Differences in left ventricular function between anterior and inferior myocardial infarction of equivalent enzymatic size

The reasons for the poorer prognosis of anterior versus inferior myocardial infarction of equivalent enzymatic size remain uncertain. We investigated whether there are differences in left ventricular function between patients with anterior and inferior infarctions of equivalent enzymatic size to account for their differing outcomes. Clinical, serum enzyme, and electrocardiographic data were prospectively recorded in a consecutive series of patients less than 70 years of age with their first myocardial infarction. At 29 +/- 6 days following infarction, ejection fraction and left ventricular wall motion were assessed by gated heart scintigraphy and functional capacity by treadmill exercise testing in 19 patients with anterior and in 23 patients with inferior myocardial infarction. Peak creatine kinase and QRS scores were used to estimate total infarct size and left ventricular infarct size respectively. The anterior infarcts were of similar size to the inferior infarcts as determined by peak creatine kinase (1444 [mean] +/- 1161 [SD] U/L versus 1484 [mean] +/- 1182 [SD] U/L, respectively, P = 0.91) and peak aspartate transaminases (174 +/- 112 U/L versus 164 +/- 102 U/L, P = 0.78). The anterior myocardial infarct group had a greater percentage of the left ventricle infarcted on QRS scoring than the inferior infarct group (25.9 +/- 14.4% versus 11.1 +/- 6.0% respectively, P = 0.0004), lower global left ventricular ejection fraction (45.8 +/- 16% versus 54.6 +/- 9.2%, P = 0.04) and greater left ventricular regional wall abnormality. A significant negative correlation existed between left ventricular ejection fraction and peak creatine kinase for both groups, but was more marked with anterior infarction (r = -0.78, P less than 0.01) compared with inferior infarction (r = -0.49, P less than 0.05). Exercise-induced ST segment elevation was more frequent in the anterior than the inferior infarct group (59% versus 18%, P less than 0.02). However, both infarct locations had similar exercise tolerance, exercise-induced angina and ST segment depression. Despite equivalence of infarct size of the two infarct locations on enzyme testing, anterior infarction was associated with greater abnormality of left ventricular function with lower resting global left ventricular ejection fraction; greater resting left ventricular regional wall abnormality and greater exercise-induced ST segment elevation. These differences probably contribute to the poorer prognosis of patients with anterior infarction compared to those with inferior infarction of equivalent enzymatic size, given the previously well-documented prognostic importance of left ventricular function.     

急性下壁心肌梗死心电图胸前导联V1-3 ST段抬高的临床意义

目的 探讨急性下壁心肌梗死患者心电图胸前导联ST段抬高与冠状动脉造影所示冠状动脉病变的关系及其临床意义.方法 187例急性下壁心肌梗死患者,按入院时18导心电图胸前导联ST段改变分为2组,ST段抬高组（16例）和非ST段压低组（171例）.所有患者均行冠状动脉造影术,病变适合行经皮腔冠状动脉成型术并检测B型钠尿肽（BNP）.结果 急性下壁心肌梗死伴胸前导联ST段抬高时多为右冠状动脉近段闭塞,尤其是圆锥支闭塞（P＜0.01）,且伴有右心功能不全和血流动力学障碍,与下壁右室心梗相比BNP差异有统计学意义（P＜0.01）.结论 急性下壁心肌梗死合并胸前导联ST抬高表明为右冠状动脉近段或开口闭塞且多伴右室心肌梗死和心功能不全.     

急性下壁心肌梗死患者心电图胸前导联ST段改变的临床意义

目的探讨急性下壁心肌梗死患者心电图胸前导联ST段改变与冠状动脉造影(CAG)所见冠状动脉病变部位的关系及其临床意义。方法 187例急性下壁心肌梗死患者,按入院时18导心电图胸前导联ST段改变分为3组,ST段无变化组(47例),ST段抬高组(16例),ST段压低组(124例);所有患者均行CAG。结果急性下壁心肌梗死伴胸前导联ST段抬高时多为右冠状动脉(RCA)近段闭塞(14例,82.3%),尤其是伴圆锥支动脉闭塞,与RCA中远端闭塞(2例,5.9%)比较差异有统计学意义(P0.01),且14例(73.7%)伴有右心功能不全和血流动力学障碍。下壁心肌梗死胸前导联ST段压低者可见于RCA、回旋支(LCX)闭塞及RCA、LCX闭塞与前降支(LAD)、对角支(D)病变的不同组合,其中LCX闭塞伴RCA病变者多表现为朐前ST V_4～V_6的压低,RCA闭塞伴LAD近端病变多有胸前ST V_1～V_6的压低,RCA伴D病变胸前ST V_1～V_3压低,与对照组比较差异有统计学意义(P0.05)。结论急性下壁心肌梗死合并胸前导联ST段抬高表明为RCA近段或丌口闭塞且多伴右心室心肌梗死和心功能不全;下壁心肌梗死伴胸前导联ST段压低提示为多支病变,ST V_1～V_3压低多伴有对角支严重狭窄,STV_1～V_6压低多伴有前降支的严重狭窄。     

