Left ventricular remodelling and brain natriuretic peptide after first myocardial infarction

OBJECTIVE—To investigate the relation between brain natriuretic peptide (BNP) concentrations and left ventricular remodelling characteristics after acute myocardial infarction.
DESIGN—Consecutive sample prospective cohort study.
SETTING—District general hospital coronary care unit in the north of England.
PATIENTS—133 initial survivors of a first myocardial infarction who received thrombolytic treatment.
INTERVENTIONS—Patients had transthoracic echocardiography and BNP concentrations measured at three to seven days (early) and two months (late).
MAIN OUTCOME MEASURES—Wall motion index  1.2, end systolic left ventricular volume index and mortality at one year.
RESULTS—Patients with an early wall motion index of  1.2 had higher early and late BNP concentrations (early BNP mean (SEM) 629 (76.2) pg/ml v 334 (20.8) pg/ml, p = 0.001 and late BNP 584 (79.5) pg/ml v 343 (25.0) pg/ml, p = 0.001). Patients with an increase in end systolic left ventricular volume index of > 10% also had higher early and late BNP concentrations (early BNP p = 0.034 and late BNP p = 0.001). Early BNP was significantly associated with one year mortality (p = 0.003).
CONCLUSIONS—Higher BNP concentrations early after first myocardial infarction are associated with adverse left ventricular remodelling characteristics. This may help explain why BNP is such a strong predictor of outcome after myocardial infarction.


Keywords: brain natriuretic peptide; wall motion index; left ventricular volume index; myocardial infarction     

N-terminal pro-B-type natriuretic peptide and matrix metalloproteinases in early and late left ventricular remodeling after acute myocardial infarction

N-terminal pro-B-type natriuretic peptide (NT-pro-BNP) is a predictor of left ventricular remodeling. Matrix metalloproteinases (MMPs) contribute to collagen breakdown that is associated with ventricular remodeling after acute myocardial infarction (AMI). We assessed the association between circulating levels of NT-pro-BNP, MMP-2, and MMP-9 and their inhibitor (tissue inhibitor of metalloproteinase-1) early (24 and 72 hours) and late (7 and 30 days) after AMI in 108 patients who had ST-elevation AMI (90 men; mean age 60 years). Serum MMP-2 levels measured 24 and 72 hours after AMI were inversely associated with NT-pro-BNP levels, whereas MMP-9 serum levels were positively related. During late-stage remodeling after AMI, circulating concentrations of tissue inhibitor of metalloproteinase-1 were independently associated with NT-pro-BNP levels 7 and 30 days after AMI. This study shows that, in patients who have ST-elevation AMI, circulating levels of NT-pro-BNP are associated with MMPs in a species-specific and time-dependent manner.     

N-terminal pro B-type natriuretic peptide in the early evaluation of suspected acute myocardial infarction

Background

Myocardial ischemia is a strong trigger of N-terminal pro-B-type natriuretic peptide (NT-proBNP) release. As ischemia precedes necrosis in acute myocardial infarction, we hypothesized that NT-proBNP might be useful in the early diagnosis and risk stratification of patients with suspected acute myocardial infarction.

Methods

In a prospective multicenter study, NT-proBNP was measured at presentation in 658 consecutive patients with acute chest pain. The final diagnosis was adjudicated by 2 independent cardiologists. Patients were followed long term regarding mortality.

Results

Acute myocardial infarction was the adjudicated final diagnosis in 117 patients (18%). NT-proBNP levels at presentation were significantly higher in acute myocardial infarction as compared with patients with other final diagnoses (median 886 pg/mL vs 135 pg/mL, P <.001). The diagnostic accuracy of NT-proBNP for acute myocardial infarction as quantified by the area under the receiver operating characteristic curve (AUC) was 0.79 (95% confidence interval [CI], 0.75-0.83). When added to cardiac troponin T, NT-proBNP significantly increased the AUC from 0.89 (95% CI, 0.84-0.93) to 0.91 (95% CI, 0.88-0.94; P = .033). Cumulative 24-month mortality rates were 0% in the first, 1.3% in the second, 8.3% in the third, and 23.3% in the fourth quartile of NT-proBNP (P <.001). NT-proBNP (AUC 0.85, 95% CI, 0.81-0.89) predicted all-cause mortality independently of and more accurately than both cardiac troponin T (AUC 0.66, 95% CI, 0.58-0.74; P <.001) and the Thrombolysis in Myocardial Infarction risk score (AUC 0.79, 95% CI, 0.74-0.84; P <.001). Net reclassification improvement (Thrombolysis in Myocardial Infarction vs additionally NT-proBNP) was 0.188 (P <.009), and integrated discrimination improvement was 0.100 (P <.001).

