Ventricular Aneurysm Formation Research Articles

Effect of coronary collateral circulation on myocardial ischemia and ventricular dysfunction.

Although a functional role of coronary collaterals has been continuously debated, we observed the following facts in our studies during intracoronary thrombolytic therapy: (a) Myocardial ischemia is important for the development of collateral circulation, (b) collaterals can perfuse the infarcted myocardium, and (c) the presence of collaterals prevents the left ventricular aneurysm formation in acute myocardial infarction, even when the amount of the salvaged tissue is small. Thus, coronary collaterals are not merely markers of severe ischemia but help to preserve the functional integrity of the myocardium in the presence of coronary obstruction. We then attempted to promote collateralization to treat patients with angina pectoris. Patients with chronic stable effort angina were treated with heparin followed by treadmill exercise twice a day for 10 days. Treadmill capacity was found to improve in association with an increase in coronary collateral circulation. Heparin treatment of ischemic patients was found to be a noninvasive alternative to percutaneous transluminal coronary angioplasty and coronary bypass surgery for patients who are not candidates for invasive procedures.

Tetralogy of Fallot and Pulmonary Atresia/Ventricular Septal Defect

Surgical repair of tetralogy of Fallot is associated with excellent results. Long-term complications include arrhythmias, sudden death, and right ventricular aneurysm formation. Reoperation is necessary in approximately 5% of patients for residual ventricular septal defect, pulmonary regurgitation, or pulmonary stenosis. Pulmonary atresia/ventricular septal defect is a more complex situation, and the anatomy needs careful delineation by cardiac catheterization prior to any surgical intervention. Palliation with a shunt or first-stage repair may be effective, or radical repair may be considered in those with adequate pulmonary distribution.

Functional significance of coronary collateral vessels in patients with previous ‘Q’ wave infarction: relation to aneurysm, left ventricular end diastolic pressure and ejection fraction

The importance of coronary collateral circulation in relation to the left ventricular function, aneurysm formation and size was investigated in 100 patients with previous ‘Q’ wave myocardial infarction who underwent coronary angiography. Aneurysms were present in 20% of patients. The majority of these (80%) patients had severe or total occlusion of the left anterior descending artery. Thirty four percent of patients without aneurysm had significant collaterals whereas 25% of patients with aneurysms had collaterals ( P > 0.05). However, the size of the aneurysm was smaller when adequate collateral circulation was present (Collateral Index 2 or above). The incidence of hypertension and diabetes was similar in both groups. Collateral circulation was more frequently seen in the anterior (60%) as compared to inferior myocardial infarction (40%), but Collateral Index was higher in right coronary artery disease. The number of patients with an elevated left ventricular end-diastolic pressure (> 12) or poor ejection fraction was similar in the two groups with and without collaterals. Thus, there was no beneficial effect of collateral circulation on left ventricular function. The incidence of aneurysm was not significantly lower, although the size of the aneurysm was significantly smaller in the presence of collateral circulation.

Transient left ventricular aneurysm in a patient with hypertrophic cardiomyopathy and myocarditis

Left ventricular wall motion abnormalities, aneurysm formation, and progression to global hypokinesis have been described in patients with myocarditis and in patients with hypertrophic cardiomyopathy. We document a case of reversible aneurysm formation, cardiogenic shock, and complete recovery in a patient with myocarditis and hypertrophic cardiomyopathy. Pathophysiologic mechanisms of myocardial injury and recovery are discussed.

Sandwich repair with two sheets of equine pericardial patch for acute posterior post-infarction ventricular septal defect.

A 74-year-old man, who had posterior post-infarction ventricular septal defect, was treated successfully by early surgical repair with a sandwich technique involving two sheets of equine pericardial patch. In this technique the ventricular septal defect (VSD) was exposed through a trans-infarction approach. The inside patch covered the VSD and ventriculotomy from the inside. The outside patch generously covered the infarcted myocardium. The two patches completely sandwiched the infarcted myocardium including the VSD and ventriculotomy with eighteen interrupted sutures. This technique ensures strong fixation of the VSD, reducing the risk of bleeding and recurrence of VSD, and also maintains the proper shape and size of the left ventricle without the danger of ventricular aneurysm formation.

