Apical Thrombus Research Articles

Presence of left ventricular apical thrombus predicts lack of myocardial viability: A dobutamine stress echocardiography study

Presence of left ventricular apical thrombus predicts lack of myocardial viability: A dobutamine stress echocardiography study

Response of six patients with idiopathic hypereosinophilic syndrome to interferon alfa*

Response of six patients with idiopathic hypereosinophilic syndrome to interferon alfa*

Embolic Accident Following Heparin Therapy for a Left Ventricular Clot Diagnosed by TEE:

There are few data available on the incidence of embolic events inpatients with systemic anticoagulation. We describe a 40‐year‐old woman in congestive heart failure who was shown by transesophageal echocardiography to have an apical thrombus in the left ventricle without concomitant aneurysm. The patient was started on heparin immediately after the diagnosis was established. Twelve hours later she developed an embolic cerebrovascular accident. We believe that heparin dislodged the thrombus as occurs occasionally with thrombolytic agents used in the treatment of acute myocardial infarction.transesophageal echocardiography, paradoxical embolization with heparin treatment, left ventricular thrombus

Improved echocardiographic detection and characterization of left ventricular apical thrombi with a 5.0 MHz short-focus transducer.

Transthoracic echocardiography is a frequently used technique for detecting ventricular thrombi. This study compares the usefulness of a 5.0 MHz short focal length transducer (5-short) with standard frequency (2.5 or 3.5 MHz) transducers for the detection of left ventricular thrombi. In addition, the effect of body habitus on study quality was evaluated. A consecutive series of 101 patients sent for echocardiographic imaging with the diagnosis of myocardial infarction, dilated cardiomyopathy, or recent suspected embolic event were imaged in the apical four-chamber, apical long-axis, and apical two-chamber views with a standard transducer and also with the 5-short. Out of this group, 16 apical thrombi were identified, six with the 5-short only, three with standard transducers only, and seven by both techniques. The areas of the seven thrombi detected by both transducers were consistently larger when measured on 5-short images compared with standard transducer images (4.6 +/- 2.3 vs 3.7 +/- 2.3 cm2, p = 0.02). In the three studies positive only with the standard transducers, the 5-short demonstrated only prominent trabeculae but no thrombus. The studies positive only with the 5-short had significantly smaller calculated thrombi areas than those visualized by the standard transducers (1.6 +/- 1.2 vs 4.2 +/- 2.1 cm2, p = 0.02). No thrombus was detected by either technique in a normally contracting left ventricular apex. There were significantly fewer studies having near-field artifact when performed by the 5-short compared with those performed with standard transducers (14/101 vs 40/101, p = 0.00004).(ABSTRACT TRUNCATED AT 250 WORDS)

Diagnosis of papillary fibroelastoma of the mitral valve complicated by non-Q-wave infarction with apical thrombus: Transesophageal and transthoracic echocardiographic study

Diagnosis of papillary fibroelastoma of the mitral valve complicated by non-Q-wave infarction with apical thrombus: Transesophageal and transthoracic echocardiographic study

Reversible Catecholamine-lnduced Cardiomyopathy Presenting as Acute Pulmonary Edema in a Patient with Pheochromocytoma

Cardiac injury caused by elevated levels of circulating catecholamines is a well-known phenomenon. We report a patient who, secondary to transient regional left ventricular dysfunction (despite normal coronary arteries), developed acute pulmonary edema. Echocardiography showed marked anteroapical hypokinesia and an apical thrombus. The diagnosis of pheochromocytoma was made by plasma catecholamine levels, abdominal ultrasound and finally at operation. The patient recovered completely long before surgical intervention was undertaken.

