Mechanism underlying mechanical dysfunction in the border zone of left ventricular aneurysm: a finite element model study

BACKGROUND: The global left ventricular dysfunction characteristic of left ventricular aneurysm is associated with muscle fiber stretching in the adjacent noninfarcted (border zone) region during isovolumic systole. The mechanism of this regional dysfunction is poorly understood. METHODS: An anteroapical transmural myocardial infarct was created by coronary arterial ligation in an adult Dorset sheep and was allowed to mature into left ventricular aneurysm for 10 weeks. The animal was imaged subsequently using magnetic resonance imaging with simultaneous recording of intraventricular pressures. A realistic mathematical model of the three-dimensional ovine left ventricle with an anteroapical aneurysm was constructed from multiple short-axis and long-axis magnetic resonance imaging slices at the beginning of diastolic filling. RESULTS: Three model simulations are presented: (1) normal border zone contractility and normal aneurysmal material properties; (2) greatly reduced border zone contractility (by 50%) and normal aneurysmal material properties; and (3) greatly reduced border zone contractility (by 50%) and stiffened aneurysmal material properties (by 1000%). Only the latter two simulations were able to reproduce experimentally observed stretching of border zone fibers during isovolumic systole. CONCLUSIONS: The mechanism underlying mechanical dysfunction in the border zone region of left ventricular aneurysm is primarily the result of myocardial contractile dysfunction rather than increased wall stress in this region.     

Ventricular volume, chamber stiffness, and function after anteroapical aneurysm plication in the sheep

OBJECTIVE: The success of left ventricular aneurysm plication depends on how the procedure affects both end-systolic elastance and diastolic compliance and how those changes affect ventricular function (stroke work/end-diastolic volume [PRSW] and stroke volume/end-diastolic pressure [Starling] relationships). METHODS: Five male Dorsett sheep were surgically instrumented with coronary artery snares, an inferior vena caval occluder, and an ascending aortic ultrasonic flow probe. One week later an anteroapical myocardial infarction was produced by tightening the coronary snares. Ten weeks after myocardial infarction, the left ventricular aneurysm was plicated. Absolute left ventricular volume was measured by long-axis transdiaphragmatic echocardiography, and relative changes in left ventricular volume were measured with a conductance catheter. End-systolic elastance, diastolic compliance, PRSW, and Starling relationships were measured immediately before myocardial infarction, 10 weeks after myocardial infarction (immediately before plication), and immediately after and 6 weeks after aneurysm plication. RESULTS: After plication, end-diastolic and end-systolic left ventricular volumes return to preinfarction values. The slopes of end-systolic elastance, diastolic compliance, and PRSW decrease 10 weeks after myocardial infarction, increase with aneurysm plication, and then decrease 6 weeks after aneurysm plication. The Starling relationship undergoes a downward parallel shift with aneurysm plication. CONCLUSION: Aneurysm plication abruptly decreases left ventricular volume and diastolic compliance, increases end-systolic elastance and PRSW, but decreases the Starling relationship. The net effect on left ventricular function is mixed. Furthermore, left ventricular remodeling 6 weeks after aneurysm plication causes left ventricular volume, end-systolic elastance, diastolic compliance, PRSW, and the Starling relationship to return to preplication values.     

Repair of left ventricular aneurysm. Changes in ventricular mechanics, hemodynamics, and oxygen consumption.

Anteroapical left ventricular aneurysms were produced in 23 sheep by coronary arterial ligation. Plication of the aneurysm does not change stroke volume or cardiac output and does not significantly change left ventricular oxygen consumption from the preoperative value of 5.1 +/- 2.6 ml/100 gm per minute. Plication, however, does increase left ventricular end-systolic elastance from 3.2 +/- 0.9 to 4.4 +/- 1.5 mm Hg/mm (p = 0.005). In nine of these sheep the midsagittal plane of the left ventricle was imaged by means of an array of sonomicrometry crystals before and after plication of the aneurysm. Regional wall stresses at end-systole and end-diastole and changes in diastolic function were calculated for anterior and posterior ventricular walls in the border zone adjacent to the aneurysm and in more basilar myocardium remote from the infarct. Plication significantly reduced end-systolic wall stresses and systolic stress integrals in the posterior border zone and remote myocardium, but it did not significantly change anterior wall systolic stresses or stress integrals. Plication also decreased diastolic stretching of border zone myocardium. Plication of anteroapical left ventricular aneurysm produced a shorter, more spherical ventricle and removed the dyskinetic segments but altered deformation (strain) in both circumferential and longitudinal directions. The changes in ventricular wall geometry and deformation provide an explanation for the increased ventricular end-systolic elastance and unchanged stroke volume observed after aneurysm plication.     

