We tested the hypothesis that admission serum inflammatory biomarkers may predict risk of early left ventricular (LV) thrombus formation in patients with first-ever anterior wall ST-segment elevation myocardial infarction (STEMI). Medical records of 207 patients admitted to our department between January 2006 and April 2012 for first-ever diagnosed anterior wall STEMI and treated with primary percutaneous coronary intervention (PPCI) were reviewed. Serum C-reactive protein (CRP) and fibrinogen levels were determined from blood samples taken before PPCI. Patients underwent an initial cardiac echocardiography on days 1 or 2 of admission and a second echocardiography on days 5 to 7 of hospitalization. An early LV thrombus was detected on the second echocardiogram in 11 patients (11 of 207, 5%), 6 of whom had also displayed an LV thrombus already during their first echocardiogram. Patients with an LV thrombus had significantly higher mean serum CRP levels than those without an LV thrombus (48 mg/L vs 8.4 mg/L, p = 0.001), and a trend for higher fibrinogen levels was also observed (398 ± 135 mg/dl vs 312 ± 82 mg/dl, p = 0.063). Following adjustment to other variables and the performance of multiple logistic regression, the CRP (relative risk 4.63, p = 0.004) and fibrinogen (relative risk 1.006, p = 0.033) levels were independent predictors of LV thrombus formation. We conclude that admission serum CRP and fibrinogen levels are independent predictors for early LV thrombus formation complicating a first-ever anterior wall STEMI.
Left ventricular (LV) mural thrombus formation is a serious complication of acute myocardial infarction (MI). Its frequency, however, has been reduced following the introduction of primary percutaneous coronary intervention (PPCI). We recently demonstrated that an LV thrombus was found during the first week of hospitalization in 18 of 429 (4%) anterior ST segment elevation MI (STEMI) patients treated with PPCI. Longer time to reperfusion, low Thrombolysis In Myocardial Infarction (TIMI) flow grade (≤1) before angioplasty, and a lower left ventricular ejection fraction (LVEF) were all associated with an increased risk for LV thrombus formation. Each of those conditions alone, however, is not sufficient to predict which of the patients with acute anterior MI is prone to develop an LV thrombus, and the identification of additional factors would therefore be of considerable benefit. Moreover, because an LV thrombus can already be detected within 24 hours following acute STEMI identification of early predictors for LV thrombus formation is warranted. Peak C-reactive protein (CRP) concentrations after an acute MI have been shown to independently correlate with LV thrombus formation within 14 days. In a subanalysis of our previous patient cohort, we investigated whether admission inflammatory biomarkers levels in patients with first-ever diagnosed anterior MI may predict early (i.e., within 7 days of admission) LV thrombus formation.
Methods
We performed a retrospective, single-center study in the Tel-Aviv Sourasky Medical Center, a tertiary referral hospital with a 24-7 PPCI service. Included were all 546 consecutive patients admitted between January 2006 and April 2012 to the cardiac intensive care unit with the diagnosis of acute anterior wall STEMI. We excluded 27 patients who were treated conservatively or with thrombolysis, and those with a final diagnosis on discharge other than anterior wall STEMI (e.g., myocarditis or Takotsubo cardiomyopathy). Serum CRP and fibrinogen levels before PPCI were available in 250 of the patients. An additional 43 patients were excluded because of a previous history of MI, known collagen tissue disease, advanced liver disease, advanced renal failure, malignancy, or any known infectious disease.
The final study population included 207 patients whose baseline demographics, cardiovascular history, clinical risk factors, and treatment characteristics were retrieved from their medical files. The diagnosis of anterior wall STEMI was documented in each patient by a typical history of chest pain, diagnostic electrocardiographic changes, and serial elevation of serum cardiac biomarkers. The electrocardiographic criterion for the diagnosis of ST elevation was an ST-segment elevation of ≥1 mm in >2 adjacent leads. Blood samples were drawn before PPCI in all patients upon admission to the emergency department or at the catheterization laboratory. Complete blood count parameters were measured using a Coulter STKS electronic counter. Quantitative fibrinogen was measured by the Clauss method, and wide-range CRP analysis was performed by the Bayer wide-range assay as previously described. All patients were treated in the emergency department with dual antiplatelet therapy consisting of aspirin (a loading dose of 300 mg followed by 75 mg/day) and clopidogrel (a loading dose of 300–600/mg followed by 75 mg/day), as well as a heparin bolus (4,000 units). If not contraindicated, PPCI was performed in patients with symptoms ≤12 hours in duration as well as in patients with symptoms lasting 12 to 24 hours in duration if the symptoms continued to persist at the time of admission. Post-PPCI anticoagulation treatment was deferred unless the echocardiographic examination demonstrated an LV thrombus. Treatment with low molecular weight heparin was started and supplemented with warfarin for patients with echocardiographic evidence of an LV thrombus, aiming a target international normalized ratio of 2 to 3 for 3 to 6 months. All patients admitted to the cardiac intensive care unit with a diagnosis of STEMI underwent a screening echocardiographic examination within 24 to 48 hours from admission. A second echocardiogram was performed during days 5 to 7 in all patients whose first echocardiographic examination demonstrated a LVEF <50%. Echocardiography was performed by a Philips IE-33, GE and Vivid 3 models equipped with S5-1 transducers (Philips Healthcare, Andover, Massachusetts). Parasternal long and short axis, apical, and 2- and 4-chamber views were obtained using standard transducer positions. Special considerations were given to apical and low parasternal echocardiographic windows. Echocardiograms were interpreted independently by 2 expert investigators. An LV thrombus was defined as an echodense mass adjacent to an abnormally contracting (akinetic or dyskinetic) myocardial segment. It had to be distinguishable from the underlying myocardium, have a clear thrombus-blood interface and be visible in ≥2 transducer positions. The 16-segment model was used for scoring the severity of segmental wall motion abnormalities according to the American Society of Echocardiography. All data were summarized and displayed as mean (±SD) for continuous variables and as number (percentage) of patients in each group for categorical variables. The p values for the chi-squared test were calculated with the Fisher exact test. The p value for the t test is reported after the Levene test for equality of variance. Binary logistic regression models were performed at the Enter mode. The models were adjusted to age, male gender, LVEF, coronary artery disease severity (referenced to single-vessel disease), a proximal left anterior descending (LAD) lesion (referenced to middle and distal lesions), and a TIMI score ≤1 (referenced to a TIMI score ≥2). All of the analyses were considered significant at a 2-tailed p value <0.05. The SPSS statistical package was used to perform all statistical evaluations (SSPS, Chicago, Illinois).