Effect of spontaneous reperfusion on myocardial infarct size

The effect of perfusion of the infarct artery on myocardial infarct size was studied in 39 patients who had not received interventive therapy. At predischarge coronary angiography, 19 patients had subtotal and 20 total occlusion of the infarct artery. The early ST-segment elevation recorded on a 12-lead electrocardiogram was used as an index of the amount of initially jeopardized myocardium. Infarct size was estimated by peak serum creatine kinase and, at discharge, by a QRS score, sigma Q and sigma R on a 12-lead electrocardiogram, and by radionuclide global and infarct segment left ventricular ejection fraction. Despite a similar degree of initial ischemia (sigma ST), infarct size was smaller in the 11 patients with anterior infarction and subtotal occlusion than in the 9 patients with anterior infarction and total occlusion when measured by peak serum creatine kinase (2114 +/- 1192 U/l vs. 3653 +/- 1059 U/l, p less than 0.02), QRS score (5.0 +/- 2.7 vs. 9.6 +/- 3.5, p less than 0.01), sigma Q (3.25 +/- 2.74 mV vs. 5.92 +/- 3.56 mV, p less than 0.10), sigma R (4.36 +/- 1.25 mV vs. 2.16 +/- 0.91 mV, p less than 0.001), global left ventricular ejection fraction (45.0 +/- 12.2% vs. 33.4 +/- 6.7%, p less than 0.05), and infarct segment ejection fraction (40.4 +/- 8.2% vs. 30.3 +/- 5.4%, p less than 0.05). In the inferior infarct patients, both the degree of initial ischemia and final infarct size were similar in the 8 patients with subtotal and in the 11 patients with total occlusion.(ABSTRACT TRUNCATED AT 250 WORDS)     

Resolution of ST-segment elevation after streptokinase therapy in anterior versus inferior wall myocardial infarction

BACKGROUND: Resolution of ST-segment elevation is the best bedside predictor of myocardial reperfusion. HYPOTHESIS: This study was conducted to examine the resolution of ST-segment elevation after streptokinase therapy in anterior versus inferior acute myocardial infarction (MI) and to corroborate it with echocardiographic and coronary angiographic data. METHODS: The study population consisted of 70 patients, 35 each in the anterior and inferior MI groups. The electrocardiograms (ECGs) were recorded before, on completion of, and on Days 1 and 2 post streptokinase therapy. The resolution of ST segment determined from post-streptokinase ECGs was compared between the two groups and correlated with echocardiographic and coronary angiographic data. RESULTS: On completion of and on Day 1 post streptokinase therapy, ST-segment resolution in both groups was not significantly different. On Day 2 post streptokinase therapy, resolution of the ST segment per lead was significantly lower in anterior than that in inferior MI (61 +/- 21% anterior vs. 77 +/- 21% inferior, p 0.003). The number of patients with akinesis of infarct-related ventricular wall was significantly higher (17 anterior vs. 7 inferior, p 0.02), and left ventricular ejection fraction was significantly lower in anterior MI (39 +/- 7% anterior vs. 48 +/- 8% inferior, p < 0.01). There was no significant difference in coronary angiographic data. One patient in each group demonstrated normal coronary arteries. CONCLUSIONS: The resolution of ST-segment elevation on the completion of and on Day 1 post streptokinase therapy was comparable between anterior and inferior MI. The significantly less frequent resolution of ST-segment elevation in anterior MI on Day 2 post streptokinase could be due to more akinesis, larger infarct size, and worse systolic function rather than due to failure to open the infarct-related vessel.     