Surgical treatment of a giant left ventricular aneurysm- A case report

An aneurysm of the left ventricle is a complication of acute myocardial infarction. We report a case of a giant aneurysm of the left ventricle after myocardial infarction in a 59 year-old male patient. The surgery to correct the aneurysm was performed with the use of cardiopulmonary bypass under normothermia. A bovine pericardial patch was used for the geometric reconstruction of the ventricular wall affected by the aneurysm. After the procedure, echocardiography and magnetic resonance imaging revealed improvement in left ventricular ejection fraction and volume reduction.     

Spontaneous coronary artery dissection with left ventricular aneurysm--a case report of successful surgical repair

Spontaneous coronary artery dissection is a rare entity. To our knowledge, 86 cases have been reported, and there are 7 operative treatment. The patient was 56 year-old male with a history of the previous myocardial infarction. A selective coronary angiography demonstrated marked dilatation of both coronary arteries. The thin radiolucent lines were shown within the LAD and first diagonal branch as a result of partial separation of the intima. A very large left ventricular myocardial aneurysm was also demonstrated within anteroapical walls, he underwent open heart surgery with left ventricular myocardial aneurysmectomy and aorto-first diagonal branch saphenous vein graft. This present case is the second report which describe a successful surgical treatment for the spontaneous coronary artery dissection with left ventricular aneurysm.     

Left ventricular pseudo-false aneurysm after a myocardial infarction; application of heart positioner

We herein present the case of a pseudo-false aneurysm which developed in a patient after a myocardial infarction in the posterior left ventricular wall. A 71-year-old man experienced an acute myocardial infarction due to occlusion in the left circumflex artery. Five weeks after the myocardial infarction, echocardiography and magnetic resonance imaging (MRI) disclosed a pseudo-false aneurysm at the posterior left ventricular wall. A patch closure of the aneurysm and coronary artery bypass grafting (CABG) to both the left anterior descending artery and the left circumflex arteries were successfully performed. At surgery, the Starfish Heart Positioner, a commercially available device that is designed to lift the heart during off-pump CABG, was found to be very useful for exposing the posterior left ventricular wall by lifting and fixing the apex of the left ventricle.     

Ventricular myocardial architecture as visualised in postmortem swine hearts using magnetic resonance diffusion tensor imaging.

OBJECTIVE: The three-dimensional arrangement of the ventricular myocardial architecture remains controversial, in part because histological assessment is difficult to achieve, while anatomic dissections are, of necessity, destructive. In this study, we describe how the use of magnetic resonance diffusion tensor imaging has permitted us to reconstruct with precision the architecture of the ventricular myocardial fibres in the post-mortem swine heart. METHODS AND RESULTS: We obtained diffusion-weighted spin-echo measurements of autopsied porcine hearts using a whole body MR system. We calculated the diffusion tensor and the corresponding eigenvectors on a voxel-by-voxel basis. This permitted us to colour code the fibres, and reconstruct them by connecting voxels in direction of the largest eigenvector. Such reconstructions show that, in the middle layer of the left ventricle, most of the fibres have a circular orientation, albeit that a far from negligible component runs in a transverse direction. With increasing distance from the epicardium, the orientation of the fibres shows a continuous change in angulation with respect to an axis normal to the epicardium. CONCLUSION: Our data presented here supports the concept that the ventricular mass is arranged as a complex three-dimensional mesh of tangential and intruding fibres. The data offers no support for the concept of a "unique myocardial band". The method has the potential to detecting deviations from this basic normal architecture, being capable of reconstructing the ventricular mass so as to assess the spatial coordinates of any single fibre strand. The technique, therefore, has major potential clinical applications in the setting of the failing or malformed heart, potentially being able to identify either systematic or regional disarray of the myocardial fibres.     

A modified technique of left ventricular restoration: endoventricular spiral plication

We describe a modified technique of left ventricular restoration after anterior myocardial infarction, referred to as endoventricular spiral plication (ESP). This technique was designed for surgical ventricular restoration with a modified spiral stitch and no patch plasty. A continuous spiral stitch can reconstruct the left ventricular shape both at the short and long axis, and appropriate restoration can be achieved by adjusting the tension of the string and the degree of spiral rotation.     

