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 17,070 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In patients in whom there is clinical suspicion of pulmonary thromboembolic disease, because of the risk of inadequate treatment, definitive radiologic evaluation should be carried out. Of the diagnostic procedures available, conventional pulmonary angiography has the greatest sensitivity and specificity in the detection of pulmonary embolism or other pulmonary vascular disease. Pulmonary angiography is indicated for patients with an indeterminate lung scan, for those with a high-probability lung scan in whom confirmation is necessary because of high risk for bleeding complications from anticoagulation, if embolism is massive and embolectomy is contemplated, if thrombolytic therapy or vena cava interruption is considered or if there is significant clinical evidence for an alternative diagnosis as well as for those with low-probability scans with a high degree of clinical suspicion and to complete a workup in patients with pulmonary hypertension. Refinements in the technique have simplified and expanded its application. The hemodynamic evaluation with right-heart catheterization before and after pulmonary angiography plays an important role in the choice of treatment of pulmonary embolism. In patients with multiple bilateral lobar or segmental perfusion defects, performance of right and left pulmonary arteriography in the right and left posterior oblique projections should be carried out. In the presence of additional pulmonary hypertension, the lung in which perfusion is most abnormal is selected first for angiography with a low bolus contrast dose. The angiographic criteria for the diagnosis of pulmonary embolism are intraluminal vascular filling defects or an abrupt cutoff of a large vessel. For selective opacification of lobar pulmonary branches occlusion pulmonary angiography is helpful. The mortality of pulmonary angiography in experienced centers is approximately 0.3%. Complications may include cardiac perforation in up to 1% and subendocardial injury in less than 0.2%. In patients with pulmonary embolism but no pulmonary hypertension, treatment with heparin for ten to 14 days should be followed by coumadin anticoagulation for at least three to six months. For obstruction of greater than or equal to 50% of the pulmonary vascular cross-sectional area and pulmonary hypertension thrombolytic therapy should be given and insertion of an inferior caval filter can be considered. In those with more than 75% pulmonary vascular obstruction and corresponding hemodynamic derangement, pulmonary artery embolectomy or thrombolytic therapy should be carried out.4
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PMID:Pulmonary angiography in the diagnosis of pulmonary embolism. 265 55

Arterial embolism is usually caused by cardiac disease, and atherosclerotic coronary vascular disease is the primary precursor. Other cardiac states, as well as several uncommon causes, are part of the etiologic spectrum. The earliest signs are pain, paresthesias, pallor, and pulselessness. Severe ischemia is indicated by paralysis, a late feature. Arterial embolism and acute thrombosis can be difficult to distinguish, and deep venous thrombosis may also be suspected in the differential diagnosis. To restore arterial flow, anticoagulation treatment with heparin (Lipo-Hepin, Liquaemin) is given and surgical embolectomy is performed. Heparin infusion is continued until the patient is ambulatory, and then warfarin sodium (Coumadin, Panwarfin) is given over the long term. Fibrinolysis has also been used to treat acute arterial occlusion. Complications of embolism must be carefully guarded against, and additional procedures are sometimes necessary.
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PMID:Management of arterial emboli. Gleanings from 20 years of experience. 357 97

Two patients with end-stage renal disease from diabetes mellitus on peritoneal dialysis for 2 or more years developed sterile peritonitis secondary to splenic infarcts with associated peripheral embolic phenomena. The dialysate had WBC counts > 200/microL, of which 70% or more were polymorphonuclear cells, and RBC counts of 60/microL or less, although transient hemoperitoneum occurred in both patients. Extensive atherosclerotic vascular disease as well as hematologic abnormalities were also present in both patients. One patient had polycythemia due to decreased plasma volume. The other patient had evidence of dysfibrinogenemia. The patients responded well to anticoagulation with warfarin. When the warfarin was discontinued, recurrent emboli occurred in both patients. Splenic infarct should be included in the differential diagnosis of diabetic patients with atherosclerotic disease who present with sterile peritonitis that does not respond to antibiotic therapy, especially if hemoperitoneum occurs even transiently. The diagnosis can be confirmed with CT scan of the abdomen. Warfarin therapy is effective in preventing recurrent embolic phenomena, but may need to be continued indefinitely.
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PMID:Splenic infarct presenting as sterile peritonitis with peripheral embolic phenomena. 810 24

Although lung transplantation is considered a definitive treatment of patients with advanced pulmonary vascular disease and pulmonary hypertension, advances in the success of the medical management of patients with pulmonary hypertension make it less clear as to when to refer a patient for transplantation. Coumadin anticoagulation is associated with improved survival in all patients, and calcium channel blockers therapy with improved survival in very select patients. Chronic prostacyclin represents a newer therapy that seems to have a dramatic impact on patients' functional class and survival. As improvements continue in the medical management in pulmonary hypertension, and in survival of patients undergoing lung transplantation, the guidelines for patient selection should be constantly evolving.
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PMID:Lung transplantation for pulmonary hypertension: patient selection and maintenance therapy while awaiting transplantation. 962 Apr 61