Serum leptin levels in acute myocardial infarction

BACKGROUND: Several studies have shown an association of serum leptin levels with cardiovascular diseases. The present study was undertaken to assess levels of serum leptin in patients presenting with acute ST segment elevation myocardial infarction. METHODS AND RESULTS: Ninety-four consecutive patients presenting with acute ST segment elevation myocardial infarction were studied and 46 controls were taken from patients who presented with chest pain but had no history of myocardial infarction in the past. There were 59 patients with anterior wall infarction and 31 had inferior wall infarction and in 4 it was a combination of anterior and inferior wall infarction. The serum leptin levels in patients with myocardial infarction was 6.51 +/- 6.76 ng/ml versus 2.86 +/- 2.22 ng/ml in controls. In the multivariate analysis the odds ratio for serum leptin with myocardial infarction was 1.45 with a 95% confidence interval of 1.2 to 1.8. CONCLUSIONS: Our results suggest that serum leptin level is elevated in patients with acute ST segment elevation myocardial infarction.     

Anterior ST segment depression in acute inferior myocardial infarction as a marker of greater inferior, apical, and posterolateral damage

The clinical significance of anterior precordial ST segment depression during acute inferior myocardial infarction was evaluated in 67 consecutive patients early after onset of symptoms with gated blood pool scans, thallium-201 perfusion images, and 12-lead ECGs. Patients with anterior ST depression (n = 33) had depressed mean values for left ventricular ejection fraction (54 +/- 2% [mean +/- S.E.M.] vs 59 +/- 2%; p = 0.02), cardiac index (3.1 +/- 0.2 vs 3.6 +/- 0.2 L/m2; p = 0.03), and ratio of systolic blood pressure to end-systolic volume (2.0 +/- 0.1 vs 2.5 +/- 0.3 mm Hg/ml; p = 0.04) compared to patients with no anterior ST depression (n = 34). Patients with anterior ST depression had (1) lower mean wall motion values for the inferior, apical, and inferior posterolateral segments (p less than 0.05) and (2) greater reductions in thallium-201 uptake in the inferior and posterolateral regions (p less than 0.05). However, anterior and septal (1) wall motion and (2) thallium-201 uptake were similar in patients with and without ST depression. Thus, anterior precordial ST segment depression in patients with acute inferior wall myocardial infarction represents more than a reciprocal electrical phenomenon. It identifies patients with more severe wall motion impairment and greater hypoperfusion of the inferior and adjacent segments. The poorer global left ventricular function in these patients is a result of more extensive inferior infarction and not of remote septal or anterior injury.     

Anterior ST-segment deviation during inferior myocardial infarction: arteriographic correlations during the acute phase

Electrocardiographic changes in the anterior wall lead in inferior myocardial infarction were studied in coronary angiographic findings in the acute stage. The subjects were 40 patients with initial inferior myocardial infarction due to right coronary lesions. ST segments were elevated in 7 patients, remained unchanged in 11 and were depressed in 22. Two patients predominantly perfused in the left coronary artery showed ST elevation. All seven patients who showed elevation of the ST segments had occlusion of the ventricular branch proximal to right. However, another 15 (68%) of the patients with occlusion of the same lesion did not show elevation of any ST segment. There was no difference in left ventricular ejection fraction between the groups. The regional ejection fraction at the left ventricular inferior wall was significantly (p less than 0.01) higher in the ST elevated group than in the ST depressed group. Elevation of the ST segments in the anterior wall lead was observed only when the right ventricular free wall sustained injury, and no elevation of any ST segment was observed when the range of injury in the inferoposterior wall was wide, even in the presence of injury to the right ventricular free wall.     

Predicting cardiac mortality after uncomplicated myocardial infarction by exercise radionuclide ventriculography and exercise-induced ST segment elevation.

In 183 consecutive patients with recent, uncomplicated myocardial infarction, the following variables were associated with 4-year cardiac death: haemodynamic decompensation with exercise (P = 0.01), left ventricular ejection fraction at rest (P = 0.004) and at peak exercise (P = 0.003), persistent ST segment elevation at rest in the area of infarction = (P = 0.004), exercise-induced ST segment elevation (P = 0.02), and late aneurysmal evolution (P = 0.01). Exercise left ventricular ejection fraction was the sole variable selected by Cox regression analysis as an independent predictor of cardiac death. In 40 patients with ST segment elevation at rest, left ventricular ejection fraction was 42 +/- 17% at rest and 40 +/- 18% at peak exercise, versus 52 +/- 12% and 52 +/- 14% in the remaining patients (both P less than 0.01). Among these 40, 16 (all with anterior infarction) also had exercise-induced ST segment elevation; their ejection fraction was 32 +/- 13% at rest, 30 +/- 13% during exercise, versus 53 +/- 15% and 53 +/- 15% in 129 patients with no ST segment elevation either at rest, or during exercise (both P less than 0.01). The 4-year risk of death was 20% in the former 40 patients, 36% in the latter 16, while in the complete absence of ST segment elevation, such risk was 3%. All 14 patients with ST segment elevation only during exercise were alive after 4 years: their left ventricular ejection fraction was 47 +/- 12% at rest, 45 +/- 13% with exercise. ST segment elevation was associated with late aneurysmal evolution but not with exercise-induced ischaemia.(ABSTRACT TRUNCATED AT 250 WORDS)     

