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The article presents a study that assessed the cost-effectiveness of prophylactic fondaparinux treatment which is used to prevent thrombotic complications following a superficial vein thrombosis (SVT). The study used a decision-tree model comparing fondaparinux 2.5 milligrams daily for 45 days versus no treatment of SVT. It shows the efficacy of fondaparinux in preventing 123 VTE events and two deaths.

The article presents a case study of a 33-year-old woman who was presented with febrile neutropenia after she initiated treatment with deferiprone. She has a history of beta-thalassemia which requires monthly blood transfusions, complicated by myocardial iron deposition and iron overload. The patient was trated for retropharyngeal abscess having piperacillin-tazobactam.

The article discusses numerous pulmonary and thrombotic manifestations of systemic lupus erythematosus (SLE). It is stated that SLE is considered as archetypal systemic autoimmune disease. According to the authors, SLE is a multisystem disease that would bring the entire pulmonary system vulnerable to injury. A suggested approach in managing SLE is presented.

Background: Pulmonary vascular microthrombi are a proposed mechanism of COVID-19 respiratory failure. We hypothesized that early administration of tissue plasminogen activator (tPA) followed by therapeutic heparin would improve pulmonary function in these patients., Research Question: Does tPA improve pulmonary function in severe COVID-19 respiratory failure, and is it safe?, Study Design and Methods: Adults with COVID-19-induced respiratory failure were randomized from May14, 2020 through March 3, 2021, in two phases. Phase 1 (n = 36) comprised a control group (standard-of-care treatment) vs a tPA bolus (50-mg tPA IV bolus followed by 7 days of heparin; goal activated partial thromboplastin time [aPTT], 60-80 s) group. Phase 2 (n = 14) comprised a control group vs a tPA drip (50-mg tPA IV bolus, followed by tPA drip 2 mg/h plus heparin 500 units/h over 24 h, then heparin to maintain aPTT of 60-80 s for 7 days) group. Patients were excluded from enrollment if they had not undergone a neurologic examination or cross-sectional brain imaging within the previous 4.5 h to rule out stroke and potential for hemorrhagic conversion. The primary outcome was Pao 2 to Fio 2 ratio improvement from baseline at 48 h after randomization. Secondary outcomes included Pao 2 to Fio 2 ratio improvement of > 50% or Pao 2 to Fio 2 ratio of ≥ 200 at 48 h (composite outcome), ventilator-free days (VFD), and mortality., Results: Fifty patients were randomized: 17 in the control group and 19 in the tPA bolus group in phase 1 and eight in the control group and six in the tPA drip group in phase 2. No severe bleeding events occurred. In the tPA bolus group, the Pao 2 to Fio 2 ratio values were significantly (P < .017) higher than baseline at 6 through 168 h after randomization; the control group showed no significant improvements. Among patients receiving a tPA bolus, the percent change of Pao 2 to Fio 2 ratio at 48 h (16.9% control [interquartile range (IQR), -8.3% to 36.8%] vs 29.8% tPA bolus [IQR, 4.5%-88.7%]; P = .11), the composite outcome (11.8% vs 47.4%; P = .03), VFD (0.0 [IQR, 0.0-9.0] vs 12.0 [IQR, 0.0-19.0]; P = .11), and in-hospital mortality (41.2% vs 21.1%; P = .19) did not reach statistically significant differences when compared with those of control participants. The patients who received a tPA drip did not experience benefit., Interpretation: The combination of tPA bolus plus heparin is safe in severe COVID-19 respiratory failure. A phase 3 study is warranted given the improvements in oxygenation and promising observations in VFD and mortality., Trial Registry: ClinicalTrials.gov; No.: NCT04357730; URL: www., Clinicaltrials: gov., (Copyright © 2021 American College of Chest Physicians. Published by Elsevier Inc. All rights reserved.)

