warfarin and Aortic-Diseases

To review information regarding etiology, pathophysiology, and treatment options for aortic thrombotic disease in dogs.. Diseases resulting in hypercoagulable states can cause thrombus formation in the distal aorta, and account for the majority of cases of aortic thrombosis (ATh) in dogs, although a substantial number of cases have no identifiable underlying cause. Aortic thromboembolism (ATE) also occurs but appears to be much less frequently documented.. The presentation of ATh and ATE in dogs is more varied compared to cats. Diagnosis can be challenging due to nonspecific clinical signs. Definitive diagnosis involves direct visualization of the thrombus, which is often obtained via ultrasound; however, other imaging modalities such as computed tomography scans can be utilized.. The optimal treatment for aortic thrombotic disease in dogs has yet to be determined. Although not always possible, treatment of concurrent diseases that may promote thrombosis is an important aspect of thrombus resolution. A recent retrospective study reported positive results with long-term warfarin therapy; however, other studies have not reported similar results. Unfractionated or low-molecular weight heparins are additional anticoagulants that have been utilized. Platelet inhibitor therapy should also be considered in combination with anticoagulant therapy.. Survival for dogs with ATh or ATE is reported to be between 50% and 60%. Dogs that present with chronic clinical signs appear to have a better prognosis than those who are acutely affected or those who are severely affected.

Topics: Animals; Anticoagulants; Aortic Diseases; Dog Diseases; Dogs; Heparin, Low-Molecular-Weight; Thrombosis; Warfarin

Atrial fibrillation and severe carotid artery stenosis are the most common causes of stroke. However, several patients recognize unusual cause for their cerebral ischemia. At the beginning of the last decade after the introduction of transesophageal echocardiography (TEE) and other imaging techniques, atheromatosis of the thoracic aorta has been recognized as an important source of stroke or systemic embolism. Formerly in the pre-TEE era, this entity was included into cryptogenic strokes. Notably, aortic atheromas are found in about one quarter of patients presenting with embolic events and their grading by TEE correlates with the risk of future embolism, especially if mobile lesions or superimposed thrombi are present. Unfortunately, the diagnosis of aortic atheroma is mostly established when an embolic event has already occurred. The aim of this paper is to review the current evidence for aortic atheroma as an important independent risk factor for stroke, and to discuss the potential therapeutic options. Unfortunately, randomized studies addressing the treatment of patients with severe aortic atheroma are not yet completed. Furthermore, although warfarin and statins look promising in several retrospective series, their results are by most controversial so far. In conclusion, although the diagnostic criteria and the negative prognostic significance of aortic atheroma are almost defined, its therapeutic options are far to be clear. Therefore, clinical trials addressing this relevant pathologic condition are urgently needed.

Topics: Anticoagulants; Aorta, Thoracic; Aortic Diseases; Aspirin; Atherosclerosis; Clopidogrel; Controlled Clinical Trials as Topic; Echocardiography, Transesophageal; Fibrinolytic Agents; Follow-Up Studies; Humans; Hypolipidemic Agents; Meta-Analysis as Topic; Odds Ratio; Platelet Aggregation Inhibitors; Prognosis; Recurrence; Risk Factors; Stroke; Ticlopidine; Time Factors; Warfarin

Aortic atheromatous disease is associated with stroke in both the ambulatory and perioperative setting. In addition to atheromatous deposits, a reduction in the compliance of the aorta takes place as elastin fibers are replaced by collagen fibers. Both of these distinct processes, termed atherosclerosis, can easily be measured using transesophageal echocardiography during cardiac surgery. A review of the literature demonstrates many studies supporting the benefit of transesophageal echocardiography examination of the aorta for reducing stroke following cardiac surgery, through modification of surgical techniques. There have also been attempts by surgeons to remove atheromatous lesions from the aorta during cardiac surgery. Unfortunately, these procedures currently have a high perioperative mortality. Finally, medical therapy such as warfarin or statins may help reduce the incidence of stroke following heart surgery.

Topics: Anticoagulants; Aorta; Aortic Diseases; Atherosclerosis; Cardiac Surgical Procedures; Clinical Trials as Topic; Endarterectomy; Humans; Risk Factors; Stroke; Ultrasonography; Warfarin

Cardiac causes of stroke account for approximately 20% of strokes occurring in the United States. Transthoracic echocardiography (TTE) remains the cornerstone of non-invasive cardiac imaging, but transesophageal echocardiography (TEE) is superior for identifying potential cardiac sources of emboli, including left atrial thrombi, valvular vegetations, thoracic aortic plaque, patent foramen ovale, and spontaneous left atrial echocardiographic contrast. The diagnostic yield of TEE for potential cardiac causes of thromboembolism exceeds 50%. The impact of TEE on the clinical management of this group, however, remains undefined for most TEE-specific diagnoses. Thus, routine use of TEE in these patients has been questioned. The diagnostic yield is highest if the clinical history/physical examination suggests a cardiac source. However, the clinical scenario often dictates patient management, and TEE data are used to "validate" the clinical impression. Data from large, prospective, randomized (aspirin/warfarin) studies, in which TEE data are obtained from patients with suspected cardiac thromboembolism, are needed. If specific TEE diagnoses can be identified in which defined therapies are beneficial, "source of embolism" will continue to be the most common indication for TEE referral. In this paradigm, TEE (without initial TTE) will probably become a more direct diagnostic pathway. However, if these studies demonstrate that all patients with suspected cardiac source benefit from one (or no) therapy, independent of TEE data, referrals for TEE will decline. Results of ongoing randomized trials to evaluate the efficacy of TEE in patients with cryptogenic stroke or transient ischemic attack are awaited.

