Left Ventricular Thrombus In Patients Research Articles

The value of non-contrast harmonic transthoracic echocardiography for the detection of left ventricular thrombi in patients with cardiomyopathy: comparison with contrast-enhanced magnetic resonance imaging

We sought to assess the value of non-contrast enhanced transthoracic harmonic echocardiography (TEE) for the visualization of left ventricular thrombi in 34 patients with cardiomyopathy. Results were compared to contrast-enhanced magnetic resonance imaging as reference standard. Maximal thrombus size was quantified with both modalities. Magnetic resonance imaging demonstrated thrombi in 15 patients. In these subjects echocardiography was negative in seven patients. Thrombi were excluded in 19 patients with magnetic resonance while echocardiography was deemed positive in 5 subjects. Thrombus size by ce-CMR was not different for clots visualized or not visualized by echocardiography (P = 0.71). Moreover, observer agreement was superior for ce-CMR (kappa = 0.94) as compared to TTE (kappa= 0.71). Non-contrast-enhanced harmonic TTE has limited value for the visualization of thrombi in patients with cardiomyopathy.

Detektion und Charakterisierung linksventrikulärer Thromben mittels MRT im Vergleich zur transthorakalen Echokardiographie

Transthoracic echocardiography is the routine diagnostic procedure in assessing patients with left ventricular thrombi, but is limited by the acoustic window and poor contrast between thrombus and adjacent myocardium. This study evaluates the role of cardiac MRI in the detection of left ventricular thrombi in patients with chronic myocardial infarction compared to standard transthoracic echocardiography. In 82 patients (55 men and 27 women, age 36 to 79 years, median 59 +/- 11 years) who suffered a myocardial infarction more than 6 months earlier, transthoracic echocardiography and MRI were performed. The MRI protocol included steady state cine imaging (true FISP: TR 3.0 ms, TE 1.5 ms, FA 65 degrees ) in standard long and short axis orientation and contrast-enhanced imaging using a 3D IR-FLASH sequence with long inversion time (TR 4 ms, TE 1.43 ms, FA 10 degrees , TI 300 ms) early, and a 2D IR-FLASH sequence with optimized inversion time (TR 8 ms, TE 4.3 ms, FA 20 degrees , TI 180 - 280 ms) late after administration of gadolinium. Transthoracic echocardiography depicted 12 thrombi. Contrast-enhanced MRI confirmed these 12 thrombi and detected 23 additional thrombi. With the exception of 2 very small apical thrombi only visible on contrast-enhanced MR images, spherical thrombi were diagnosed by both techniques, whereas only contrast-enhanced MRI was able to visualize mural thrombi. Left ventricular thrombi were more frequently diagnosed in patients with moderate to severe impairment of the left ventricular systolic function, 32/42 (76 %), or in patients with left ventricular aneurysms, 21/24 (84 %). Contrast-enhanced MRI is mostly superior to transthoracic echocardiography in diagnosing mural left ventricular thrombi in patients who had suffered a myocardial infarction. Intracavitary thrombi are more frequently found in patients with impaired regional and global left ventricular function.

Comparison of frequency of left ventricular thrombi in patients with anterior wall versus non–anterior wall acute myocardial infarction treated with antithrombotic and antiplatelet therapy with or without coronary revascularization

Of 200 patients with ST-segment elevation acute myocardial infarction (AMI), all received antiplatelet and antithrombotic therapy, and 186 patients (93%) underwent coronary revascularization. Left ventricular thrombi were diagnosed by 2-dimensional echocardiography ≤1 week after AMI in 19 of 114 patients (17%) with anterior wall AMI and in 3 of 86 patients (3%) with non–anterior wall AMI (p <0.001).

Predictors of left ventricular thrombus formation in patients with dilated cardiomyopathy: role of activated protein C resistance.

