The right atrial thrombus: the sword of Damocles with real risk of massive pulmonary embolism

Cases of 6 patients admitted at the intensive care unit for massive pulmonary embolism are reported. All patients presented with dyspnea, tachypnea, and tachycardia, and 4 were hypotensive and had syncope. Lung ventilation/ perfusion scans revealed perfusion defects in 4 patients. Transthoracic echocardiography (TTE) demonstrated acute cor pulmonale. It also revealed mobile right atrial thrombi in 5 patients, adherent thrombus in the right atrium in 1 patient and patent foramen ovale in 4 patients. Thrombolytic therapy was initiated in 4 patients, and 2 patients received heparin infusion only. Effects of thrombolysis were monitored using bedside TTE during the first 24 hours and in follow-up. The outcome of 4 patients who received thrombolytic therapy was good whereas other 2 patients, who received only heparin, died. Thrombotic mass disappeared 8 to 12 hours after initiation of therapy, and 10 weeks after discharge TTE showed normalized right ventricle dimensions and function in all 4 patients.     

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 received 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 thrombi and analyze wall motion. Ejection fraction was determined by radionuclide angiography in all patients on day 7. Apical thrombi were detected on day 3 in three patients (5.5%) who received rt-PA and in eight control patients (18%) (p less than 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 less than 0.01). Ejection fractions and wall motion scores of patients without a thrombus were significantly better when compared with data from those with a thrombus. There were fewer patients with apical dyskinesis (17 of 54) in the group receiving rt-PA therapy compared with the control group (36 of 44) (p less than 0.01). Ejection fractions and wall motion scores were better in patients who received rt-PA compared with control subjects (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)     

Rapid resolution of left ventricular thrombus in antiphospholipid syndrome

A 43-year-old male with recurrent cerebral infarctions and high titers of antiphospholipid antibodies was found to have a thrombus in his left ventricular outflow tract by transthoracic echocardiography. This thrombus disappeared after less than 24 hours of intravenous heparin therapy due to resolution or asymptomatic embolism. Left ventricular thrombi in patients with antiphospholipid syndrome and rapid disappearance of left ventricular thrombi with heparin therapy are infrequently reported occurrences.     

29例急性肺栓塞临床观察及治疗研究

目的分析急性肺栓塞的临床特点,观察溶栓抗凝治疗对急性肺栓塞的临床治疗效果。方法２９例肺栓塞患者根据放射性核素肺灌注通气检查、选择性肺动脉造影或超声心动图确诊。对其中２３例肺栓塞患者行静脉溶栓加抗凝治疗２９例次;６例肝素抗凝治疗,以临床及核素检查评价其治疗效果。结果男性患者中以年轻超力型发病者较高,女性患者以更年期以后发病明显增高。院外误诊率高达７５．９％。临床上以呼吸困难为主要表现者多见;尿激酶或重组组织型纤溶酶原激活剂（ｒｔ－ＰＡ）溶栓２９例次,总有效率为６５．５％。根据本组有限病例观察溶栓效果与栓塞的面积未见差异,而与发病开始到溶栓治疗的时间密切相关（Ｐ＜０．０５）。肝素抗凝６例,１例显效,２例有效,３例无效。结论应提高对急性肺栓塞的警惕性,减少误诊率;尿激酶或ｒｔ－ＰＡ对急性肺栓塞溶栓抗凝治疗安全有效,溶栓时间越早越好;对有溶栓适应证的患者应首选溶栓治疗。     

