Lysis of left ventricular thrombi with urokinase

In 16 patients with recent myocardial infarction (3 to 12 week old) and with large left ventricular thrombi systemic thrombolysis with urokinase was performed. Left ventricular thrombi were diagnosed by two-dimensional echocardiography; in all patients the mural thrombus was located in the area of recent myocardial infarction. Each of three patients suffered an embolic episode before the initiation of thrombolytic therapy and the episode caused a stroke in one. Urokinase was infused intravenously at a rate of 60,000 U/hr for 2 to 8 days in combination with intravenous heparin (200 units/kg X 12 hr). Left ventricular thrombi were successfully lysed in 10 of 16 patients, as determined by two-dimensional echocardiography. In four of the six remaining patients only partial thrombolysis was achieved and in two thrombolytic treatment failed. There was no evidence of embolic events during thrombolysis in any of the 16 patients. The success of thrombolysis seemed to depend on the age of the thrombus: the thrombus was dissolved in eight of nine patients undergoing thrombolysis within 4 weeks of the acute myocardial infarction vs in two of seven patients receiving treatment later (p = .057). The presence of a left ventricular aneurysm or depressed left ventricular function also appeared to reduce the likelihood of successful thrombolysis. All patients were discharged on oral anticoagulants. At 6 months follow-up (n = 9) no recurrence of left ventricular thrombus was found. These results show that left ventricular thrombi can be safely lysed by intravenous urokinase. However, for better definition of the risk and benefit of this new therapy further investigation is necessary.     

Increased embolic risk in patients with left ventricular thrombi

Although left ventricular thrombi are associated with an increased embolic risk in the first few weeks after acute myocardial infarction, the long-term risk remains undefined. To ascertain the incidence of strictly defined systemic emboli, we followed 85 patients with echocardiographically documented left ventricular thrombi. At the time of the entry echocardiogram, most patients (n = 57) had remote myocardial infarction, while 19 had recent (less than 1 month) infarction, and nine had idiopathic cardiomyopathy. Because of the difficulty in classifying events as embolic in patients with advanced atherosclerosis, a matched control group of 91 patients without thrombi was also studied. The thrombus and control groups were similar with regard to recent myocardial infarction, remote infarction, anterior infarction, ejection fraction, atrial fibrillation, echocardiographic referral for source of emboli, and warfarin therapy. During a mean follow-up of 22 months after echocardiography, embolic events occurred in 13% (11 of 85) of patients with thrombi compared with 2% (two of 91) control patients (p less than .01). The actuarial probability of being embolus free at 2 years after echocardiography was 86% in patients with thrombi compared with 97% in control patients (p less than .01). All embolic events occurred greater than 1 month after myocardial infarction (range 1 to 96 months). The only clinical or echocardiographic features predictive of embolization were protrusion and mobility of thrombus (both p less than .02). We conclude that the incidence of embolic events is definitely increased in patients with left ventricular thrombi compared with control subjects during long-term follow-up.(ABSTRACT TRUNCATED AT 250 WORDS)     

Reduced incidence of left ventricular thrombi with intravenous streptokinase in acute anterior myocardial infarction: prospective evaluation by cross-sectional echocardiography

Forty-five consecutive patients with transmural anterior acute myocardial infarction were prospectively studied to determine the effect of intravenous streptokinase on the incidence of left ventricular thrombi. Three patients died. The remaining patients were divided into 2 groups. Group 1 patients (n = 22) received 750,000 units of intravenous streptokinase within 6 hours of onset of symptoms. Neither thrombolytic therapy or anticoagulants were administered to 18 patients in group 2. Cross-sectional echocardiography was performed 8 to 10 days following acute myocardial infarction to detect left ventricular thrombus. Technically satisfactory echocardiography was not possible in 2 patients. Apical akinesia or dyskinesia was observed in all patients. No patient in the treated group developed left ventricular thrombus compared with 8 of 18 (44.4%) in group 2 (P less than 0.05). One patient in the control group sustained an embolic cerebrovascular accident. Thus intravenous streptokinase significantly reduces the incidence of left ventricular thrombus formation in patients of transmural anterior acute myocardial infarction.     