The aim of this study was to investigate the association between left ventricular thrombus formation and natural anticoagulant systems including the protein C, protein S and antithrombin in patients with dilated cardiomyopathy. Sixty patients with dilated cardiomyopathy who met the inclusion criteria were included in the study. Patients were divided into two groups: group I consisted of 22 patients with left ventricular thrombus and group II consisted of 38 patients without left ventricular thrombus. Our main inclusion criteria were ejection fraction </= 35% and left ventricular end-diastolic diameter >/= 6.0 cm. These two groups were compared for clinical and hematologic parameters (activated protein C resistance, protein S and antithrombin). There were no statistically significant differences between patients with or without left ventricular thrombi with respect to left ventricular end-diastolic and end-systolic dimensions, ejection fraction, fractional shortening and left atrial diameter. There were no statistically significant differences between patients with and without left ventricular thrombus with respect to platelet count (252 +/- 64/mm3 x 10(3) compared with 260 +/- 74/mm3 x 10(3) respectively, P=0.68), prothrombin time (12.94 +/- 1.9 s compared with 12.86 +/- 1.3 s respectively, P=0.82), activated partial thromboplastin time (32 +/- 5 compared with 30 +/- 4 s respectively, P=0.32) and fibrinogen levels (36 +/- 9 mg/dl compared with 34 +/- 8 mg/dl respectively, P=0.41). None of the patients had protein S and antithrombin deficiency. Activated protein C resistance was found in 12 patients (12 out of 22, 54%) in group I and four patients (four out of 38, 9.5%) in group II (P < 0.01). It was also shown to be an independent predictor of left ventricular thrombus (P < 0.05). Activated protein C resistance is found to be an independent predictor of left ventricular thrombus in patients with dilated cardiomyopathy who have ejection fractions less then 35% and left ventricular end-diastolic dimensions > 6.0 cm.

1126-114 Clinical and magnetic resonance imaging characteristics of pathologically confirmed left ventricular thrombus in patients with cardiomyopathy

1126-114 Clinical and magnetic resonance imaging characteristics of pathologically confirmed left ventricular thrombus in patients with cardiomyopathy

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 wether 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. (Acta Cardiol 2004; 59(1): 33-39)

Factor V Leiden and its relation to left ventricular thrombus in acute myocardial infarction

Objective — The genetic defect of coagulation factor V, known as factor V Leiden, produces a resistance to degradation by activated protein C (APC) and increases the risk of venous thrombosis. However, the role of factor V Leiden in the formation of left ventricular (LV) thrombus has not been studied.We investigated whether factor V Leiden is a risk factor for LV thrombus in patients with acute myocardial infarction (AMI).Methods and results — We have analyzed clinical, echocardiographic and biochemical data in 135 consecutive patients (aged 58 ± 13 years; 31 women) with first anterior AMI. Two-dimensional echocardiographic examination was performed on days I, 3, 7, 15 and 30; LV thrombus was detected in 33 (24.4%) of 135 patients with AMI. The study also included 95 control subjects. Healthy age and sex-matched subjects without a personal or family history of ischaemic heart disease, stroke or thromboembolic disease served as a control group. Blood samples from the patients and controls were analyzed for the factor V Leiden mutation by DNA analysis, using the polymerase chain reaction. In addition, concentrations of fibrinogen, von Willebrand factor (vWF), tissue plasminogen activator (t-PA), plasminogen activator inhibitor-I (PAI-1) and D-dimer were measured in 135 patients. There was no significant difference in the prevalence of factor V Leiden between patients and control subjects. The prevalence of the factor V mutation was 9% (3/33) in patients with thrombus, and 7.7% (8/103) in patients without thrombus. The prevalence of factor V Leiden was 7.3% (7/95) in control subjects. No significant differences in plasma fibrinogen (480 ± 195 vs. 444 ± 179 mg/dl, p = 0.6), D-dimer (471 ± 256 vs. 497 ± 293 ng/dl, p = 0.7), vWF (112 ± 18 vs. 103 ± 15%, p = 0.5), PAI-I (26.7 ± 9.8 vs. 28.1 ± 10.2 ng/dl, p = 0.6), and t-PA (19.8 ± 8.7 vs. 17.2 ± 9.1 ng/dl, p = 0.7), levels are found in patients with LV thrombus when compared with those without LV thrombus. Multivariate analyses showed that peak creatine kinase level (p = 0.002) and LV wall motion score index (p = 0.003) were independent predictors of LV thrombus formation.Conclusion — Factor V Leiden mutation is not a risk factor for LV thrombus formation in patients with AMI. (Acta Cardiol 2001; 56(1 ): 1-6)

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.

