Diagnosis Of Paradoxical Embolism Research Articles

Transcranial Doppler ultrasound: Clinical applications from neurological to cardiological setting.

Transcranial Doppler (TCD) ultrasonography is a rapid, noninvasive, real-time, and low-cost imaging technique. It is performed with a low-frequency (2 MHz) probe in order to evaluate the cerebral blood flow (CBF) and its pathological alterations, through specific acoustic windows. In the recent years, TCD use has been expanded across many clinical settings. Actually, the most widespread indication for TCD exam is represented by the diagnosis of paradoxical embolism, due to patent foramen ovale, in young patients with cryptogenic stroke. In addition, TCD has also found useful applications in neurological care setting, including the following: cerebral vasospasm following acute subarachnoid hemorrhage, brain trauma, cerebrovascular atherosclerosis, and evaluation of CBF and cerebral autoregulation after an ischemic stroke event. The present review aimed to describe the most recent evidences of TCD utilization from neurological to cardiological setting.

Clot Through the Heart

We present the case of a 67-year-old man with concomitant stroke and pulmonary embolism 1 day after radiofrequency catheter ablation for refractory atrial tachycardia. A chest computed tomographic angiogram revealed "thrombus-in-transit" across a patent foramen ovale, confirming the diagnosis of paradoxical embolism. Paradoxical embolism is a rare definitive diagnosis. Our case is a key demonstration of the even rarer instance where such a diagnosis is confirmed at multidetector computed tomography.

Paradoxical embolism: role of imaging in diagnosis and treatment planning.

Paradoxical embolism (PDE) is an uncommon cause of acute arterial occlusion that may have catastrophic sequelae. The possibility of its presence should be considered in all patients with an arterial embolus in the absence of a cardiac or proximal arterial source. Despite advancements in radiologic imaging technology, the use of various complementary modalities is usually necessary to exclude other possibilities from the differential diagnosis and achieve an accurate imaging-based diagnosis of PDE. In current practice, the imaging workup of a patient with symptoms of PDE usually starts with computed tomography (CT) and magnetic resonance (MR) imaging to identify the cause of the symptoms and any thromboembolic complications in target organs (eg, stroke, peripheral arterial occlusion, or visceral organ ischemia). Additional imaging studies with modalities such as peripheral venous Doppler ultrasonography (US), transcranial Doppler US, echocardiography, and CT or MR imaging are required to detect peripheral and central sources of embolism, identify cardiac and/or extracardiac shunts, and determine whether arterial disease is present. To guide radiologists in selecting the optimal modalities for use in various diagnostic settings, the article provides detailed information about the imaging of PDE, with numerous radiologic and pathologic images illustrating the wide variety of features that may accompany and contribute to the pathologic process. The roles of CT and MR imaging in the diagnosis and exclusion of PDE are described, and the use of imaging for planning surgical treatment and interventional procedures is discussed.

Thrombus in Transit within a Patent Foramen Ovale: Gone with the Cough!

Pulmonary embolism and concomitant right atrial thrombus entrapped in a patent foramen ovale (PFO) is a rare, unusual finding in echocardiography. The diagnosis of paradoxical embolism is usually presumptive when PFO is detected by echocardiography. We herein reported a case of a 53-year-old patient presenting with pulmonary embolism in which a thrombusin-transit through a PFO was found and disappeared during transesophageal echocardiography.

Caught in the act: entrapped embolus through a patent foramen ovale

A patent foramen ovale (PFO) is detected frequently by transesophageal echocardiography. The diagnosis of paradoxical embolism is usually presumptive when arterial emboli occur in the appropriate clinical setting. Presumably, paradoxical embolism of small thrombi arise in the venous system and pass through the PFO during a transient right-to-left shunt; however, cases demonstrating a thrombus traversing the PFO are relatively few.

Intraoperative identification of both a paradoxical embolism and its probable etiologic site

We report a case of upper extremity arterial ischemia in a 41-year-old man. Intraoperative transesophageal echocardiography identified a paradoxical embolization that traversed a patent foramen ovale as the probable etiology. The diagnosis of paradoxical embolism with intraoperative identification of the etiologic site of the deep venous thrombosis is a rare event. This case presents the use of transesophageal echocardiography beyond its monitoring function in helping diagnose the cause of arterial ischemia.