Background: Antithrombotic therapy in valvular disease is important to mitigate thromboembolism, but the hemorrhagic risk imposed must be considered., Methods: The methods of this guideline follow those described in Methodology for the Development of Antithrombotic Therapy and Prevention of Thrombosis Guidelines. Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines in this supplement., Results: In rheumatic mitral disease, we recommend vitamin K antagonist (VKA) therapy when the left atrial diameter is > 55 mm (Grade 2C) or when complicated by left atrial thrombus (Grade 1A). In candidates for percutaneous mitral valvotomy with left atrial thrombus, we recommend VKA therapy until thrombus resolution, and we recommend abandoning valvotomy if the thrombus fails to resolve (Grade 1A). In patients with patent foramen ovale (PFO) and stroke or transient ischemic attack, we recommend initial aspirin therapy (Grade 1B) and suggest substitution of VKA if recurrence (Grade 2C). In patients with cryptogenic stroke and DVT and a PFO, we recommend VKA therapy for 3 months (Grade 1B) and consideration of PFO closure (Grade 2C). We recommend against the use of anticoagulant (Grade 1C) and antiplatelet therapy (Grade 1B) for native valve endocarditis. We suggest holding VKA therapy until the patient is stabilized without neurologic complications for infective endocarditis of a prosthetic valve (Grade 2C). In the first 3 months after bioprosthetic valve implantation, we recommend aspirin for aortic valves (Grade 2C), the addition of clopidogrel to aspirin if the aortic valve is transcatheter (Grade 2C), and VKA therapy with a target international normalized ratio (INR) of 2.5 for mitral valves (Grade 2C). After 3 months, we suggest aspirin therapy (Grade 2C). We recommend early bridging of mechanical valve patients to VKA therapy with unfractionated heparin (DVT dosing) or low-molecular-weight heparin (Grade 2C). We recommend long-term VKA therapy for all mechanical valves (Grade 1B): target INR 2.5 for aortic (Grade 1B) and 3.0 for mitral or double valve (Grade 2C). In patients with mechanical valves at low bleeding risk, we suggest the addition of low-dose aspirin (50-100 mg/d) (Grade 1B). In valve repair patients, we suggest aspirin therapy (Grade 2C). In patients with thrombosed prosthetic valve, we recommend fibrinolysis for right-sided valves and left-sided valves with thrombus area < 0.8 cm(2) (Grade 2C). For patients with left-sided prosthetic valve thrombosis and thrombus area ≥ 0.8 cm(2), we recommend early surgery (Grade 2C)., Conclusions: These antithrombotic guidelines provide recommendations based on the optimal balance of thrombotic and hemorrhagic risk.

An 8-year-old boy was admitted to the hospital with multiple abdominal and pelvic injuries following a motor vehicle accident. During hospitalization, signs of stroke developed. Evaluation discovered the cause to be emboli originating from a large left ventricular thrombus, most probably as a result of cardiac injury. Anticoagulation therapy was initiated, the cardiac mass resolved completely within 3 days, and neurologic status subsequently improved. When possible, echocardiography should be used as part of the workup of pediatric patients after multiple trauma, even without obvious signs of chest involvement.

Background: In patients who have experienced acute myocardial infarction (MI), primary percutaneous coronary intervention (PCI) has been shown to be of benefit in terms of clinical outcomes. However, the value of performing routine PCI in patients with early MI (ie, an MI occurring > 12 h to < or = 7 days before patient presentation) or recent MI (ie, an MI occurring > or = 8 days to < 30 days before patient presentation) has not been established. The purposes of this prospective observational study were to evaluate the impact of PCI on outcomes, and to delineate the predictors of lack of response to reperfusion and the prognostic determinants in patients with this clinical condition., Methods and Results: A total of 377 consecutive unselected patients who had experienced early or recent MI underwent PCI. Successful reperfusion (ie, Thrombolysis in Myocardial Infarction flow grade 3 of the infarct-related artery [IRA]) was achieved in 90.2% of patients. By multiple stepwise logistic regression analysis, high-burden thrombus formation (odds ratio [OR], 15.53; 95% confidence interval [CI], 6.09 to 39.60; p < 0.0001) in the IRA, early PCI (ie, < or = 3 days) [OR, 4.10; 95% CI, 1.79 to 7.36; p = 0.0008], advanced congestive heart failure (CHF) [OR, 4.10; 95% CI, 1.70 to 9.91; p = 0.002], and diabetes (OR, 3.03; 95% CI, 1.03 to 7.06; p = 0.010) were independent predictors for lack of response to reperfusion. The 30-day mortality rate was 6.8%. The only variables that were independently related to the 30-day mortality rate were advanced CHF (OR, 29.85; 95% CI, 7.84 to 113.7; p < 0.0001), lack of response to reperfusion (OR, 7.57; 95% CI, 2.29 to 25.07; p = 0.0009), early PCI (OR, 4.81; 95% CI, 1.60 to 14.41; p = 0.005), and multivessel disease (OR, 9.22; 95% CI, 1.63 to 52.04; p = 0.0119). The surviving 351 patients were discharged from the hospital and followed-up for a mean (+/- SD) 38.9 +/- 14.2 months. Coronary angiographic follow-up was performed in 285 patients (81.2%). Restenosis of the IRA was found in 101 patients (35.4%). Reinterventions of the IRA were required in 69 patients (24.2%). Follow-up measurements of left ventricular ejection fraction (LVEF) showed significantly more improvement than the initial LVEF (59.3 +/- 13.8% vs 50.4 +/- 13%; p < 0.0001). The total cumulative mortality rate after hospital discharge was 6.5% for the entire group. Only advanced CHF (OR, 3.46; 95% CI, 1.26 to 9.52; p = 0.016) and old age (ie, > or = 70 years of age) [OR, 4.41; 95% CI, 1.59 to 12.24; p = 0.004] were independent predictors of long-term mortality., Conclusion: The performance of PCI on > or = day 4 in patients after they had experienced an MI was safe and had a high rate of success. The clinical benefits of a relative low mortality rate associated with successful PCI for patients with early and recent MI was maintained during the long-term follow-up. However, patients with advanced CHF along with old age continued to have a poor prognosis.

