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.     

Right ventricular infarction complicating left ventricular infarction secondary to coronary heart disease: Frequency, location, associated findings and significance from analysis of 236 necropsy patients with acute or healed myocardial infarction

Right ventricular infarction associated with left ventricular infarction was identified by gross examination at necropsy in 33 (14 percent) of 236 patients with transmural myocardial infarction. Right ventricular infarction occurred exclusively as a complication of posterior left ventricular infarction. Associated right ventricular infarction occurred in none of the 97 patients with isolated anterior wall infarction of the left ventricle, but in 33 (24 percent) of the 139 patients with posterior left ventricular infarction. Transmural infarction of the posterior ventricular septum was an additional prerequisite for right ventricular infarction. Of the 139 patients with infarction of the posterior left ventricular wall, 74 had no transmural infarction of the ventricular septum and none of these 74 had associated right ventricular infarction. In contrast, of the 65 patients with infarction of the posterior left ventricular wall and transmural infarction of the ventricular septum, 33 (50 percent) had associated right ventricular infarction.

Among the 33 patients with right ventricular infarction, the infarct was limited to the posterior right ventricular free wall in 27 (82 percent); in the other 6 patients (18 percent) it extended to involve the anterolateral right ventricular free wall. Among patients with a posterior left ventricular infarct, those with a right ventricular infarct had right ventricular dilatation nearly three times (P < 0.05) more frequently than the patients without a right ventricular infarct. Comparison of the same two groups disclosed no differences in the patients' age, sex, extent of coronary arterial luminal narrowing, right ventricular hypertrophy, right ventricular thrombi or duration of symptoms of myocardial ischemia.

Hemodynamic data in four patients with a right ventricular infarct disclosed previously reported characteristic hemodynamics of right ventricular infarction in only one patient. Recognition of right ventricular infarction is important because it implies specific therapy, namely, aggressive volume administration. Clinical evidence of posterior left ventricular infarction and right ventricular dilatation should arouse strong suspicion of associated right ventricular infarction.     

Reduction of infarct size in patients with inferior infarction with intravenous glyceryl trinitrate. A randomised study

Glyceryl trinitrate was previously said to be contraindicated in patients with acute myocardial infarction. Its intravenous administration during acute infarction, however, was associated with a beneficial effect as determined by ST segment mapping. Most recently in a selected group of patients with acute infarction and abnormal haemodynamics, intravenous glyceryl trinitrate was shown to reduce infarct size estimated by enzymes. The present study was performed to verify the safety of intravenous glyceryl trinitrate in patients with infarction under conventional clinical conditions without invasive monitoring and to determine its effect on infarct size in a prospective randomised trial involving 85 patients with infarction (43 treated and 42 control). Treated patients received glyceryl trinitrate within 10 hours of the onset of symptoms (mean 6.0 hours), and the dose was titrated to preset limits for changes in heart rate and blood pressure. In patients with inferior infarction, infarct size estimated by enzymes in the treated was only 12.2 +/- 1.8 versus 19.1 +/- 3.6 CK gram equivalents per metre squared in the placebo group. A similar but statistically insignificant trend was observed for subendocardial infarction but no difference was observed for anterior infarction. Ventricular arrhythmias determined from 24 hour tapes were more frequent in treated patients though this was not statistically significant. Lignocaine requirements in treated and control (1692 +/- 250 vs 1512 +/- 232 mg/24 h) were similar, as were the requirements for morphine (11.4 +/- 1.8 vs 12.2 +/- 2.2 mg/24 h). Results indicate that intravenous glyceryl trinitrate can be administered safely during evolving infarction without invasive monitoring and reduces infarct size in patients with inferior infarction.     

Reduction of infarct size in patients with inferior infarction with intravenous glyceryl trinitrate. A randomised study.