使用磁共振弥散张量成像技术对心肌带结构的初步研究

目的初步研究用磁共振弥散张量成像(MRDTI)技术显示离体猪心心肌带结构的可能性。方法以MRDTI技术为基础,检测5个成年离体猪心,在猪心离体后2h内使用25个方向的弥散张量成像(DTI)序列扫描心室部分,之后使用脑白质纤维束成像重建方式显示心肌纤维的走行、分布和排列方式。结果MRDTI可以清晰显示离体1h心室肌纤维整体具有一定的连续性,在空间上螺旋、缠绕而形成左、右心室;左室壁的心肌纤维大体呈现心内膜下纵向排列、心肌中层斜行排列和心外膜下环行排列,这与心肌带理论相符合。结论MRDTI技术可以显示离体心肌纤维的完整性和排列方式,并能部分地证实心肌带理论的真实性。     

Off-pump anteroapical aneurysm plication following left ventricular postinfarction aneurysm: effect on cardiac function,clinical status and survival

Background

In patients with coronary disease and aneurysm, ventricular reconstruction with revascularization is a surgical option. Details of patient selection and optimal surgical technique are still debated. We report our results with off-pump aneurysm plication after ventricular aneurysm with relative wall thinning.

Methods

We retrospectively reviewed the records of 248 patients who had an operation for postinfarction left ventricular aneurysm. Reconstruction was accomplished by off-pump anteroapical aneurysm plication. The following variables were recorded: preoperative clinical, angiographic and echocardiographic findings and operative procedures. Outcomes were early mortality, long-term survival and poor 5-year result, defined as the need for transplantation or repeated hospitalization for congestive heart failure. Risk factors were pinpointed using the t test and survival curves. Independent risk factors were identified using Cox regression methods.

Results

Hospital mortality was low (2.0%). Mean follow-up was 5.8 (standard deviation [SD] 3.8) years. Actuarial survival at 1 and 5 years was 94% and 84%. Among the 232 survivors, 200 were in functional class I or II, and the average increase in ejection fraction was 14.0% (SD 3.1%). As determined by multivariable analysis, factors predicting poor outcome were advanced age, ejection fraction less than 0.35, conicity index less than 1, end-systolic volume index greater than 80 mL/m², advanced New York Heart Association functional class and congestive heart failure.

Conclusion

Using wall thinning as a criterion for patient selection, the technique of off-pump anteroapical aneurysm plication can be performed with low operative mortality and provides good symptomatic relief and long-term survival.     

Restraining acute infarct expansion decreases collagenase activity in borderzone myocardium

Background. After acute myocardial infarction, regional myocardial wall strains and stresses change and a complex cellular and biochemical response is initiated to remodel the ventricle. This study tests the hypothesis that changes in regional ventricular wall strains affect regional collagen accumulation and collagenase activity.

Methods. Fourteen sheep had acute anteroapical infarction that progressively expands into left ventricular aneurysm within 8 weeks. In 7 sheep, infarct expansion was restrained by prior placement of mesh over the area at risk. Fourteen days after infarction, and after hemodynamic and echocardiographic measurements, animals were euthanized for histology, measurements of hydroxyproline, matrix metalloproteinase-1 (MMP-1 or collagenase) and MMP-2 (gelatinase) activity, as well as collagen type I and III in infarcted, borderzone, and remote myocardium.

Results. Restraining infarct expansion does not change collagen content or MMP-1 or MMP-2 activity in the infarct, but significantly increases the ratio of collagen I/III. In borderzone and remote myocardium infarct, restraint significantly increases collagen content and significantly reduces MMP-1 activity. MMP-2 activity is reduced (p = 0.059) in borderzone myocardium only. Between groups, the ratio of type I/III fibrillar collagen does not change in borderzone myocardium.

Conclusions. Fourteen days after acute myocardial infarction, restraining infarct expansion increases collagen accumulation in borderzone and remote myocardium, which may prevent expansion of hypocontractile, fully perfused “remodeling myocardium” adjacent to the infarct. This study demonstrates that changes in regional myocardial wall strain alter the cellular and biochemical processes involved in postinfarction ventricular remodeling.     