Prevalence of early left ventricular thrombus after primary coronary intervention for acute myocardial infarction.

The prevalence of left ventricular (LV) thrombus after acute myocardial infarction (AMI) has been reported high at 20-60%. Current reperfusion therapies such as thrombolysis have shown a trend toward reducing the incidence of LV thrombosis. However, the prevalence of LV thrombus after primary percutaneous coronary intervention (PCI) for AMI has not been systematically studied. At Massachusetts General Hospital 71 consecutive patients who underwent primary PCI for acute ST elevation MI were reviewed for the prevalence of LV thrombus evaluated by echocardiography. Echocardiography was performed within 5 days of infarction. PCI was successful in all patients. The time delay from symptom onset to intervention was 191 minutes. Thrombolysis in Myocardial Infarction (TIMI) grade 3 flow was achieved in more than 80% of cases. Only 3 patients (4%) had echocardiographic evidence of LV thrombus. All 3 patients had anterior infarctions. The incidence among patients with anterior MI was 10% (3 of 30 patients). The prevalence of LV thrombus in patients treated with primary PCI for AMI is low (4%).

Left ventricular thrombosis after anterior myocardial infarction with and without thrombolytic treatment

To examine the incidence of left ventricular thrombus in patients with anterior myocardial infarction, with and without streptokinase treatment. To identify predictors of thrombus development. Consecutive patients prospectively studied during the hospitalized period. Echocardiography was performed within 3 days of admission and before discharge. Umeå University Hospital, a teaching hospital in Northern Sweden. Ninety-nine patients with anterior myocardial infarction of whom 74 were treated with streptokinase. Left ventricular thrombus and left ventricular segmental myocardial function. During the hospital stay, a thrombus developed in 46% (95% confidence interval [CI], 35-57%) of the patients in the thrombolysis group and in 40% (95% CI, 21-59%) of the patients in the non-thrombolysis group. No difference in left ventricular segmental myocardial function was found between the thrombolysis and non-thrombolysis groups at hospital discharge. No embolic events were observed. The occurrence of a left ventricular thrombus at hospital discharge was significantly associated with previous myocardial infarction, peak enzyme levels, left ventricular global and segmental dysfunction and an increased dose of peroral diuretics or use of parenteral diuretics. In a multiple logistic regression model, left ventricular segmental dysfunction was the most important predictor of left ventricular thrombus. Thrombolytic treatment with streptokinase does not prevent the development of a left ventricular thrombus but the risk of embolic complications is low. The left ventricular segmental myocardial score can be used to assess the risk of thrombus development, also, after thrombolysis.

Safety of high doses of low molecular weight heparin (Fragmin) in acute myocardial infarction. A dose - finding study

We postulated that low molecular weight heparin (LMWH) in doses producing plasma levels in the range of 0,6 – 1,0 anti-Xa U/ml may reduce the incidence of left ventricular thrombi (LVT) secondary to acute anterior wall myocardial infarction (AAMI). In an open, dose-finding study, 72 patients with acute myocardial infarction (AMI) were treated with Fragmin (KABI) 240–360 anti-Xa U/kg/24h subcutaneously for 6 – 10 days. 300 anti-Xa U/kg/24h given as 2 or 3 injections resulted in a mean plasma concentration of about 0,8 anti-Xa U/ml. There were 3 minor haemorrhages, all in a subgroup of 22 patients also being treated with 0,3 g aspirin orally per day after 1,5 mill. U streptokinase intravenously on admission. In the 38 patients with AAMI receiving 300 anti-Xa U/kg/24h there were only 3 LVT during the period of treatment (8 %). In conclusion, 300 anti-Xa U Fragmin/kg/24h s.c to patients with AMI appears safe, but minor haemorraghe may occur in patients receiving aspirin concomitantly. Although these data are limited, the low incidence of LVT in patients with AAMI suggests efficacy of this dose of Fragmin to prevent LVT.