Glyceryl trinitrate was previously said to be contraindicated in patients with acute myocardial infarction. Its intravenous administration during acute infarction, however, was associated with a beneficial effect as determined by ST segment mapping. Most recently in a selected group of patients with acute infarction and abnormal haemodynamics, intravenous glyceryl trinitrate was shown to reduce infarct size estimated by enzymes. The present study was performed to verify the safety of intravenous glyceryl trinitrate in patients with infarction under conventional clinical conditions without invasive monitoring and to determine its effect on infarct size in a prospective randomised trial involving 85 patients with infarction (43 treated and 42 control). Treated patients received glyceryl trinitrate within 10 hours of the onset of symptoms (mean 6.0 hours), and the dose was titrated to preset limits for changes in heart rate and blood pressure. In patients with inferior infarction, infarct size estimated by enzymes in the treated was only 12.2 +/- 1.8 versus 19.1 +/- 3.6 CK gram equivalents per metre squared in the placebo group. A similar but statistically insignificant trend was observed for subendocardial infarction but no difference was observed for anterior infarction. Ventricular arrhythmias determined from 24 hour tapes were more frequent in treated patients though this was not statistically significant. Lignocaine requirements in treated and control (1692 +/- 250 vs 1512 +/- 232 mg/24 h) were similar, as were the requirements for morphine (11.4 +/- 1.8 vs 12.2 +/- 2.2 mg/24 h). Results indicate that intravenous glyceryl trinitrate can be administered safely during evolving infarction without invasive monitoring and reduces infarct size in patients with inferior infarction.     

Assessment of myocardial infarct size in clinical practice

The myocardial infarct size was assessed on the basis of serial analyses of serum creatine phosphokinase (CPK) in 70 patients with first transmural myocardial infarction. Clinical symptoms of heart failure (Killip II-III) were found in patients with infarcts larger than 50 CPK-g-equ; in patients with lung oedema the infarct size averaged 104.2 CPK-g-equ. Patients without clinical and roentgenological evidence of left heart failure (Killip I) had infarct sizes always lesser than 50 CPK-g-equ, averaging 31.7 CPK-g-equ. Precordial mapping of the QRS complex in patients with anterior wall infarction revealed a significant correlation (r = 0.916) between the sum of voltages of Q waves on a 30-lead map recorded 24 hours after hospitalization and the enzymically assessed infarct size. Exact skiagraphic and auscultatory examinations of the heart and lungs, together with precordial mapping of the QRS complex, in patients with anterior wall infarct allow a relatively accurate quantification of the infarct size for prognostic classification of the patients.     

Relation between electrocardiography and coronary angiography findings in the infarct stage

One hundred and fifty-two patients underwent cardiac catheterization and coronary arteriography within 6.3 +/- 6.0 hours from onset of acute myocardial infarction. All had a standard 12-lead electrocardiogram recorded within 1.5 hours of cardiac catheterization. The electrocardiographic abnormalities present were correlated with the infarct related artery as determined by coronary arteriography. ST segment elevation was the most common finding in patients with the left anterior descending (LAD), or right coronary artery (RCA) as the infarct related artery. ST segment depression was the most common abnormality in patients with left circumflex artery (CX) as the infarct related artery. A typical pattern of anterior acute myocardial infarction was seen in 93% of all patients with the LAD as the infarct related artery. A typical pattern of acute inferior myocardial infarction was seen in 53% of all patients with RCA or CX narrowing taken as one group. The pattern of true posterior or posterolateral wall acute myocardial infarction in the absence of typical changes in the inferior leads was highly specific and predictive of CX narrowing. In contrast, the pattern of an inferior wall myocardial infarction, in the absence of true posterior or lateral wall changes, was highly specific and predictive of right coronary artery narrowing. Fifty-six percent of patients with CX artery as the infarct related artery presented with non-classical electrocardiographic abnormalities. The electrocardiographic pattern in patients with subtotal occlusions were similar to those of patients with total occlusions. Thus the electrocardiogram obtained in the first few hours of acute myocardial infarction is reliable in localizing the LAD as the infarct related artery.(ABSTRACT TRUNCATED AT 250 WORDS)     

Comparison of coronary angiography and early oral dipyridamole thallium-201 scintigraphy in patients receiving thrombolytic therapy for acute myocardial infarction