Influence of left ventricular aneurysm on survival following the coronary bypass operation

Patients having coronary bypass and aneurysm resection (N = 40) or aneurysm plication (N = 32) were compared with patients having coronary bypass without aneurysm (N = 2782). Unlike other series, the primary indication for surgery in the aneurysm patients was angina pectoris, with heart failure playing a secondary role. Multivessel disease was present in 83% of the patients with aneurysm. Total occlusion of the anterior descending coronary artery was more prevalent in the group of patients who had aneurysmectomy (75%) than in rhe group of patients who had plication (38%), and more grafts/patient could be performed in the plication group (2.6 vs 2.0). Location of the aneurysm was most often anteroapical (N = 55) and infrequently inferior (N = 6). Septal wall motion was akinetic or aneurysmal in 47% of the aneurysmectomy group, and 10% of the plication group. Postoperative requirements for inotropes or intra-aortic balloon assist was much higher in the aneurysm group (aneurysmectomy or plication) than in patients without aneurysm having bypass. Hospital mortality for aneurysm patients was 2.7% versus 1.4% in patients without aneurysms having coronary bypass. The actuarial survival rate at 42 months for all aneurysm patients was 90%. Improvement in anginal symptoms after plication and coronary bypass (96%) was more frequent than with aneurysmectomy and coronary bypass (76%) and this was attributed to larger viable muscle mass and greater revascularization. Although two-thirds of patients having surgery for aneurysms had improvement in heart failure symptoms after operation, 30% of those having aneurysmectomies and 35% of those having plications said they were unimproved after surgery. However, this could be explained by the finding that a significant number (35% of the aneurysmectomy and 45% of the plication group) were in heart failure Class I prior to operation. Hospital mortality has been progressively reduced and late survival increased by the surgical treatment of left ventricular aneurysm, primarily through early operation at a time when coronary bypass can be used as an adjunct to aneurysm resection or plication.     

Reverse remodeling and improved regional function after repair of left ventricular aneurysm

BACKGROUND: Changes in regional left ventricular mechanics after anteroapical aneurysm repair in human subjects can be studied noninvasively by means of magnetic resonance tagging. We hypothesized that left ventricular intramyocardial function would improve throughout the left ventricle after repair. METHODS: We studied 6 male patients with a left ventricular anteroapical aneurysm (mean age +/- SD, 63 +/- 5 years) using magnetic resonance tagging 3 +/- 1 weeks before and 6 +/- 1 weeks after aneurysm repair, coronary artery bypass grafting, and mitral valve repair (n = 2). Breath-hold tagged imaging spanned the left ventricle in the short axis from apex to base. Left ventricular mass, end-diastolic and end-systolic volume, and ejection fraction were measured. Two-dimensional strain analysis was applied; averaged for the apical, middle, and basal left ventricle and the whole left ventricle; and expressed as greatest lengthening (similar to wall thickening), greatest shortening, and angular deviation of the lengthening strain from the radial direction. RESULTS: After aneurysm repair, left ventricular mass decreased from 373 +/- 27 to 333 +/- 25 g (P <.05), end-diastolic volume from 212 +/- 22 to 168 +/- 18 mL (P <.005), and end-systolic volume from 188 +/- 26 to 113 +/- 18 mL (P <.005); ejection fraction improved from 13% +/- 4% to 23% +/- 4% (P <.005). For the whole left ventricle, lengthening strain increased from before to after the operation (8% +/- 1% to 10% +/- 1%, P <.01). Most of the improved lengthening occurred at the middle left ventricle (8% +/- 1% to 11% +/- 1%, P <.01), in the base (8% +/- 1% to 10% +/- 1%, P <.05), and in the inferior wall (9% +/- 1% to 12% +/- 1%, P <.05). Lengthening tended to become more radially oriented, decreasing from 31 degrees +/- 3 degrees to 27 degrees +/- 3 degrees (P =.10). Shortening strain did not change (10% +/- 1% to 11% +/- 1%, P = not significant). CONCLUSIONS: Left ventricular aneurysm repair is associated with reverse remodeling and an improvement in the extent and orientation of intramyocardial function, especially at the middle and basal left ventricle and inferior wall.     