Management of mobile right heart thrombi: a prospective series

BACKGROUND: Mobile right heart thrombi (MRHT) are uncommon but their true prevalence is unknown. The aim of our study was to assess the prevalence of MRHT by a systemic use of transthoracic echocardiography in a prospective series of consecutive patients admitted for acute severe pulmonary embolism (PE) and to adopt intravenous thrombolysis with recombinant tissue plasminogen activator (rt-PA) as the first line intention to treat patients with proven MRHT. METHODS AND RESULTS: We performed a systematic transthoracic echocardiogram from November 1997 to June 1999 in 335 consecutive patients admitted for suspected acute massive PE in whom the diagnosis was subsequently confirmed by perfusion lung scan or angiography. MRHT was identified in 12 of the 335 patients (4%). Nine patients presented a coil form and three patients a ball form. The thrombolytic employed in all cases was rt-PA according to the following protocol: 10 mg in a bolus and 40 mg over 2 h, followed by 50 mg over 5 h, up in a total dose of 100 mg, associated with a bolus of 5000 units of heparin. Control echocardiograms were performed 12 h after the initiation of treatment and at 12-month follow-up. Three patients died before the onset of thrombolytic infusion. The nine remaining patients were submitted to thrombolytic therapy using rt-PA. In seven of the nine remaining patients, MRHT was no longer observed after 12 h and the echocardiographic signs of RV overload had disappeared. The two last patients required adjunctive surgery because of evidence of persistent thrombus in a pulmonary artery. After 24 h, both scintigraphy and angiography demonstrated improved pulmonary perfusion. At 1-year follow-up, all patients were alive and the pulmonary artery pressure estimated by Doppler echocardiography was <30 mm Hg. CONCLUSIONS: The incidence of right heart thrombus is low in patients admitted for acute PE. Thrombolytic therapy with rt-PA appears to be rapidly effective in most patients with MRHT. The thrombus usually resolves and pulmonary perfusion is rapidly improved. Systematic echocardiogram appears to be useful for rapidly detecting MRHT in patients with suspected massive PE.     

Effect of early anticoagulation on the frequency of left ventricular thrombi after anterior wall acute myocardial infarction

To determine the effect of early anticoagulation on the incidence of left ventricular thrombi complicating anterior acute myocardial infarction (AMI), 82 consecutive patients admitted within 12 hours of symptom onset and with electrocardiographic changes consistent with anterior AMI were randomly assigned to 1 of 2 treatment groups. Group 1 patients received high-dose intravenous heparin to maintain the whole blood clotting time between 15 and 20 minutes, and commenced warfarin therapy within 48 hours. Group 2 patients received low-dose subcutaneous heparin and warfarin therapy if the peak creatine kinase level was more than 1,000 U/liter. Eighteen group 2 patients received warfarin, but none had a therapeutic prothrombin ratio within 5 days. The presence and morphologic characteristics of thrombus were assessed by serial 2-dimensional echocardiography. Thirty patients were excluded because AMI was not confirmed or because of technically unsatisfactory echocardiograms, death, surgery or, in group 1 patients, inadequate anticoagulation. Thrombi were identified in 29 of 52 patients (56%): in 14 of 25 group 1 patients (56%) and 15 of 27 group 2 patients (56%). Twenty-three thrombi formed within 3 days. Thrombi were protruding rather than mural only in 3 group 2 patients. The groups did not differ in baseline characteristics or in incidence, time of appearance or morphologic characteristics of thrombus (p greater than 0.05, beta for more than 25% reduction in incidence with group 1 treatment less than 0.10). Systemic embolism occurred only in 1 group 2 patient with mural thrombus.(ABSTRACT TRUNCATED AT 250 WORDS)     

Large right atrial thrombus with pulmonary embolism

We present the cases of two patients, aged 67 and 77 years, who were admitted for the evaluation of rapidly progressive dyspnea and syncope, respectively. Both patients developed large right atrial thrombi with pulmonary embolism. The first patient received recombinant tissue plasminogen activator and survived with an uneventful result, whereas the second patient received operative thrombectomy followed by intravenous heparin and died 15 days later of pulmonary infarction with pulseless electrical activity. Data from these limited experiences suggest that thrombolytic therapy might be considered in patients with right heart thrombi with pulmonary embolism.     

Free floating right atrial thrombus leading to acute pulmonary embolism

The presence of right heart thrombi appears to increase the risk of mortality compared to the presence of pulmonary thromboemboli alone. The increased use of two-dimensional echocardiography has led to increased detection of these thromboemboli, particularly in patients with suspected or confirmed pulmonary emboli. The optimal management of the right heart thromboemboli remains unclear, but thrombolytic therapy with rt-PA appears to be rapidly effective in most patients resulting with complete resolution of the thrombus and improvement of pulmonary perfusion. Here, we present a case of free floating, worm-like thrombus in the right atrium which was lysed successfully by fibrinolytic therapy in a patient presenting with acute massive pulmonary embolism.     