Topics: Anticoagulants; Aorta, Thoracic; Aortic Diseases; Arteriosclerosis; Aspirin; Cerebrovascular Disorders; Echocardiography, Transesophageal; Heart Atria; Heart Diseases; Heart Septal Defects, Atrial; Heart Valve Diseases; Humans; Intracranial Embolism and Thrombosis; Ischemic Attack, Transient; Medical History Taking; Physical Examination; Platelet Aggregation Inhibitors; Prospective Studies; Randomized Controlled Trials as Topic; Referral and Consultation; Reproducibility of Results; Thrombosis; Treatment Outcome; Warfarin

Severe atherosclerosis in the aortic arch is associated with a high risk of recurrent vascular events, but the optimal antithrombotic strategy is unclear.. This prospective randomized controlled, open-labeled trial, with blinded end point evaluation (PROBE design) tested superiority of aspirin 75 to 150 mg/d plus clopidogrel 75 mg/d (A+C) over warfarin therapy (international normalized ratio 2-3) in patients with ischemic stroke, transient ischemic attack, or peripheral embolism with plaque in the thoracic aorta>4 mm and no other identified embolic source. The primary end point included cerebral infarction, myocardial infarction, peripheral embolism, vascular death, or intracranial hemorrhage. Follow-up visits occurred at 1 month and then every 4 months post randomization.. The trial was stopped after 349 patients were randomized during a period of 8 years and 3 months. After a median follow-up of 3.4 years, the primary end point occurred in 7.6% (13/172) and 11.3% (20/177) of patients on A+C and on warfarin, respectively (log-rank, P=0.2). The adjusted hazard ratio was 0.76 (95% confidence interval, 0.36-1.61; P=0.5). Major hemorrhages including intracranial hemorrhages occurred in 4 and 6 patients in the A+C and warfarin groups, respectively. Vascular deaths occurred in 0 patients in A+C arm compared with 6 (3.4%) patients in the warfarin arm (log-rank, P=0.013). Time in therapeutic range (67% of the time for international normalized ratio 2-3) analysis by tertiles showed no significant differences across groups.. Because of lack of power, this trial was inconclusive and results should be taken as hypothesis generating.. http://www.clinicaltrials.gov. Unique identifier: NCT00235248.

Topics: Aged; Aged, 80 and over; Anticoagulants; Aorta, Thoracic; Aortic Diseases; Aspirin; Brain Ischemia; Clopidogrel; Drug Therapy, Combination; Embolism; Female; Humans; Male; Middle Aged; Plaque, Atherosclerotic; Platelet Aggregation Inhibitors; Prospective Studies; Single-Blind Method; Stroke; Ticlopidine; Treatment Outcome; Warfarin

Aortic arch plaques are a risk factor for ischemic stroke. Although the stroke mechanism is conceivably thromboembolic, no randomized studies have evaluated the efficacy of antithrombotic therapies in preventing recurrent events.. The relationship between arch plaques and recurrent events was studied in 516 patients with ischemic stroke who were double-blindly randomized to treatment with warfarin or aspirin as part of the Patent Foramen Ovale in Cryptogenic Stroke Study (PICSS), based on the Warfarin-Aspirin Recurrent Stroke Study (WARSS). Plaque thickness and morphology were evaluated by transesophageal echocardiography. End points were recurrent ischemic stroke or death over a 2-year follow-up. Large plaques (> or =4 mm) were present in 19.6% of patients; large complex plaques (those with ulcerations or mobile components) were seen in 8.5%. During follow-up, large plaques were associated with a significantly increased risk of events (adjusted hazard ratio [HR], 2.12; 95% confidence interval [CI], 1.04 to 4.32), especially those with complex morphology (HR, 2.55; 95 CI, 1.10 to 5.89). The risk was highest among cryptogenic stroke patients, both for large plaques (HR, 6.42; 95% CI, 1.62 to 25.46) and large complex plaques (HR, 9.50; 95% CI, 1.92 to 47.10). Event rates were similar in the warfarin and aspirin groups in the overall study population (16.4% versus 15.8%; P=0.43).. In patients with stroke, especially cryptogenic stroke, large aortic plaques remain associated with an increased risk of recurrent stroke and death at 2 years despite treatment with warfarin or aspirin. Complex plaque morphology confers a slight additional increase in risk.

Topics: Adult; Aged; Aged, 80 and over; Aorta, Thoracic; Aortic Diseases; Aspirin; Atherosclerosis; Death; Double-Blind Method; Female; Fibrinolytic Agents; Humans; Male; Middle Aged; Risk; Secondary Prevention; Stroke; Treatment Outcome; Warfarin

Patients with atrial fibrillation and with documented aortic plaque who were assigned to adjusted-dose warfarin therapy (international normalized ratio 2.0 to 3.0) had an annual rate of cholesterol embolization of 0.7% (95% confidence interval [CI] 0.1% to 5.3%/patient-year). Warfarin-assigned patients with plaque had a lower rate of embolic events (5.9%/year; 95% CI 3.0 to 12) than those on combination low-dose warfarin (international normalized ratio <1.5) plus aspirin (17.3%/year; 95% CI 11 to 27; p = 0.01).