Conclusions

Use of NT-proBNP improves the early diagnosis and risk stratification of patients with suspected acute myocardial infarction.     

急性心肌梗死后左心室重构及其防治

本文简述了急性心肌梗死后左心室重构的发生机制、时间、后果、影响因素及防治措施等     

Intravenous atrial natriuretic peptide prevents left ventricular remodeling in patients with first anterior acute myocardial infarction

OBJECTIVES: The study evaluates the effect of atrial natriuretic peptide (ANP) compared with nitroglycerin (GTN) on left ventricular (LV) remodeling after first anterior acute myocardial infarction (AMI). BACKGROUND: Compared with GTN, ANP suppresses the renin-angiotensin-aldosterone system and endothelin-1 (ET-1), which stimulate LV remodeling. METHODS: Sixty patients with a first anterior AMI were randomly divided into the ANP (n = 30) or GTN (n = 30) groups after direct percutaneous transluminal coronary angioplasty. We evaluated LV ejection fraction (LVEF), end-diastolic volume index (LVEDVI) and end-systolic volume index (LVESVI) at the acute phase and after one month. We also measured neurohumoral factors during study drug infusion. RESULTS: There was no difference in the baseline characteristics or LVEF (46.9+/-1.0 vs. 46.8+/-1.3%) between the two groups. Although there was no difference in hemodynamics during the infusion periods, the LVEF was significantly improved after one month compared with the baseline value in both groups, but it was improved more in the ANP group than in the GTN group (54.6+/-1.1%, 50.8+/-1.3%, p < 0.05). Left ventricular enlargement was prevented in the ANP group (LVEDVI, 85.8+/-3.1 ml/m2 to 87.3+/-2.7 ml/m2; p = ns, LVESVI, 45.6+/-1.8 ml/m2 to 41.0+/-2.1 ml/m2, p < 0.05) but not in the GTN group (LVEDVI, 86.2+/-4.1 to 100.2+/-3.7, p < 0.01; LVESVI, 46.3+/-2.8 ml/m2 to 51.1+/-3.0 ml/m2, p = ns). During the infusion, ANP suppressed plasma levels of aldosterone, angiotensin II and ET-1 compared with GTN. CONCLUSIONS: These findings indicate that in patients with a first anterior AMI, an ANP infusion can prevent LV remodeling better than can GTN, and effectively suppresses aldosterone, angiotensin II and ET-1.     

同型半胱氨酸、N-末端脑钠肽前体与急性心肌梗死后左心室重构的关系

目的 探讨急性心肌梗死（acute myocardical infarction,AMI）患者同型半胱氨酸（homocysteine,Hcy）、N-末端脑钠肽前体（N-terminal pro-brain natriuretic peptide,NT-proBNP）浓度对心肌梗死后左心室重构的预测价值及对AMI患者临床预后的影响.方法 选择2009年6月至2011年6月在广州市第一人民医院心内科住院并诊断为急性ST段抬高型心肌梗死（STEMI）的患者266例,根据入院后空腹Hcy浓度的三分位数间距将患者分为A组（Hcy＜15.6μmol/L）83例,B组（15.6～24.6 μmol/L）组93例和C组（Hcy＞24.6μmol/L）90例.测定患者入院时即刻NT-proBNP浓度,并于入院48 h内及半年后行超声心动图测定患者左心室舒张末期内径（LVEDd）、左心室舒张末期容积（LVEDV）,左心室收缩末期容积（LVESV）,左心室射血分数（LVEF）.动态追踪观察3组患者随访期间内（6个月）的主要心血管事件（MACE）的发生情况.结果 三组患者随Hcy浓度升高,NT-proBNP浓度升高,左心室舒张末期容积和左心室收缩末期容积显著增加,左心室射血分数降低（P＜0.05 or P＜0.01）.ST段抬高型心肌梗死患者Hcy与NT-proBNP浓度呈正相关（r=0.380,P＜0.05）.直接经皮冠状动脉介入治疗随访6个月,Kaplan-Meier生存分析发现三组患者累积无主要心血管事件生存率比较,差异有统计学意义（91.6％ vs.86.0％ vs.77.8％,Log rank=6.630,P=0.036）.多因素Logistic回归分析显示Hcy、NT-proBNP均是ST段抬高型心肌梗死患者近期主要心血管事件发生的独立预测因子.结论 AMI患者Hcy、NT-proBNP浓度与梗死后心室重构密切相关,Hcy、NT-proBNP对患者的近期预后具有预测意义.     