Long-term prospective assessment of left ventricular thrombus in anterior wall acute myocardial infarction and implications for a rational approach to embolic risk

To prospectively assess the predictive value of left ventricular (LV) thrombus anatomy for defining the embolic risk after acute myocardial infarction (AMI), 2 comparable groups of patients with a first anterior AMI (group A, 97 thrombolysed patients; group B, 125 patients untreated with antithrombotic drugs [total 222]) underwent prospective serial echocardiography (follow-up 39 +/- 13 months) at different time periods. LV thrombi were detected in 26 patients in group A (27%) and in 71 in group B (57%; p <0.005). Embolism occurred in 12 patients (5.4%; 1 in group A [1%] vs 11% in group B [9%], p < 0.04). At multivariate analysis, thrombus morphologic changes were the most powerful predictor of embolism (p <0.001), followed by protruding shape (p <0.01) and mobility (p <0.02). In patients untreated with thrombolysis, a higher occurrence of thrombus morphologic changes (48% vs 8%, p <0.002) and protruding shape (69% vs 31%, p <0.002) were observed, whereas thrombus mobility was similar in the 2 groups (18% vs 8%, p = NS). Thrombus resolution occurred more frequently in thrombolysed patients (85% vs 56%, p <0.002). Thus, after anterior AMI, changes in LV thrombus anatomy frequently occur and appear the most powerful predictor of embolization. A minor prevalence of thrombus, a more favorable thrombus anatomy, and a higher resolution rate may contribute to reduce embolic risk after thrombolysis.     

Intraventricular thrombi with systemic embolization: two clinical cases.

Ventricular thrombi are a frequent complication of dilated cardiomyopathy and acute myocardial infarction, with variable risk of embolization according to the clinical setting and thrombus morphology. The authors report two cases of patients admitted on the same day for acute myocardial infarction and dilated cardiomyopathy respectively, with high embolic risk left ventricular thrombi that embolized to the lower limbs after admission. Echocardiography, considered the gold standard diagnostic tool for intraventricular thrombi, is also the mainstay of embolic risk evaluation, for characterizing their size, mobility and echostructure. In the absence of evidence-based guidelines, management options--anticoagulation therapy, thrombolysis or thrombectomy--must be decided according to each specific case, taking account of embolic, bleeding and surgical risk.     

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

Abstract. Objectives. 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. Design. Consecutive patients prospectively studied during the hospitalized period. Echocardiography was performed within 3 days of admission and before discharge. Setting. Umeå University Hospital, a teaching hospital in Northern Sweden. Subjects. Ninety-nine patients with anterior myocardial infarction of whom 74 were treated with streptokinase. Main outcome measures. Left ventricular thrombus and left ventricular segmental myocardial function. Results. 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. Conclusion. 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.     

Left ventricular thrombus in anterior acute myocardial infarction after thrombolysis. A GISSI-2 connected study

BACKGROUND. Streptokinase reduces the incidence of left ventricular thrombosis after acute myocardial infarction. However, it is unknown whether a similar effect can be obtained with different thrombolytic agents and whether subcutaneous calcium heparin can have an additional efficacy. METHODS AND RESULTS. To compare the effects of two different thrombolytic agents combined or not with heparin on the incidence and features of left ventricular thrombi and their related embolic events, we performed a GISSI-2 ancillary echocardiographic study (the first echocardiogram obtained within 48 hours of symptoms onset and the second before hospital discharge) that enrolled 180 consecutive patients (mean age, 63 +/- 11 years, 142 men) with a first anterior acute myocardial infarction. Patients were randomized into four groups of treatment: recombinant tissue-type plasminogen activator (rt-PA) (n = 47), rt-PA plus heparin (n = 45), streptokinase (n = 39), and streptokinase plus heparin (n = 49). Left ventricular thrombosis was observed in 51 of 180 patients (28%). No significant differences were found concerning the incidence of thrombi in the four treatment groups. Mural shape of left ventricular thrombi was found more frequently than the protruding shape (71% versus 29% at the first examination, 64% versus 36% at the second), particularly in heparin-treated patients (93% versus 7% at first examination, 70% versus 30% at the second). Only one embolic event (0.5%) occurred during the hospitalization. CONCLUSIONS. We conclude that 1) the rate of left ventricular thrombi does not differ in patients with acute myocardial infarction treated either with streptokinase or rt-PA, 2) subcutaneous heparin, when begun 12 hours after intravenous thrombolysis, does not appear to further reduce the occurrence of thrombi but seems to influence the shape of left ventricular thrombi, and 3) during the predischarge period, embolic events are rare in patients treated by thrombolysis.     