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.     

Q-wave evolution of a first acute myocardial infarction without significant ST segment elevation

BACKGROUND: Some patients with acute myocardial infarction presenting without significant ST segment elevation develop a Q-wave infarction. It is unclear whether these patients can be identified from the admission electrocardiogram (ECG) and whether they differ in their in-hospital prognosis from those who retain a non-Q-wave myocardial infarction. METHODS: In 432 consecutive patients admitted to our centre with a first acute myocardial infarction without Q waves and with ST segment amplitudes < or =0.1 mV on admission, we assessed the frequency, the electrocardiographic predictors and the short-term implications of a Q-wave evolution. RESULTS: In 94 patients (22%), a Q-wave myocardial infarction evolved before hospital discharge (14 anterior, 26 inferior, six lateral, and 48 posterior). Minor anterior ST segment elevation was 36% sensitive and 95% specific in predicting anterior Q waves; minor inferior ST segment elevation, 42% and 89%, respectively, for inferior Q waves; and a maximal ST segment depression > or =0.2 mV in leads V2-V3 with upright T waves and without remote ST segment depression, 38% and 97%, respectively, for posterior R waves. Although patients with a Q-wave evolution had a greater creatinkinase MB peak than those retaining a non-Q-wave pattern (191+/-113 vs. 105+/-77 IU/l, respectively, P<0.001), they experienced a benign in-hospital course, with similar risk of severe complications after adjustment for the baseline clinical predictors than non-Q-wave patients. CONCLUSIONS: About one fifth of patients with a first acute myocardial infarction without a significant ST segment elevation develop a Q-wave infarction and the admission ECG can help identify them. This evolution, however, is not associated with a worse in-hospital outcome.     

Exercise-induced ST segment elevation 2 weeks after uncomplicated myocardial infarction: contributing factors and prognostic significance

To define the prevalence and clinical significance of exercise-induced ST segment elevation during predischarge treadmill testing after uncomplicated acute myocardial infarction confirmed by serum MB creatine kinase (CK) activity, 241 consecutive patients were prospectively investigated with quantitative exercise thallium-201 scintigraphy, rest radionuclide ventriculography and coronary angiography at 10 +/- 3 days. All patients received customary care, and in none was thrombolytic therapy or emergency coronary angioplasty employed. Eighty-two patients (34%) had exercise-induced ST segment elevation of greater than or equal to 1 mm above rest baseline. These patients were similar to the 159 patients without this finding with respect to history of prior infarction, the Norris coronary prognostic index, exercise duration, metabolic equivalents (METs) achieved and peak heart rate-blood pressure product. The frequency of inducible myocardial ischemia and extent of angiographic coronary disease was also comparable in the two groups. Findings associated with larger infarct size and transmural extent of infarction were more common in patients with exercise-induced ST segment elevation than in those without, including higher peak CK values (1,235 +/- 1,037 versus 942 +/- 915 mumol/min per liter, p less than 0.026), lower left ventricular ejection fraction (43 +/- 12 versus 51 +/- 10%, p less than 0.001), a higher prevalence of pathologic Q waves in greater than or equal to 2 contiguous infarct-related leads (80 versus 55%, p less than 0.001), more persistent thallium-201 defects (2.2 +/- 1.1 versus 1.4 +/- 1.1, p less than 0.001), abnormally increased lung uptake of thallium (33 versus 18%, p less than 0.01) and a greater number of akinetic or dyskinetic segments (3.2 +/- 2.5 versus 1.4 +/- 1.9, p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)     

