Coexistence of prothrombic risk factors and its relation to left ventricular thrombus in acute myocardial infarction

OBJECTIVE: Within the last few years a number of thrombophilic mutations have been identified. Pre-symptomatic testing for these established genetic risk factors identifies individuals predisposed to a disease and often allows to select suitable prophylactic interventions in time. We investigated whether or not the prothrombin G20210A allele, the factor V Leiden G1691A, and MTHFR C677T allele are risk factors for left ventricular thrombus (LV) in patients with myocardial infarction (AMI) or not. METHODS AND RESULTS: We analysed clinical, echocardiographic and biochemical data in 183 consecutive patients (aged 58 +/- 12 years; 34 women) with a first anterior acute myocardial infarction. Two-dimensional echocardiographic examination was performed on days 1, 3, 7, 15, and 30. LV thrombi were detected in 42 (23%) of the 183 patients with acute myocardial infarction. We have used multiplex assays based on PCR and DNA hybridization in microtitre plates for the simultaneous analysis of three mutations (FV Leiden G1691A, prothrombin G20210A, and MTHFR C677T). No significant differences in allele frequencies of FV Leiden G1691A (9.5% vs. 8.5%, p = 0.75), prothrombin G20210A (9.5% vs 7.1%, p = 0.74) and MTHFR C677T (47.6% vs. 50.3%, p = 0.74) were found in patients with LV thrombus when compared with those without LV thrombus. No significant differences in haemostatic factor levels were found in patients with LV thrombus when compared with those without LV thrombus. CONCLUSION: FV Leiden, prothrombin 20210 variant, and MTHFR mutation are no risk factors for left ventricular thrombus in patients with myocardial infarction.The presence of multiple mutations did not influence the development and outcome of LV thrombus in patients with myocardial infarction     

Factor V Leiden mutation and its relation to left atrial thrombus in chronic nonrheumatic atrial fibrillation

The genetic defect of coagulation factor V, known as factor V Leiden, produces a resistance to degradation by activated protein C and increased venous thrombosis. However, the role of factor V Leiden in the formation of left atrial thrombus with nonrheumatic atrial fibrillation has not been studied. We investigated whether factor V Leiden is a risk factor for left atrial thrombus in patients with nonrheumatic atrial fibrillation. We analyzed clinical, echocardiographic, and biochemical data in 105 consecutive patients with nonrheumatic atrial fibrillation. These patients were divided into two groups: group A (n = 37) with left atrial thrombus and group B (n = 68) without left atrial thrombus. The study also included 42 control subjects. Left atrial thrombus was investigated by using both transthoracic echocardiography and transesophageal echocardiography. Blood samples from the patients and controls were analyzed for the factor V Leiden mutation by DNA analysis, using the polymerase chain reaction. There was no significant difference in the prevalence of factor V Leiden between the patients and control subjects. The prevalence of factor V Leiden mutation was 8.1% (3/37) in patients with left atrial thrombus, and 8.8% (6/68) in patients without left atrial thrombus. The prevalence of factor V Leiden was 7.1% (3/42) in control subjects. The prevalance of factor V Leiden was 10% (2/20) in patients with spontaneous echo contrast and 8% (7/85) in patients without spontaneous echo contrast. Multivariate analyses showed that left ventricular ejection fraction was an independent predictor of left atrial thrombus. Factor V Leiden mutation is not a risk factor for left atrial thrombus formation and spontaneous echo contrast in patients with nonrheumatic atrial fibrillation.     