Left ventricular thrombi after short-term high-dose anticoagulants in acute myocardial infarction

To examine the effect of short-term, high-dose anticoagulationon the subsequent occurrence of left ventricular (LV) thrombiafter a first anterior wall acute myocardial infarction (AMI),21 patients received placebo and 21 high-dose anticoagulantsduring the first 10 days of the acute infarction. They werestudied with cross-sectional echocardiography 10 days and 1-3and 6 months post infarction. At 1 month, 6 of 7 thrombi presentin the placebo group at 10 days were still visible. No thrombiwere detected at 10 days in the anticoagulation group, but 6patients had developed a LV thrombus at 1 month. These 12 patientswith LV thrombi were subsequently treated with oral warfarinfor 2 months, after which all thrombi had disappeared. Warfarinwas then discontinued, and a thrombus had recurred in 5 patientsafter 6 months. Apical akinesis at 10 days a predictor for thrombuswith a sensitivity and specificity of 100% and 72.2% respectively. Three of the 13 patients with LV thrombi suffered stroke incontrast to none without thrombi (P=0.025). We conclude that after discontinuation of short-term high-doseanticoagulation therapy in anterior AMI, LV thrombi may developrapidly and lead to embolic complications, particularly in patientswith persisting apical akinesis.     

Left ventricular thrombi after short-term high-dose anticoagulants in acute myocardial infarction

To examine the effect of short-term, high-dose anticoagulationon the subsequent occurrence of left ventricular (LV) thrombiafter a first anterior wall acute myocardial infarction (AMI),21 patients received placebo and 21 high-dose anticoagulantsduring the first 10 days of the acute infarction. They werestudied with cross-sectional echocardiography 10 days and 1-3and 6 months post infarction. At 1 month, 6 of 7 thrombi presentin the placebo group at 10 days were still visible. No thrombiwere detected at 10 days in the anticoagulation group, but 6patients had developed a LV thrombus at 1 month. These 12 patientswith LV thrombi were subsequently treated with oral warfarinfor 2 months, after which all thrombi had disappeared. Warfarinwas then discontinued, and a thrombus had recurred in 5 patientsafter 6 months. Apical akinesis at 10 days a predictor for thrombuswith a sensitivity and specificity of 100% and 72.2% respectively. Three of the 13 patients with LV thrombi suffered stroke incontrast to none without thrombi (P=0.025). We conclude that after discontinuation of short-term high-doseanticoagulation therapy in anterior AMI, LV thrombi may developrapidly and lead to embolic complications, particularly in patientswith persisting apical akinesis.     

Influence of thrombolytic therapy on the incidence of left ventricular thrombi after acute anterior myocardial infarction: role of successful reperfusion.

BACKGROUND: Previous studies have reported controversial results regarding the effectiveness of systemic thrombolysis in preventing left ventricular (LV) thrombus after acute myocardial infarction (MI). HYPOTHESIS: This study was performed to evaluate the influences of thrombolysis, and particularly successful reperfusion, on the incidence of LV thrombus formation after acute anterior MI. METHODS: In all, 191 patients suffering from a first attack of acute anterior MI were prospectively evaluated by two-dimensional echocardiography and coronary angiography, performed at the end of the first week and within the first two weeks of MI, respectively. Of these, 98 who presented within 12 h of onset of symptoms received intravenous streptokinase (1.5 million IU), while the remaining 93 patients who, either because of contraindications or late admission, did not receive thrombolytic treatment served as control group. All patients received aspirin and full-dose anticoagulation with intravenous heparin. Successful reperfusion in the streptokinase group was assessed by enzymatic and electrocardiographic evidence. RESULTS: The overall incidence of LV thrombi was 24.6% (47/191). When all patients were evaluated, no statistically significant difference was found between the frequency of LV thrombi in the patients who had thrombolysis (22.4%) and those who did not (26.8%), despite a trend toward the formation of fewer thrombi in the initial group (p > 0.05). However, the patients who had successful reperfusion with streptokinase (n = 64) had significantly reduced incidence of LV thrombi compared with those who did not receive thrombolytic therapy (20 vs. 26.8%, p < 0.05). Stepwise multivariate analysis suggested that LV abnormal wall motion score (p = 0.01) and presence of LV aneurysm were independent predictors of LV thrombus formation in patients with acute anterior MI. CONCLUSION: Not all patients who received streptokinase for acute anterior MI, but only those with successful reperfusion had reduced incidence of LV thrombi. The favorable effects of thrombolysis on LV thrombus formation are probably due to the preservation of global LV systolic function.     