Study Objectives: Most left ventricular (LV) thrombi that occur after acute myocardial infarction (AMI) are formed within 2 weeks, when inflammatory cells have infiltrated into the necrotic myocardium. Inflammatory changes on the endocardial surface may induce platelet deposition and fibrin net formation through interaction with proinflammatory cytokines. We sought to determine the significance of the inflammatory response reflected by serum C-reactive protein (CRP) elevation in LV thrombus formation after AMI., Design: We examined 160 patients with first anterior AMI. Peak serum creatine kinase (CK) and CRP levels were determined by serial measurements. Echocardiography was performed 10 to 14 days after the onset. We assessed the association between the elevation of serum CRP levels and LV thrombus formation after AMI., Results: LV thrombus was observed in 13 patients (8%). There was no difference in age, sex, coronary risk factors, preinfarction angina, use of revascularization therapy and anticoagulant therapy, platelet count, and fibrinogen level on hospital admission between the two groups. The mean (+/- SD) peak serum CRP level was markedly increased in patients with LV thrombus compared to those without (18.0 +/- 12.6 vs 9.4 +/- 8.1 mg/dL; p = 0.001), despite their having similar peak CK levels. Multivariate analysis showed that a peak CRP level of > or =20 mg/dL was an independent predictor of thrombus formation (relative risk, 4.82; p = 0.037) among variables including older age (> or =60 years old), peak CK level (> or =3,000 IU/L), and peak WBC count (> or =12,000 cells/ microL)., Conclusion: A greater elevation of serum CRP level was associated with a higher incidence of LV thrombus after AMI, suggesting an important role of the inflammatory response in mural thrombus formation.

The exploration of coagulation led to identifying inflammation as a major factor in arterial disease throughout life. "Integrative molecular physiology" reflects our emerging understanding of how coagulation and inflammation integrate with one another, in both normal physiology and in pathophysiology. Our own responses to environmental challenge provide much of the damage that cumulatively results in chronic cardiovascular disease. Only by intervening in exquisitely precise ways can we hope to effectively and safely modify the course of lifelong chronic diseases, such as atherosclerosis.

In addition to its primary role in hemostasis and blood coagulation, thrombin is a potent mitogen capable of inducing cellular functions. Therefore, it should come as no surprise that thrombin has proved to be of importance in the behavior of cancer. In this review, we focus on the ability of tissue factor (TF) and thrombin to influence tumor angiogenesis. Both exert their influence on angiogenesis through clotting-dependent and clotting-independent mechanisms: (1). directly affecting signaling pathways that mediate cell functions, and (2). mediating clot formation, thereby providing a growth media for tumor cells. Therefore, anticoagulant drugs may prove efficacious in cancer treatment due to their ability to reduce the characteristic hypercoagulability of cancer and alter the fundamental biology of cancer.

