Author + information
- Miguel A. Quinones, MD∗ ()
- ↵∗Reprint requests and correspondence:
Dr. Miguel A. Quinones, Department of Cardiology, Houston Methodist DeBakey Heart & Vascular Center, Houston Methodist Hospital, Smith Tower, 6550 Fannin, Suite 1901, Houston, Texas 77030.
Mural thrombus formation on an infarcted segment of the left ventricle (LV) is a well-recognized complication of a myocardial infarction (MI). A majority of these thrombi occur within the first 30 days after an anterior ST-segment elevation myocardial infarction (STEMI) and are considered a cause of embolic strokes during the post-MI period. Such strokes can be devastating to patients and families. In 1976, when serving as a cardiologist in the military, I treated a 48-year-old master sergeant who presented with acute right hemiparesis that left him permanently disabled. An electrocardiogram suggested a recent anterior MI, and an M-mode echocardiogram demonstrated accentuated contraction of the basal LV segments. As I scanned down into the LV, I could see reduced mobility of the more distal segments but could never visualize the thrombus. It was not until the advent of transthoracic 2-dimensional (2D) echocardiography in the early 1980s that we had the amazing ability to visualize and detect LV mural thrombi noninvasively (1). During the decade of the 1980s, 2D echocardiography became the imaging standard for detection of post-MI thrombi. These were located mostly at the apex and occurred in the setting of an anterior MI. Their appearance was often described as round, protruding, mobile, or layered. Serial evaluation by 2D echocardiography demonstrated frequent reduction in size or resolution over several months regardless of treatment with anticoagulant drugs. More recently, the accuracy of 2D echocardiography was enhanced with the use of intravenous ultrasound contrast agents, particularly in patients with suboptimal image quality (2).
In recent years, delayed-enhancement cardiac magnetic resonance (DE-CMR) has emerged as a highly accurate imaging technique for thrombi detection, more sensitive than echocardiography (3,4). In this issue of iJACC, Weinsaft et al. (5) used DE-CMR as the “gold standard” against which they evaluated the accuracy of 2D echocardiography and contrast-2D for thrombi detection. They studied 201 patients with acute STEMI with CMR and echocardiography performed between 7 and 30 days post-MI (mean, 28 days) and within 24 h of each other. The authors found 17 cases of thrombi, an overall incidence of 8% (15% of left anterior descending coronary artery infarcts), not much different from that reported in the pre-thrombolysis/percutaneous coronary intervention era, when fewer anticoagulant and antiplatelet agents were administered. All thrombi were located in apical segments with severe wall motion abnormalities. The authors also found a rather low sensitivity of 2D echocardiography for thrombus detection (35%), which improved to 64% with the use of ultrasound contrast. Specificity was ≥98%. Patients with thrombi frequently had preserved function at the base that worsened progressively toward the apex and a wide range of ejection fractions, with only 12% having an ejection fraction ≤30%.
One must ask whether the lower sensitivity of echocardiography found by Weinsaft et al. (5) is representative of the accuracy of the technique across all laboratories or is unique to the authors’ institution. In the GISSI-3 (Gruppo Italiano per lo Studio della Sopravivenza nell’Infarto Miocardico) database of 8,326 patients (6), the incidence of LV thrombus in patients treated with fibrinolytic therapy by 2D echocardiography was much lower than that reported by Weinsaft et al. (5) (5.1 % overall and 11.5 % of those with anterior MI), a finding that suggests underdetection by echocardiography. We have, at our institution, seen patients with apical thrombi found by DE-CMR that were missed by 2D echocardiography and contrast 2D echocardiography. Thus, I am inclined to accept the authors’ findings as real, although the exact sensitivity of 2D echocardiography may vary from one laboratory to another and is likely to be affected by image quality. The authors found a higher sensitivity and concordance with DE-CMR for 2D echocardiography studies of good quality than for those of lesser quality. However, no such relation was found when contrast was used, thus leaving open other plausible explanations for the lower sensitivity of echocardiography. In our own experience, foreshortening the apex and failure to obtain an imaging plane that cuts through the thrombus are common reasons for missing the abnormality. At times, one has to use unusual off-axis planes to visualize a thrombus (Figure 1). Thus, it might be possible to improve thrombi detection with 2D echocardiography by combining additional views with selective use of contrast (2).
In the study by Weinsaft et al. (5), a summation of wall motion scores for the 5 apical segments of ≥5 for 2D echocardiography (≥7 for contrast 2D echocardiography) had 100% sensitivity for thrombus detection and was therefore proposed by them as a screening tool for high-risk patients. In their series, 20% of the patients with this finding had an apical thrombus by DE-CMR. The authors suggested that applying the proposed algorithm in their own series would have avoided the use of DE-CMR in 56% of the MI population. On the other hand, 46% of the patients would still have required cardiac magnetic resonance (CMR). If we were to apply this algorithm to the large number of MIs that occur each year in the United States, we could add more than 50 million dollars annually in costs to our health-care system (estimated using only Centers for Medicare and Medicaid Services reimbursement figures for our region). In addition, we would need to equip every hospital in America with CMR capabilities.
The increase in cost that would result from greater use of DE-CMR could be justified if one could identify and provide anticoagulation therapy for every patient with a mural thrombus and by so doing prevent a majority of post-MI strokes. The risk of embolization in patients with known thrombi has been reported to be between 10% and 15%, with most events occurring in the first 4 months. Stratton and Resnick (7) reported a risk of 13% in patients with thrombi versus 2% in a matched control group without thrombi. Although there are no randomized trials, observational studies suggest that treatment with warfarin reduces the risk of embolization in these patients by as much as 85% (8). The approach recommended by Weinsaft et al. (5) needs to be tested prospectively through a large, randomized trial to compare it to the current practice of relying on echocardiography to identify and guide the use of warfarin in post-MI patients. Given the limited availability of hospitals with expertise in CMR, it is doubtful that we will see much interest in conducting such a trial at this time. An alternative approach that would not require CMR is for patients in the high-risk group (i.e., those with an apical thrombus by 2D echocardiography or an apical wall motion score ≥5, or ≥7 for contrast 2D echocardiography) to receive anticoagulation with warfarin for 3 to 6 months. Although there are current proponents of a similar approach (9), in my opinion, we would need a randomized controlled trial comparing it to our current practice, given the risk of bleeding with warfarin when it is added to dual-antiplatelet therapy in STEMI patients treated with an intracoronary stent. For now, it may be more reasonable to use 2D echocardiography as a screening tool for thrombi in patients with anterior MIs, using contrast and additional views as needed to improve accuracy, and cautiously treat those patients with evidence of a thrombus with warfarin for 3 to 6 months. CMR, if available, should be used selectively when the results of the 2D echocardiography are inconclusive.
↵∗ Editorials published in JACC: Cardiovascular Imaging reflect the views of the authors and do not necessarily represent the views of JACC: Cardiovascular Imaging or the American College of Cardiology.
Dr. Quinones has reported that he has no relationships relevant to the contents of this paper to disclose.
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