Treatment of massive cardiac thrombi in a patient with protein C and protein S deficiency.

Myocarditis and dilated cardiomyopathy is characterized by dilatation of all four cardiac chambers and decreased systolic function of the heart, especially in the left ventricle. In this report we presented a patient with myocarditis or dilated cardiomyopathy and deficiency of protein C and protein S with biventricular multiple intracardiac thrombi. Standard heparin infusion and acetyl salicylic acid was begun. On the 10th day of hospitalization the right ventricular thrombus disappeared, and on the 24th day all thrombi in the left ventricle disappeared. During the treatment we did not observe any complication such as hemorrhagia or embolism. We think that patients with dilated cardiomyopathy or myocarditis should be evaluated for hemostatic disorders, and should be anticoagulated if any of these disorders are presented.     

A case of peripartum cardiomyopathy with recurrent left ventricular apical thrombus.

Peripartum cardiomyopathy (PPCM) is a disorder of unknown cause in which heart failure occurs during the peripartum period. A 32-year-old woman was diagnosed with PPCM 10 days after delivery. One month after the initial diagnosis, a newly formed left ventricular (LV) apical thrombus was revealed and warfarin was started. One week later, the thrombus became mobile and she underwent surgical thrombectomy. Warfarin was restarted on postoperative day (POD) 1; however, thrombi recurred at POD 3. Intravenous heparin was then supplemented, which subsequently resolved the thrombi without any embolism. Although there is currently no consensus as to whether patients with depressed LV function and sinus rhythm should be anticoagulated to prevent thrombus formation, PPCM presents a higher risk and might need aggressive and pre-emptive anticoagulation once diagnosis is made.     

Lysis of a left ventricular thrombus with recombinant tissue plasminogen activator

A 23-year-old woman with peripartum cardiomyopathy presented with a 2.1 x 2.5-cm pedunculated, mobile, left ventricular thrombus and evidence of systemic embolization. Due to the patient's poor left ventricular function, thrombectomy was not a viable option. Treatment with high-dose IV heparin was initially utilized but was unsuccessful as the thrombus appeared to enlarge on echocardiography. An accelerated weight-adjusted dose of recombinant tissue plasminogen activator (rt-PA) successfully lysed the thrombus without evidence of embolization. Although rt-PA has been used for primary lysis of high-risk ventricular thrombi, this is the first documentation of successful lysis of a left ventricular thrombus in a patient with peripartum cardiomyopathy.     

Treatment of canine embolic pulmonary hypertension with recombinant tissue plasminogen activator. Efficacy of dosing regimes

We investigated effects of two dosing regimes of recombinant tissue plasminogen activator (rt-PA) and sodium heparin on pulmonary thrombolysis in a canine model of pulmonary hypertension, induced by injection of radioactive blood clots. By continuously counting over both lung fields with a mobile gamma camera, we correlated rate and extent of pulmonary thrombolysis with corresponding pulmonary hemodynamics. Treatment with heparin, over a 3-hour interval, did not result in significant thrombolysis or in a decrease in mean pulmonary artery pressure (PAP). In contrast, rt-PA caused marked pulmonary thrombolysis. While total clot lysis was similar when 1 mg/kg rt-PA was infused over 15 (rt-PA15) or 90 (rt-PA90) minutes (47% and 42%, respectively), rate of lysis during infusion was markedly increased with rt-PA15 (56% vs. 27%/hr, p less than 0.001). Corresponding to the increased rate of thrombolysis with rt-PA15, relative PAP decrease was greater at 15 and 30 minutes. At 4 hours, PAP decreased most with rt-PA90. However, two of the six dogs given rt-PA15 had an increase in PAP and lung radioactivity 1 hour after rt-PA. This was associated with dislodgment of a previously trapped clot. These results suggest that rt-PA may be appropriate therapy for pulmonary embolism and support further studies designed to optimize dosing regimes.     