Acute Myocardial Infarction and Left Ventricular Aneurysm in a Patient with Normal Coronary Arteries

A 25-year-old young man was admitted with typical manifestations of acute myocardial infarction. Cardiac catheterization performed 2 weeks later showed a left ventricular aneurysm and normal coronary arteries. Because of the unusual clinical features, an endomyocardial biopsy was done and revealed histopathological changes of acute myocarditis. Acute myocarditis presenting as acute myocardial infarction with left ventricular aneurysm formation at the same time was never reported before. The long-term prognosis of the patient with left ventricular aneurysm caused by myocarditis still needs further observation.

Transesophageal echocardiographic detection of abnormalities of the tricuspid valve in adults associated with spontaneous closure of perimembranous ventricular septal defect

Perimembranous defects are the most frequent types of ventricular septal defect. Spontaneous closure of these defects occurs often in childhood. The mechanism of closure is controversial, but recent pathologic and clinical studies in children suggest that it occurs by reduplication and adhesion of the septal leaflet of the tricuspid valve to the margins of the defect. 1–2 Closure of the defect is frequently associated with the formation of a ventricular septal aneurysm, a term that describes an outpouching in the region of the membranous septum. 3 The adherent tricuspid valve protrudes into the right ventricle during ventricular systole, accounting for its aneurysmal appearance. Less frequently, prolapse of an aortic valve leaflet reduces the size of the defect and can result in aortic insufficiency. 1 Early pathologic studies demonstrated deformity of the tricuspid valve resulting from ventricular septal aneurysm formation. 4 Chordal shortening and fusion, and leaflet deformity have been demonstrated in necropsy examinations of patients with ventricular septal aneurysms. Functional abnormalities resulting from tricuspid valve involvement in the formation of the aneurysm were recently described in pediatric studies.2 However, these abnormalities have not been described in adults, and the use of transesophageal echocardiography for the detection of ventricular septal aneurysms was not previously reported.

Structural remodeling of human myocardial tissue after infarction. Quantification with ultrasonic backscatter.

Remodeling of myocardial tissue after infarction may culminate in the development of either a well-healed scar or a thin, expanded heart wall segment that predisposes to ventricular aneurysm formation, congestive heart failure, or ventricular tachycardia. The three-dimensional architecture of mature human infarct tissue and the mechanisms that determine it have not been elucidated. We have previously shown that quantitative ultrasonic backscatter can be used to define the transmural organization of human myofibers in the normal ventricular wall by measuring the dependence of backscatter on the angle of insonification, or ultrasonic anisotropy. We propose that measurement of ultrasonic anisotropy of backscatter may permit quantitative characterization of the transmural architecture of tissue from areas of myocardial infarction and facilitate identification of fundamental mechanisms of remodeling of the ventricular wall. We measured integrated backscatter in 33 transmural sections from 12 cylindrical biopsy specimens (1.4-cm diameter) sampled from central regions of mature infarction in six explanted fixed human hearts. Tissue samples were insonified in two-degree steps around their entire circumference at successive transmural levels with a 5-MHz broad-band piezoelectric transducer. Backscatter radio frequency data were gated from the center of each specimen, and spectral analysis was performed on the gated radio frequency for the computation of integrated backscatter. Histological morphometric analysis was performed on each specimen for determination of the predominant fiber orientation and the percentage of tissue infarcted at consecutive transmural levels. The average percentage of tissue infarcted for all transmural levels was 49 +/- 3% (range, 13-80%). Histological attributes varied from patchy fibrosis to extensive confluent zones of scar tissue. The angle-averaged integrated backscatter for all transmural levels in infarct tissue was approximately 5 dB greater than that previously measured in normal tissue in our laboratory (-48.3 +/- 0.5 versus -53.4 +/- 0.4 dB, infarct versus normal). Marked anisotropy of backscatter was observed in tissue from areas of infarction and was characterized by a sinusoid-like dependence on the angle of insonification at each transmural level. Insonification perpendicular to infarct fibers yielded values for integrated backscatter 14.8 +/- 0.5 dB greater than those for insonification parallel to these fibers. Juxtaposition of the sinusoid-like anisotropy functions from all consecutive transmural levels demonstrated a progressive shift in the orientation of scar tissue elements from epicardial to endocardial levels of 14.6 +/- 1.5 degrees/mm of tissue. The transmural shift in fiber orientation per millimeter of tissue from the area of infarction exceeded that previously measured for normal tissue (9.2 +/- 0.7 degrees/mm) by 59%. This marked augmentation in angular shift per millimeter of tissue results from a generalized structural rearrangement (or reorientation) of fibers across the entire ventricular wall in the infarct zone that we hypothesize is determined in part by dynamic mechanical forces, imposed by the surrounding functional normal tissue, that tether the "infarcted" tissue. Myocardial tissue from areas of myocardial infarction manifests substantial anisotropy of ultrasonic scattering that may be useful for quantitative characterization of the alignment and overall three-dimensional anatomic organization of mature infarct scars.