重组人脑利钠肽对大鼠心肌梗死后心室重构的影响

目的 探讨重组人脑利钠肽(心活素)对大鼠心肌梗死后心室重构的影响. 方法建立雄性Wistar大鼠心肌梗死后心室重构模型.随机分为模型组、治疗组、假手术组.治疗组给予心活素15μg/kg,每天腹腔注射1次,假手术组及模型组仅以等体积的生理盐水腹腔注射.5周后检测心室重构指标、心功能参数及电镜观察. 结果模型组左室质量(LVAW)(883.09±35.15)mg、左室质量指数(LVRW)(2.40±0.13)mg/g、左室舒张压(LVEDP)(32.1±4.0)mm Hg,较治疗组LVAW(827.15±44.10)mg、LVRW(2.26±0.14)mg/g、LVEDP(26.1±2.0)mm Hg和假手术组的LVAW(759.70±43.82)mg、LVRW(2.04±0.09)mg/g、LVEDP(20.9±6.6)mm Hg水平增高(F=11.892、14.341、7.765,P=0.002、0.001、0.023);模型组球形指数(SI)(1.32±0.14)、收缩压(104.4±3.2)mm Hg、舒张压(71.8±5.1)mm Hg、左室收缩压(LVSP)(116.8±7.8)mm Hg、及左室内压最大上升和下降速率(±dp/dt)(5.7±0.9、3.6±0.3)mm Hg/ms较治疗组SI(1.47±0.08)、收缩压(111.2±4.6)mm Hg、舒张压(80.4±6.3)mm Hg、LVSP(129.2±5.3)mm Hg、及(±dp/dt)(5.7±0.9、3.6±0.3)mm Hg/ms和假手术组SI(1.63±0.15)、收缩压(118.5±5.8)mm Hg、舒张压(95.6±3.7)mm Hg、LVSP(138.0±4.2)mm Hg、及±dp/dt(6.9±0.4、5.25±0.1)mm Hg/ms明显降低(F=7.350、11.037,39.253、8.495、11.775、16.947,P=0.011、0.002、0.000、0.007、0.002、0.000);治疗组与模型组比较,LVAW、LVRW减小(t=11.489、6.439,P=0.003、0.019),SI增大(t=5.133,P=0.024);收缩压、舒张压、LVSP、±dp/dt明显增高(t=16.685、13.057、21.127、13.619、35.614,P=0.000、0.002、0.000、0.001、0.000),LVEDP显著降低(t=28.160,P=0.000);心肌细胞超微结构损伤程度明显减轻. 结论心活素能减轻心肌梗死大鼠心室重构后心肌细胞损伤,明显抑制心室重构发展,改善心功能.     

血氨基末端脑钠肽前体对急性心肌梗死远期心功能的评估价值

目的观察血氨基末端脑钠肽前体（NT-proBNP）对急性心肌梗死患者的远期预测价值。方法本研究入选了58例发病24h以内ST段抬高的急性心肌梗死患者。所有病例既往均无明显心功能不全临床表现。于入院即刻、24h及1周测NT-proBNP,高敏C反应蛋白（HS-CRP）,随访1年的病死率、心血管事件住院率及心力衰竭住院率,并于1年后复查超声心动图。结果所有急性心肌梗死患者的NT-proBNP峰值均高于正常,高峰见于入院24h。一年随访中病死率、所有心血管事件住院率和心力衰竭住院率分别为6.9%、20.7%和13.8%。死亡病例、所有心血管事件住院病例和因心力衰竭住院病例研究入组时的NT-proBNP峰值均高于其余病例。发生心血管事件病例研究入组时的HS-CRP峰值也高于其余病例,但仅在死亡病例中有统计学意义。在急性心肌梗死病例中,研究入组时的血NT-proBNP峰值与1年后的左室射血分数值（r=0.383,P=0.003）及左室舒张末期直径（r=0.280,P=0.035）呈线性相关关系。结论高NT-proBNP的急性心肌梗死患者容易再发急性心血管事件,并且与远期心力衰竭的发生密切相关。     