Serum lipoprotein(a) and its relation to left ventricular thrombus in patients with acute myocardial infarction

It is well known that the incidence of left ventricular (LV) thrombosis is high in patients with acute myocardial infarction (AMI). Due to the high degree of structural homology with plasminogen, lipoprotein(a) may produce thrombogenic effects by modulating the fibrinolytic system. However, the role of Lp(a) level in the formation of LV thrombus has not been studied. This study sought to determine whether Lp(a) is a risk factor for LV thrombus in patients with AMI. We have analyzed clinical, echocardiographic and biochemical data in 102 consecutive patients (aged 58+/-12 years, 92 men / 10 women) with first anterior AMI. Two-dimensional examination was performed on days 1, 3, 7, 15, and 30. Blood samples were obtained within 12 h after the onset of symptoms and before beginning the therapy. Plasma levels of fibrinogen and Lp(a) were measured using enzyme-linked immunosorbent assay and immunonephelometric methods, respectively. LV thrombus was detected in 20 (20.3%) patients. No significant difference was found for admission Lp(a) levels between patients with or without thrombus (30.5+/-17.2 vs 32.3+/-22.4 mg/dl, p = 0.7). Univariate analysis showed that patients with LV thrombus had a higher wall motion score index (1.8+/-0.3 vs 1.4+/-0.3, p = 0.002), a higher peak creatine kinase level (2945+/-898 vs 1805+/-1336, I / U p = 0.004), a larger end-diastolic volume (139.7+/-38.6 vs 114.1+/-41.8 ml, p = 0.04), a larger end-systolic volume (83.1+/-34.3 vs 59.2+/-30.6 ml, p = 0.02 ), and a lower ejection fraction (38+/-12 vs 47+/-11, p = 0.04). In multivariate analyses, only peak creatine kinase level (p = 0.04) and LV wall motion score index (p = 0.002) were independent predictors of left ventricular thrombus formation. These results suggest that Lp (a) is not a risk factor for LV thrombus in patients with AMI. Our data demonstrate that the best predictors of LV thrombus formation after AMI are a high peak creatine kinase level and a high LV wall motion score index.     

Magnesium dynamics and relation to left ventricular function in acute myocardial infarction

The present study investigated the serial changes in serum magnesium (Mg) and erythrocyte concentration of Mg in patients with acute myocardial infarction (AMI) and the relationship between these changes and left ventricular ejection fraction (LVEF) at 1 month after the onset of infarction. The study group comprised 26 patients with AMI (mean age, 57.9+/-8.9 years). Serum Mg and erythrocyte Mg were measured on hospital days 1, 2, 4, 7 and 21. The change in erythrocyte Mg during the acute phase was calculated as a ratio: [(erythrocyte Mg at day 2)-(erythrocyte Mg at day 1)]/(erythrocyte Mg at day 1). The change in serum Mg was calculated similarly. The following results were obtained. (1) Serum Mg tended to increase from the onset of myocardial infarction (day 1: 1.86+/-0.19, day 2: 1.93+/-0.22, day 4: 2.17+/-0.23; day 7: 2.25+/-0.20; day 21: 2.12+/-0.15 mg/dl). (2) Erythrocyte Mg on day 2 and day 4 showed a significant decrease compared with day 1 (day 1: 2.45+/-0.40, day 2: 2.09+/-0.41, day 4: 2.07+/-0.37, day 7: 2.22+/-0.33, day 7: 2.34+/-0.28 mg/dl per 400x10(4)/mm3 cells). (3) A significant positive correlation was observed between the change in serum Mg and LVEF (r=0.55, p<0.05), and a significant negative correlation was observed between the change in erythrocyte Mg and LVEF (r=-0.57, p<0.05). Thus, it was concluded that an extracellular shift in intracellular Mg occurred during the first 2 days after the onset of myocardial infarction. This responsive increase in the extracellular Mg level may be an important factor for maintaining left ventricular function in patients 1 month after the onset of AMI.     