Reversible and irreversible elongation of ischemic, infarcted, and healed myocardium in response to increases in preload and afterload.

Left ventricular aneurysm formation after myocardial infarction (MI) has been associated with elongation of infarcted tissue in response to wall stress. Such elongation most commonly occurs in acutely infarcted or partially healed regions during the early post-MI period; however, recent reports have indicated that mature (15-week-old) healed infarct regions also undergo elongation after stress. To assess factors contributing to post-MI left ventricular aneurysm formation, we subjected isolated strips (n = 50) of rabbit myocardial tissue from acutely ischemic (noninfarcted left ventricular), acutely infarcted (24 hours after MI), and healed infarct (3 and 15 weeks after MI) regions to a range of loading conditions and measured the reversible and irreversible length changes that occurred. The isolated strips were repetitively stretched for 1 hour at 4 Hz to impose cyclical physiological peak and resting stresses of 2.0 and 0.2 g/mm2. During a second hour, either peak stress ("afterload") or resting stress ("preload") was tripled, and the increase in strip length (strain) was measured. During a third hour, peak and resting stresses were returned to the initial values to assess the reversibility of length changes occurring during increased load. Elongation was expressed as the increase in natural strain from the first hour. Increasing afterload caused similar irreversible length increases of 4-5%/hr in acutely infarcted and 3- and 15-week-old healed infarct strips; acutely ischemic tissue length increased by 7.4%/hr (p less than 0.05 versus acutely infarcted tissue and scars). Increasing preload in acutely ischemic and acutely infarcted tissue caused a reversible length increase of less than 1%/hr. (Scar strips were not tested for the effect of preload.) Since an irreversible length increase may represent an early event in aneurysm formation, our results suggest that 1) afterload increases are more likely to lead to aneurysm development than preload increases, 2) acutely ischemic tissue is the most vulnerable to increased afterload, and 3) for a given wall stress level, healing scar tissue is as susceptible to irreversible length changes as is acutely infarcted tissue. The observation that even mature post-MI scar elongated in response to increases in afterload implies that long-term pharmacological management of afterload in post-MI patients may be beneficial in preventing tissue elongation and aneurysm formation and that factors that increase wall stress (e.g., hypertension and exercise stress) have the potential to promote aneurysm formation in healed infarct scars.

MRI of cardiac pseudoaneurysm and other complications of myocardial infarction

The purpose of this paper is to review the spectrum of pathology revealed by cardiac magnetic resonance (MR) in the evaluation of myocardial infarction. In addition, the paper is intended to provide a concise introduction to the capabilities and limitations of MR in the evaluation of myocardial infarction and its complications. To provide this introductory guide, three cases of infarction are reviewed in detail, including one unusual case of infarction with both true and false ventricular aneurysm formation. A selected review of the literature is included to demonstrate the current role of MR in the work-up and follow-up of acute infarction.

Bivalent effects of human growth hormone in experimental myocardial infarcts. Protective when administered alone and aggravating when combined with beta blockers.

Human growth hormone (hGH) administered alone revealed itself as a useful drug to prevent ventricular aneurysm formation in experimental myocardial infarctions in rats and is also able to diminish and change the usually expected pattern of wall necrosis. A protective action on the collagen framework of myocytes has been confirmed as one of the main causes responsible for the above mentioned findings. There are other positive metabolic actions on the myocardial cell although not completely known yet. These actions are revealed by an atypical picture of infarction which appears regionally reduced and with a patchy intracellular distribution. In an opposite fashion, when hGH was administered together with beta blockers, a rapid and extensive deleterious action occurred at the ventricular wall, a very high incidence of ventricular aneurysms and an increased extension of myocardial infarcts were the most outstanding features. The histologic picture in this series resembles that of a rapidly evolving diabetic cardiomyopathy.