Enhancement of thrombolysis with tissue-type plasminogen activator by pretreatment with heparin

The effect of pretreatment with heparin on lysis of arterial thrombi by tissue-type plasminogen activator (rt-PA) was studied in 19 dogs. Copper coil-induced carotid artery thrombi were weighed, inserted into the femoral arteries, and exposed to a 15 min infusion of rt-PA at 10 micrograms/kg/min either with (n = 6 thrombi) or without pretreatment with a 200 unit/kg bolus of heparin (n = 6 thrombi). The infusion of rt-PA without pretreatment reduced the thrombus weight by 27.6 +/- 7.4%, while infusion of rt-PA with pretreatment reduced it by 79.1 +/- 12.3% (p less than .0001). To test the hypothesis that heparin enhanced thrombolysis by preventing continued incorporation of new fibrin into the thrombus during thrombolysis we repeated the experiments using pretreatment with 8 U/kg of ancrod, which rapidly depletes fibrinogen. Pretreatment with ancrod (n = 6 thrombi) depleted fibrinogen and enhanced the lytic effect of rt-PA to a similar degree as pretreatment with heparin, resulting in a 67.6 +/- 12.3% (NS) decrease in thrombus weight. We conclude that heparin significantly enhances the thrombolytic effect of rt-PA, probably by preventing new fibrin formation and its incorporation into the thrombus during lysis.     

Recurrent left ventricular mural thrombi in a patient with acute myocarditis

Summary A case of acute myocarditis with recurrent left ventricular mural thrombi in a 59-year-old man is reported. Two-dimensional echocardiogram demonstrated left ventricular mural thrombus with apical dyskinesis on the 2nd day after the onset of chest oppression. No hemoagglutination abnormalities were present. Anticoagulation treatment with heparin was initiated. A two-dimensional echocardiogram obtained on the 15th day showed that the left ventricular wall motion had become normal and that the thrombus had disappeared. However, on the 38th day, a new pedunculated free mobile thrombus was found in the apical part of the left ventricle despite the normal wall motion. By the 46th day, the new thrombus had disappeared.The present case suggests that mural thrombi can occur in the absence of left ventricular dyskinesis and dilatation. Anticoagulation therapy resolved the mural thrombi but could not prevent the recurrence at the apex. Thus, in acute myocarditis, a mural thrombus may appear as a result of the endocardial damage, even when blood stasis is absent.     

Thromboses of the right atrium: echocardiographic aspects, practical management. Apropos of 8 cases

Right atrial (RA) thrombosis is rare. The aim of this study was to determine their clinical and echocardiographic features and therapeutic implications. In the last 7 years, 16 RA masses were detected by 2D echocardiography. The diagnosis of thrombosis was made in 8 cases based on anatomo-pathological examination (6 cases) or their disappearance with medical treatment (2 cases). The clinical presentations were: pulmonary embolism (4 cases), anterior myocardial infarction (2 cases), Ebstein's anomaly (1 case), thrombosis of a Leveen catheter (1 case). Only 1 patient had atrial fibrillation. Two echocardiographic appearances were observed: 1) a long, very mobile thrombus floating between the RA and right ventricle (4 cases), 2) a relatively immobile mass (4 cases). The 4 patients with relatively immobile thrombi survived: 2 underwent surgery and 2 were treated medically. All cases of floating thrombi had pulmonary embolism: 2 patients underwent surgery but the postoperative course was complicated; 2 patients died suddenly before surgery. These cases show that 2D echo is the diagnostic method of choice for detection of RA thrombosis. The floating RA thrombus is a therapeutic emergency and has a poor prognosis.     