Simulated left ventricular aneurysm and aneurysm repair in swine

Patch reconstruction of left ventricular aneurysm may be superior to linear closure, but this hypothesis has not been tested experimentally. Accordingly, six anesthetized domestic pigs were instrumented to measure regional left ventricular wall thickening, stroke volume, systolic left ventricular pressure, and myocardial oxygen consumption. With total bypass and cardioplegia, a 6 by 8 cm Dacron patch was inserted into the anteroapical left ventricle. Simulations were as follows: left ventricular aneurysm, patch open; patch reconstruction, 50% patch plication; standard repair, ventriculotomy edges approximated. Global function, from stroke work (stroke volume x integral of left ventricular pressure)-left ventricular end-diastolic pressure curves, was depressed in all three simulations compared with control. A tendency for stroke work to be greater for standard repair than for left ventricular aneurysm and patch reconstruction at higher preloads was not statistically significant. Mechanical efficiency, from stroke work/myocardial oxygen consumption (joules per milliliter oxygen per beat), was 2.43 +/- 0.52 (mean +/- standard error of the mean) (control), 2.22 +/- 0.94 (standard repair), 1.27 +/- 0.39 (patch reconstruction), and 1.09 +/- 0.37 (left ventricular aneurysm) (no significant differences). Regional work was calculated as regional left ventricular wall thickening x integral of left ventricular pressure. The slope of the regional work-end-diastolic wall thickness relation decreased in the posterior wall 14.0 +/- 2.9 (control) versus 8.4 +/- 2.0 (left ventricular aneurysm), 6.9 +/- 1.4 (patch reconstruction), and 7.4 +/- 1.4 (standard repair) (p less than 0.05). In the anterior wall, contractility did not change significantly (7.4 +/- 1.2, control; 7.8 +/- 2.7, left ventricular aneurysm; 5.0 +/- 0.4, patch reconstruction; and 5.3 +/- 0.4, standard repair). Decreased end-diastolic wall thinning anteriorly suggested tethering. These results in the normal left ventricle suggest that patch ventriculoplasty is of no greater benefit than linear repair. Either repair may impede function of adjacent myocardium through restriction of regional diastolic lengthening.     

心肌梗死后室壁瘤及二尖瓣反流的外科治疗

目的 总结心肌梗死后室壁瘤和二尖瓣反流的外科治疗经验,以提高手术疗效和生存率.方法 回顾性分析2000年12月～2007年6月间收治的37例心肌梗死后室壁瘤及中度以上二尖瓣反流患者的临床资料,大多数患者行冠状动脉旁路移植术加室壁瘤切除后左心室重建、二尖瓣成形或置换术.结果 术后死亡3例,死亡率8.1%,其中死于肾功能衰竭2例,脑部并发症1例.随访30例,随访率88.2%(30/34),4例失访;随访时间1个月至6年.随访期间死亡2例,其中1例死于抗凝治疗失败并发的大面积脑梗死,1例死于肺部感染和心力衰竭.术后6个月复查心脏彩色超声心动图提示:左心房内径较术前明显缩小(30.1±3.5mm vs.39.3±3.7mm, P=0.004),左心室舒张期末内径较术前明显缩小(48.4±4.3mm vs.61.2±5.1mm, P=0.003),旷置的室壁瘤大小无明显变化(直径＜5 cm),二尖瓣成形和旷置者无反流或轻微反流12例,轻度反流2例,中度反流1例.结论 对不同类型的心肌梗死后室壁瘤和二尖瓣反流患者制定相应的手术治疗方案,能取得良好的近、远期疗效,绝大部分患者心功能改善明显,生存率提高.     

Contrast-enhanced magnetic resonance imaging guided decision making after primary percutaneous coronary intervention for acute ST-elevation inferior myocardial infarction

Coronary occlusion of large epicardial branches leads to profound ischemia at the infarct core, resulting in simultaneous necrosis of myocytes and endothelial cells. This process leads to microvascular obstruction in the infarct core, described as the no-reflow region in basic studies and documented in humans by contrast-enhanced magnetic resonance imaging and ultrasound. After coronary occlusion, contrast-enhanced magnetic resonance identifies myocardial infarction as a hyperenhanced region containing a hypoenhanced core. There is growing interest in incorporating its assessment into the evaluation of acute myocardial infarction because it is the key in defining specific therapeutic strategies and in directing the interventional therapy. We report a rare case of right ventricular infarction where contrast-enhanced magnetic resonance produced detailed images of myocardial perfusion pattern and tissue damage and directed the treatment after acute myocardial infarction.     