Clinical predictors of early left ventricular thrombus formation in acute myocardial infarction

OBJECTIVE: Clinical epidemiological and echocardiographic risk factors relating to the development of a left ventricular thrombus were studied retrospectively in patients with acute myocardial infarction. METHODS AND RESULTS: The data on 1833 consecutive patients treated for acute myocardial infarction during a 10-year period were processed retrospectively. Transthoracic echocardiography was performed on each patient 65.0 +/- 5.5 hours after hospital admission. A left ventricular thrombus was detected in 145 patients (7.9%). The patients with acute myocardial infarction and a left ventricular thrombus had significantly lower frequencies of 1) myocardial infarction in their family history (3% versus 11%, respectively), 2) hospital admission within 24 hours from the onset of chest pain (17% versus 50%, respectively), 3) thrombolytic therapy (8% versus 23%, respectively) and 4) current smoking (24% and 35%, respectively) than those without a left ventricular thrombus. In contrast, anterior infarction (81% versus 38%, respectively), left ventricular dilatation (30% versus 19%, respectively), dyskinesis of the left ventricular wall (23% versus 10%, respectively), an aneurysm (22% versus 7%, respectively) and a reduced systolic left ventricular function (ejection fraction < 40%) (28% versus 17%, respectively) were more frequent in the presence of a left ventricular thrombus after myocardial infarction. Multivariate analysis of the results revealed that the presence of anterior myocardial infarction and an aneurysm is associated with significantly increased hazard ratios. On the other hand, early hospitalization and a positive family history of infarction significantly lowered the hazard ratio. The frequency of a left ventricular thrombus was significantly higher in spring and winter. CONCLUSIONS: The results presented in this paper confirm the significant hazard of certain parameters [location of infarction (anterior) and aneurysm] as concerns left ventricular thrombus formation among patients with acute myocardial infarction. Early hospitalization was found to lower the risk of thrombus formation.These echocardiographic and clinical parameters may be useful in the establishment of the individual risk of intracavital thrombus formation and may be of help in everyday medical practice.     

Usefulness of high-dose anticoagulants in preventing left ventricular thrombus in acute myocardial infarction

Fifty-three patients with a suspected first anterior wall acute myocardial infarction (AMI) were randomized to intervention with intravenous heparin followed by oral warfarin (26 patients) or matching placebo (27 patients). The regimen was started within 12 hours after the onset of AMI. Anticoagulation was maintained at a therapeutic level (for heparin, activated partial thromboplastin time 70 to 140 seconds; for warfarin, thrombotest 5 to 10%) for 10 days, and no bleeding episodes occurred. The baseline characteristics of the 2 study groups were well matched. In 7 patients in the placebo group and in none in the anticoagulant group, left ventricular thrombus developed during the study, as detected by serial 2-dimensional echocardiography. Early intervention with high-dose anticoagulant drugs may prevent the development of left ventricular thrombus in anterior wall AMI.     

Influence of coronary arterial thrombus location on left ventricular function in acute myocardial infarction

In 238 patients with acute myocardial infarction studied during intracoronary streptokinase therapy, the circumferential extent of left ventricular hypokinesis was measured by 5 methods and correlated with the location of the infarct-related coronary artery segment and with 1-year survival. Of the 5 methods, 1 focused only on the infarct region, and 4 varied in the complexity of the noise filter. Hypokinetic segment length measurements by all 5 methods correlated significantly with the location of occlusion along the left anterior descending coronary artery. No method yielded measurements that correlated with occlusion location along the right coronary artery. Measurements by all methods correlated significantly with survival, but the method that focused on the infarct region performed least well. Thus, the circumferential extent of hypokinesis in patients with acute myocardial infarction is greater for proximal than mid- or distal occlusions of the left anterior descending but not the right coronary artery. Survival is influenced by the function of periinfarct and noninfarct regions and by the function of the infarct region. Complex noise filters provide no advantage over simpler filters in measuring the extent of hypokinesis.     