Background: The presence of right heart thromboemboli complicating pulmonary thromboemboli carries with it an increased mortality rate compared to pulmonary thromboemboli alone, but little is known about the optimal management of this difficult clinical situation. This fact is highlighted in the case study of a patient with a 19-cm right atrial thrombus complicating bilateral pulmonary thromboemboli., Study Objectives: We sought to determine the effects of anticoagulation therapy, thrombolysis, and surgical embolectomy on mortality rate in patients with right heart thromboemboli., Design: Retrospective analysis of all reported cases in the English language literature (1966 to 2000) of right heart thromboembolism in which age, sex, therapy, and outcome were reported., Measurements and Results: We analyzed 177 cases of right heart thromboembolism. Pulmonary thromboembolism was present in 98% of the cases. The patients were evenly divided by gender with an average age of 59.8 years (SD, 16.6 years) years. Dyspnea (54.2%), chest pain (22.6%), and syncope (17.5%) were the most common presenting symptoms. The treatments administered were none (9%), anticoagulation therapy (35.0%), surgical procedure (35.6%), or thrombolytic therapy (19.8%). The overall mortality rate was 27.1%. The mortality rate associated with no therapy, anticoagulation therapy, surgical embolectomy, and thrombolysis was 100.0%, 28.6%, 23.8%, and 11.3%, respectively. Using multivariate modeling with survival as the primary outcome, age and gender were not associated with mortality rate, but thrombolytic therapy was associated with an improved survival rate (p < 0.05) when compared either to anticoagulation therapy or surgery., Conclusion: The presence of right heart thromboemboli may have diagnostic and therapeutic implications in pulmonary thromboembolism patients. A well-designed prospective, randomized trial is needed to determine the optimal treatment of right heart thromboemboli.

Airway obstruction due to presence of blood clot occurs in a variety of clinical settings; however, it is not always preceded by hemoptysis. The impact on respiratory function may be minimal or result in life-threatening ventilatory impairment. Three illustrative cases and a comprehensive literature review are presented. The presence of endobronchial blood clot is suggested by the clinical and radiographic findings of focal airway obstruction. The diagnosis is established by direct endoscopic evaluation. Initial efforts at removal of the airway clot, if warranted, involve lavage, suctioning, and forceps extraction through a flexible bronchoscope. If unsuccessful, further management options include rigid bronchoscopy, Fogarty catheter dislodgment of the clot, and topical thrombolytic agents.

Vinorelbine tartrate (Navelbine [Burroughs Wellcome; Research Triangle Park, NC; Pierre Fabre Medicament; Paris, France]) is used in the treatment of non-small cell lung cancer (NSCLC), breast cancer, and some gynecologic malignant neoplasms. The reported prevalence of adverse effects involving the respiratory system is less than 5% and involves mostly dyspnea with occasional interstitial infiltrates. A patient with a hypercoagulable state and diffuse pulmonary NSCLC developed acute respiratory failure soon after vinorelbine infusion. Physicians should be aware of possible increased pulmonary toxicity of vinorelbine in patients with diffuse pulmonary NSCLC.

We present a case of primary systemic amyloidosis complicated by multiple thrombotic events and initially presenting with a massive thrombosis of the inferior vena cava. Widespread infiltration of the vascular tree by amyloid was found at the time of autopsy. In addition, we report successful treatment of the massive inferior vena cava thrombosis with systemic thrombolysis.

Congenital anomalies of the inferior vena cava (IVC) are common and usually of little clinical significance. We report the unusual cases of two patients with pulmonary embolism from thrombosis of part of a duplicated IVC. Both caval anomalies were easily identified with ultrasound, and the patients were successfully treated with anticoagulants. We encourage the reporting of similar cases since knowledge of the contribution of IVC duplication to thromboembolic disease is unknown.

A 78-year-old-woman was admitted to the hospital with bilateral femoral arterial occlusion. Her medical history disclosed atrial fibrillation and a left thoracoplasty performed 50 years earlier for treatment of tuberculosis. A transesophageal echocardiogram demonstrated intraluminal thrombus in a left pulmonary vein. The patient recovered after thromboembolectomy. This case documents another uncommon cause of cardiac thromboembolism in which a transesophageal echocardiogram was essential to make the diagnosis.