We evaluated 50 consecutive patients who received thrombolytic therapy for acute myocardial infarction using thallium-201 single photon emission computed tomography in combination with oral dipyridamole (300 mg) to assess the frequency of residual myocardial ischemia. Thallium studies were performed early after myocardial infarction at a mean of 4.6 days (range 3 to 11) in 50 patients. The time from the onset of chest pain to the administration of thrombolytic therapy was 2.6 hours (range 0.5 to 5.5). Q wave myocardial infarction was evident in 46 patients; four patients had a non-Q wave infarction (anterior infarction in 31 patients and inferior infarction in 19 patients). The serum mean peak creatinine kinase was 1503 IU/L (range 127 to 6500). Coronary angiography was performed in all patients at a mean of 3.1 days (range 2 to 10) and revealed the infarct-related vessel to be patent in 36 patients (72%). The ejection fraction was 48% (range 26% to 67%). After dipyridamole administration, 13 patients (26%) developed angina that was easily reversed with the administration of intravenous aminophylline. Systolic blood pressure decreased from 122 to 115 mm Hg (p less than 0.05) and the heart rate increased from 76 to 85 beats/min (p less than 0.05). None of the patients had significant hypotension, arrhythmias, or evidence of infarct extension. Perfusion abnormalities were present on the initial thallium images in 48 patients. Redistribution suggestive of ischemia was present in 36 patients (72%). Ischemia confined to the vascular distribution of the infarct vessel was evident in 22 patients. Seven patients had ischemia in the infarct zone as well as in a remote myocardial segment. Thus 29 patients (58%) had ischemia in the distribution of the infarct vessel. Ischemia in the infarct zone was evident in 19 of 36 patients (53%) with open infarct vessels and in 10 of 14 patients (71%) with occluded infarct vessels. In conclusion, thallium-201 single photon emission computed tomography using oral dipyridamole was safely performed in patients with recent myocardial infarctions who receive thrombolytic therapy.(ABSTRACT TRUNCATED AT 250 WORDS)     

Prognostic significance of location and type of myocardial infarction: independent adverse outcome associated with anterior location

To determine the relative prognostic significance of location (anterior or inferior) and type (Q wave or non-Q wave) of infarction, the hospital course and follow-up outcome (mean duration 30.8 months) of 471 patients with a first infarction were analyzed. Analyses were performed grouping the patients according to infarct location (anterior, n = 253; inferior, n = 218), infarct type (Q wave, n = 323; non-Q wave, n = 148), and both location and type (inferior non-Q wave, n = 85; inferior Q wave, n = 133; anterior non-Q wave, n = 63; and anterior Q wave, n = 190). Patients with anterior infarction had a substantially worse in-hospital and follow-up clinical course compared with those with inferior infarction, evidenced by a larger infarct size (21.2 versus 14.9 g Eq/m2 creatine kinase, MB fraction [MB CK], p less than 0.001), lower admission left ventricular ejection fraction (38.1 versus 55.3%, p less than 0.001) and higher incidence of heart failure (40.7 versus 14.7%, p less than 0.001), serious ventricular ectopic activity (70.2 versus 58.9%, p less than 0.05), in-hospital death (11.9 versus 2.8%, p less than 0.001) and total cumulative cardiac mortality (27 versus 11%, p less than 0.001). Patients with Q wave infarction similarly experienced a worse in-hospital course compared with patients with non-Q wave infarction, evidenced by a larger infarct size (20.7 versus 12.7 MB CK g Eq/m2, p less than 0.001), lower admission left ventricular ejection fraction (43.7 versus 50.6%, p less than 0.001), and a higher incidence of heart failure (31.9 versus 21.6%, p less than 0.05) and in-hospital death (9.3 versus 4.1% p less than 0.05). However, there was no increased rate of reinfarction or mortality in hospital survivors with non-Q wave infarction compared with those with Q wave infarction, and total cardiac mortality was similar (16 versus 21%, p = NS). To evaluate the role of infarct location and type independent of infarct size, patients were grouped according to quartile of infarct size, and outcome was reanalyzed within each group. Patients with anterior infarction demonstrated a lower left ventricular ejection fraction on admission and after 10 days than did patients with inferior infarction, even after adjustment for infarct size, as well as a higher incidence of congestive heart failure and cumulative cardiac mortality.(ABSTRACT TRUNCATED AT 400 WORDS)     

Dual radionuclide study of acute myocardial infarction: comparison of thallium-201 and technetium-99m stannous prophosphate imaging in man.