Elucidation of the natural history of ventricular septal defects by serial Doppler color flow mapping studies

Two-dimensional echocardiography has provided information to aid in the diagnosis and management of infants with ventricular septal defect, but its inability to resolve very small ventricular septal defects and problems with defining ventricular septal defect orifice size (because of overlying muscle or tricuspid tissue) have made it unsuitable as a standard for defining the natural history of ventricular septal defect. In this study, 114 serial two-dimensional Doppler color flow mapping studies were performed to define ventricular septal defect anatomy, location and color flow diameter as an indicator of shunt size in 66 patients (over a 40 month period).Twenty-five patients first studied at 6 months of age (mean age at most recent study 15.9 months) had congestive heart failure and 41 (mean age 45 months) did not. In the congestive heart failure group, there were 24 perimembranous and 1 muscular ventricular septal defect and aneurysm formation was present in 17. Mean (±SD) color flow diameter was 8.2 ± 1.9 mm and color flow diameter/aortic root diameter ratio was 0.63. In the 30 patients who underwent cardiac catheterization, color flow diameter bore a close relation to angiographic diameter (r = 0.96) and pulmonary/systemic flow ratio (Qp/Qs) (r = 0.88). In the patients with congestive heart failure, 4 of the 25 ventricular septal defects, all with aneurysm present or positioned adjacent to the tricuspid valve, became smaller but none closed.Of the 41 patients without congestive heart failure, 21 had a perimembranous defect (15 with aneurysm), 18 had a muscular ventricular septa) defect and 2 had a supracristal ventricular septal defect. Mean color flow diameter was 3.9 ± 1.7 mm, and color flow diameter/aortic root ratio was 0.27 (both p < 0.05 compared with values in the congestive heart failure group). Follow-up Doppler color flow map studies of the noncongestive heart failure group showed that 4 of 21 perimembranous defects and 6 of 18 muscular defects had closed, whereas 4 perimembranous and 3 muscular defects showed significant diminution in color flow diameter.Two-dimensional echocardiography and color flow mapping diameter observations aid in predicting which patients with a ventricular septal defect might develop congestive heart failure, and suggest which ventricular septal defects will become smaller or close spontaneously.

Importance of collateral circulation for prevention of left ventricular aneurysm formation in acute myocardial infarction.

The effect of preexistent coronary collateral perfusion on the prevention of left ventricular aneurysm formation was examined in 47 patients undergoing an intracoronary thrombolysis within 6 hours after the onset of a first acute anterior myocardial infarction. Left ventricular aneurysm formation and wall motion were analyzed with cineventriculography. A left ventricular aneurysm was determined as well-defined demarcation of the infarcted segment from normally contracting myocardium. In 25 patients with successful thrombolysis (group A), a left ventricular aneurysm was observed in one patient (4%) during the chronic stage of infarction. In 10 patients who had a significant collateral circulation to the infarct-related coronary artery and unsuccessful reperfusion (group B), the left ventricular aneurysm was observed in only one patient (10%). In the remaining 12 patients with unsuccessful recanalization in the absence of a significant collateral perfusion (group C), there was a higher incidence (seven of 12, 58%) of left ventricular aneurysm formation than in groups A and B (p less than 0.05). In group A, both the global ejection fraction and regional wall motion in the infarct areas improved significantly (p less than 0.05) between the acute and chronic stages of infarction. By contrast, in groups B and C, these indexes on the ventricular function did not change significantly during the convalescent period. Thus, although the collateral perfusion existing at the onset of acute myocardial infarction may not improve ventricular function, it exerts a beneficial effect on the prevention of left ventricular aneurysm formation.

Electrophysiologic effects of thrombolytic therapy in patients with a transmural anterior myocardial infarction complicated by left ventricular aneurysm formation

To assess the effects of early thrombolytic therapy on the incidence of clinical and induced ventricular arrhythmias in high risk postmyocardial infarction patients, 32 patients with a transmural anterior myocardial infarction complicated by left ventricular aneurysm formation were prospectively evaluated. Sixteen patients (Group A) received routine care because of contraindication to thrombolytic therapy or other factors and 16 (Group B) received either tissue plasminogen activator or streptokinase within 6 h of the onset of chest pain. The two groups were similar in left ventricular ejection fraction (mean ± SD, 28 ± 9% [Group A] versus 30 ± 8% [Group B]) and occurrence of spontaneous nonsustained ventricular tachycardia, new bundle branch block and congestive heart failure. Group B patients had higher peak creatine kinase MB levels (446 ± 336 versus 205 ± 120 IU; p = 0.017) and earlier time to peak creatine kinase values (13.4 ± 6.6 versus 19.1 ± 6.1 h; p = 0.006).Twenty patients who had no clinical sustained ventricular arrhythmias underwent electrophysiologic study 13 ± 6 days after infarction. Ventricular tachycardia was induced during the study in 7 (88%) of 8 Group A patients, but in only 1 (8%) of 12 Group B patients given thrombolytic therapy (p = 0.0008).During a mean follow-up period of 11 ± 8 months, eight Group A patients (50%) died suddenly or were resuscitated from sustained ventricular tachycardia; all Group B patients are alive and have had no clinical arrhythmic events (p = 0.002). Four of the 8 patients with inducible ventricular tachycardia at electrophysiologic study have had a clinical arrhythmic event, whereas the 12 patients without inducible tachycardia are arrhythmia free (p = 0.020).Thus, patients with a transmural anterior myocardial infarction and subsequent left ventricular aneurysm formation had an improved arrhythmic outcome if they received early thrombolytic therapy. Furthermore, thrombolytic therapy dramatically improved electrical stability as elucidated by electrophysiologic study. These results were observed despite the failure of thrombolytic therapy to significantly improve global left ventricular ejection fraction or affect clinical variables normally associated with a poor prognosis.