Left ventricular mural thrombi complicating acute myocardial infarction. Long-term follow-up with serial echocardiography

To determine the clinical significance of left ventricular thrombi, we used two-dimensional echocardiography to study 261 patients with acute transmural myocardial infarction. Mural thrombi were found in 46 patients. This complication occurred in 34% (44 of 130) of anterior wall infarctions but in only 1.5% (2 of 131) of inferior wall infarctions. An apical wall motion abnormality was present in all patients with thrombus. Severe depression of left ventricular function was not a prerequisite for thrombus formation: the mean left ventricular ejection fraction was 37 +/- 1.5%. Forty-three patients with left ventricular thrombi were followed for a mean duration of 15 months with serial echocardiography. None of the 25 patients who received anticoagulation treatment had an embolic event. Embolization occurred in 7 of 18 patients who had not received anticoagulation treatment. All embolic events occurred within 4 months of infarction. Although anticoagulation treatment appeared to provide protection against embolic events, the prevalence of left ventricular thrombi on follow-up echocardiographic study was essentially the same whether or not this treatment was used.     

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)     

Increased occurrence of left ventricular thrombi during early treatment with timolol in patients with acute myocardial infarction

To examine whether early intervention with timolol influences the occurrence of left ventricular thrombi in acute anterior myocardial infarction, 40 patients with acute anterior myocardial infarction admitted to hospital within 6 hr of onset of symptoms were randomly assigned to receive intravenous followed by oral timolol maleate or placebo. Five (25%) of 20 patients in the placebo group and 14 (73.7%) of 19 patients with confirmed infarction in the timolol group developed a left ventricular apical thrombus as detected by two-dimensional echocardiography from 2 to 10 days after inclusion (p less than .005). Patients received anticoagulants only after a left ventricular thrombus had been diagnosed. Only one patient with thrombus suffered peripheral embolization (timolol group). The treatment groups were comparable with respect to location of regional left ventricular dysfunction, electrocardiographic changes, and infarct size estimated by creatine kinase release. However, computer-assisted regional wall motion analysis demonstrated significantly reduced apical wall motion in the timolol group compared with the placebo group (p less than .01). Also, the mean heart rate during the first 10 days after the acute infarction was reduced by 13% in the timolol group (p less than .001). The reduction in heart rate and left ventricular apical wall motion caused by timolol in patients with acute anterior myocardial infarction may increase the occurrence of left ventricular thrombi.     

Saddle embolism of the aorta. A complication of streptokinase therapy

Streptokinase was given to a patient with an unsuspected left ventricular aneurysm as treatment for acute pulmonary embolism. After 2 days of therapy, a large thrombus dislodged from the left ventricular aneurysm and produced an acute saddle embolic occlusion of the abdominal aorta. Detection of mural thrombi by two-dimensional echocardiography in patients with evidence of previous myocardial infarction might prove helpful in identifying those at risk for this complication of streptokinase therapy.     

Risk factors for embolisation in patients with left ventricular thrombi and acute myocardial infarction

Risk factors for systemic embolisation in patients with ventricular thrombi caused by an acute myocardial infarction were studied in 150 consecutive patients with an infarction of the anterior wall. Serial echocardiograms were performed 2-10 days after the acute event and patients were followed up for three months. Anticoagulation treatment was started only after the detection of thrombi. Of the 55 patients in whom a thrombus developed, 15 (27%) had peripheral emboli between 6-62 days; but only two (2%) of 95 patients without thrombus had emboli. Among 15 variables, the best single predictors of embolisation were age greater than 68 years (80% sensitive, 85% specific), pendulous thrombus (60%, 93%), and independent thrombus mobility (60%, 85%). Logistic regression analysis showed that a formula that included patient age, thrombus area, and the length of thrombus in the ventricular lumen predicted embolisation (sensitivity 87%, specificity 88%). There was no correlation between age and the thrombus variables. The risk of embolisation from left ventricular thrombi in acute anterior myocardial infarction can be accurately assessed from patient age and echocardiographic features. The risk of peripheral emboli is high in patients with left ventricular thrombi and those aged greater than 68.     