Lactate metabolism in acute myocardial infarction and its relation to regional ventricular performance

Myocardial metabolism was assessed in 20 patients with acute anterior myocardial infarction using lactate uptake (defined as (aortic lactate - great cardiac venous lactate)/aortic lactate X 100) as an index. The regional ejection fraction of the anterior wall was obtained from left ventriculography. There was a linear relation between lactate uptake and regional ejection fraction (r = 0.79, p less than 0.001). Four patients without total occlusion in the infarct vessel had a higher lactate uptake (19.6 +/- 6.7 versus 4.2 +/- 13.4%, p less than 0.05) and regional ejection fraction (26.3 +/- 7.9 versus 14.9 +/- 7.0%, p less than 0.05) than did 16 patients with total occlusion. The latter group of patients underwent intracoronary infusion of urokinase, which resulted in reperfusion in 13 patients. Lactate uptake before urokinase infusion (sample I), just after reperfusion (sample II), 30 minutes after reperfusion (sample III) and 4 weeks after reperfusion (sample IV) was 5.7 +/- 13.2, -13.9 +/- 14.7, 2.9 +/- 15.2 and 20.2 +/- 11.0%, respectively (sample I versus II and II versus III, p less than 0.01; sample I versus IV and III versus IV, p less than 0.05). The decrease in lactate uptake immediately after reperfusion, which was accompanied by an increase in creatine kinase-MB isoenzyme release into the blood, was considered to be the result of a "washout" effect. Lactate uptake was ameliorated 4 weeks later, accompanied by an improvement (from 15.1 +/- 7.1 to 23.4 +/- 7.2%, p less than 0.01) in the regional ejection fraction. It is concluded that the degree of asynergy was closely related to the extent of metabolic deterioration in myocardial infarction.     

Usefulness of mitral regurgitation in protecting against left ventricular thrombus after acute myocardial infarction

In conclusion, we documented an increased incidence of LV thrombus in patients with MR after AMI.     

Prospective two-dimensional echocardiographic evaluation of left ventricular thrombus and embolism after acute myocardial infarction

To determine whether two-dimensional echocardiography can identify patients with left ventricular thrombus after myocardial infarction who are prone to embolism, clinical and echocardiographic variables in 541 patients with a first infarction between 1979 and 1983 were studied prospectively. The first echocardiogram showed definite thrombus in 115 patients (Group 1, 21%) and no thrombus in 426 (Group 2, control). In Group 1, 27 patients (23%) had clinical evidence of systemic embolism related to the thrombus before referral (Group 1a) and 88 did not (Group 1b); these two groups were similar in age, gender and infarct location, but more Group 1a patients were within 1 month of the acute infarction. In both Groups 1a and 1b, the thrombus was found in apical views over asynergic zones, with no difference (p greater than 0.05) between the two groups in the size (average area from two views being 5.3 versus 4.5 cm2), type (protruding in apical views 30% versus 27%), location (apical 83% versus 86%; septal 11% versus 11%; posterior 4% versus 2%), extent of asynergy (31% versus 33%) and ejection fraction (33% versus 34%). However, the frequency of anticoagulant therapy was less (26% versus 63%, p less than 0.005), adjacent hyperkinesia greater (100% versus 49%, p less than 0.005) and thrombus mobility greater (81% versus 19%, p less than 0.005) in Group 1a than in Group 1b. Serial echocardiograms revealed a decreased size of the thrombus by 6 months in both Groups 1a and 1b, and little or no trace in 85% by 24 months. Thus, ventricular thrombus size, location and protrusion in apical views on echocardiography did not correlate with embolism. In contrast, thrombus mobility, the presence of adjacent hyperkinesia and thrombus protrusion assessed in multiple views appeared to be strong discriminators of thrombus prone to embolism. These echocardiographic features might provide a guide for the duration of anticoagulant therapy.     

Catecholaminergic activation in acute myocardial infarction: time course and relation to left ventricular performance