Topics: Aged; Anticoagulants; Aorta, Thoracic; Aortic Diseases; Arteriosclerosis; Aspirin; Atrial Fibrillation; Drug Therapy, Combination; Echocardiography, Transesophageal; Female; Fibrinolytic Agents; Follow-Up Studies; Humans; Safety; Thromboembolism; Treatment Outcome; Warfarin

Transesophageal echocardiography (TEE) visualizes potential sources of embolism in patients with atrial fibrillation, but the clinical significance of TEE findings has not been prospectively established.. To define TEE predictors of stroke in patients with atrial fibrillation and to examine response to antithrombotic therapy.. Prospective correlation of TEE findings at study entry with subsequent ischemic stroke during 1.1-year mean follow-up of participants in a randomized trial.. 18 echocardiography laboratories.. 382 patients with atrial fibrillation at high risk for thromboembolism.. Adjusted-dose warfarin (international normalized ratio, 2 to 3) or low-intensity warfarin (international normalized ratio, 1.2 to 1.5) plus aspirin (325 mg/d).. Size of left atrium and left atrial appendage, flow velocity, spontaneous echocardiographic contrast, thrombus, and plaque on the aortic arch.. 23 ischemic strokes occurred. In patients with dense spontaneous echocardiographic contrast (20%), the rate of stroke was 18.2% per year with combination therapy (2.9 times the rate in patients without this finding; P = 0.06) and 4.5% per year with adjusted-dose warfarin (P = 0.09 for rate reduction). Appendage thrombus, detected in 10% of patients, was associated with dense spontaneous echocardiographic contrast (P < 0.001), was seen more frequently after 2 weeks of combination therapy (15%) than after 2 weeks of adjusted-dose warfarin (4%) (P = 0.004), and tripled the overall rate of stroke (P = 0.04). Patients with complex aortic plaque (35%) had a fourfold increased rate of stroke compared with plaque-free patients (P = 0.005); adjusted-dose warfarin decreased risk by 75% (P = 0.02). Dense spontaneous echocardiographic contrast and complex aortic plaque were independent of each other as predictors of thromboembolism.. In high-risk patients with atrial fibrillation, subsequent rates of thromboembolism are correlated with dense spontaneous echocardiographic contrast, thrombus of the atrial appendage, and aortic plaque. Adjusted-dose warfarin reduces the rate of stroke among patients with dense contrast and complex plaque. In patients with atrial fibrillation, the pathogenesis of stroke is multifactorial, and warfarin seems effective for the diverse mechanisms.

Topics: Aged; Anticoagulants; Aortic Diseases; Arteriosclerosis; Aspirin; Atrial Fibrillation; Drug Therapy, Combination; Echocardiography, Transesophageal; Female; Follow-Up Studies; Heart Atria; Heart Diseases; Humans; Male; Platelet Aggregation Inhibitors; Prospective Studies; Risk Factors; Thromboembolism; Warfarin

Cisplatin is one of the key drugs that is frequently used for treating various types of malignancies. Although renal and digestive toxicities are well-known cisplatin-related toxicities, attention should also be paid to acute aortic thrombosis, a relatively rare but potentially fatal disorder caused by cisplatin. Additionally, D-dimer is mainly measured to detect venous thromboembolism or disseminated intravascular coagulation, whereas its usefulness for detecting aortic thrombosis remains unclear. Here, we report a case of squamous cell lung cancer treated with cisplatin-based chemotherapy, wherein acute aortic thrombosis was diagnosed based on elevated D-dimer levels.. A 65-year-old man with stage IV squamous cell lung cancer presented with elevated D-dimer levels during treatment with second-line chemotherapy with cisplatin and S-1. Contrast-enhanced computed tomography (CT) revealed an intramural thrombus, which had not been previously identified, extending from the abdominal aorta to the common iliac artery.. We diagnosed the patient as having acute aortic thrombosis caused by cisplatin.. The patient received intravenous administration of unfractionated heparin for 9 days followed by oral warfarin.. One month after initiating treatment, the patient's D-dimer levels decreased to the normal range, and contrast-enhanced CT revealed that the thrombi had nearly completely disappeared without any sequelae or organ damage.. Our findings revealed that cisplatin can cause acute aortic thrombosis and that regular measurements of D-dimer levels before and during chemotherapy may contribute to the early detection of acute aortic thrombosis.

Topics: Administration, Intravenous; Administration, Oral; Aged; Anticoagulants; Antineoplastic Agents; Aortic Diseases; Carcinoma, Squamous Cell; Cisplatin; Fibrin Fibrinogen Degradation Products; Heparin; Humans; Lung Neoplasms; Male; Neoplasm Staging; Thrombosis; Tomography, X-Ray Computed; Treatment Outcome; Warfarin

Topics: Adult; Anticoagulants; Aorta, Thoracic; Aortic Diseases; Computed Tomography Angiography; Echocardiography, Transesophageal; Female; Humans; Infarction, Middle Cerebral Artery; Magnetic Resonance Imaging; Thrombosis; Warfarin

Topics: Aged, 80 and over; Anticoagulants; Aortic Diseases; Aortic Valve Stenosis; Bicuspid Aortic Valve Disease; Humans; Male; Sinus of Valsalva; Thrombosis; Transcatheter Aortic Valve Replacement; Treatment Outcome; Warfarin

The aim of this study was the analysis of the risk associated with direct oral anticoagulants (DOACs) in patients undergoing non-elective operations on the proximal aorta due to aortic disease.. Data from the department's register of cardiac surgery was analysed retrospectively with emphasis on operative mortality. 135 non-elective operations for proximal aortic disease (October 2016 to 2018) were identified, of which 19 died during the first 90 days. DOAC use was the top-ranked risk factor in the univariate analysis with a HR of 9.6 (3.1 to 29), p=0.00007. Using a Cox proportional hazards model including the most relevant risk factors, the risk associated with DOAC use remained significant with a HR of 6.1 (1.4 to 26.3), p=0.015. We did not find increased risk associated with warfarin use.. In patients undergoing non-elective operations on the proximal aorta due to aortic disease, the use of DOAC is associated with increased operative mortality.