We evaluated dual imaging with thalium-201 (201TI) and technetium-99m (99mTc) pyrophosphate in 80 patients with documented acute myocardial infarction (55 transmural, 25 nontransmural infarction). Color-coded isocount display of 201TI images was essential for interpretation in 16 patients. Combined 201 TI and 99mTc-pyrophosphate imaging for infarct detection was 100% sensitive; however, either was falsely negative in 12 of 80 patients. False-negative individual 201TI or 99mTc-pyrophosphate infarct images were most common in patients with small infacts or left ventricular hypertrophy. Thallium-201 images correctly localized the site of acute transmural infarction in all 51 patients with a positive image, while 99mTc-pyrophosphate localized the site of infarction in 49 of 53 with an abnormal image. Comparison of the size of the imaged infarct region revealed size discordance in 25 of 49 patinets, with 99mTc-pyrophosphate larger in 21 of 49 and 201TI larger in only four of 49. Thus dual radionuclide imaging provides definition of the presence and location of acute myocardial infarction.     

Infarct size determined by emission computed tomography using 99mTc-PYP: effect of coronary thrombolysis

Emission computed tomography with 99mTc-PYP was used to estimate infarct size in 38 patients with documented acute myocardial infarction. In the present study, the effect of thrombolysis with Urokinase on infarct size and on left ventricular function was assessed. Fourteen patients with acute myocardial infarction who underwent intracoronary thrombolysis within six hours after the onset of symptoms, and 24 patients who underwent conventional therapy were the subjects of this study. Infarct size was measured by drawing a region of interest around the myocardial pyrophosphate uptake for each tomographic slice. The boundary was then defined as 65% of the maximal count within the region of interest as determined by phantom volume studies. The total number of voxels was obtained by adding those in all slices and multiplying the sum by the voxel volume (0.205 ml per one voxel) to determine the infarct volume. Measurement of the 99mTc-PYP uptake on the tomographic image revealed an average infarct size of 100.1 +/- 36.0 ml (ranged 45 to 198). The calculated infarct volume correlated significantly with sigma CPK (p less than 0.01) and with left ventricular ejection fraction (p less than 0.01), but not with the peak CPK. In patients with acute inferior myocardial infarction, the mean infarct volume was 78.4 +/- 29.1 ml in the coronary thrombolysis group, and 105.1 +/- 33.7 ml in the conventional bypass graft treatment group (p less than 0.05). We concluded that successful intracoronary thrombolysis may reduce infarct size. ECT imaging with 99mTc-PYP to determine infarct size may be clinically applicable in patients with acute myocardial infarction.     

Creatine kinase release in acute myocardial infarction: correlation with clinical, electrocardiographic, and pathological findings.

Creatine kinase (CK) release curves were analysed in 40 patients with acute myocardial infarction. Three groups could be identified. Group A (duration of CK release less than 30 hours) comprised 15 patients whose CK release was completed within 22.8 hours. In these patients chest pain was noted on the first hospital day and necropsy in three showed a homogeneous myocardial infarction. Group B (duration of CK release greater then 30 hours) comprised 16 patients who had a significantly longer CK release time of 42.2 hours (P less than or equal to 0.05). Their chest pain persisted for two to three days and pathological examination in five patients showed a heterogeneous composition of the infarcted myocardium. Group C comprised nine patients who had a second rise of serum CK. This was always associated with chest pain. It reflected an extension of the infarct which accounted on average for 24 per cent of the size of the final infarct. We concluded that a CK release of short duration indicated infarction without extension, CK release of longer duration indicated a gradual extension of infarction, and a repeated CK release resulted from a sudden extension of an infarct. According to these criteria an extension of the infarct occurred in 62 per cent of our patients.     

