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      In vivo Magnetic Resonance Imaging and Surgical Histopathology of Intracardiac Masses: Distinct Features of Subacute Thrombi

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          We evaluated intracardiac masses in vivo, in situ and histologically to determine tissue properties revealed by magnetic resonance (MR) imaging. In 15 consecutive patients scheduled for cardiotomy, the cardiac chambers were studied preoperatively with MR imaging and echocardiography. Visual examination of one or more chambers was performed during cardiotomy for mitral valve replacement, aneurysmectomy, atrial septal repair and atriotomy. Six thrombi (1 atrial appendage, 5 ventricular) and 2 atrial myxomas were removed and subjected to histological analysis. All masses were detected preoperatively by MR imaging. The smallest was a subacute 3-mm mural clot in the left ventricle and was undetected by transesophageal and transthoracic echocardiography. The 3 subacute clots had homogeneously low MR signals, did not enhance with gadolinium and exhibited magnetic susceptibility effects; histopathology confirmed these clots to be avascular and laden with dense iron deposition related to hemoglobin breakdown products. The 3 organized clots had intermediate and heterogeneous MR signals and multiple areas of gadolinium enhancement. The 2 myxomas had low MR signals and gadolinium enhancement in the core and septal attachment; these areas had dense neovascular channels. Subacute thrombi appear to have MR features that are distinct from organized thrombi and myxomas, and MR images of subacute thrombi contrast sharply with normal cardiac structures, enabling detection of thin mural clots that may be echographically occult. These findings may be of value, because a subacute clot may be more likely than an organized thrombus to give rise to an embolus.

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          Ventricular dysfunction and the risk of stroke after myocardial infarction.

          In patients who have had a myocardial infarction, the long-term risk of stroke and its relation to the extent of left ventricular dysfunction have not been determined. We studied whether a reduced left ventricular ejection fraction is associated with an increased risk of stroke after myocardial infarction and whether other factors such as older age and therapy with anticoagulants, thrombolytic agents, or captopril affect long-term rates of stroke. We performed an observational analysis of prospectively collected data on 2231 patients who had left ventricular dysfunction after acute myocardial infarction who were enrolled in the Survival and Ventricular Enlargement trial. The mean follow-up was 42 months. Risk factors for stroke were assessed by both univariate and multivariate Cox proportional-hazards analysis. Among these patients, 103 (4.6 percent) had fatal or nonfatal strokes during the study (rate of stroke per year of follow-up, 1.5 percent). The estimated five-year rate of stroke in all the patients was 8.1 percent. As compared with patients without stroke, patients with stroke were older (mean [+/-SD] age, 63+/-9 years vs. 59+/-11 years; P<0.001) and had lower ejection fractions (29+/-7 percent vs. 31+/-7 percent, P=0.01). Independent risk factors for stroke included a lower ejection fraction (for every decrease of 5 percentage points in the ejection fraction there was an 18 percent increase in the risk of stroke), older age, and the absence of aspirin or anticoagulant therapy. Patients with ejection fractions of < or = 28 percent after myocardial infarction had a relative risk of stroke of 1.86, as compared with patients with ejection fractions of more than 35 percent (P=0.01). The use of thrombolytic agents and captopril had no significant effect on the risk of stroke. During the five years after myocardial infarction, patients have a substantial risk of stroke. A decreased ejection fraction and older age are both independent predictors of an increased risk of stroke. Anticoagulant therapy appears to have a protective effect against stroke after myocardial infarction.
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            Transesophageal echocardiography.


              Author and article information

              S. Karger AG
              May 2001
              25 May 2001
              : 95
              : 1
              : 40-47
              aDepartment of Neurology, University of Massachusetts Medical School, Worcester, Mass.; Departments of bMedicine, cSurgery and dRadiology, St. Elizabeth’s Medical Center and Tufts University School of Medicine, Boston, Mass.; eDepartment of Neurology, Cleveland Clinic Foundation, Cleveland, Ohio, USA
              47342 Cardiology 2001;95:40–47
              © 2001 S. Karger AG, Basel

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              Page count
              Figures: 5, Tables: 1, References: 23, Pages: 8
              Diagnostic Cardiology


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