The aim of the present study was to investigate the prevalence of left ventricular (LV) thrombus formation and important determinants in patients with acute ST elevation myocardial infarction localized to the anterior wall treated with percutaneous coronary intervention (PCI) and dual-antiplatelet therapy. One hundred selected patients with ST elevation myocardial infarctions revascularized with PCI in the left anterior descending coronary artery were included. The patients participated in the Autologous Stem Cell Transplantation in Acute Myocardial Infarction (ASTAMI) trial. All were treated with aspirin 75 mg/day and clopidogrel 75 mg/day and underwent serial echocardiography and magnetic resonance imaging during the first 3 months after PCI. After 4 to 5 days, the ejection fraction and infarct size in percentage of the left anterior descending coronary artery area were assessed using single photon-emission computed tomography in addition to the ejection fraction by echocardiography. LV thrombi were detected in 15 patients during the first 3 months, 2/3 of them within the first week. No differences in baseline characteristics between the groups with and without LV thrombi were shown. However, in the thrombus group, significantly higher peak creatine kinase levels (6,128 vs 2,197 U/L, p <0.01), larger infarct sizes (82.5% vs 63.8%, p <0.01), and lower ejection fractions on single photon-emission computed tomography (35.5% vs 40.0%, p = 0.03) and on echocardiography (43.0% vs 46.0%, p = 0.03) were found compared to patients without LV thrombi. In conclusion, LV thrombus formation is a frequent finding in patients with anterior wall ST elevation myocardial infarction treated acutely with PCI and dual-antiplatelet therapy and should be assessed by echocardiography within the first week.
Left ventricular (LV) thrombus formation is a serious complication of acute myocardial infarction (AMI). In the prethrombolytic era, LV thrombi were reported in up to 60% of patients with large anterior wall myocardial infarctions. Studies have shown that systemic thrombolysis may reduce the formation of LV thrombus, but it is still a frequent finding in patients with large anterior wall myocardial infarctions. Embolization of LV thrombi has been reported in up to 20% of patients with AMI. Today, most patients with acute ST elevation myocardial infarctions are treated with percutaneous coronary intervention (PCI) and antiplatelet medications with limited or no effect on the coagulation system. The primary aim of the present study was to investigate LV thrombus formation and important clinical determinants in selected patients with acute anterior wall ST elevation myocardial infarctions successfully revascularized with PCI and stenting, all treated with aspirin and clopidogrel.
Methods
We examined patients (n = 100) participating in the Autologous Stem Cell Transplantation in Acute Myocardial Infarction (ASTAMI) trial included at Ullevål University Hospital and Rikshospitalet University Hospital (Oslo, Norway). Patients were aged 40 to 75 years, of both genders, with acute anterior wall ST elevation myocardial infarctions and culprit lesions located in the left anterior descending coronary artery, proximal to the diagonal branch. All patients were treated successfully with PCI and stent implantation and dual-antiplatelet therapy within 2 to 12 hours of symptom onset. Primary PCI was performed in 71 patients, facilitated PCI in 15 patients, and rescue PCI in 14 patients. The inclusion criteria were peak creatine kinase (CK)–MB >3 times the upper reference level and hypokinesia or akinesia in >2 of 16 segments of the left ventricle determined by echocardiography. Patients with cardiogenic shock, previous Q-wave infarctions, and considerable co-morbidities with short life expectancies were excluded from the study. The regional committee for medical research ethics approved the study protocol, and written informed consent was obtained from all patients. The study is registered at ClinicalTrials.gov ( NCT 00199823 ).
The treatment procedure in the ASTAMI study has been described in detail. In brief, 100 patients were randomized 1:1 to receive intracoronary injections of autologous mononuclear bone marrow cells (mBMC) or to a control group. Only the mBMC group was aspirated for 50 ml bone marrow from the iliac crest under local anesthesia 4 to 7 days after acute PCI, and the next day, a median of 6 days after the AMI, they received intracoronary injections of mBMC in the left anterior descending coronary artery. Patients in the control group did not undergo any further coronary intervention. All patients were treated with a loading dose of clopidogrel 300 mg and thereafter 75 mg/day in addition to an initial dose of aspirin 300 mg followed by 75 mg/day. Patients with LV thrombi were treated with low–molecular weight heparin and further warfarin with a target international normalized ratio of 2.0 to 2.5 for ≥3 to 6 months. In accordance with the study protocol, screening echocardiographic examinations of all eligible patients were performed within the first 1 to 3 days after acute PCI. Thereafter, echocardiography was performed using a Vivid 7 scanner (GE Vingmed Ultrasound AS, Horten, Norway) of all included patients 4.5 ± 1.1 days after the acute AMI, with assessment of the ejection fraction according to the modified Simpson’s rule and repeated after 3 months. Additional echocardiographic examinations were performed between the predefined time points when clinically indicated. In addition, magnetic resonance imaging was performed with a 1.5-T scanner (Siemens Medical Solutions, Erlangen, Germany) 18.8 ± 4.3 days after acute PCI. The LV ejection fraction and infarct size were assessed using electrocardiographically gated single photon emission computed tomography (using 4D-MSPECT software; GE Medical Systems, Milwaukee, Wisconsin) 4.0 ± 1.4 days after the AMI.