老年急性心肌梗死患者发病时间与梗死部位及ST段偏移的相关性

目的 探讨老年急性心肌梗死患者发病时间与梗死部位及ST段偏移的相关性. 方法 对909例老年急性心肌梗死患者(其中包括412例前壁和423例下壁的急性心肌梗死患者)发病时间、部位和ST段抬高及冠状动脉造影等临床资料进行分析. 结果 老年急性心肌梗死患者在清晨6时至中午12时发病为525例(57.8%).24时至清晨6时发生下壁心肌梗死138例(32.6%),与其他时间比较,差异有统计学意义(P<0.01),从清晨6时至中午12时,发生前壁心肌梗死156例(37.9%),与其他时间段比较,差异有统计学意义(P<0.01),516例冠状动脉造影的AMI患者中,24时至清晨6时发病的急性下壁心肌梗死118例,其病变累及右冠状动脉多于累及左冠状动脉[分别为85.6%(101/118)和14.0%(17/118),P<0/013,清晨6时至24时发病的急性下壁心肌梗死275例,其病变累及右冠状动脉与左冠状动脉分别为54/2%(149/275)和45.8%(126/275)(P>0.05);732例急性ST段抬高患者在清晨6时至中午12时发病率最高为44.0%(263/644),265例非ST段抬高的心肌梗死24时至清晨6时发病率最高为36.6%(96/265). 结论 老年急性心肌梗死患者中,夜间非ST段抬高的发生率高于ST段抬高.由于夜间右冠状动脉闭塞所引起的急性下壁心肌梗死多于左冠状动脉,所以睡眠对老年患者的左冠状动脉累及和急性非ST段抬高性心肌梗死的保护作用是有限的.     

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.     

Influence of infarct artery patency on the relation between initial ST segment elevation and final infarct size.

Thirty seven patients with acute myocardial infarction were studied to determine the effect of perfusion of the infarct artery on the relation between the extent of initial ST segment elevation and final electrocardiographic infarct size. The sum of the initial peak ST elevations in all leads correlated with electrocardiographic infarct size in patients with anterior infarction and total occlusion of the infarct artery without collaterals. In patients with anterior infarction and subtotal occlusion of the infarct artery and in all patients with inferior infarction, infarct size was smaller than predicted from the extent of initial ST segment elevation. Collaterals to the infarct artery were present in eight of the 10 patients with inferior infarction and total occlusion. In patients with a persistently occluded infarct artery without collaterals the final infarct size correlated with the extent of initial peak ST segment elevation. This study provides further evidence that spontaneous reperfusion by anterograde flow or via collaterals may salvage jeopardized myocardium.     

Influence of infarct artery patency on the relation between initial ST segment elevation and final infarct size

Thirty seven patients with acute myocardial infarction were studied to determine the effect of perfusion of the infarct artery on the relation between the extent of initial ST segment elevation and final electrocardiographic infarct size. The sum of the initial peak ST elevations in all leads correlated with electrocardiographic infarct size in patients with anterior infarction and total occlusion of the infarct artery without collaterals. In patients with anterior infarction and subtotal occlusion of the infarct artery and in all patients with inferior infarction, infarct size was smaller than predicted from the extent of initial ST segment elevation. Collaterals to the infarct artery were present in eight of the 10 patients with inferior infarction and total occlusion. In patients with a persistently occluded infarct artery without collaterals the final infarct size correlated with the extent of initial peak ST segment elevation. This study provides further evidence that spontaneous reperfusion by anterograde flow or via collaterals may salvage jeopardized myocardium.     

Acute non-Q wave myocardial infarction associated with early ST segment elevation: evidence for spontaneous coronary reperfusion and implications for thrombolytic trials

The clinical significance of early ST segment elevation in patients with non-Q wave infarction is unknown. Therefore, 150 consecutive patients with creatine kinase isoenzyme-confirmed acute uncomplicated myocardial infarction who had ST segment elevation of 1 mm or more in at least two contiguous leads on the admission electrocardiogram were analyzed. None received thrombolytic therapy or acute coronary angioplasty. Predischarge angiography, radionuclide ventriculography and exercise thallium-201 scintigraphy were performed 10 +/- 3 days after myocardial infarction. Based on serial electrocardiograms (on days 1, 2, 3 and 10), all 150 infarcts were classified as Q wave (n = 115 [77%]) or non-Q wave (n = 35 [23%]). Although patients with Q wave infarction exhibited greater ST elevation, the amount observed in the non-Q wave group was appreciable, as reflected by the number of leads with ST elevation (3.8 +/- 1.8 versus 3.1 +/- 1.2, p = 0.007) and the sum of the ST elevation (9.6 +/- 7.4 versus 6.2 +/- 6.2 mm, p = 0.016). When compared with the Q wave group, patients with non-Q wave infarction had a shorter time to peak creatine kinase (23.0 +/- 9.1 versus 15.8 +/- 7.9 hours, p = 0.0001), a higher infarct vessel patency rate (24 versus 57%, p = 0.001), lower peak creatine kinase values based on 4 hour sampling (1,372 +/- 964 versus 664 +/- 924 IU/liter, p = 0.0002) and a higher left ventricular ejection fraction (46 +/- 12% versus 54 +/- 9%, p = 0.0003).(ABSTRACT TRUNCATED AT 250 WORDS)     