Nonpenetrating Traumatic Rupture of the Tricuspid Valve: Formation of Ventricular Septal Aneurysm and Subsequent Septal Necrosis: Recognition by Two-Dimensional Doppler Echocardiography

A 26-year old man was admitted with blunt trauma to the chest following a high-speed deceleration injury. A two-dimensional Doppler echocardiogram demonstrated traumatic rupture of the tricuspid valve and a hematoma in the basilar portion of the interventricular septum. Serial two-dimensional Doppler echocardiographic analyses demonstrated evolutionary formation of a septal aneurysm and subsequent rupture with formation of a ventricular septal defect. The usefulness of the two-dimensional Doppler echocardiogram as a screening tool for cardiac contusion is discussed.

Determinants of left ventricular aneurysm formation after anterior myocardial infarction: A clinical and angiographic study

To determine factors involved in left ventricular aneurysm formation after transmural anterior myocardial infarction, 79 patients with a first myocardial infarction who underwent cardiac catheterization within 6 months of infarction were evaluated. Patients who had received thrombolytic therapy were excluded. Patients were divided into four groups depending on the status of the left anterior descending artery and the presence or absence of a left ventricular aneurysm: Group I (n = 25): aneurysm with occluded left anterior descending artery; Group II (n = 27): no aneurysm and occluded left anterior descending artery; Group III (n = 23): no aneurysm and patent left anterior descending artery; and Group IV (n = 4): aneurysm with patent left anterior descending artery. Single vessel disease was more common in Group I (aneurysm) compared with Groups II and III (no aneurysm) (chi 2(4) = 12.8; probability value equal to 0.012). Collateral blood supply in the presence of an occluded left anterior descending artery was significantly less in Group I (aneurysm) compared with Group II (no aneurysm) (0.9 versus 2.4, p less than 0.001). The extent of coronary artery disease and collateral blood supply in Groups I and II were directly related (p = 0.012). Neither age, sex nor risk factors for coronary disease correlated with aneurysm formation. At a mean follow-up of 48 months, no differences were observed in the incidence of recurrent angina, new myocardial infarction, embolic events or sudden death. More patients in Group II underwent coronary artery bypass surgery. Total occlusion of the left anterior descending artery in association with inherent poor collateral blood supply is a significant determinant of aneurysm formation after anterior myocardial infarction. Multivessel disease with either good collateral circulation or a patent left anterior descending artery is uncommonly associated with the development of left ventricular aneurysm.

Incidence, timing and prognostic value of left ventricular aneurysm formation after myocardial infarction: A prospective, serial echocardiographic study of 158 patients

Serial 2-dimensional echocardiography was performed prospectively in 158 consecutive patients with first acute myocardial infarction (AMI) to determine the incidence of left ventricular (LV) aneurysm formation and the time course required for, and the clinical significance of, onset of LV aneurysm formation. Studies were performed throughout the first 5 days and after 3 months and 1 year. LV aneurysm was defined as an abnormal bulge in the LV contour during both systole and diastole. Eighty-four patients had anterior, 68 posterior and 6 anteroposterior AMI defined echocardiographically. During the study period, LV aneurysm was found in 35 of 158 patients (22%); in anterior AMI in 27, in posterior AMI in 6 and in anteroposterior AMI in 2. No new aneurysm developed after 3 months. Early aneurysm formation, during the first 5 days after AMI, was seen in 15 patients with anterior infarction. Twelve of these 15 (80%) died within 1 year (10 within 3 months), in contrast to 5 (25%) of the remaining 20 patients with LV aneurysm (p < 0.05). Dyskinesia of the anterior wall in the acute stage usually resulted in aneurysm formation. Thus, LV aneurysm formation is seen in 22% of mostly anterior AMI and occurs within 3 months after AMI. Early aneurysm formation is associated with a high 3 month (67%) and 1-year (80%) mortality rate.