Results
Two hundred seven consecutive patients (mean age 62 ± 14 years, range 25–96, 79% male) met the inclusion criteria of this study, and their data were included in the analyses. The median duration of hospitalization was 6.4 ± 2.8 days (range 5–33). The first echocardiogram was performed within 1.41 ± 1.13 days of admission, and the second echocardiogram was performed after 5.34 ± 1.47 days. Early LV thrombus formation was detected on the second echocardiogram in 11 of the 207 patients (5%), 6 of whom had already displayed an LV thrombus on their first echocardiogram ( Figure 1 ). Wall motion abnormalities were identified in all 11 of these patients (100%). Normal LV function (LVEF ≥55%) without segmental wall motion abnormalities was demonstrated in 30 of the 196 patients without evidence of an LV thrombus (15%). The characteristics of the patients with and without an LV thrombus are summarized in Table 1 . Table 2 shows the relationship between the presence or absence of an LV thrombus and the results of blood tests. Serum CRP levels were significantly higher in patients with an LV thrombus (48 ± 68 mg/L vs 8.4 ± 21 mg/L, p = 0.001), and a trend for higher fibrinogen levels was also observed (398 ± 135 mg/dl vs 312 ± 82 mg/dl, p = 0.063). In addition, patients with an LV thrombus that had been detected on both the first and second echocardiography examinations had higher serum CRP levels compared with patients in whom an LV thrombus was present at only the second examination (66 ± 35 mg/L vs 28 ± 15 mg/L). There were no other significant differences in laboratory data between the groups ( Table 2 ). Binary logistic regression analysis showed that serum CRP, as well as fibrinogen levels were independent predictors of an LV thrombus ( Table 3 ).
| Variable | LV Thrombus | p Value ∗ | |
|---|---|---|---|
| + | 0 | ||
| n = 11 | n = 196 | ||
| Age (yrs; mean ± SD) | 64 ± 8 | 61 ± 14 | NS |
| Men | 9 (82%) | 153 (78%) | NS |
| Diabetes mellitus | 2 (17%) | 33 (18%) | NS |
| Dyslipidemia | 4 (36%) | 79 (40%) | NS |
| Hypertension | 3 (25%) | 75 (39%) | NS |
| Smoker | 4 (36%) | 99 (51%) | NS |
| Family history of CAD | 3 (27%) | 31 (16%) | NS |
| Number of coronary arteries involved | |||
| 1 | 6 (54%) | 95 (49%) | NS |
| 2 | 3 (27%) | 61 (31%) | NS |
| 3 | 2 (18%) | 39 (20%) | NS |
| Proximal LAD narrowing | 6 (55%) | 107 (55%) | NS |
| Ejection fraction (mean ± SD) | 40 ± 4 | 44 ± 8 | 0.007 |
| TIMI Flow ≤1 | 10 (91%) | 120 (62%) | 0.047 |
∗ The p values for the chi squared test were calculated with the Fisher’s exact test. The p value for the t -test is reported following Levene’s test for equality of variance.
| Variable | LV Thrombus | p Value ∗ | |
|---|---|---|---|
| + | 0 | ||
| (n = 11) | (n = 196) | ||
| Hemoglobin (g/dl; mean ± SD) | 14.1 ± 1.9 | 14.2 ± 1.5 | 0.674 |
| WBC (10 3 /μl; mean ± SD) | 11.3 ± 3.4 | 11.4 ± 3.6 | 0.95 |
| Platelets(10 3 /μl; mean ± SD) | 240 ± 51 | 261 ± 79 | 0.232 |
| Fibrinogen (mg/dl; mean ± SD) | 398 ± 135 | 312 ± 82 | 0.063 |
| Troponin (ng/ml; mean ± SD) | 26 ± 44 | 12 ± 37 | 0.45 |
| Creatinine (mg/dl; mean ± SD) | 1.3 ± 0.40 | 1.05 ± 0.21 | 0.13 |
| CRP (mg/L; mean ± SD) | 48 ± 68 | 8.4 ± 21 | 0.001 |
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