急性心肌梗死后心室重塑与脑钠肽的关系

目的 通过观察血浆脑钠肽(BNP)水平在急性心肌梗死(AMI)后的改变,了解BNP与心室重塑的关系,探讨血浆BNP测定可否作为预测AMI早期心室重塑的方法.方法 AMI组AMI患者37例,仅接受强化内科保守治疗;正常组为32例健康对照者.分别在AMI后72 h、1个月及3个月,采用免疫荧光测定血浆BNP,并应用超声心动图检查测定射血分数(EF)、左室快速充盈速度(VE)、左房收缩峰值速度(VA)及VE/VA比值、左室舒张末期内径(LVEDd)、左室舒张末期容积(LVEDV);比较不同时期AMI组与正常对照组间各指标的差异.结果 AMI后72 h、1个月、3个月血浆BNP均值与对照组比较差异有统计学意义(P＜0.01),均高于对照组,同时各AMI组之间差异亦有统计学意义(P＜0.01);AMI 72 h内血浆BNP水平与AMI后1个月、3个月心脏超声心功能指标之间的直线相关关系与EF、VE/VA表现为负相关,与LVEDd、LVEDV均表现为正向变化.结论 心肌梗死患者72 h内的血浆BNP与近期心肌梗死(心肌梗死后1个月、3个月)EF、VE/VA呈负相关,而与LVEDd、LVEDV呈正相关.心肌梗死患者早期血浆BNP水平可预测AMI近期心室重塑.     

N-端心房利钠肽与N-端脑利钠肽对预测左室收缩功能障碍的价值

目的比较N-端心房利钠肽(心钠素NT-proANP)和N-端脑钠肽(NT-proBNP)对左室收缩功能障碍(LVSD)预测效率,依据二者特性确定适用范围并界定最佳下限(cut-off)值。方法入选心血管病患者380例(病例组),依据左室射血分数(LVEF)将患者划分为LVSD组(LVEF≤40%,n=90)及非LVSD组(LVEF40%,n=290)。另选136名健康体检者作为对照组。超声心动图测定LVEF;ELISA法测定血浆NT-proANP和NT-proB-NP浓度。描记NT-proANP和NT-proBNP预测左室收缩功能障碍受试者工作特征(ROC)曲线。依据年龄(以65岁为分界)、性别及原发心血管疾病种类划分亚组,分别描记各组患者NT-proANP和NT-proBNP预测左室收缩功能障碍ROC曲线;确定最佳cut-off值。结果病例组血浆NT-proANP和NT-proBNP浓度均显著高于对照组log(NT-proANP):(3.30±0.41)vs(2.98±0.16),P0.01;log(NT-proBNP):(2.71±0.30)vs(2.49±0.13),P0.01。NT-proANP和NT-proBNP对不同程度LVSD(LVEF≤40%或LVEF≤30%)患者诊断ROC曲线下面积(AUC)均大于0.73(P0.01);对LVEF≤40%的患者,NT-proANPAUC大于NT-proBNP(0.820vs0.738);对LVEF≤30%的患者,NT-proANPAUC明显小于NT-proBNP(0.853vs0.877)。根据各亚组ROC曲线确定cut-off值,NT-proANP为1676.92pmol/L时对各组LVSD预测敏感度88.9%～100%;特异度14.0%～58.7%;阳性预测值9.04%～30.04%;阴性预测值96.96%～98.77%。NT-proBNP为417.37pmol/L时,敏感度77.8%～94.4%;特异度10.0%～55.8%;阳性预测值7.07%～48.88%;阴性预测值94.46%～98.87%。结论 NT-proBNP与NT-proANP均能够反映心力衰竭高危人群心脏功能状态,可作为LVSD的诊断指标,对于LVEF≤40%的预测,NT-proANP效果优于NT-proBNP,有助于早期发现LVSD患者。     