Effects of intravenous recombinant tissue-type plasminogen activator therapy on the incidence and associations of left ventricular thrombus in patients with a first acute Q wave anterior myocardial infarction

Consecutive survivors of a first Q wave anterior myocardial infarction were studied to observe the impact of recombinant tissue-type plasminogen activator (rt-PA) therapy on the incidence and associations of left ventricular thrombus. Fifty-four patients recelved rt-PA within 4 hours after the onset of cardiac pain, followed by heparin infusion. Forty-four patients who did not qualify for rt-PA therapy but who were anticoagulated with heparin served as a control group. Two-dimensional echocardiography was performed in all patients on days 3 and 7 to detect thrombl and analyze wall motion. Election fraction was determined by radionuclide angiography in all patients on day 7. Apical thrombl were detected on day 3 in three patients (5.5%) who recelved rt-PA and in eight control patients (18%) ( p < 0.05). All patients with a thrombus had apical dyskinesis and 8 of 11 (73%) had an aneurysm. Of the 87 patients without thrombosis, apical dyskinesis and aneurysm were present in 42 (48%) and 11 (13%) patients, respectively ( p < 0.01). Ejection fractions and wall motion scores of patients without a thrombus were significantly better when compared with data from those with thrombus. There were fewer patients with apical dyskinesis (17 of 54) in the group recelving rt-PA therapy compared with the control group (36 of 44) ( p < 0.01). Ejection fractions and wall motion scores were better in patients who recelved rt-PA compared with control subjects ( p < 0.01). Thus rt-PA reduced the incidence of ventricular thrombosis by 70% in patients with anterior myocardial infarction by preserving apical wall motion, and this decrease in relative risk was significant in comparison with the risk in patients recelving heparin therapy.

The Effects of Long-term Antithrombotic Treatment on Left Ventricular Thrombi in Patients After an Acute Myocardial Infarction

The Effects of Long-term Antithrombotic Treatment on Left Ventricular Thrombi in Patients After an Acute Myocardial Infarction

The effects of long-term antithrombotic treatment on left ventricular thrombi in patients after an acute myocardial infarction

Sixty patients (48 men and 12 women; aged 36 to 72 years, mean 48 +/- 9), who survived an acute anterior myocardial infarction and in whom left ventricular thrombus was detected by cross-sectional echocardiography 1 to 2 days before they were discharged from the hospital, were prospectively studied. All had evidence of left apical wall motion abnormalities. They were randomly divided into three groups of 20 patients each. Group A was given a full dose of oral anticoagulants, group B was given aspirin, 650 mg/day, and group C received no antithrombotic therapy. Echocardiography was performed every 3 months in all patients, and they were followed for 9 to 24 months (mean 16 +/- 5 months). Twelve patients in group A had complete resolution of the thrombus and three had a significant decrease in the size of the thrombus (greater than or equal to 50% of initial thickness) during the first trimester after acute infarction. In group B the thrombus resolved in nine patients and was significantly diminished in four during the first trimester of follow-up. In group C the thrombus resolved in two patients during the first trimester and showed a significant decrease in size in two patients during the second trimester of follow-up. Two patients in group C initially had recurrent transient cerebral ischemic attacks, which did not recur after aneurysmectomy. One patient in group C had a peripheral embolic episode in the femoral artery.(ABSTRACT TRUNCATED AT 250 WORDS)

Diagnosis of left ventricular thrombi by magnetic resonance imaging and comparison with angiocardiography, computed tomography and echocardiography