A CASE OF LEFT VENTRICULAR ANEURYSMAL CHANGE AFTER REPAIR OF A CARDIAC STAB WOUND

The patient, a 25-year-old man, had received a stab wound to the left anterior chest with a kitchen knife and was transported to our center. As plane chest roentgenography showed left hemothorax and his blood pressure was decreased, thoracotomy was urgently carried out. An approximatoly 3cm stab wound was recognized on the left side of the anterior descending branch of the left coronary artery, and hemostasis was performed by 4-acus interrupted suture using 3-0 Ticron® thread. Although the postoperative blood circulation was stable, ECG and enzymological examination showed suspicion of myocardial infarction and coronary arteriography showed occlusion of the anterior descending branch of the left coronary artery. Furthermore, left ventricular arteriography showed anteroseptal dyskinesis and ventricular aneurysmal changes. The patient is uneventfully under observation of the course. In the present case, the thrombotic occlusion and so on, which were caused by direct ligation of the coronary artery with suture thread or distortion or flexion of the coronary artery with ligature were considered to be the cause of ventricular aneurysm formation. With regard to the indication for surgery, the procedure for ventricular aneurysm after myocardial infarction is though to be applied to this case.

Late effects of intracoronary streptokinase on regional wall motion, ventricular aneurysm and left ventricular thrombus in myocardial infarction: Results from the Western Washington randomized trial

To determine whether intracoronary streptokinase improves late regional wall motion or reduces left ventricular aneurysm or thrombus formation in patients with acute myocardial infarction, two-dimensional echocardiography was performed at 8 +/- 3 weeks after infarction in 83 patients randomized to streptokinase (n = 45) or standard therapy (n = 38) in the Western Washington Intracoronary Streptokinase Trial. Among the patients treated with streptokinase, the average time to treatment was 4.7 +/- 2.5 hours after the onset of chest pain, and 67% had successful reperfusion. Regional wall motion was assessed in nine left ventricular segments on a scale of 1 to 4 (normal, hypokinetic, akinetic and dyskinetic). Left ventricular thrombus formation was interpreted as positive, equivocal or negative. All patients received anticoagulant therapy in the hospital and 52 received such therapy after hospital discharge. The mean (+/- SD) global (1.5 +/- 0.4 in both groups) and regional wall motion scores in the streptokinase-treated and control groups were not significantly different. The prevalence of aneurysm was 16% in both groups. Left ventricular thrombus was identified in only five patients (positive identification in four, and equivocal in one), all in the streptokinase-treated group (p = NS). There were also no differences between streptokinase and control treatment in any of the echocardiographic variables in subgroups of patients with anterior infarction, inferior infarction, no prior infarction or reperfusion with streptokinase. It is concluded that intracoronary streptokinase given relatively late in the course of acute myocardial infarction does not result in improved global or regional wall motion or a reduction in left ventricular thrombus or aneurysm formation in survivors studied 2 months after myocardial infarction.

Contractile properties of the left ventricle with aneurysm

Twenty-five patients with an anterior wall acute myocardial infarction (AMI) were studied by 2-dimensional echocardiography (2-D echo) 3 to 5 days after the onset of chest pain, and serially over 3 to 24 months to determine if a particular pattern of contractility may predispose to left ventricular (LV) aneurysm formation. No subject had a prior AMI. In 8 subjects LV aneurysm eventually developed (group I), usually within 2 to 4 weeks of AMI; in 17 patients LV aneurysm did not develop (group II). Percent fractional shortening of the basal and midventricular segments was significantly better in group I subjects than in group II subjects (29 ± 2% vs 20 ± 2%, p < 0.01, respectively, for the basal segment, and 23 ± 1% vs 17 ± 2%, p < 0.02, respectively, for the midventricular segment). Infarct size as determined by peak creatine kinase isoenzyme levels was large in both groups, and there was no statistically significant difference between their mean values (2,099 ± 620 IU vs 1,334 ± 249 IU for groups I and II, respectively). Severe asynergy of the infarcted myocardium was present in all group I subjects and in 9 of 17 group II subjects on the initial 2-dimensional echocardiographic study. These results indicate that LV aneurysm formation depends on a critical imbalance of myocardial forces where strong LV segments cause bulging of weakened ones.