A 47-year-old man experienced recurrent pulmonary embolism resistant to aggressive medical and surgical prophylaxis. Although paraneoplastic hypercoagulability was suspected, no endoscopic or radiologic signs of malignancy were detected. Death was the result of electromechanical dissociation, which was attributed to right ventricular outflow obstruction. At autopsy, anaplastic lung carcinoma was found in the left basal segment with superimposed pulmonary infarction. A huge pedunculated thrombus was attached to the left ventricular apex and extended into the ascending aorta, obstructing the left ventricular outflow. To our knowledge, this is the first case of electromechanical dissociation due to left ventricular thrombus in a patient with pulmonary embolism. Radiologic and echocardiographic evaluation of such patients should take into account possible masking of the underlying neoplasm by embolic or hemorrhagic phenomena, or both, and the presence of left-sided cardiac thombi, which may cause catastrophic events.

The prevalence of left atrial spontaneous echo contrast (SEC) and the occurrence of systemic embolism were prospectively studied in 176 consecutive patients. All had significant mitral regurgitation (MR) and underwent transesophageal echocardiographic (TEE) studies. Left ventriculography was performed in all patients to document the severity of MR. The underlying causes of MR included rheumatic heart disease in 84 patients, ruptured chordae tendineae in 37, mitral valve prolapse in 18, infective endocarditis in 20, coronary artery disease in 8, congenital heart disease in 5, and dilated cardiomyopathy in 4. No patient was found to have left atrial thrombus. Left atrial SEC was observed in three patients (1.7 percent), all of whom had atrial fibrillation, concomitant mitral stenosis, and huge left atria. Color flow mapping revealed that left atrial SEC was prominent in regions where the turbulent flow of MR was not present. Systemic embolism occurred in ten patients (5.7 percent). The underlying disease was infective endocarditis, rheumatic heart disease, and dilated cardiomyopathy in 6, 3, and 1 patient, respectively. The sites of embolization involved the central nervous system in eight patients and the spleen in the remaining two. Three patients with rheumatic heart disease and the one with dilated cardiomyopathy were in atrial fibrillation and had dilated left atria (diameter > 45 mm) when systemic embolism occurred. Only one patient with rheumatic heart disease was found to have left atrial SEC. The remaining six, with infective endocarditis, all had sinus rhythm. In conclusion, left atrial SEC or thrombus detected by TEE is uncommon in patients with significant MR. Clinical conditions may be of help to identify the subsets of patients at higher risk for systemic embolism.

Three months after splenic infarct, a 50-year-old woman underwent arteriography for persistent low-grade fever and abdominal complaints. After 5 months of corticosteroid therapy for "polyarteritis nodosa," another arteriogram confirmed embolic disease; transesophageal echocardiography (TEE) showed a pedunculated mobile thrombus in the aortic arch. We suggest this represents "pseudovasculitis" from an aortic thrombus.

We report the case of a woman treated with urokinase for acute pulmonary embolism with a right-sided heart thrombus. She developed life-threatening acute cor pulmonale which dramatically improved within 4 h with recombinant tissue plasminogen activator (rtPA). We emphasize the clinical interest of rtPA for the treatment of life-threatening pulmonary embolism.

Two cases of difficult ventilation are presented, the first caused by endotracheal tube obstruction with nasal turbinate, and the second caused by tracheobronchial obstruction with blood clots. The clinical presentation in each case was characterized by extreme difficulty in ventilating and severe hypercapnia despite vigorous ventilatory efforts with either a mechanical ventilator or resuscitator bag. A simple manipulation of the endotracheal tube cuff helped to differentiate between increased impedance caused by endotracheal tube obstruction as opposed to increased respiratory system impedance beyond the tip of tube. In the second patient, in whom even a short interruption of ventilation was poorly tolerated, simultaneous rigid bronchoscopy (for removal of intratracheal masses) and ventilation via endotracheal tube were successfully performed.

An unusual case is reported of right atrial thrombus associated with cardiogenic shock. The role of two-dimensional echocardiography in detection of blood clots is highlighted.

A 74-year-old woman presented with a stroke. Transesophageal echocardiography showed evidence of a thrombus attached to the wall of the ascending aorta that was not detected by the transthoracic approach. The thrombus was no longer present after treatment with heparin with no recurrent embolic event. To our knowledge, this is the first report of a thrombus attached to the ascending aorta that was no longer present after treatment with heparin, was detected by transesophageal echocardiography, and was thought to be the source of cerebral embolic event.