Peripheral emboli from left ventricular thrombi of different echocardiographic appearance in acute myocardial infarction

In four patients with anterior wall acute myocardial infarction (AMI) and left ventricular thrombi diagnosed by two-dimensional (2-D) echocardiography, disappearance of left ventricular thrombi was demonstrated by 2-D echocardiography immediately after the patients had suffered peripheral emboli. Two thrombi were pendulous with free motion during the cardiac contractions; one of these consisted of two separated pendulous clots that disappeared after two episodes of embolization six and 16 days, respectively, after the onset of AMI. Two thrombi were initially broad based, flat, and without intracavitary motion. One thrombus caused two episodes of peripheral emboli; the other began as a flat thrombus without intracavitary motion but progressed to show central echolucency and, then, vigorous intracavitary motion of the margin prior to embolization. Five of six embolic episodes occurred when these patients were receiving high-dose anticoagulants. These anticoagulants were administered once the thrombi were diagnosed. Left ventricular thrombi of very different appearance on 2-D echocardiography may cause embolization, which may occur during therapeutic anticoagulation administered after thrombi have developed in patients with AMI.     

Risk factors for embolisation in patients with left ventricular thrombi and acute myocardial infarction.

Risk factors for systemic embolisation in patients with ventricular thrombi caused by an acute myocardial infarction were studied in 150 consecutive patients with an infarction of the anterior wall. Serial echocardiograms were performed 2-10 days after the acute event and patients were followed up for three months. Anticoagulation treatment was started only after the detection of thrombi. Of the 55 patients in whom a thrombus developed, 15 (27%) had peripheral emboli between 6-62 days; but only two (2%) of 95 patients without thrombus had emboli. Among 15 variables, the best single predictors of embolisation were age greater than 68 years (80% sensitive, 85% specific), pendulous thrombus (60%, 93%), and independent thrombus mobility (60%, 85%). Logistic regression analysis showed that a formula that included patient age, thrombus area, and the length of thrombus in the ventricular lumen predicted embolisation (sensitivity 87%, specificity 88%). There was no correlation between age and the thrombus variables. The risk of embolisation from left ventricular thrombi in acute anterior myocardial infarction can be accurately assessed from patient age and echocardiographic features. The risk of peripheral emboli is high in patients with left ventricular thrombi and those aged greater than 68.     

Effects of full-dose heparin anticoagulation on the development of left ventricular thrombosis in acute transmural myocardial infarction

The incidence of left ventricular thrombosis after acute transmural myocardial infarction has been evaluated with two-dimensional echocardiography. To assess the preventive action of early anticoagulation with full-dose heparin, 90 patients, admitted within 5.2 +/- 4.6 hours after the onset of symptoms of their first episode of acute myocardial infarction (46 anterior and 44 inferior), were prospectively studied. Patients were randomly assigned either to therapeutic anticoagulation with heparin or to no anticoagulant therapy. Serial two-dimensional echocardiograms were recorded on the day of admission, the next day, days 4 to 7 and days 20 to 50 to detect left ventricular thrombus and to assess global left ventricular performance. On the first echocardiogram (10.3 +/- 8.0 hours after the onset of symptoms) no thrombus was visualized. In 44 patients with inferior myocardial infarction (23 receiving heparin and 21 not receiving heparin) no further left ventricular thrombus developed. In 46 patients with anterior myocardial infarction, 21 additional thrombi developed (45.6%) within 4.3 +/- 3.0 days after the acute event. Thrombus developed in 8 (38%) of 21 patients receiving heparin, compared with 13 (52%) of 25 patients not receiving heparin. This difference in ventricular thrombosis was not statistically significant (chi-square with the Yates correction = 0.76; NS). No difference was found between the subgroups in terms of clinical variables, infarct size, hemodynamic impairment, intensity of the inflammatory process and quantitative two-dimensional echocardiographic and cineangiographic left ventricular function. It is concluded that early anticoagulation with heparin reduced by 27% the incidence of left ventricular thrombus formation in anterior acute transmural myocardial infarction, and this relative risk reduction was not statistically significant when compared with findings in the untreated group.     