AIM: The study was designed to assess (1) the time course of catecholaminergic activation in acute myocardial infarction (AMI) as estimated by adrenaline (ADR) and noradrenaline (NOR) concentrations, and (2) to relate activation of these hormones to predict the outcome of cardiac performance. PATIENTS AND METHODS: Eighteen patients with first AMI were studied. Blood samples were drawn within the first 4-18 h, after 18-24 h, on day 2, day 3 and on day 6 as well as after 1 year. Radionuclide ventriculography was performed on the day of discharge and after 1 year to determine left-ventricular ejection fraction (LVEF). RESULTS: In the study group as a whole, the concentrations of ADR decreased from (mean +/- SEM) 0.80 +/- 0.12 nmol/l on admission to 0.33 +/- 0.03 nmol/l at discharge (p < 0.05). NOR decreased from 4.19 +/- 0.78 to 2.44 +/- 0.33 nmol/l (p < 0.05). Initial peak concentrations of both ADR and NOR on admission were correlated to LVEF at discharge (r = -0.56, p < 0.05 and r = -0.72, p < 0.05, respectively). If NOR was normal (<3 nmol/l) at admission, the LVEF was normal or almost normal (= 0.46) at discharge. The mean plasma level of ADR and NOR after 1 year follow-up was 0.34 +/- 0.04 and 1.95 +/- 0.25 nmol/l, respectively. The values after 1 year were unchanged compared to values at discharge, at day 6 (n.s.). Mean LVEF was 0.50 +/- 0.03 (range: 0.23-0.69) at discharge and unchanged 0.46 +/- 0.05 (range: 0.18-0.72) at 1 year follow-up (n.s.). During hospitalisation, the group with LVEF <0.50 had an 86% higher initial ADR and an 82% higher initial NOR concentration compared to values in patients with LVEF >0.50 (p < 0.05). CONCLUSION: (1) Catecholaminergic activation, as measured by plasma ADR and NOR in AMI, is acute and restricted to the first 5 days. Thereafter, the hormone levels are normal and stable. (2) The magnitude of the early catecholaminergic activation correlates with left ventricular systolic performance. (3) Normal NOR values at admittance predicts normal or almost normal LVEF at discharge.     

Persistent ST-segment elevation after primary stenting for acute myocardial infarction: its relation to left ventricular recovery

BACKGROUND: Early restoration of coronary artery patency in acute myocardial infarction (AMI) has been linked to improvement in survival. However, early recanalization of an occluded epicardial coronary artery by either thrombolytic agents or percutaneous transluminal coronary angioplasty (PTCA) does not necessarily lead to left ventricular (LV) function recovery. HYPOTHESIS: The aim of this study was to evaluate the relation between persistent ST elevation shortly after primary stenting for acute myocardial infarction (AMI) and LV recovery. METHODS: Thirty-one patients with primary stenting for AMI were prospectively enrolled. To evaluate the extent of microvascular injury, serial ST-segment analysis on a 12-lead electrocardiogram recording just before and at the end of the coronary intervention was performed. Persistent ST-segment elevation (Persistent Group, n = 11) was defined as > or = 50% of peak ST elevation and resolution (Resolution Group, n = 20) was defined as < 50% of peak ST elevation. Echocardiography was performed on Day 1 and 3 months after primary stenting. RESULTS: At 3 months, infarct zone wall-motion score index (WMSI, 2.1 +/- 0.6 vs. 2.7 +/- 0.3, p < 0.05) was smaller in the Resolution Group than in the Persistent Group, whereas wall motion recovery index (RI, 0.4 +/- 0.3 vs. 0.1 +/- 0.2, p < 0.05) and ejection fraction (58 +/- 5 vs. 43 +/- 10%, p < 0.05) were larger in the Resolution Group than in the Persistent Group. The extent of persistent ST elevation (% ST) shortly after successful recanalization of the infarct-related artery was significantly related to RI at 3 months (r = -0.4, p < 0.05). However, time to reperfusion was not related to RI at 3 months. There was also significant correlation between corrected TIMI frame count and %ST (r = 0.4, p < 0.05). CONCLUSIONS: Persistent ST-segment elevation shortly after successful recanalization (> or = 50% of the peak value), as a marker of impaired microvascular reperfusion, predicts poor LV recovery 3 months after primary stenting for AMI.     