Objective: The aim of the study was to investigate if evidence at transthoracic echocardiography (TTE) of left atrial (LA) thrombus and LA spontaneous echo-contrast (LA SEC), which are potential precursors of embolization, can be predicted by clinical and TTE variables in nonanticoagulated mitral valve stenosis (MS)., Design: Clinical (age, NYHA class, rhythm, previous embolization) and TTE variables were related to transesophageal echocardiography (TEE) evidence of LA thrombus and/or LA SEC., Setting: Nonanticoagulated MS was the setting., Patients: Fifty-nine patients had MS, and they were not receiving anticoagulant or antiplatelet therapy (24 in sinus rhythm and 35 in atrial fibrillation). Previous arterial embolization had occurred in 12 patients (20.3 percent)., Measurements: The following TTE variables were analyzed: mitral orifice area (pressure half-time method), mitral gradient (Bernouilli's equation), LA end-systolic area, and mitral regurgitation (color Doppler grading). LA thrombus and LA SEC were analyzed by monoplane TEE., Results: LA thrombus was found by TEE in 12 patients (20.3 percent). Of these 12, 11 (91.6 percent) were in atrial fibrillation. LA SEC was found by TTE in 2 patients (3.5 percent) and by TEE in 40 (67.8 percent) (p < 0.001). Previous embolization had occurred only in patients with LA SEC, of whom 5 had and 7 did not have LA thrombus. Patients with LA SEC, compared with those without LA SEC, were characterized by more frequent advanced NYHA class, atrial fibrillation, smaller mitral valve area, and larger LA size. By multivariate regression analysis, atrial fibrillation and LA end-systolic area were factors related to both LA thrombus and LA SEC, whereas mitral area was related only to LA SEC. However, whereas LA SEC was accurately predicted by the presence of atrial fibrillation (sensitivity: 87.5 percent; specificity: 100 percent) and a LA area > or = 30 cm2 (sensitivity: 72.5 percent; specificity: 89.5 percent), among patients with LA SEC no clinical or TTE variable accurately identified those with actual LA thrombus., Conclusions: TEE is not necessary in many patients with MS in order to recognize LA SEC. However, when actual LA thrombus detection is necessary for clinical decision making, TEE should be performed.

The association of left-sided pleural effusion and subcapsular splenic hematoma was reported in 1980. We describe a patient in whom a left-sided pleural effusion resulted from splenic vein thrombosis, a relationship not previously reported. Splenectomy was performed, demonstrating the spleen to be enlarged and hemorrhagic. The pleural effusion did not recur after splenectomy. The three effusions due to splenic hematomas reported previously cleared only after splenectomy, suggesting splenectomy may be necessary to prevent reaccumulation. We propose possible pathophysiologic mechanisms and recommend that splenic vein thrombosis be considered in the differential diagnosis of unexplained left-sided pleural effusions.

A 68-year-old man was admitted with congestive heart failure. He was treated with diuretics and digitalis; thereafter, the two-dimensional echocardiogram suggested a pedunculated and mobile left ventricular thrombus. He underwent surgical thrombectomy because of the high risk of systemic embolization. To our knowledge, this is the first case of dilated cardiomyopathy with a mobile left ventricular thrombus that was attached to ruptured false tendons.

It is extremely rare for a thrombus to form in a normal functioning left ventricle. We present two patients in whom this occurred without any plausable explanation. In both instances the patients presented with systemic emboli and had no heart disease or hypercoagulable state. The diagnosis was made by two-dimensional echocardiography and subsequently confirmed during surgery.

A case of idiopathic pulmonary hypertension is associated with portal venous thrombosis. The patient's chest roentgenogram revealed numerous nodular densities which at necropsy were found to have been caused by an exuberant fibroblastic reaction around small pulmonary arterioles. This is an example of the unusual association of idiopathic pulmonary hypertension and portal venous thrombosis, and to our knowledge, the first report of roentgenographically visible pulmonary nodules secondary to the pathologic alterations of idiopathic pulmonary hypertension.