B型尿钠肽水平对急性心肌梗死患者心源性死亡的预测价值

目的 探讨急性心肌梗死（AMI）患者血B型尿钠肽（BNP）水平预测死亡的价值。方法对264例AMI患者随访（14．7±5．3）个月,随访率为87．1％。检测肌酸激酶同工酶（CK—MB）、肌钙蛋白（TnT）、左室舒张末径、左室射血分数和BNP,并绘制受试者工作特性曲线（ROC）对比评价BNP等指标对AMI后心源性死亡的预测价值。结果ROC曲线显示仅BNP能预测心源性死亡。据ROC曲线定864ng／L为最佳分界值时,预测AMI后1、6个月和1年时心源性死亡的敏感性、特异性、准确度、阳性和阴性预测值分别为76．2％-92．9％、84．3％-85．6％、82．2％-86．1％、21．3％-36．2％和97．3％-98．9％。多元回归分析显示BNP是预测AMI后近、远期心源性死亡的独立危险因素（P〈0．01）。BNP≤864ng／L组1年无心源性死亡生存率显著高于BNP〉864ng／L组（97．3％比72．3％,P〈0．001）,死亡者中位生存时间在前者亦显著长于后者（16．0比10．7个月,P〈0．01）,且与急诊PCI和ST段抬高与否无关。结论 与传统指标相比BNP水平能预测AMI患者心源性死亡,且预测作用最佳。     

Clinicopathological study of left ventricular remodeling after first acute myocardial infarction

The morphological characteristics of post-infarction ventricular remodeling were determined by comparison of infarct location and histological changes of noninfarcted myocardium at autopsy. A total of 94 cases of first acute myocardial infarction with clinical courses of 0 to 37 days were studied. Hearts were sliced on the short axis at the level of 1/3 of the distance from the atrioventricular ring to the apex. Wall thicknesses of the infarcted and noninfarcted areas, and the endocardial and epicardial perimeter lengths of the left ventricle were measured. Myocyte diameter and number of myocytes in the noninfarcted area were measured. Infarcts were classified into 3 groups based on infarct location (51 anterior, 22 posterior, and 21 nontransmural circumferential) and each group was further divided according to the clinical course of less than 72 hours or longer. Fifty two patients died within 72 hours. Cardiac rupture was the most common cause of death in the anterior group. Patients in the posterior group chiefly died due to cardiogenic shock and in the circumferential group chiefly died to pump failure. According to the number of stenosed coronary arteries, cardiac rupture was the most common cause of death in single-vessel disease in both anterior and posterior groups (62.1% and 55.6%, respectively). In double-vessel disease, the most common cause of death in the anterior group was still cardiac rupture (50.0%). On the other hand, 50.0% of the posterior group died of cardiogenic shock in double-vessel disease. Patients with triple-vessel disease mainly died due to heart failure in all groups. Wall thickness of the infarcted myocardium was decreased in the anterior group after 72 hours (11.8 +/- 3.5 vs 7.8 +/- 2.5 mm). Endocardial perimeter length was increased in the anterior and circumferential groups (83.6 +/- 25.6 vs 116.3 +/- 29.5 mm, 75.2 +/- 12.0 vs 117.6 +/- 3.1 mm, respectively). Endocardial/epicardial perimeter length ratio increased with longer clinical course in the anterior group. No specific change in wall thickness or perimeter length was found in the posterior group. Noninfarcted wall thickness was preserved in both the anterior and posterior groups. Myocyte diameter and number of myocytes in the noninfarcted area showed no significant difference after 72 hours. The nature of ventricular remodeling differs with infarct location. Ventricular dilation occurred during the clinical course in the anterior group. The transmural and adjacent areas are more important than the remote noninfarcted area in post-infarction remodeling within this period.     

Left ventricular remodeling in patients with stress hyperglycemia after acute myocardial infarction