Topics: Administration, Oral; Aged; Aged, 80 and over; Anticoagulants; Aortic Diseases; Factor Xa Inhibitors; Female; Humans; Male; Middle Aged; Postoperative Hemorrhage; Registries; Retrospective Studies; Risk Assessment; Risk Factors; Time Factors; Treatment Outcome; Vascular Surgical Procedures; Warfarin

A 54-year-old man underwent decompressive craniectomy following a stroke. He further developed right lower limb ischaemia, and CT aortography revealed extensive aortic atherosclerotic disease. Urgent embolectomy prevented him from having a major amputation. He subsequently developed pulmonary embolism. This was initially treated with heparin followed by warfarin apart from antiplatelets and statin. A follow-up aortography at 3 months interval showed near complete resolution of atheromatous disease of the aorta. This report raises the possibility that apart from antiplatelets and lipid-lowering agents, anticoagulation may be responsible for resolution of such an extensive atheromatous disease and whether this can be considered as part of regular treatment.

Topics: Anticoagulants; Aorta, Thoracic; Aortic Diseases; Brain; Carotid Stenosis; Drug Therapy, Combination; Heparin; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Infarction, Middle Cerebral Artery; Male; Middle Aged; Plaque, Atherosclerotic; Pulmonary Embolism; Simvastatin; Stroke; Warfarin

A 65-year-old man was diagnosed with advanced non-small, non-squamous lung cancer. He was treated with chemotherapy containing bevacizumab as well as cisplatin and pemetrexed. After 2 courses of treatment, computed tomography revealed that his abdominal aortic artery was almost occluded by a thrombus; however, he had no ischemic symptoms. Heparin infusion and warfarin reduced the size of the arterial thrombus and the patient was subsequently treated with chemotherapy without bevacizumab. No thrombotic events occurred during the subsequent treatment. We later noticed a small organized abdominal arterial clot and calcification on a computed tomography scan taken before bevacizumab treatment. Atherosclerotic changes should be evaluated before the administration of bevacizumab.

Topics: Aged; Antineoplastic Combined Chemotherapy Protocols; Aortic Diseases; Bevacizumab; Carcinoma, Non-Small-Cell Lung; Cisplatin; Heparin; Humans; Lung Neoplasms; Male; Pemetrexed; Thrombosis; Treatment Outcome; Warfarin

Topics: Anticoagulants; Aortic Diseases; Aspirin; Clopidogrel; Female; Humans; Male; Platelet Aggregation Inhibitors; Stroke; Ticlopidine; Warfarin

The development of aortic thrombosis without the presence of atheroscrelosis, dissection, or aneurysms is rare. A cancer-related hypercoagulable state is a well-known risk factor for venous thrombosis, however, atrial thrombosis has rarely been reported in cancer patients. Cisplatin-based chemotherapy is known to cause various side-effects. Detecting aortic thrombosis is important because it is a fatal condition. We herein present the first reported case of endo-aortic thrombosis occurring during cisplatin-based chemotherapy for gastric cancer.

Topics: Acute Disease; Anticoagulants; Antineoplastic Combined Chemotherapy Protocols; Aortic Diseases; Aortography; Arterial Occlusive Diseases; Carcinoma, Signet Ring Cell; Cisplatin; Dexamethasone; Drug Combinations; Heparin; Humans; Oxonic Acid; Stomach Neoplasms; Tegafur; Thrombosis; Tomography, X-Ray Computed; Warfarin

The optimal treatment strategy for patients with aortic atheroma is not well established because data regarding medical treatment for such patients are lacking, especially with respect to the Japanese population. The purpose of this study was to clarify the effects of medical treatment on the risk of embolic events and mortality in patients with severe aortic plaque.. We retrospectively investigated 75 consecutive patients with severe aortic plaque detected on transesophageal echocardiography (TEE) between 1995 and 2005. The occurrence of embolic events and all-cause death in the period after TEE was assessed. The cumulative incidence of subsequent embolic events and death was evaluated in relation to specific medical treatments, including statins, antiplatelet drugs and warfarin.. Embolic events occurred in 27 patients (36%) and death occurred in 37 patients (49%) during follow-up (5.6±3.0 years). The patients who experienced embolic events had a significantly higher prevalence of previous embolic events, atrial fibrillation and hemodialysis than the patients who did not experience embolic events. Univariate and multivariate analyses showed that the use of statins and/or antiplatelet drugs was significantly associated with a low incidence of death but not with a low incidence of embolic events. On the other hand, warfarin exhibited neither beneficial nor harmful effects on the incidence of embolic events or death.. Statin and antiplatelet drugs have beneficial effects on the prognosis of patients with severe aortic plaque diagnosed on TEE.

Topics: Aged; Aged, 80 and over; Aorta; Aortic Diseases; Atrial Fibrillation; Death, Sudden; Echocardiography, Transesophageal; Embolism; Female; Follow-Up Studies; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Japan; Male; Middle Aged; Multivariate Analysis; Platelet Aggregation Inhibitors; Prevalence; Prognosis; Regression Analysis; Renal Dialysis; Retrospective Studies; Risk; Stroke; Treatment Outcome; Warfarin

Topics: Aged, 80 and over; Aneurysm, False; Anticoagulants; Aortic Diseases; Echocardiography; Humans; Male; Tomography, X-Ray Computed; Vascular Surgical Procedures; Warfarin

In vitro, transglutaminase-2 (TG2)-mediated activation of the β-catenin signaling pathway is central in warfarin-induced calcification, warranting inquiry into the importance of this signaling axis as a target for preventive therapy of vascular calcification in vivo.. The adverse effects of warfarin-induced elastocalcinosis in a rat model include calcification of the aortic media, loss of the cellular component in the vessel wall, and isolated systolic hypertension, associated with accumulation and activation of TG2 and activation of β-catenin signaling. These effects of warfarin can be completely reversed by intraperitoneal administration of the TG2-specific inhibitor KCC-009 or dietary supplementation with the bioflavonoid quercetin, known to inhibit β-catenin signaling. Our study also uncovers a previously uncharacterized ability of quercetin to inhibit TG2. Quercetin reversed the warfarin-induced increase in systolic pressure, underlying the functional consequence of this treatment. Molecular analysis shows that quercetin diet stabilizes the phenotype of smooth muscle and prevents its transformation into osteoblastic cells.. Inhibition of the TG2/β-catenin signaling axis seems to prevent warfarin-induced elastocalcinosis and to control isolated systolic hypertension.