Thrombus-in-transit causing paradoxical embolism in cerebral and coronary arterial circulation

We describe the case of an elderly man who was admitted to our hospital with the diagnosis of an acute anterior myocardial infarction, together with an acute bioccipital ischaemic stroke. Coronary angiography revealed embolization of the distal left anterior descendens and the first septal branch. The definite diagnosis of paradoxical embolism was made by means of a transoesophageal echocardiography which demonstrated a large snake-like floating thrombus crossing a patent foramen ovale. This diagnosis was also supported by the presence of deep venous thrombosis as a probable origin of the intra-atrial thrombus and the secondary pulmonary embolism which contributed to the elevated right heart pressure.The patient was treated with full-dose heparin and subsequently oral anticoagulation. After discharge, follow-up by transoesophageal echocardiography was organized and once the intracardiac thrombus had disappeared, elective transcatheter closure of the patent foramen ovale was performed.

Thrombus-in-transit causing paradoxical embolism in cerebral and coronary arterial circulation.

We describe the case of an elderly man who was admitted to our hospital with the diagnosis of an acute anterior myocardial infarction, together with an acute bioccipital ischaemic stroke. Coronary angiography revealed embolization of the distal left anterior descendens and the first septal branch. The definite diagnosis of paradoxical embolism was made by means of a transoesophageal echocardiography which demonstrated a large snake-like floating thrombus crossing a patent foramen ovale. This diagnosis was also supported by the presence of deep venous thrombosis as a probable origin of the intra-atrial thrombus and the secondary pulmonary embolism which contributed to the elevated right heart pressure.The patient was treated with full-dose heparin and subsequently oral anticoagulation. After discharge, follow-up by transoesophageal echocardiography was organized and once the intracardiac thrombus had disappeared, elective transcatheter closure of the patent foramen ovale was performed.

Surgical Closure of Patent Foramen Ovale for Stroke Prevention: Vancouver General Hospital Experience

95 Background and Purpose Patent foramen ovale (PFO) is implicated as a potential cause of stroke, particularly in young patients with otherwise cryptogenic events. The natural history, risk of stroke recurrence and optimal secondary stroke prevention remains uncertain. Therapeutic options include long-term antiplatelet therapy, anti-coagulation therapy, and PFO closure by surgery or device. We report the results of 53 patients treated with surgical closure. Methods and Materials We have followed 53 consecutive surgically treated patients (23 men and 30 female). All patients were evaluated by a stroke neurologist, a cardiologist with expertise in adult congenital disease and a cardiovascular surgeon. Patients who met the following criteria were included: 1) embolic TIA or stroke, 2) PFO or PFO and atrial septal aneurysm (ASA), 3) investigations included cerebral angiography, transesophageal echocardiography, and hypercoagulable studies, 4) presumptive clinical diagnosis of paradoxical embolism with no other etiology detected. Follow up was obtained by clinic visit and standardized telephone questionnaire. Results Prior to surgery 27 patients had stroke and 26 had TIAs; 12 had multiple cerebrovascular events. The mean age at symptom onset was 41.8 ± 9.3 yrs (range 19 to 59). 22 patients had an isolated PFO and 31 had both a PFO and an ASA. Average PFO size measured at surgery was 8.8 ± 7.7 mm. 40 were treated with primary closure, 13 with suture and patch closure. Average post-surgical hospital stay was 4 days. There was no surgical mortality or major morbidity. Minor perioperative morbidity occurred in 13 patients. Average follow up postsurgery was 22.2 ± 17.4 months (range 0.7 to 90.8 months). There were no recurrent strokes and 1 recurrent TIA. Conclusions Surgical closure of PFO can be safely performed with low morbidity and mortality. In this group of carefully selected patients, there have been no recurrent strokes. Further studies are necessary to define high-risk patients for recurrent stroke who may benefit from surgical closure.

Surgical Closure of Patent Foramen Ovale for Stroke Prevention: Vancouver General Hospital Experience

95 Background and Purpose Patent foramen ovale (PFO) is implicated as a potential cause of stroke, particularly in young patients with otherwise cryptogenic events. The natural history, risk of stroke recurrence and optimal secondary stroke prevention remains uncertain. Therapeutic options include long-term antiplatelet therapy, anti-coagulation therapy, and PFO closure by surgery or device. We report the results of 53 patients treated with surgical closure. Methods and Materials We have followed 53 consecutive surgically treated patients (23 men and 30 female). All patients were evaluated by a stroke neurologist, a cardiologist with expertise in adult congenital disease and a cardiovascular surgeon. Patients who met the following criteria were included: 1) embolic TIA or stroke, 2) PFO or PFO and atrial septal aneurysm (ASA), 3) investigations included cerebral angiography, transesophageal echocardiography, and hypercoagulable studies, 4) presumptive clinical diagnosis of paradoxical embolism with no other etiology detected. Follow up was obtained by clinic visit and standardized telephone questionnaire. Results Prior to surgery 27 patients had stroke and 26 had TIAs; 12 had multiple cerebrovascular events. The mean age at symptom onset was 41.8 ± 9.3 yrs (range 19 to 59). 22 patients had an isolated PFO and 31 had both a PFO and an ASA. Average PFO size measured at surgery was 8.8 ± 7.7 mm. 40 were treated with primary closure, 13 with suture and patch closure. Average post-surgical hospital stay was 4 days. There was no surgical mortality or major morbidity. Minor perioperative morbidity occurred in 13 patients. Average follow up postsurgery was 22.2 ± 17.4 months (range 0.7 to 90.8 months). There were no recurrent strokes and 1 recurrent TIA. Conclusions Surgical closure of PFO can be safely performed with low morbidity and mortality. In this group of carefully selected patients, there have been no recurrent strokes. Further studies are necessary to define high-risk patients for recurrent stroke who may benefit from surgical closure.