Usefulness of transesophageal echocardiography in identifying small left ventricular apical thrombus

Objectives. The aim of this study was to determine whether transesophageal echocardiography could clarify the nature of equivocal echodense structures in the left ventricular apical region frequently found on transthoracic echocardiography by directing the ultrasound beam from the left ventricular base to the apex and achieving better image quality.Background. Transthoracic echocardiography often reveals an echogenic structure suggesting thrombus in the left ventricular apical region because of limited near-field resolution and echo vibration artifact in apical views.Methods. Thirty-six patients with coronary artery disease or dilated cardiomyopathy who had apical wall motion abnormalities and equivocal transthoracic echodense structures were studied with transesophageal echocardiography using special manipulation of the transesophageal probe for adequate imaging of the apical region. Left ventricular thrombus was defined when echogenic structures with a cleariy delineated margin adjacent to but distinct from the endocardium were observed in at least two different tomographic views in the four-chamber and left ventricular long-axis views during both systole and diastole.Results. Left ventricular thrombus (mean size 1.3 ± 0.7 cm2) was defined by transesophageal echocardiography in 19 (53%) of 36 patients with suspected thrombus on transthoracic echocardiography in the four-chamber or left ventricular long-axis view. Heavy trabeculation or extremely high echo reflection, or both, was observed in the apical region in 12 patients (33%). No extra structures in the apical region were found in five patients. In 19 patients with transesophageal echocardiographically defined thrombus, 6 patients (31%) experienced arterial embolic events before the transesophageal procedure. In contrast, none of 17 patients without transesophageal echocardiographically defined thrombi had systemic embolism (p < 0.03).Conclusions. 1) Transesophageal echocardiography is useful in identifying left ventricular apical thrombus in patients with unclear echogenic structures on transthoracic apical images; and 2) the high incidence of arterial embolism in patients with transesophageal echocardiographically detected left ventricular thrombus indicates the clinical importance of such thrombus.

Superiority of transesophageal echocardiography in detecting cardiac source of embolism in patients with cerebral ischemia of uncertain etiology

The diagnostic yield of transesophageal and transthoracic echocardiography for identifying a cardiac source of embolism was compared in 79 patients presenting with unexplained stroke or transient ischemic attack. There were 35 men and 44 women with a mean age of 59 years (range 17 to 84); 52% had clinical cardiac disease. Both transthoracic and transesophageal echocardiograms were performed using Doppler color flow and contrast imaging.Transesophageal echocardiography identified a potential cardiac source of embolism in 57% of the overall study group compared with only 15% by transthoracic echocardiography (p < 0.0005). Compared with transthoracic echocardiography, transesophageal echocardiography more frequently identified atrial septal aneurysm associated with a patent foramen ovale (9 versus 1 of 79 patients, p < 0.005), left atrial thrombus or tumor (6 versus 0 of 79 patients, p < 0.05) and left atrial spontaneous contrast (13 versus 0 of 79 patients, p < 0.0005). All cases of left atrial thrombus or spontaneous contrast were identified in patients with clinically identified cardiac disease.In the 38 patients with no cardiac disease, transesophageal echocardiography identified isolated atrial septal aneurysm and alrial septal aneurysm with a patent foramen ovale more frequently than transthoracic echocardiography (8 versus 2 of 38 patients, p < 0.05). The two techniques had a similar rate of identifying apical thrombus and mitral valve prolapse. Overall, transesophageal echocardiography identified abnormalities in 39% of patients with no cardiac disease versus 19% for transthoracic echocardiography (p < 0.005).Thus, transesophageal echocardiography identifies potential cardiac sources of embolism in the majority of patients presenting with unexplained stroke. Even in patients with no clinical heart disease the diagnostic yield of transesophageal echocardiography is 39%. The use of transesophageal echocardiography in patients with unexplained stroke, even in those with a normal transthoracic echocardiogram, should be recommended.