急性心肌梗死合并左心室附壁血栓患者经皮冠状动脉介入术后的抗栓治疗

目的分析急性心肌梗死（AMI）并发左心室附壁血栓（LvT）行经皮冠脉介入治疗（PCI）患者的临床特征及抗栓治疗。方法收集煤炭总医院2005年8月至2012年2月确诊为急性心肌梗死并发左室附壁血栓并行PCI治疗的12例患者的临床资料,对其进行回顾性分析。结果广泛前壁心肌梗死、前壁心肌梗死9例（75％）,左室射血分数低于40％共7例（58％）,冠脉造影检查三支及以上血管病变7例（58％）。6例给予华法林、阿司匹林、氯吡格雷三联抗栓,2例给予西洛他唑、阿司匹林及氯吡格雷三联抗血小板治疗,随访期间血栓均消失。4例双联抗血小板治疗者l例发生脑梗死后加用华法林,3例患者血栓消失,1例血栓机化。12例患者均未出现严重出血现象。结论急性心肌梗死并发左心室附壁血栓并接受PCI治疗患者,充分衡量获益及出血风险,按照个体化原则给予抗栓治疗安全有效。     

Successful resolution of a left ventricular thrombus with apixaban treatment following acute myocardial infarction

A 62-year-old man was admitted to our emergency department owing to prolonged chest pain that had lasted for 3 h. An electrocardiogram showed ST elevation in leads I, aV_L, and V1-6, and the patient’s laboratory revealed elevated myocardial necrosis marker levels. Emergency coronary angiography showed total occlusion of the proximal left anterior descending coronary artery. Subsequent percutaneous coronary intervention was performed by balloon angioplasty followed by stent implantation, and the patient showed improvement. However, echocardiographic examination 2 weeks after the percutaneous coronary intervention showed a thrombus (40 × 14 mm) in the apex of the left ventricle. In addition to dual antiplatelet therapy, apixaban was administered as anticoagulant therapy for the left ventricular thrombus. The size of the thrombus gradually decreased, and magnetic resonance imaging performed approximately 6 weeks after the initial apixaban administration showed no thrombus without a thromboembolic event. This case demonstrates that left ventricular thrombus can be resolved with apixaban treatment. Apixaban may be an effective alternative to vitamin K antagonist for some patients with acute myocardial infarction complicated by left ventricular thrombus.     

The relation between supraventricular tachyarrhythmias and left ventricular dysfunction after acute myocardial infarction

The clinical characteristics of supraventricular tachyarrhythmias (SVTA) and their relation to left ventricular dysfunction were assessed in 208 consecutive patients with recent myocardial infarction. Arrhythmias were quantified on hospital discharge by 24 hour electrocardiographic recording. All the variables were evaluated between the second and the fourth week after infarction. SVTA occurred in 113 (54%) patients: Supraventricular premature beats (SVPB) in 49 (24%), frequent or repetitive SVPB in 37 (18%), atrial or junctional tachycardia in 23 (11%), atrial flutter or fibrillation in 4 (2%). Most of these arrhythmias occurred in the absence of symptoms, and the most complex forms were always selflimiting. No relation was found among the presence of different forms of SVTA and sex, coronary risk factors, previous history of ischemic heart disease, type or site of acute myocardial infarction, NYHA functional class. Age, left atrial dimension (LAD), cardio-thoracic ratio (CTR) and left ventricular ejection fraction (LVEF) at rest differed significantly among three groups of patients: those without SVTA, those with SVPB less than 100 per hour and those with frequent-repetitive SVPB or atrial-junctional tachycardia. The more SVTA complexity, the worse LAD, CTR, LVEF and the higher the age. Multivariate discriminant analysis showed that CTR was directly and LVEF inversely related to the occurrence of SVPB less than 100 per hour, while the presence of frequent-repetitive SVPB or supraventricular tachycardia was closely related to increasing age, LAD, CTR and decreasing LVEF. Patients with atrial fibrillation always showed the worst values of LAD, CTR, LVEF and age. The results of the present study show that different types of SVTA occurring at discharge from hospital after myocardial infarction are clinically benign, but always suggestive of different degrees of left ventricular dysfunction.