Background To investigate the association between left ventricular remodeling and stress hyperglycemia (SH) inpatients with acute anterior wall myocardial Infarction. Methods Patients with acute anterior myocardial infarction and a successful primary percutaneous coronary intervention (PCI) were enrolled and divided into two groups according to the presence or absence of SH. Patients with diabetes mellitus were excluded. Echocardiographic studies were performed on discharge and at 6 month follow-up. Left ventricular (LV) ejection fractions (EF), LV end-diastolic volume (EDV) and LV end-systolic volume (ESV) were obtained at baseline and at 6 month. Differences between changes of ESV (ΔESV) and changes of EDV (ΔEDV) in the two groups as well as EF improvement rate (ΔEF %) over six month were obtained. Correlation between SH and LV remodeling was investigated. Results (1) At baseline, the level of hemoglobin A1c was significantly higher in SH group (6.9±1.4 vs 6.2±0.8 P=0.04). Other baseline characteristics, including peak serum creatine kinase MB and LV function, were similar between two groups; (2) EF increased significantly over 6 months in both group with SH((41.1±7.2)% vs (52.7±8.4)%, P=0.02) and group without SH. ((43.6±8.7)% vs (54.5±9.3)%, P=0.03) (3) Only in SH group, EDV increased significantly at 6 month (139.6±26.7 vs 126.1±26.7 P=0.04); (4) There was a weak correlation between ΔEDV and the level of fasting plasma glucose on admission.(Pearson's r=0.35, P0.01). Conclusions (1) Previous glucose metabolism disorder is at least partially responsible for hyperglycemia on admission; (2) Given successful primary PCI within recommended time interval, left ventricular function improved regardless of whether SH is present or not; (3) The degree of glucose metabolic dysfunction on admission is weakly associated with the remodeling process in 6 months     

N末端脑钠肽前体、超敏C-反应蛋白和血清CD137对急性心肌梗死患者左心室重构的预测价值

目的探讨急性心肌梗死(AMI)患者N末端脑钠肽前体(NT-proBNP)、超敏C-反应蛋白(hs-CRP)和血清白细胞分化抗原137(CD137)的表达及其与左心室重构(LVR)的关系。方法选择2017年1月至2018年5月于宜兴市人民医院心血管内科确诊为急性心肌梗死的住院患者124例,入院常规检测血常规、生化、心肌酶、血清肌钙蛋白T(cTNT)、NT-proBNP、hs-CRP、血清CD137等指标,入院期间及出院12个月行超声心动图检查。随访12个月后根据是否存在LVR分为LVR组(n=38)和非LVR组(n=86)。采用SPSS 16.0统计软件进行数据分析。相关性分析采用Pearson相关分析法。采用多因素二分类logistic回归法分析LVR的独立危险因素。采用受试者工作特征(ROC)曲线评估NT-proBNP、hs-CRP、血清CD137对LVR的预测价值。结果 LVR组患者入院时NT-proBNP、hs-CRP、血清CD137均明显高于非LVR组,差异具有统计学意义(P0.05)。Pearson相关分析表明,NT-proBNP(r=0.419)、hs-CRP(r=0.209)和血清CD137(r=0.604)水平与左心室舒张期末内径增加值呈正相关(均P0.05)。二分类logistic回归分析显示,NT-proBNP、hs-CRP和血清CD137水平是AMI后发生LVR的独立危险因素(P0.05)。NT-proBNP、hs-CRP和血清CD137水平预测LVR发生的ROC曲线下面积(AUC)分别为0.753,0.722,0.690,三者联合预测的AUC为0.805(均P0.05)。结论 NT-proBNP、hs-CRP和血清CD137水平与急性心肌梗死后LVR密切相关,三者联合检测对急性心肌梗死后LVR有一定的预测价值。     

Left ventricular thrombus formation after first anterior wall acute myocardial infarction

The characteristics of the left ventricle and coronary arteries associated with left ventricular (LV) thrombus in patients with recent anterior acute myocardial infarction were defined. Of 77 patients studied, 35 (46%) had LV thrombi. The presence of LV thrombus was not correlated to the extent of coronary artery disease. The frequency of LV thrombus progressively increased with groups of increasing wall motion abnormality as determined by the extent of akinesia and dyskinesia (%AD) (%AD 0 to 14, thrombus present in 3 of 16 [19%], %AD 15 to 29, thrombus in 8 of 27 [30%]; %AD greater than or equal to 30%, thrombus in 24 of 34 [71%]; p less than 0.001) and with increasingly severe degrees of early ventricular shape change (normal or mildly abnormal contour, 16% with thrombus; moderately abnormal contour, 36% with thrombus; severely abnormal contour, 70% with thrombus; p less than 0.001). Patients with thrombi had higher diastolic (249 +/- 55 vs 225 +/- 48 ml; p less than 0.05) and systolic (158 +/- 48 vs 120 +/- 45 ml; p less than 0.001) volumes than patients without thrombi, respectively. A stepwise discriminant analysis identified ejection fraction, extent of early shape change and LV end-diastolic pressure as independent correlates of LV thrombus after acute myocardial infarction.