Natural history of left ventricular thrombi: their appearance and resolution in the posthospitalization period of acute myocardial infarction

A series of 198 consecutive patients with acute myocardial infarction were prospectively studied before hospital discharge and during 24.0 +/- 8.6 months of follow-up. A predischarge thrombus was found in 38 (31%) of 124 patients with anterior infarction but in none of 74 patients with inferior infarction (p less than 0.001). Early thrombolytic therapy in 34 patients did not decrease the rate of thrombus occurrence. Acute anterior infarction, ejection fraction less than or equal to 35% and apical dyskinesia or aneurysm (but not akinesia) were significantly related to the appearance of thrombus during hospitalization by stepwise logistic regression analysis. Echocardiographic follow-up of 159 patients for at least 6 months (mean 26.6 +/- 8.4) revealed that thrombus disappeared in 14 (48%) of 29. Disappearance of thrombus was related to predischarge apical akinesia (but not dyskinesia) and to warfarin therapy during the follow-up period. A new thrombus first appeared after hospital discharge in 13 of 130 patients, and in 7 of the 13 it resolved during further follow-up. Thus, 30% (13 of 42) of thrombi in these patients appeared after discharge from the hospital. Three factors were related to occurrence of new thrombi during the follow-up period: deterioration in left ventricular ejection fraction, predischarge ejection fraction less than or equal to 35% and ventricular aneurysm or dyskinesia. Systemic embolism occurred in six patients, all with a predischarge thrombus (p less than 0.001). Mobility of the thrombus was the only variable significantly related to subsequent embolic events (p = 0.001) by logistic regression analysis. Thus, the predischarge echocardiogram identifies patients with thrombus and those at highest risk of embolic events. It can indicate patients who are likely to have thrombus resolution and those at risk of developing a new thrombus after hospital discharge. Follow-up echocardiograms may help in guiding the length of long-term anticoagulant therapy. Four additional patients with a predischarge apical mobile thrombus (not part of the consecutive series) received thrombolytic therapy. In two of the four, lysis of thrombus was achieved without complications, but systemic embolism occurred in the other two, and proved fatal in one.     

Ventricular thrombi in the chronic infarct stage: echocardiographic findings, clinical aspects, relations to anticoagulation

In 10% (n = 139) of 1,383 patients in the chronic phase of myocardial infarction left ventricular mural thrombi on a-/dyskinetic segments were present in the 2D-echocardiogram. Thrombi were more often seen in patients with anterior wall infarct (14% of 734) or combined anterior-posterior infarcts (11% of 337) than in those with posterior wall infarct (0.6% of 312). Thrombi were most frequent in patients with left ventricular aneurysm (26% of 362). Generally, our patients with left ventricular thrombi had suffered large infarctions, involving on average 42% of the wall segments. Accordingly, signs of severe left ventricular damage were found in most of these patients: in 69% global ventricular dilation was present in the echocardiogram, in 64% the global heart size, determined by chest-ray was enlarged, in 42% the exercise tolerance on the bicycle ergometer was limited to 25 watts or less, 29% had congestive heart failure, and 17% severe ventricular arrhythmias. Systemic embolization had occurred in 7.9% of the 132 thrombus patients, but in only 0.7% of the 1,244 patients without thrombi. At the time of the thrombus diagnosis by means of 2D-echocardiography, 90% of the thrombus patients had not received effective anticoagulant therapy. Follow-up was possible in 65 of these patients and showed thrombus regression in 45 patients, 93% of whom were effectively anticoagulated. Of the 20 patients with persisting thrombi only 20% were under an effective anticoagulant drug management. If anticoagulant therapy has to be stopped, a former thrombus patient runs a high risk of developing thrombi also in the chronic phase of myocardial infarction.