Clinical, echocardiographic and evolutive aspects of right atrial thrombosis

The clinical and echocardiographic features of right atrial thrombi were examined in 9 patients, 5 men and 4 women aged 16 to 86 years. The 2D echocardiographic diagnosis was confirmed at autopsy (4 cases) or by the association of severe recurrent pulmonary embolism (5 cases). Three patients had associated ischaemic heart disease and on patient had dilated cardiomyopathy. The clinical presentation was: acute cor pulmonale (5 cases including 2 patients which biventricular myocardial infarction), chronic post-embolic cor pulmonale (1 case), tricuspid valve obstruction (1 case), general ill health with pyrexia (1 case) and heparin-induced thrombocytopenia (1 case). Predisposing factors included: absence of anticoagulent therapy (7 cases), previous supraventricular arrhythmias (2 cases) and right ventricular failure (6 cases, including 2 of right ventricular infarction). In 2 patients the thrombi were relatively immobile and had a wide base of implantation on the interatrial septum; in 1 patient, multiple thrombi were observed lining the right heart cavities from the inferior vena cava to the pulmonary infundibulum. In the other 6 patients, the thrombi were very mobile with a visible pedicule of implantation (2 cases) or totally free (4 cases). The variable polylobulated appearances, completely irregular whirling motion and intermittent prolapse into the tricuspid valve were characteristic features of the latter 4 cases. They disappeared spontaneously (2 cases) or after fibrinolytic therapy (2 cases) in under 36 hours. Three patients were operated with one postoperative death. The global hospital mortality was 22%. The present occasional detection of right atrial thrombosis will certainly become more common if patients with pulmonary embolism, right ventricular infarction or deep venous thrombosis are systematically examined by 2D echocardiography in the acute phase of their illness.     

Silent Pulmonary Embolism of a Large Right Atrial Thrombus

We report the case of a patient who was admitted to the hospital with acute pulmonary embolism 2 weeks after a complicated pelvis fracture. Echocardiography revealed a large, long, and mobile thrombus in the right atrium. The patient was scheduled to undergo urgent surgical thrombectomy. Preoperative echocardiography did not detect any thrombi in the right heart and pulmonary artery. The obvious embolism of this large thrombus in the pulmonary circulation was silent as the patient remained asymptomatic and hemodynamically stable. We discuss the contribution of echocardiography to the appropriate therapeutic management of right atrial thrombi and particularly to the cancellation of urgent operative thrombectomy.     

Right atrial mobile thrombi: two-dimensional echocardiographic diagnosis and clinical outcome

Four patients with pulmonary embolism and right atrial mobile thrombi (RAMT) are described. One patient died during intravenous heparin treatment because of a "saddle" pulmonary artery embolus, another died from surgical complications after successful embolectomy. One of the two survivors was treated with intravenous streptokinase and the other with intravenous heparin. Echocardiographically detected RAMT seems a reliable sign of impending massive pulmonary embolism. Pulmonary angiography is unnecessary and may be dangerous. Surgical removal of RAMT, fibrinolytic treatment or intravenous heparin introduced promptly may be lifesaving.     

Echocardiography Detects and Demonstrates Disappearance of Right Atrial and Pulmonary Artery Thrombus: Case Report

We present the case of a patient with acute pulmonary embolism and a large right atrial and a smaller pulmonary artery thrombus. Thrombi were successfully treated with intravenous heparin. Echocardiography was used to document the morphological evolution of thrombi and to evaluate the medical treatment.     

Free floating right atrial thrombus with massive pulmonary embolism:near catastrophic course following thrombolytic therapy

A 28-year-old policeman presented with left lower limb deep vein thrombus, pulmonary embolism and a highly mobile right atrial clot. Thrombolytic therapy with IV Tenecteplase was administered. Within a few minutes after the Tenecteplase bolus, the patient's condition worsened dramatically with severe hypotension and hypoxemia. Immediate bedside transthoracic echocardiogram revealed that the mobile right atrium clot had disappeared completely presumably having migrated to the pulmonary circulation thus worsening the clinical condition. With intensive supportive measures the patient's condition was stabilized and he made a complete recovery. Prior to discharge, the echocardiogram revealed normal right ventricular function and a CT pulmonary angiogram performed after 2 months revealed near complete resolution of pulmonary thrombi. Thrombolytic therapy for right heart thrombus with pulmonary embolism can be a reasonable first line therapy but may be associated with hemodynamic worsening due to clot migration.