Early detection of left ventricular mural thrombi after acute Q wave myocardial infarction using 111In oxine-labelled autologous platelets

Autologous 111In oxine-labelled platelet scintigraphy was used to detect left ventricular thrombi in 20 patients with anterior and 18 patients with inferior Q wave myocardial infarction within 48-72 h. Left ventricular thrombi were found in 8/20 patients with anterior myocardial infarction and in 1/18 patients with inferior myocardial infarction, giving a total incidence of 24%. Patients with left ventricular thrombi were older (64.3 versus 58.2 years), had higher peak creatinine kinase (CK) levels (4523 versus 2749 IU 1-1), lower ejection fraction (19.5 versus 37.8%, P less than 0.005) and were more likely to have an enlarged left ventricle than those without left ventricular thrombi (87.5 versus 54.5%, P less than 0.001). Left ventricular thrombi were found overlying sites of myocardial infarction in 8 out of 9 patients. Apical left ventricular thrombi were 1.7 times more common than septal left ventricular thrombi. All patients received minidose heparin for prevention of deep venous thrombosis. This technique is complementary to echocardiography and may provide additional information in the difficult cases where the decision about full-dose anticoagulation is in doubt.

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 < 0.001). Early thrombolytic therapy in 34 patients did not decrease the rate of thrombus occurrence. Acute anterior infarction, ejection fraction ≤ 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 ≤ 35% and ventricular aneurysm or dyskinesia. Systemic embolism occurred in six patients, all with a predischarge thrombus (p < 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.

Prediction of apical thrombus formation in acute myocardial infarction based on left ventricular spatial flow pattern

The predictive value of the left ventricular spatial flow pattern for thrombus formation was determined in 62 patients with acute myocardial infarction. A normal flow pattern by pulsed Doppler echocardiography was characterized by 1) simultaneous onset of blood motion at the mitral valve and apical level, and 2) a discontinuous Doppler signal along the lateral wall and interventricular septum. The flow pattern was assessed by these criteria, within 24 h after the onset of complaints and after 6 and 12 weeks. In 46 of the 62 patients, a normal flow pattern was found at the first examination; none of these 46 patients developed a thrombus during the study period. An abnormal flow pattern was seen at the first examination in 16 patients; this pattern normalized during follow-up in 6 patients, none of whom developed a thrombus. In the other 10 patients the abnormal flow pattern persisted, and 7 of these developed a thrombus. These findings suggest that a normal left ventricular flow pattern in the setting of acute myocardial infarction is not associated with subsequent thrombus formation. This observation may be of importance if anticoagulation is considered.

Flow characteristics in the dilated left ventricle with thrombus: Qualitative and quantitative doppler analysis

In an attempt to determine whether mural thrombus in a dilated left ventricle is associated with specific flow patterns, a study was undertaken to assess qualitatively and quantitatively the flow characteristics by conventional pulsed and two-dimensional Doppler color flow examination. Forty patients with cardiomyopathy formed the study group (20 with an apical thrombus and 20 without). The groups did not differ with respect to age, gender, origin of ventricular dysfunction, ventricular size and ejection fraction. Guided by the Doppler color flow pattern, a quantitative analysis of flow velocity profile in the ventricular inflow and outflow “compartments” was performed by serial pulsed wave Doppler sampling.Inflow velocity at the ventricular apex was significantly lower in the thrombus group than in the no thrombus group (11.7 ± 15.3 versus 28.3 ± 10.5 cm/s, p < 0.0001). Flow velocities were generally lower in the thrombus group at the other levels in the inflow compartment (that is, mitral anulus, leaflet tips and papillary muscle level). The systolic flow velocity at the apex was similarly significantly lower in the thrombus group than in the no thrombus group (7.1 ± 8.1 versus 15.3 ± 7.0 cm/s, p < 0.001). Additionally, a higher prevalence of mitral regurgitation was noted in the no thrombus group (14 patients) than in the thrombus group (3 patients).Thus, specific abnormal flow profiles are associated with a left ventricular thrombus. Whether the abnormal flow is a primary event in the genesis of left ventricular thrombus or occurs secondary to development of the thrombus cannot be determined from this study.