Left ventricular (LV) thrombi are common in patients with acute and healed anterior myocardial infarction. Although the reported incidence of clinically diagnosed embolism varies widely, 1–3 diagnosis of thrombus seems to carry an increased risk for this potentially life-threatening complication. It is not entirely clear whether long-term anticoagulation can reduce the embolism rate in patients with chronic aneurysms with an acceptable risk of bleeding. However, it is widely assumed that this is so; thus, the diagnosis of LV thrombus has far-reaching consequences. It is difficult to diagnose LV thrombus using currently available imaging techniques. LV angiography carries the risk of precipitating systemic emboli and has a low sensitivity in most reported studies. 4 Echocardiography has been reported to be fraught with false-positive results. 5,6 Indium-111 platelet scintigraphy reflects thrombus activity but has suboptimal sensitivity, especially for small thrombi. 7 More recently, computed tomography (CT) 8 and magnetic resonance imaging (MRI) 9,10 have shown encouraging results in the detection of LV thrombi. However, the diagnostic accuracy of MRI has not been evaluated with independent confirmation by surgery or autopsy. This study describes the sensitivity and specificity of MRI in the diagnosis of LV thrombi in patients with LV aneurysms undergoing surgical aneurysmectomy, and compares the results with those of angiography, 2-dimensional echocardiography and CT performed in the same patients.

Fate of left ventricular thrombi in patients with remote myocardial infarction or idiopathic cardiomyopathy.

Although left ventricular thrombi that form acutely after myocardial infarction frequently resolve spontaneously or with anticoagulant therapy, the fate of left ventricular thrombi in patients with remote myocardial infarction or with idiopathic cardiomyopathy remains unknown. To determine the natural history of such chronic left ventricular thrombi, we performed serial echocardiograms on 51 patients with remote myocardial infarction (greater than or equal to 3 months; mean, 31 +/- 41 months) and on nine patients with idiopathic dilated cardiomyopathy. Mean follow-up was 24 +/- 22 months during which 3.5 +/- 1.4 echocardiograms were obtained. Studies were interpreted by blinded observers, and an increase or decrease of more than 5 mm in maximal thrombus thickness was defined as significant. Among all 60 patients left ventricular thrombi were unchanged in 24 (40%), completely resolved in 24 (40%), decreased in size in four (7%), increased in size in five (8%), and decreased and then increased in size in three (5%). Results in patients with remote infarction and idiopathic cardiomyopathy were similar. Warfarin therapy, which was at the discretion of the primary physician, was associated with a higher prevalence of thrombus resolution compared with no therapy (59% vs. 29%, p = 0.02). Definite systemic emboli occurred in seven patients (12%), all at times while they were not anticoagulated. Among the 48 thrombi that were present on two or more echocardiograms, changes in thrombus shape (classified as protruding or flat) occurred in only 16%, and changes in thrombus movement (classified as mobile or immobile) occurred in only 10%.(ABSTRACT TRUNCATED AT 250 WORDS)

Prognostic significance and natural history of left ventricular thrombi in patients with acute anterior myocardial infarction: a two-dimensional echocardiographic study.

Fifty-eight patients with transmural anterior myocardial infarction were prospectively studied with serial two-dimensional echocardiography to determine the clinical implications and prognostic significance of detection of left ventricular thrombus during acute myocardial infarction, the incidence of systemic embolization, and the possible occurrence of spontaneous regression of left ventricular thrombi. Patients were not treated with anticoagulants or platelet inhibitors during the acute phase of infarction or during follow-up. Two-dimensional echocardiograms were obtained within 24 hr of myocardial infarction, every 24 hr until day 5, every 48 hr until day 15, and every month for a follow-up of 2 to 11 months (mean 7), in the surviving patients; a total of 774 echocardiograms were obtained. Left ventricular thrombi were identified in 24 (41%) of the 58 study patients, and developed within 48 hr of infarction in 11 of these patients. Ten (91%) of the 11 patients with early thrombus formation died during hospitalization or during follow-up, while only two (15%) of the 13 who developed a thrombus after 48 hr of infarction died (p less than .005). Incidence of Killip class III or IV, total lactic dehydrogenase values, and extent of wall motion abnormalities were significantly higher in patients who developed a thrombus within 48 hr of infarction than in patients without thrombus. On the other hand, in patients who developed a thrombus after 48 hr of infarction, these parameters were not significantly different from those in patients who did not develop a thrombus. Spontaneous regression of thrombi was documented in three (20%) of the 15 patients who survived the acute phase of myocardial infarction.(ABSTRACT TRUNCATED AT 250 WORDS)