Topics: Animals; Aorta; Aortic Diseases; beta Catenin; Blood Pressure; Cell Line; Disease Models, Animal; Dose-Response Relationship, Drug; Enzyme Activation; Enzyme Inhibitors; Gene Expression Regulation; Glycogen Synthase Kinase 3; Glycogen Synthase Kinase 3 beta; GTP-Binding Proteins; Isoxazoles; Male; Mice; Mice, Inbred C57BL; Mice, Knockout; Muscle, Smooth, Vascular; Osteogenesis; Phosphorylation; Protein Glutamine gamma Glutamyltransferase 2; Quercetin; Rats; Rats, Wistar; Signal Transduction; Transglutaminases; Vascular Calcification; Warfarin

The pathogenesis and presentation of aortic thrombosis (AT) in dogs is not well characterized and an effective antithrombotic therapy for AT in dogs has not been identified. Our goal is to report the clinical presentation and results of therapies in dogs with AT.. Twenty-six client-owned dogs.. Retrospective review of medical records of dogs diagnosed with AT between 2003 and 2010.. Twenty-six dogs had an apparent primary mural aortic thrombus. None had structural heart disease at diagnosis. Twenty dogs were ambulatory with varying degrees of pelvic limb dysfunction. Duration of ambulatory dysfunction was 7.8 weeks (range 1 day-52 weeks). A majority of dogs (58%) had no concurrent conditions at diagnosis. Fourteen dogs were treated with a standard warfarin protocol for a median period of 22.9 months (range 0.5-53 months). Ambulatory function improved in all dogs treated with warfarin. Time until clinical improvement was 13.9 days (range 2-49 days). Dogs treated with warfarin did not become non-ambulatory, die or undergo euthanasia related to AT, or have a known serious hemorrhagic event.. The pathogenesis of AT in dogs is distinct from that of aortic thromboembolism (ATE) in cats. Aortic thrombosis in dogs is more likely to involve local thrombosis in the distal aorta with embolization to the arteries of the pelvic limb resulting in chronic progressive ambulatory dysfunction. Chronic warfarin administration is well-tolerated and appears to be an effective short-term and long-term therapy for dogs with AT.

Topics: Animals; Anticoagulants; Aortic Diseases; Dog Diseases; Dogs; Female; Male; Retrospective Studies; Thrombosis; Treatment Outcome; Warfarin

We report an uncommon case of thrombogenesis in the distal aortic arch after apicoaortic conduit (AAC) for severe aortic stenosis (AS). A 71-year-old woman underwent AAC with a bioprosthetic valve for severe AS because of heavy calcification of the ascending aorta. Although anticoagulant therapy with warfarin was performed, a postoperative computed tomographic (CT) scan revealed a thrombus in the distal aortic arch. Cine magnetic resonance imaging (MRI) revealed stagnation of the blood flow at that site. Administration of warfarin was continued. A follow-up CT-scan showed a marked reduction of the thrombus at six months after the surgery. A follow-up MRI revealed that the antegrade flow through the native aortic valve was decreased at one year after the surgery. We suggest that thrombogenesis may occur after AAC because of stagnation of the blood flow and that the distribution of the blood flow may change during the follow-up period. Therefore, we recommend that postoperative anticoagulant therapy should be initiated immediately, even when a bioprosthetic valve is used.

Topics: Aged; Anticoagulants; Aortic Diseases; Aortic Valve Stenosis; Aortography; Bioprosthesis; Blood Vessel Prosthesis; Blood Vessel Prosthesis Implantation; Calcinosis; Female; Heart Valve Prosthesis; Heart Valve Prosthesis Implantation; Humans; Magnetic Resonance Imaging, Cine; Severity of Illness Index; Thrombosis; Tomography, X-Ray Computed; Warfarin

Topics: Anticoagulants; Aortic Diseases; Aspirin; Atherosclerosis; Fibrinolytic Agents; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Risk; Secondary Prevention; Stroke; Warfarin

Ascending aorta and aortic arch thrombosis is rare in a young man with no risk factor. Here, we report the case of a young male patient with factor V Leiden mutation who developed ascending aorta and aortic arch thrombosis and subsequent emboli.

Topics: Adult; Anticoagulants; Aortic Diseases; Arterial Occlusive Diseases; Blood Coagulation; Blood Coagulation Disorders, Inherited; Echocardiography, Transesophageal; Embolism; Factor V; Humans; Lower Extremity; Male; Mutation; Thrombosis; Tomography, X-Ray Computed; Treatment Outcome; Vascular Surgical Procedures; Warfarin

Topics: Anticoagulants; Aorta, Thoracic; Aortic Diseases; Female; Heparin; Humans; Middle Aged; Radiography; Thrombosis; Warfarin

The effect of atorvastatin on warfarin-induced aortic medial calcification and systolic blood pressure (SBP) of rats induced by warfarin was studied. Thirty healthy and adult rats were randomly divided into Warfarin group (n=10), Atorvastatin group (n=10) and normal control group (n=10). Caudal arterial pressure of rats was measured once a week, and 4 weeks later, aorta was obtained. Elastic fiber, collagen fiber and calcium accumulation in tunica media of cells were measured by Von Kossa staining. The results showed that warfarin treatment led to elevation of systolic blood pressure and aortic medial calcification. The chronic treatment also increased collagen, but decreased elastin in the aorta. However, the atorvastatin treatment had adverse effects. It was concluded that treatment with atorvastatin presented evidence of blood pressure lowing and calcification reducing. These data demonstrate that atorvastatin protected aortic media from warfarin-induced calcification and elevation of systolic blood pressure.

