 7 of 13 Group II patients (difference not significant). The patient with the greatest amount of stress-induced S-T elevation (S-T 11.5 mm) had no evidence of ischemia during the stress test. However, Group I patients did have larger anterolateral plus septal initial thallium uptake defect scores than did those of Group II (10 of 15 with defect score ≥ 350 in Group I versus 1 of 13 in Group II, p <0.002). Similarly, resting left ventricular ejection fraction ≥ 30% was present in only 4 of 15 Group I patients versus 13 of 13 in Group II (p <0.001). Finally, multiple stepwise linear regression analysis demonstrated that ΔST correlated best with the extent of initial anterolateral plus septal thallium uptake defect score (F = 17.3, p < 0.001) and to a lesser extent with resting ejection fraction (F = 5.2, p < 0.05) and change in heart rate from rest to peak stress (F = 8.1, p < 0.01; corrected multiple correlation coefficient = 0.76, p < 0.001). Thus, in patients with previous anterior MI (1) exercise-induced myocardial ischemia occurs as often with as without S-T segment elevation, (2) myocardial ischemia is not required for the production of stress-induced S-T segment elevation, and (3) stress-induced S-T elevation primarily reflects the extent of previous anterior wall damage and to a lesser extent an increase in heart rate between rest and peak stress.