Left ventricular thrombi diagnosed by echocardiography in patients with acute myocardial infarction treated with intracoronary streptokinase followed by intravenous heparin

Thirty patients with acute myocardial infarction (AMI) treated with intracoronary streptokinase (7 × 10 5 ± 3 × 10 5 IU) followed by 10 days of intravenous heparin (800 to 1,500 IU/hour) therapy were prospectively studied by serial 2-dimensional echocardiography for left ventricular (LV) thrombus. Within the first 24 hours, evidence of a thrombolytic state appeared as indicated by fibrin and fibrinogen degradation products (123 ± 45 mg/dl at 24 hours). Throughout the course of this study partial thromboplastin times were maintained within therapeutic range (40 to 100 seconds). Apical LV thrombus developed in 8 of 30 patients (27%). Apical thrombus developed within 24 hours in 3 patients with anterior AMI and persisted through day 10. By day 10, apical thrombus developed in 3 additional patients with anterior AMI and 2 patients with inferior AMI. In these patients, anterior AMI and apical dysfunction were significant (p < 0.01 for both) determinants of LV thrombus formation. Hence, the incidence of LV thrombus in patients treated with streptokinase/heparin is similar to that reported earlier in comparable patients not receiving thrombolytic therapy.

Frequency and embolic potential of left ventricular thrombus in dilated cardiomyopathy: Assessment by 2-dimensional echocardiography

Left ventricular (LV) thrombus at autopsy and systemic emboli during life have been frequent findings in patients with dilated Cardiomyopathy. Since anticoagulation has substantial risk, noninvasive identification of those patients likely to have emboli is important. Therefore, wide-angle 2-dimensional (2-D) echocardiograms in 123 patients (average age 56 ± 6 years) with chronic dilated Cardiomyopathy were analyzed for the presence of LV thrombus; these findings were compared with the clinical course in 96 patients. On 2-D echocardiography, thrombus was present in 44 patients (36%). Events compatible with systemic emboli occurred in 11 patients (11%), and were not more frequent in those patients with than in those without LV thrombus. In addition, neither the presence of thrombus nor the frequency of systemic emboli differed between patients with and those without associated coronary artery disease. Thus, although 2-D echocardiography shows a high frequency of LV thrombus in patients with dilated Cardiomyopathy irrespective of the presence of coronary artery disease, clinical events compatible with systemic emboli are not more frequent in those with than those without LV thrombus.

Regional stasis of blood in the dysfunctional left ventricle: echocardiographic detection and differentiation from early thrombosis.

SUMMARY In two-dimensional echocardiographic studies of left ventricular thrombus in patients, an unusual pattern of dynamic left ventricular intracavitary echoes was identified in some hearts with severe apical dysfunction. These intracavitary echoes were noted in the apical region and were distinct from left ventricular thrombi. Certain features of the intracavitary echoes suggested that they were generated by regional stasis of blood. To study this phenomenon, echocardiography was performed in 1I dogs with experimental anteroapical infarction and associated left ventricular thrombus and in six dogs with infarction but no thrombus. The dynamic intracavitary echo pattern suggesting blood stasis was identified in the ischemic apex in dogs of both groups. These echoes had characteristics suggesting a fluid or semifluid state and could be distinguished from thrombi. In real time, the echoes moved in a slow, circular fashion at the apex and lacked well-defined borders; their configuration and acoustic intensity changed over short periods of time, and they could be rapidly altered bv ectopic or mechanical contraction of the heart and by dopamine infusion. Postmortem examination showed that liquid blood produced the echoes. Additional studies demonstrated the echogenicitv of static blood. Echocardiography of dog hearts with KCI-induced mechanical-asystole showed the rapid development of diffuse echogenicity of the intraventricular rontents; in vitro studies confirmed the echogenicity of static blood.These observations indicate that a spectrum of echocardiographic features characterizes ventricular blood under various conditions of flow and with frank thrombosis. The ability of echocardiographv to detect in vivo stasis of blood in the left ventricle and to distinguish this from thrombosis has important clinical and investigational implications.