Left Ventricular Wall Motion Abnormalities in Subarachnoid Hemorrhage: An Echocardiographic Study

Although electrocardiographic (ECG) abnormalities and autopsy evidence of myocardial necrosis are associated with subarachnoid hemorrhage, their relation to in vivo measures of left ventricular function in this condition has not been established. Thirteen patients with subarachnoid hemorrhage and no prior history of heart disease were studied by two-dimensional echocardiography, performed initially 10 to 48 h (mean 18) after admission and serially for less than or equal to 14 days. Serum creatine kinase (total and myocardial isoenzyme) was determined 5 times over the first 48 h; ECGs were performed daily. Neurologic state was assessed with the use of a standard grading system. Four patients (Group I) exhibited left ventricular wall motion abnormalities in one to eight segments. In two of these patients there was also left ventricular apical mural thrombus that embolized in one patient, leading to further neurologic deterioration. The initial creatine kinase myocardial isoenzyme was higher in Group I than in Group II (patients without wall motion abnormalities) (10.3 versus 2.1 U/liter, p less than 0.001), initial heart rate was higher (91 versus 61 beats/min, p less than 0.01), neurologic grade was higher (2.5 to 4.5 versus 1 to 2, p less than 0.001) and inverted T waves were more common (4 of 4 versus 1 of 9). Three of the four patients in Group I died; two of the three underwent autopsy and were found to have no significant coronary artery disease. No other patients died.(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.

Left ventricular mural thrombi secondary to acute myocardial infarction: predisposing factors and embolic phenomenon.

Twenty-five patients with acute myocardial infarction were examined for ventricular thrombi using two-dimensional echocardiography. Six of 10 patients (60%) with an anterior wall infarction had an apical or apical-septal thrombus within the first week of hospitalization. None of the fifteen patients with an inferior wall myocardial infarction had a mural thrombus. Although the size of infarction in the patients with a thrombus was not significantly larger than in those who had an anterior wall infarction without a thrombus (43% +/- 10% vs. 31% +/- 7%, P less than 0.1), the severity and extent of dyskinesia or akinesia were more marked in the former group. Left ventricular function as determined by the nuclear blood pool scan ejection fraction was also significantly less for the former group than for the latter group (21% +/- 6% vs. 40% +/- 11%, P less than 0.02). Three of six patients with an intracavitary thrombus on echocardiography had systemic embolic during their hospital course. Postinfarction ventricular thrombi tend to occur in those patients with an anterior wall myocardial infarction who have far advanced wall motion abnormalities of the affected area, and overall poor left ventricular function. Although the number of patients was small, the high incidence of systemic embolization in the infarction subjects with echocardiographically proven thrombi indicates that these patients are at increased risk for such events.

Left Ventricular Thrombi Identified by Cross-Sectional Echocardiography

We studied 25 patients with anterior myocardial infarction and two with congestive cardiomyopathy to evaluate two-dimensional echocardiography in the diagnosis of left ventricular thrombi. Five coronary patients had systemic emboli. Four of these patients manifested apical filling defects on cineangiogram, while a levophase cine was equivocal for clot in the fifth patient. Neither echocardiography nor cineangiography visualized ventricular thrombi in the nonembolus coronary patients. Echoes from a distinct apical mass, however, were visualized in all five patients in the embolus group by two-dimensional echocardiography at the cardiac apex. Apical thrombi were confirmed in all four patients in the embolus group undergoing surgery. The irregular configuration of recent thrombi in the coronary patients differed from the circumscribed appearance of chronic thrombi in the cardiomyopathy patients on two-dimensional echocardiogram. Thus, two-dimensional echocardiography can be used to detect and characterize left ventricular thrombi.

Unusual complications of coronary bypass surgery

Five patients after coronary bypass surgery developed unusual complications. Three developed new apical thrombi which are thought to be due to the trauma of the left ventricular vent or deterioration of the left ventricular contraction. Significant new mitral regurgitation in one patient probably is secondary to papillary muscle dysfunction as the result of stenosis distal to anastomoses. The leakage of angoigraphic material around distal anastomatic site is due to technical error. Although these unusual complications are very rare, however, they should be considered as potential source of morbidity in asymptomatic patients who leave the hospital after bypass surgery.