Creatine kinase release in acute myocardial infarction: correlation with clinical, electrocardiographic, and pathological findings.

Creatine kinase (CK) release curves were analysed in 40 patients with acute myocardial infarction. Three groups could be identified. Group A (duration of CK release less than 30 hours) comprised 15 patients whose CK release was completed within 22.8 hours. In these patients chest pain was noted on the first hospital day and necropsy in three showed a homogeneous myocardial infarction. Group B (duration of CK release greater then 30 hours) comprised 16 patients who had a significantly longer CK release time of 42.2 hours (P less than or equal to 0.05). Their chest pain persisted for two to three days and pathological examination in five patients showed a heterogeneous composition of the infarcted myocardium. Group C comprised nine patients who had a second rise of serum CK. This was always associated with chest pain. It reflected an extension of the infarct which accounted on average for 24 per cent of the size of the final infarct. We concluded that a CK release of short duration indicated infarction without extension, CK release of longer duration indicated a gradual extension of infarction, and a repeated CK release resulted from a sudden extension of an infarct. According to these criteria an extension of the infarct occurred in 62 per cent of our patients.     

急性脑梗死患者血清基质金属蛋白酶9及外周白细胞计数的变化

目的探讨急性脑梗死患者血清基质金属蛋白酶-9(MMP-9)及外周白细胞(WBC)计数的变化。方法选择急性脑梗死患者124例(脑梗死组),分别测定其发病后24 h内、51、4天的血清MMP-9、外周WBC,健康体检者40例(对照组),测空腹血清MMP-9和外周WBC,分析其与脑梗死面积的关系。结果脑梗死组与对照组比较,24 h内血清MMP-9、WBC明显升高(P<0.05),5天达高峰(P<0.01),14天已明显下降,脑梗死组中大面积梗死表现最为明显;血清MMP-9、WBC有相关性,相关系数r=0.78(P<0.01)。结论急性脑梗死患者血清MMP-9及外周WBC明显升高,并与病灶大小呈正比;MMP-9与WBC在动态变化中呈正相关。     

苯那普利对急性心肌梗塞后梗塞面积及心功能的近期和远期影响

目的对急性前壁心肌梗塞患者加用苯那普利治疗，观察其对梗塞面积及左室收缩功能的近期与远期效果。方法８８例ＡＭＩ患者随机分为苯那普利组（４５例）和常规治疗组（４３例）作为对照。入院即刻、３日、３周、６个月及１年作心电图ＱＲＳ评分，３周、６个月及１年作ＵＣＧ或心血池核素测定以判断左室收缩功能。结果１．苯那普利组ＱＲＳ评分明显降低；２．梗塞面积一直保持在２５．３％左右，未见扩大，而对照组均比苯那普利组扩大；３．ＬＶＥＦ测定在３周、６个月、１年均比对照组明显升高。结论苯那普利对梗塞面积、心电图评分、及心功能方面有明显改善的作用。     

Coronary arteriography in acute transmural myocardial infarction

Coronary arteriography was performed 16 ± 3 days (range 7 to 21 days) in 106 patients with acute transmural myocardial infarction (61 posterior infarct, 45 anterior infarct). Coronary arteriography was performed without serious complications. Only 44 per cent of patients with anterior infarct had total occlusion of the left anterior descending artery while a significant stenosis of the vessel was observed in the others ?27 per cent had a single vessel disease, 49 per cent had two lesions and 22 per cent had three lesions; one patient had angiographically normal coronary arteries. Among the patients with posterior infarction, 21 per cent had one vessel disease and double or triple lesions accounted for 39 per cent of each.Sixty per cent of patients with anterior infarction and 45 per cent with posterior infarction had no collateral vessels. In the others patients collateral circulation had a protective effect only in anterior infarction. Age has no effect on the distribution and number of lesions nor on the development of a collateral circulation. The location and severity of the lesions were not different in patients who presented with arrythmias and those who did not.     