Variables are expressed as proportions or as medians with 25th and 75th percentiles. Differences between groups were assessed using the Mann-Whitney test. Categorical data were analyzed using chi-square tests. A trend analysis was performed using the chi-square test to evaluate the peak level of CK in relation to LV thrombus. All tests were 2 sided, and p values <0.05 were considered statistically significant. SPSS version 16.0 for Windows (SPSS, Inc., Chicago, Illinois) was used for data analyses.
Results
LV thrombi were detected in 15 of the 100 patients within the first 3 months after the AMI: 6 of the patients allocated to the mBMC group and 9 of those allocated to the control group (p = 0.58 for the difference between the groups). One of the patients experienced a minor cerebral stroke. As visualized in Figure 1 , most of the LV thrombus formation was detected within the first week after acute PCI. LV thrombi were diagnosed by echocardiography in 13 patients and by magnetic resonance imaging in 2 patients. No between-group differences regarding the characteristics of the patients could be detected ( Tables 1 and 2 ). However, the LV thrombus group had significantly larger infarct sizes (p <0.01) and lower ejection fractions assessed by single photon-emission computed tomography (p = 0.03) and echocardiography (p = 0.03) compared to patients without thrombus formation ( Table 3 ). In addition, we found significantly higher peak levels of CK in the thrombus group compared to patients without LV thrombi (p <0.01; Table 3 ). Trend analysis through quartiles of peak CK levels showed an increase in the number of LV thrombi with increasing peak CK level. Patients with peak CK levels in the upper quartile (4,912 U/L) had significantly higher risk for developing LV thrombi (odds ratio 12.1%, 95% confidence interval 3.3 to 44.3, p <0.01).
| Variable | LV Thrombus | p Value ‡ | |
|---|---|---|---|
| No (n = 85) | Yes (n = 15) | ||
| Age (years) | 57 (50–64) | 63 (50–69) | 0.18 |
| Women | 15 (18%) | 1 (7%) | 0.49 |
| Current smokers | 37 (44%) | 7 (47%) | 0.20 |
| Hypertension ⁎ | 27 (32%) | 7 (47%) | 0.41 |
| Hyperlipidemia † | 39 (46%) | 9 (60%) | 0.47 |
| Diabetes mellitus | 6 (7%) | 2 (13%) | 0.76 |
| Previous myocardial infarction | 4 (5%) | 0 (0%) | 0.89 |
| Weight (kg) | 84.0 (74.5–92.5) | 80 (77.0–92.0) | 0.99 |
| Systolic blood pressure (mm Hg) | 130 (120–144) | 135 (130–150) | 0.33 |
⁎ Previous treatment with antihypertensive medication and/or previous measured blood pressure >140/90 mm Hg.
† Baseline fasting total cholesterol >5.5 mmol/L and/or previous use of cholesterol-lowering medication.
‡ Differences between the LV thrombus group and patients without thrombus formation.
| Variable | LV Thrombus | p Value ⁎ | |
|---|---|---|---|
| No (n = 85) | Yes (n = 15) | ||
| Time to PCI (minutes) | 210 (180–330) | 240 (150–315) | 0.78 |
| Primary PCI | 59 (69%) | 12 (80%) | 0.54 |
| Thrombolysis | 26 (31%) | 3 (20%) | 0.60 |
| Rescue PCI | 12 (14%) | 2 (13%) | 0.55 |
| Culprit proximal LAD | 51 (60%) | 10 (67%) | 0.84 |
| TIMI flow grade 0 before PCI | 51 (60%) | 12 (80%) | 0.31 |
| TIMI flow grade 3 after PCI | 80 (94%) | 12 (80%) | 0.16 |
| GP IIb/IIIa receptor blockers | 42 (49%) | 7 (47%) | 1.00 |
Stay updated, free articles. Join our Telegram channel
Full access? Get Clinical Tree