Topics: Animals; Aortic Diseases; Atorvastatin; Blood Pressure; Calcinosis; Heptanoic Acids; Hypertension; Male; Pyrroles; Random Allocation; Rats; Rats, Wistar; Warfarin

The case of a 66-year-old patient with acute intramural haematoma in descending aorta, receiving anticoagulant treatment with warfarin for chronic atrial fibrillation, is presented. Transoesophageal echocardiography was fundamental in the diagnosis of the intramural haematoma, assessment of the cardioembolic risk of atrial fibrillation and in follow-up the evolution of the intramural haematoma, which facilitated therapeutic management. Although no established recommendation exists on anticoagulation in aortic intramural haematoma, individual risk-benefit assessment of anticoagulation and follow-up with imaging techniques are essential to elect the most appropriate therapeutic management.

Topics: Aged; Anticoagulants; Aorta, Thoracic; Aortic Diseases; Atrial Fibrillation; Diagnosis, Differential; Echocardiography, Transesophageal; Female; Hematoma; Humans; Warfarin

Topics: Abciximab; Antibodies, Monoclonal; Aorta, Abdominal; Aortic Diseases; Calcinosis; Combined Modality Therapy; Drug Therapy, Combination; Femoral Artery; Heparin; Humans; Immunoglobulin Fab Fragments; Ischemia; Magnetic Resonance Imaging; Male; Middle Aged; Platelet Aggregation Inhibitors; Sensation Disorders; Spinal Cord; Thrombosis; Urinary Incontinence; Warfarin

We sought to determine whether carbonic anhydrase (CA), which plays an important role in bone resorption, contributes to vascular mineral loss induced by an endothelin receptor antagonist.. Wistar rats were compared with rats receiving warfarin and vitamin K1 (WVK) for 8 weeks alone or in association with the endothelin receptor antagonist darusentan (30 mg/kg per day), the CA inhibitor acetazolamide (100 mg/kg per day), or both for the last 4 weeks. Rats were also treated with WVK for 5 or 6 weeks, and darusentan was added for the last week or last 2 weeks of treatment, respectively. Treatment with WVK produced medial elastocalcinosis in the aorta and carotid arteries. Immunohistochemistry revealed that CA II was already abundant in the adventitia and in calcified areas of aortic sections from WVK-treated rats. Darusentan did not significantly modify its abundance or distribution. In contrast, CA IV immunostaining, which was weak in WVK-treated rats, became apparent after 1 week of darusentan treatment and declined toward basal levels thereafter. These findings were confirmed by a parallel increase in CA IV protein abundance and activity in the aorta. The mineral loss induced by darusentan was blunted by acetazolamide treatment, confirming the functional relevance of the biochemical findings. Moreover, CA IV immunostaining was enhanced much later in the carotids, where darusentan did not cause regression of elastocalcinosis.. Vascular mineral loss induced by the blockade of endothelin receptors seems dependent on the activation of membrane-bound CA IV, suggesting that mineral loss may proceed via local changes in pH similar to that seen in bone resorption.

Topics: Animals; Aorta; Aortic Diseases; Calcinosis; Calcium; Carbonic Anhydrase II; Carbonic Anhydrase IV; Carotid Arteries; Endothelin Receptor Antagonists; Enzyme Activation; Hemodynamics; Male; Phenylpropionates; Pyrimidines; Rats; Rats, Wistar; Remission Induction; Vitamin K 1; Warfarin

Floating thrombus in a non-aneurysmal and non-atherosclerotic thoracic aorta is a rare event with potentially catastrophic complications. Especially younger patients have a higher risk of embolization. Transesophageal echocardiography is the diagnostic method of choice. However, the treatment of this pathology is still controversial and includes both medical and surgical options. We report our experience with a 43-year-old patient and a review of the literature, and make a proposal for therapeutic interventions.

Topics: Adult; Anticoagulants; Aorta, Thoracic; Aortic Diseases; Echocardiography, Transesophageal; Electrocardiography; Heparin; Humans; Male; Thrombosis; Warfarin

Topics: Abdominal Abscess; Anticoagulants; Aortic Diseases; Arterial Occlusive Diseases; Arteriosclerosis; Calcinosis; Conversion Disorder; Diagnostic Errors; Female; Humans; Hypesthesia; Ischemia; Leg; Middle Aged; Muscle Denervation; Paraplegia; Peripheral Nerves; Thrombosis; Tibial Arteries; Tomography, X-Ray Computed; Warfarin

We have previously shown that an endothelin receptor antagonist can regress medial arterial calcification in a rat model. The aim of this study was to characterize the phenotypic changes of vascular smooth muscle cells during calcification and mineral loss, in order to understand better the underlying mechanisms. Control Wistar rats were compared with rats treated only with warfarin/ vitamin K1 (15 mg/kg per day) for 8 weeks, or in combination with darusentan (30 mg/kg per day) for the final 4 weeks. Vascular smooth muscle cell, bone cell and macrophage phenotypes were evaluated by the local expression of alpha-actin, tartrate-resistant acid phosphatase and ED-1, respectively. Proteins involved in the modulation of bone resorption like osteopontin and osteoprotegerin were also evaluated by immunohistochemistry. The warfarin/vitamin K1 treatment increased medial arterial calcification ninefold (P < 0.05). At sites of calcification, there was a decrease in alpha-actin localization, and an appearance of osteopontin immunostaining. Histochemical and immunostaining for osteoclast and macrophage markers, as well as for osteoprotegerin, were negative. Although the extent of calcification foci was reduced by darusentan, protein localization in the calcified areas was not modified. Thus, the development of medial arterial calcification produces a phenotypic change in vascular smooth muscle cells that does not appear to be normalized in regions remaining calcified during mineral loss.