Measurement of infarct size using single photon emission computed tomography and technetium-99m pyrophosphate: a description of the method and comparison with patient prognosis

The application of dual tracer transaxial emission computed tomography of the heart was studied with use of technetium-99m pyrophosphate and technetium-99m-labeled red blood cells for measuring infarct size in 20 patients with acute myocardial infarction and 10 without infarction. Imaging was performed with a standard gamma camera and with a multidetector transaxial emission computed tomographic body scanner 3 hours after injection of technetium-99m pyrophosphate. Immediately after the scanning procedure, technetium-99m pertechnetate was injected to label red blood cells, and the scanning protocol was repeated. Technetium-99m pyrophosphate was detected in the anterior wall with involvement of the interventricular septum or lateral wall in patients with electrocardiographic criteria for anterior infarction, whereas uptake was detected in the diaphragmatic left ventricular wall with involvement of the posterior, posteroseptal or posterolateral left ventricle or of the right ventricle in patients with electrocardiographic criteria for inferior or posterior infarction. Infarct size measured from transaxial images ranged from 14.0 to 117.0 g in weight. There was a direct relation between infarct size and patient prognosis in that, of the 13 patients with infarct greater than 40 g, 11 (85 percent) had complications, whereas only 2 (29 percent) of 7 patients with an infarct less than 40 g had complications during a follow-up period averaging 17.8 months (p less than 0.05).     

前循环梗死患者影像学梗死模式和发病机制初探

目的 从磁共振弥散加权成像(diffusion-weighted imaging,DWI)角度,分析颈内动脉(internal carotid artery,ICA)、大脑中动脉(middle cerebral artery,MCA)重度狭窄或闭塞患者脑梗死的影像学模式特点,探讨其相应的梗死机制.方法 回顾性分析88例经全脑血管造影证实存在ICA、MCA中重度狭窄或闭塞的急性缺血性梗死患者,将其分为ICA病变组和MCA病变组.根据DWI将梗死模式分为单发和多发,前者再分为穿支动脉梗死(perforating artery infarct,PAI)、皮质支梗死(pial infarct,PI)、分水岭梗死和大面积梗死.结果 MCA供血区梗死模式可分为11种.DWI多发梗死模式占所有患者的62.5%(55/88).ICA病变组更多出现PI伴发分水岭梗死(11/45,P=0.040),而MCA病变组更多出现PI伴发PAI(10/43,P=0.037).结论 在伴有ICA或MCA重度狭窄或闭塞的脑梗死患者中,大多数表现为多发梗死模式,提示栓塞、低灌注/栓子清除能力下降以及局部穿支闭塞等机制是其发生梗死的主要机制.ICA病变组梗死的主要机制为栓塞合并低灌注/栓子清除能力下降,而MCA病变组则为栓塞合并局部穿支闭塞.     

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.     

Myocardial salvage with direct coronary angioplasty for acute infarction.

To assess the changes in myocardial function following direct coronary angioplasty, we evaluated 323 consecutive patients undergoing coronary angioplasty without antecedent thrombolytic therapy for acute myocardial infarction. Left ventricular function was evaluated using contrast ventriculography immediately preangioplasty and at the time of predismissal follow-up angiography (a mean of 7 days after infarction). The global ejection fraction increased from 52.6% to 58.9% (p less than 0.0005). Multivariate correlates of improved global left ventricular function included baseline ejection fraction less than or equal to 45%, and a patent infarct vessel at the time of predischarge follow-up angiography. Systolic function in the infarct zone improved by a mean of 30%. Logistic regression analysis identified sustained infarct vessel patency and anterior myocardial infarction as multivariate correlates of improved regional function in the infarct zone. In patients presenting with baseline ejection fractions less than or equal to 40%, the mean ejection fraction increased from 28% to 42%. Long-term survival was compromised in patients with global ejection fractions of less than or equal to 40% at the time of dismissal. Thus significant improvement in left ventricular function can be expected in the majority of patients undergoing direct infarct angioplasty. The myocardial salvage appears to be most significant in patients suffering large infarctions, and in those with sustained infarct vessel patency.