We studied the etiology of subcortical hemorrhage in 55 patients (30 males, 25 females), aged 19-83 years (mean 60 years). CT scan was made in all patients on admission, with the use of intravenous infusion of contrast agent in 35 patients. Cerebral angiography was performed in 37 patients and MRI was performed in 22 patients. Forty-one patients underwent surgery and the other fourteen patients were treated conservatively. The cause of bleeding had been discovered before surgery in 12 cases; 10 arteriovenous malformations and 2 brain tumors. They were discovered by meticulous neuroradiological investigations including cerebral angiography, MRI, dynamic MRI, MRA and enhancing CT. The cause of bleeding was newly discovered after surgery in 7 cases; all of amyloid angiopathy. It remained unknown in the other 22 surgical cases although hypertensive angiopathy was suspected in eleven of them. Among the 14 patients who received conservative therapy, hemorrhagic diathesis including the use of Warfarin and DIC was the cause of bleeding in four cases and the etiology remained unknown in other ten, although hypertensive angiopathy was suspected in eight of them. The 32 patients in whom the etiology remained unknown had been observed as long as 12-120 months (mean, 40 months) and although bleeding has occurred at different locations in two of these patients, there has been no recurrence of bleeding at the same location in any of them. In conclusion, surgery is not indicated to determine the etiology of subcortical hemorrhage when meticulous neuroradiological investigations fail to disclose any vascular or tumorous lesions.
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PMID:[Indications for surgery to determine the etiology of subcortical hemorrhage]. 988 45

There are no clear data regarding whether to use warfarin, aspirin, or no therapy in patients with left ventricular systolic dysfunction. Aspirin use is widespread in patients with vascular disease but it can decrease renal blood flow in low output states. Warfarin may be used in patients with advancing heart failure due to the perceived risk of in situ thromboembolism. However, we know that ejection fraction and symptom class do not always match and that the regulation of warfarin dosing is more difficult in worsening heart failure. Drug use must be individualized, based on knowledge of underlying heart failure etiology, functional class, drug side effects, and renal function. We await ongoing studies to elucidate the differential effects of these drugs on global outcome as well as on the mechanisms by which they achieve their results.
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PMID:Anticoagulation and heart failure. 1113 2

Intracerebral hemorrhage (ICH), which constitutes 10 to 15% of all strokes and affects approximately 65,000 people each year in the United States, has the highest mortality rate of all stroke subtypes. Hypertension, cerebral amyloid angiopathy, and anticoagulation underlie the majority of cases of ICH. Warfarin not only increases the risk but also increases the severity of ICH by causing hematoma expansion. With the advent of gradient-echo magnetic resonance imaging, patients with underlying cerebral amyloid angiopathy or hypertensive vasculopathy can be identified, and measures can be taken to prevent ICH. Initiating an antihypertensive regimen in a patient with nonlobar microbleeds suggestive of hypertensive vasculopathy, and withholding warfarin in patients with lobar microbleeds suggestive of cerebral amyloid angiopathy, are emerging prevention strategies. Although a treatment for cerebral amyloid angiopathy does not exist, agents targeting beta-amyloid metabolism and bioactivity are promising candidates. Strategies for preventing warfarin-associated hemorrhage include strict monitoring of anticoagulation levels and using agents such as direct thrombin inhibitors. The future of ICH management lies in therapies targeted at the pathophysiological steps in ICH. Potential treatments include glutamate receptor antagonists for preventing glutamate excitotoxicity, matrix metalloproteinase and thrombin inhibitors for preventing perihematomal edema, and recombinant activated factor VII for preventing hematomal expansion.
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PMID:Treatment and prevention of primary intracerebral hemorrhage. 1634

Patients with aortic stenosis (AS) have an increased prevalence of coronary risk factors, coronary artery disease, and other atherosclerotic vascular disease and an increased incidence of coronary events and death. Statins may reduce the progression of AS. Angina pectoris, syncope or near syncope, and heart failure are the three classic manifestations of severe AS. Prolonged duration and late peaking of an aortic systolic ejection murmur best differentiate severe AS from mild AS on physical examination. Doppler echocardiography is used to diagnose the presence and severity of AS. Once symptoms develop, aortic valve replacement (AVR) should be performed in patients with severe or moderate AS. Warfarin should be administered indefinitely after AVR in patients with a mechanical aortic valve and in patients with a bioprosthetic aortic valve who have either atrial fibrillation, prior thromboembolism, left ventricular systolic dysfunction, or a hypercoagulable condition. Patients with a bioprosthetic aortic valve without any of these four risk factors should be treated with aspirin 75-100 mg daily.
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PMID:Aortic stenosis. 1802 9

Cholesterol crystal embolization (CCE) can result in end-organ ischemia. Retrospective review of clinicopathologic data. The first patient was anticoagulated with coumadin for chronic atrial fibrillation and presented subacutely with a solid mass. The second patient suffered from coronary artery disease post-angioplasty/stenting and presented with acute pancreatitis and pancreatic cystification. CCE should be considered in patients with significant vascular disease, arrhythmias or vascular manipulation who present with a pancreatic mass.
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PMID:Cholesterol crystal embolization presenting as either solid or cystic pancreatic lesion. 2097 33

Internal jugular vein thrombosis (IJVT) is an elusive vascular disease that is rarely seen, with potentially lethal complications such as sepsis and pulmonary embolism. Spontaneous IJVT is considered when no apparent predisposing cause of thrombosis is present. A previously healthy, 31-year-old woman presented to the university-based emergency department because of painless swelling in the right anterior side of her neck. Physical examination revealed a painless, soft and immobile mass in the right anterior side of her neck beneath the sternocleidomastoid muscle, without hyperemia or local heat. On ultrasonographic examination, a hyperechogenic mass was visualized around the thoracic entrance of the right internal jugular vein, which was suggestive of a thrombus. The patient was administered intravenous antibiotic and low-molecular-weight heparin followed by oral coumadin as anticoagulant therapy. Her complaints were relieved within 5 days. She was completely well after 6 months. Venous thrombosis generally results from impaired blood flow locally or systemically that leads to activation of coagulation. Primary care physicians should sustain a high index of suspicion in patients who present with undiagnosed swelling in the neck, or other signs and symptoms attributed to IJVT.
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PMID:Spontaneous internal jugular vein thrombosis: a case report. 2118 18


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