Surgical treatment of ischemic mitral regurgitation might not influence ventricular remodeling

OBJECTIVES: Surgical treatment for ischemic mitral regurgitation has become more aggressive. However, no clinical study has demonstrated that surgical correction of chronic ischemic mitral regurgitation improves survival. We used 4 well-developed ovine models of postinfarction left ventricular remodeling to test the hypothesis that ischemic mitral regurgitation does not significantly contribute to postinfarction left ventricular remodeling. METHODS: Infarction of 21% to 24% of the left ventricular mass was induced by means of coronary ligation in 77 sheep. Infarctions varied only by anatomic location in the left ventricle: anteroapical, n = 26; anterobasal, n = 16; laterobasal, n = 9; and posterobasal, n = 20. Six additional sheep had ring annuloplasty before posterobasal infarction. End-systolic and end-diastolic left ventricular volume, end-systolic muscle-to-cavity area ratio, left ventricular sphericity, ejection fraction, and degree of ischemic mitral regurgitation, as determined by means of quantitative echocardiography, were assessed before infarction and at 2, 5, and 8 weeks after infarction. RESULTS: All infarcts resulted in significant postinfarction remodeling and decreased ejection fraction. Anteroapical infarcts lead to left ventricular aneurysms. Only posterobasal infarcts caused severe and progressive ischemic mitral regurgitation. Remodeling because of posterobasal infarcts was not more severe than that caused by infarcts at other locations. Furthermore, prophylactic annuloplasty prevented the development of mitral regurgitation after posterobasal infarction but had no effect on remodeling. CONCLUSION: The extent of postinfarction remodeling is determined on the basis of infarct size and location. The development of ischemic mitral regurgitation might not contribute significantly to adverse remodeling. Ischemic mitral regurgitation is likely a manifestation rather than an important impetus for postinfarction remodeling.     

Spinal cord diffusion tensor imaging and fiber tracking can identify white matter tract disruption and glial scar orientation following lateral funiculotomy

Diffusion tensor magnetic resonance imaging (DTI) provides data concerning water diffusion in the spinal cord, from which white matter tracts may be inferred, and connectivity between spinal cord segments may be determined. We evaluated this potential application by imaging spinal cords from normal adult rats and rats that received cervical lateral funiculotomies, disrupting the rubrospinal tract (RST). Vitrogen and fibroblasts were transplanted into the surgical lesion at time of injury in order to fill the cavity. At 10 weeks, animals were sacrificed; the spinal cords were dissected out and then imaged in a 9.4-Tesla magnet. DTI tractography demonstrated the disruption of the rubrospinal tract axons while indicating which axon tracts were preserved. Additionally, DTI imaging could identify the orientation of glial processes in the gray matter adjacent to the site of injury. In the injured animals, reactive astrocytes in adjacent gray matter appeared to orient themselves perpendicular to white matter tracts. In summary, DTI identified not only white matter disruption following injury, but could distinguish the orientation of the accompanying glial scar.     

Survival following free rupture of left ventricular aneurysm: report of a case.

A 50-year-old man sustained free rupture of the left ventricle four weeks following a massive anterior myocardial infarction. The rupture occurred at the junction between a bulging left ventricular aneurysm that was not yet fibrotic and normal myocardium without evidence of fresh myocardial infarction. Accurate preoperative diagnosis aided by echocardiography and right heart catheterization made possible a planned surgical approach. Postoperative support with intraaortic balloon pumping appeared to be beneficial in maintaining statisfactory cardiac function until an adequate stroke volume could be reestablished, presumably by an increase in left ventricular volume.     

Myocardial perfusion in ST-elevation myocardial infarction treated successfully with primary angioplasty

OBJECTIVES: To study myocardial perfusion in ST-elevation myocardial infarction (STEMI) treated successfully with primary angioplasty. Additionally, to evaluate the predictive value of perfusion on subsequent infarct size. DESIGN: Fifty patients with acute STEMI and restoration of normal epicardial flow after primary angioplasty were included in the study. TIMI myocardial perfusion (TMP) grades were determined at the end of the procedure. Contrast enhanced magnetic resonance imaging (MRI) including first-pass perfusion and delayed enhancement imaging were performed within five days and after three months. RESULTS: The patients were divided into two groups: A=TMP 0-1, B=TMP 2-3. The early MRI showed significantly reduced myocardial perfusion in the infarct zone compared to remote myocardium in both groups (p<0.001), but the reduction was more pronounced in group A. The infarct sizes were smaller (p=0.0017) and the ejection fractions higher (p=0.0001) in group B than in group A at follow-up. CONCLUSIONS: In STEMI, early impairments in myocardial perfusion were observed in spite of successful treatment with angioplasty. Marked early impairments in perfusion were associated with larger infarct sizes on MRI after three months.