Pulmonary veno-occlusive disease is a rare and usually fatal condition in which there is gradual obliteration of the pulmonary veins and venules. Without a lung biopsy the clinical diagnosis of this disease is difficult. If there is pulmonary hypertension with roentgenographic signs of pulmonary edema and of congestion in the absence of signs of increased left atrial pressure, the diagnosis must be considered. The morphologic picture of the lungs is characteristic. The small veins, and sometimes also the major veins, are narrowed or occluded by fibrous tissue, almost certainly on the basis of organized thrombi. Nodular areas of congestion, interstitial fibrosis, and pneumonitis are regularly present. A viral etiology has been suggested in a number of cases. If we may assume, however, that thrombosis of pulmonary veins is the initial event, the possibility has to be considered that this may be elicited by a virus in some patients and by toxic factors or by clotting disorders in others. Pulmonary veno-occlusive disease might then well be a syndrome rather than an etiologic entity.

Acquired tricuspid valve incompetence was caused by a mobile thrombus attached to a permanent right ventricular endocardial electrode wire. The rarity of this complication is noted and the importance of its consideration in the proper setting is stressed. Diagnosis was made by angiography and confirmed at surgery.

The clinical, echocardiographic, and pathologic features of a discrete calcified left ventricular thrombus are presented in a young adult man with a two-year history of transient visual field defects leading to eventual loss of vision in his left eye. M-mode and cross-sectional echocardiographic studies suggested a large mass extending across the left ventricle. These findings were confirmed at surgery when a calcified mass pathologically consistent with a calcified thrombus was removed. The pertinent literature on the echocardiographic diagnosis of left ventricular thrombi is reviewed.

A 55-year-old man who had been asymptomatic after replacement of his aortic valve with a Bjork-Shiley prosthesis, suddenly developed heart failure. The clinical suspicion of prosthetic malfunction was not only confirmed, but specified as being a stuck disc secondary to a large thrombus. Surgical removal of the clot resulted in restoration of normal function and return to the expected findings on echocardiogram. The value of echocardiography in such instances, as well as in routinely following-up patients with prostheses postoperatively, is emphasized.

Two infants with thrombosis of the abdominal aorta are discussed. In each case the presentation was indistinguishable from that in coarctation of the aorta, with heart failure and absent femoral pulses. Surgery in one infant successfully relieved the obstruction. The diagnosis may not be suspected from the history. Aggressive management is indicated.

A woman presented with acute left leg pain requiring urgent left femoral embolectomy. Echocardiography showed a large, pedunculated left ventricular mass, but no additional cardiac abnormality. Clinical evaluation including cardiac catheterization and open heart surgery demonstrated no cardiac pathologic findings. At surgery, a large thrombus was removed from the left ventricle. We suggest that all patients with arterial embolic disease have echocardiography, even if heart disease is not suspected.

Degos' disease (malignant atrophic papulosis) is a rare multisystemic disease with characteristic cutaneous lesions, abdominal symptoms and often rapidly fatal course. Our review of the reported intrathoracic involvement in the more than 60 reported cases of Degos' disease suggests that pleuritis and pericarditis are manifestations of the underlying pathophysiologic process. Seventeen of these reported cases were said to have intrathoracic lesions, which were, in most cases, incidental findings at autopsy. We present an illustrative report of a case in which chronic pleuritis and pericarditis were the major causes of morbidity in a 32-year-old woman with Degos' disease.

A patient with rheumatic heart disease, mitral stenosis, and mitral insufficiency is described. The thrombosed giant left atrium paralyzed the left vocal cord and completely obstructed the bronchi to the middle and lower lobes of the right lung. The giant left atrium mimicked a mediastinal tumor on the chest x-ray film.

This report describes three cases of massive mobile right heart thrombus and reviews the available literature to better define the pathophysiology, natural history and most appropriate therapy of the syndrome. The clinical presentation of most patients has been severe cardiopulmonary dysfunction and the diagnosis has been made by echocardiographic study. The most likely source of these cardiac thrombi is the large systemic veins. The associated mortality risk is very high. Therapy has, heretofore, been individualized. Embolectomy has been most favored, with a survival rate of 80 percent. The role of thrombolytic therapy remains to be delineated. Therapy should, however, be initiated rapidly because of the precipitous nature of the mortality risk.

A 54-year-old woman with the Noonan syndrome was admitted with congestive heart failure and a giant right atrial thrombus with atrial septal defect detected by two-dimensional echocardiography. The thrombus vanished on oral anticoagulant therapy with warfarin. The thrombus is considered to result from hemostasis in the right atrium due to congestive heart failure and to her specific skeletal characteristics. This report describes the first case of Noonan syndrome with right atrial thrombus.