Topics: Animals; Aorta, Thoracic; Aortic Diseases; Calcinosis; Disease Models, Animal; Endothelin Receptor Antagonists; Endothelin-1; Macrophages; Male; Muscle, Smooth, Vascular; Myocytes, Smooth Muscle; Osteoclasts; Osteopontin; Osteoprotegerin; Phenotype; Phenylpropionates; Pyrimidines; Rats; Rats, Wistar; Receptors, Endothelin; Vitamin K 1; Warfarin

Topics: Anticoagulants; Aorta, Thoracic; Aortic Diseases; Arteriosclerosis; Atrial Fibrillation; Electric Countershock; Heart Rate; Humans; Risk Factors; Stroke; Thromboembolism; Warfarin

Topics: Acute Disease; Adult; Aged; Amputation, Surgical; Anticoagulants; Aortic Diseases; Arterial Occlusive Diseases; Aspirin; Clopidogrel; Diagnosis, Differential; Echocardiography, Transesophageal; Female; Follow-Up Studies; Humans; Ischemia; Leg; Male; Middle Aged; Spain; Thrombectomy; Thrombosis; Ticlopidine; Tomography, X-Ray Computed; Treatment Outcome; Warfarin

Severe aortic plaques seen on transesophageal echocardiography (TEE) are a high-risk cause of stroke and peripheral embolization. Evidence to guide therapy is lacking. Retrospective information was obtained regarding the occurrence of embolic events (stroke, transient ischemic attacks, or peripheral emboli) in 519 patients with severe thoracic aortic plaque seen on TEE since 1988. Treatment with statins, warfarin, or antiplatelet medications was noted. Treatment was not randomized. In a matched-paired analysis, each patient taking each class of therapy was matched for age, gender, previous embolic event, hypertension, diabetes, congestive failure, and atrial fibrillation to someone not taking that medication. Multivariate analysis was also performed. An embolic event occurred in 111 patients (21%). Multivariate analysis showed that statin use was independently protective against recurrent events (p = 0.0001). Matched analysis also showed a protective effect of statins (p = 0.0004; absolute risk reduction 17%, relative risk reduction 59%, number needed to treat [n = 6]). No protective effect was found for warfarin or antiplatelet drugs. The odds ratio for embolic events was 0.3 (95% confidence interval [CI] 0.2 to 0.6) for statin therapy, 0.7 (95% CI 0.4 to 1.2) for warfarin, and 1.4 (95% CI 0.8 to 2.4) for antiplatelet agents. Thus, there is a protective effect of statin therapy, and no significant benefit of warfarin or antiplatelet drugs on the incidence of stroke and other embolic events in patients with severe thoracic aortic plaque on TEE.

Topics: Aged; Anticoagulants; Aorta, Thoracic; Aortic Diseases; Arteriosclerosis; Echocardiography, Transesophageal; Embolism; Female; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Incidence; Longitudinal Studies; Male; Multivariate Analysis; Odds Ratio; Platelet Aggregation Inhibitors; Retrospective Studies; Stroke; Treatment Outcome; Warfarin

The present experiments were carried out to test the hypothesis that artery calcification is linked to bone resorption by determining whether the selective inhibition of bone resorption with the bisphosphonates alendronate and ibandronate will inhibit artery calcification. Artery calcification was first induced by treatment of 42-day-old male rats with warfarin, a procedure that inhibits the gamma-carboxylation of matrix Gla protein and has been shown to cause extensive calcification of the artery media within 2 weeks. These experiments revealed that ibandronate (0.05 mg. kg(-1). d(-1)) and alendronate (0.1 mg x kg(-1) x d(-1)) completely inhibited calcification of all arteries and heart valves examined after 2 and 4 weeks of warfarin treatment. A 10-fold lower dose of alendronate reduced artery calcification by 50% (P<0.005). These bisphosphonate doses are comparable to those that inhibit bone resorption in rats of this age. More rapid artery calcification was induced by treatment with warfarin together with high doses of vitamin D, a procedure that causes extensive artery calcification by 84 hours. Alendronate and ibandronate again completely inhibited calcification of all arteries and heart valves examined. The subcutaneous doses of alendronate and ibandronate necessary to inhibit artery calcification are comparable to the daily subcutaneous doses of these drugs that have previously been shown to inhibit bone resorption in rats of the same age, with 50% inhibition of artery calcification at 20 microg alendronate x kg(-1) x d(-1) and at 1 microg ibandronate x kg(-1) x d(-1) x Bisphosphonate treatment did not affect serum calcium and phosphate, and so the inhibition of artery calcification cannot be due to a simple lowering of the serum calcium phosphate ion product. We conclude that bisphosphonates inhibit the calcification of arteries and heart valves at doses comparable to the doses that inhibit bone resorption. These results support the hypothesis that artery calcification is linked to bone resorption. The mechanism of this linkage remains to be established, however, and an alternative explanation for the present results is also considered.