Trapped Venous Embolus in a Patent Foramen ovale Causing Recurrent Paradoxical Embolism

The combination of deep venous thrombosis, patent foramen ovale and arterial emboli suggests the diagnosis of paradoxical embolism. In these cases, only very rarely, a causal relationship between the venous thrombus and the patent foramen can be established. An instructive case of trapped venous embolism within the foramen ovale is described proving a causal relationship between arterial embolism and its venous origin.

Transoesophageal echocardiography in the diagnosis of paradoxical embolism

Two patients with systemic embolism were studied with transoesophageal contrast echocardiography which demonstrated its probable paradoxical nature. In both cases paradoxical embolism was associated with pulmonary embolism. Precordial contrast echocardiography demonstrated a right-to-left shunt in one patient but was unable to demonstrate a shunt in the second. Transoesophageal echocardiography suggested that the shunt was across a patent foramen ovale in both cases and revealed large thrombi in the pulmonary arteries in one. When precordial contrast echocardiography reveals a right-to-left shunt or when it is technically inadequate in patients suspected of having one, transoesophageal contrast echocardiography can demonstrate the nature of the shunt and is an alternative to cardiac catheterisation techniques. In addition, it can reveal large thrombi in the pulmonary arteries.

Stroke due to paradoxical embolism

We present a case of stroke in a young girl, preceded by a deep vein thrombosis and pulmonary embolism, both clinically asymptomatic, and accompanied by upper limb acute ischemia. Diagnosis of paradoxical embolism through a patent foramen ovale was made on clinical grounds and with contrast echocardiography. We discuss the main points leading to diagnosis, stressing the importance of contrast echocardiography. We also suggest that paradoxical embolism could be a more frequent cause of stroke than usually suspected.

Diagnosis of paradoxical embolism with contrast echocardiography

Contrast echocardiography is useful in detecting rightto-left intracardiac shunting. Clinical events that cause reversal of the normal interatrial pressure gradient can lead to transient right-to-left shunting across a patent foramen ovale, creating conditions conducive to paradoxical embolism. We present a patient with pulmonary embolism and associated systemic embolization. During the acute stage, contrast echocardiography demonstrated right-to-left shunting at the atria1 level throughout the respiratory cycle. After the patient’s clinical recovery, contrast echocardiography demonstrated atrial right-toleft shunting only upon release of Valsalva’s maneuver. A 60-year-old woman was transferred to Moffitt Hospital, University of California, San Francisco, because of left arm pain, a pulseless left upper extremity, and increasing dyspnea. The day before her admission, the patient had been admitted to another hospital with a complaint of weakness over a 3-week period and acute right arm pain. Physical examination revealed a pulseless right upper extremity and angiography revealed an occlusion of the right axillary artery. A Fogarty embolectomy was successful in removing a pathologically confirmed thrombus. The morning of the transfer, the patient complained of acute shortness of breath and left arm pain. Arterial blood gases on 2 L of nasal oxygen revealed a PO, of 30 mm Hg, PcoZ of 29 mm Hg, and pH of 7.54. The patient was transferred to Moffitt Hospital. There was no history of pleuritic chest pain, hemoptysis, calf tenderness, immobilization, fever, chills, or sweats. The patient did not smoke. She had undergone varicose vein stripping and a hysterectomy several years previously, but was otherwise healthy and active. Physical examination in the emergency department revealed an alert, anxious woman in moderate respiratory distress. Her temperature was 38°C and pulse 110 bpm and regular. Respirations were 3O/min; blood pressure was 110/70 mm Hg in the right arm and unobtainable in the left arm, and paradoxical pulse was 3 mm Hg. The lungs were clear without rubs or assymetrlc breath sounds. Jugular venous pressure was 12 cm H,O with A wave accentuation. The carotid pulse was of normal upstroke and contour. There was a l+ left parasternal precordial lift, and the point of maximal impulse was in the midclavicular line. S, was normal; S, was