Reciprocal ST change in acute myocardial infarction: assessment by electrocardiography and echocardiography

To evaluate the incidence, time course and significance of reciprocal change, 25 consecutive patients admitted with their first acute transmural myocardial infarction were studied with serial electrocardiography and two-dimensional echocardiography. Reciprocal change was noted in all patients with inferior infarction (mean maximal ST segment depression 3.53 +/- 1.97 mm) and 70% of patients with anterior infarction (mean maximal ST depression 1.45 +/- 0.8 mm, p = 0.001). When initially present, reciprocal change had resolved within 24 hours in 59% of patients. The sum of reciprocal ST depression correlated with the sum of ST elevation in anterior (r = 0.92, p less than 0.001) and inferior (r = 0.55, p = 0.035) infarction, and this relation persisted when maximal ST depression and elevation were considered. Echocardiographic evidence of contraction abnormalities in areas of the left ventricle remote from the infarction was seen in 45% of patients. However, its presence did not correlate with the presence of reciprocal change. Although reciprocal change progressively diminished on serial electrocardiograms (maximal ST depression 2.73 +/- 1.77 mm at 19 hours after onset of symptoms; 1.0 +/- 0.92 mm at 2 to 3 days; and 0.22 +/- 0.26 mm at 7 to 10 days; p less than 0.05), the corresponding serial echocardiograms showed no change in the function of the remote wall (remote wall motion index 1.87 +/- 0.65, 1.81 +/- 0.62, 1.86 +/- 0.47, respectively, p = NS). These data, therefore, do not support the hypothesis that reciprocal ST depressions during early acute transmural myocardial infarction reflect remote ischemia. Rather, these changes are influenced by factors determining the degree of acute ST elevation, previously shown to include infarct size, shape, location, transmurality and duration.     

ST segment elevation in leads V1 to V3 due to isolated right ventricular branch occlusion during primary right coronary angioplasty.

It is rare to observe ST elevation in anterior derivations caused by isolated right ventricular branch occlusion. We described the case with acute inferior and right ventricular myocardial infarction (MI) who developed ST segment elevation in precordial leads V(1) to V(3) due to isolated right ventricular branch occlusion during primary right coronary angioplasty.     

Early peak activity of creatine kinase in non-thrombolysed myocardial infarction: prognostic factor?

The time elapsed between the onset of pain and serum creatine kinase (CK) peak activity is an indirect marker of reperfusion in the thrombolytic treatment of myocardial infarction, and some authors regard this time as a prognostic factor in infarctions not treated with thrombolysis. CK activity was measured in 90 consecutive patients (mean age 66.9 +/- 13.7 years) with acute myocardial infarction (anginal pain + ECG signs + CK greater than 160 3U/l, including 40 p. 100 of CK MB). Measurements began at the time of admission to the intensive care unit and were repeated 6-hourly until CK levels returned to normal. Mean time of CK peak activity was 19.30 +/- 7.15 h after the initial pain (8 to 55 hours prior to admission). This time was not influenced by age, sex, presence or absence of risk factors and history of coronary disease, nor by the anterior or transmural location of the infarct. In contrast, an early arrival at the intensive care unit was associated with an early CK peak: patients who reached the unit within 6 hours or less had a peak at 18.15 +/- 6 h, whereas those who arrived after 6 h had a peak at 22.30 +/- 9.30 h (p less than 0.01). In addition, cases of infarction without Q wave and with an initially elevated ST segment had an earlier peak than the others (16.30 +/- 5.30 h vs 19 +/- 6.45 h in transmural infarctions and vs 24.30 +/- 7.30 h in infarctions with initially depressed ST; p less than 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)