Topics: Alendronate; Animals; Aortic Diseases; Bone Resorption; Calcification, Physiologic; Calcinosis; Diphosphonates; Drug Administration Schedule; Etidronic Acid; Female; Humans; Ibandronic Acid; Male; Muscle, Smooth, Vascular; Osteoporosis; Rats; Rats, Sprague-Dawley; Vitamin D; Warfarin

To investigate the relationship among lipids, coagulation and thrombosis in the absence of atherosclerosis, spontaneous or dietary-induced hyperlipidemic (FHL) rats were studied. FHL showed higher levels of coagulation factors VII, IX, X, VIII and XII and a shortening of the occlusion time (OT) of an artificial arterial prosthesis as compared with normolipidemic (FNL) animals. Damage of abdominal aorta of FHL was followed by increased fibrin deposition in the vascular intima as compared to FNL. After 5 months of cholesterol-rich diet FNL showed increased cholesterol, triglycerides and factor II, VII, IX, X, XII levels. A significant shortening of the OT and increased fibrin deposition was also observed. Two-month diet withdrawal restored the initial condition. Warfarin treatment, at a dose decreasing vitamin K-dependent factor to levels found in FNL, prolonged the OT and reduced fibrin deposition, without modifying F XII or changing lipid profile. An increase in the activated form of F VII was observed. In contrast, no difference was found in F VII clearance. High lipid levels favour the process of thrombus formation by increasing the activation of vitamin K-dependent coagulation factors. Low-dose warfarin treatment reverts the prothrombotic effect of hyperlipidemia.

Topics: Administration, Oral; Animals; Anticoagulants; Aorta, Abdominal; Aortic Diseases; Blood Coagulation Factors; Blood Vessel Prosthesis; Cholesterol, Dietary; Diet, Atherogenic; Disease Models, Animal; Enzyme Activation; Factor VII; Hypercholesterolemia; Hyperlipidemias; Hypertriglyceridemia; Postoperative Complications; Rats; Rats, Inbred Strains; Rats, Sprague-Dawley; Thrombophilia; Thrombosis; Vitamin K; Warfarin

The present studies demonstrate that growth and vitamin D treatment enhance the extent of artery calcification in rats given sufficient doses of Warfarin to inhibit gamma-carboxylation of matrix Gla protein, a calcification inhibitor known to be expressed by smooth muscle cells and macrophages in the artery wall. The first series of experiments examined the influence of age and growth status on artery calcification in Warfarin-treated rats. Treatment for 2 weeks with Warfarin caused massive focal calcification of the artery media in 20-day-old rats and less extensive focal calcification in 42-day-old rats. In contrast, no artery calcification could be detected in 10-month-old adult rats even after 4 weeks of Warfarin treatment. To directly examine the importance of growth to Warfarin-induced artery calcification in animals of the same age, 20-day-old rats were fed for 2 weeks either an ad libitum diet or a 6-g/d restricted diet that maintains weight but prevents growth. Concurrent treatment of both dietary groups with Warfarin produced massive focal calcification of the artery media in the ad libitum-fed rats but no detectable artery calcification in the restricted-diet, growth-inhibited group. Although the explanation for the association between artery calcification and growth status cannot be determined from the present study, there was a relationship between higher serum phosphate and susceptibility to artery calcification, with 30% higher levels of serum phosphate in young, ad libitum-fed rats compared with either of the groups that was resistant to Warfarin-induced artery calcification, ie, the 10-month-old rats and the restricted-diet, growth-inhibited young rats. This observation suggests that increased susceptibility to Warfarin-induced artery calcification could be related to higher serum phosphate levels. The second set of experiments examined the possible synergy between vitamin D and Warfarin in artery calcification. High doses of vitamin D are known to cause calcification of the artery media in as little as 3 to 4 days. High doses of the vitamin K antagonist Warfarin are also known to cause calcification of the artery media, but at treatment times of 2 weeks or longer yet not at 1 week. In the current study, we investigated the synergy between these 2 treatments and found that concurrent Warfarin administration dramatically increased the extent of calcification in the media of vitamin D-treated rats at 3 and 4 days. There was a close parallel

Topics: Aging; Animals; Anticoagulants; Aorta; Aortic Diseases; Arteries; Calcinosis; Drug Combinations; Drug Synergism; Male; Rats; Rats, Sprague-Dawley; Time Factors; Vascular Diseases; Vitamin D; Warfarin

The clinical presentation of patients with acute lower-limb ischemia and primary aortic thrombus prompted this review. Following recognition of the first case in early 1994, relevant patients (n = 6) were kept in a database and were reviewed for presentation, treatment, and follow-up. The median age was 41 and five patients were male. Angiography, computed tomography, and/or magnetic resonance angiography demonstrated one or more aortic sessile or pedunculated thrombus(i) without associated atherosclerotic disease. In two cases, a retropancreatic intraaortic mural thrombus was associated with severe pancreatitis. All other cases presented with acute lower-limb emboli requiring limb salvage embolectomy. Because of significant patient illness, systemic anticoagulation was chosen acutely to prevent recurrent emboli. Interestingly, serial studies demonstrated aortic thrombus resolution. Failure to continue warfarin therapy resulted in recurrent problems (n = 1) unless the instigating event had resolved (n = 3). There were no deaths or amputations. We concluded that surgical embolectomy, when required, with subsequent anticoagulation, results in limb salvage and allows for eventual resolution of the primary aortic thrombus. Long-term anticoagulation is required unless the etiologic process resolves. The literature describes patients with atherosclerosis and overlying thrombus but fails to describe the approach to patients with primary thrombus formation.

Topics: Acute Disease; Adult; Aged; Anticoagulants; Aorta, Abdominal; Aortic Diseases; Embolectomy; Embolism; Female; Heparin; Humans; Leg; Male; Pancreatitis; Thrombosis; Warfarin

Vitamin K2(K2), a therapeutic agent osteoporosis, is prohibited for patients with thrombosis who are receiving warfarin (WF). However, because some aged patients with thrombosis have osteoporosis, some patients treated with WF may be administered K2 concomitantly. We investigated here the interaction between K2 and WF on thrombosis in a rat aorta loop model. Administration of WF at 0.58, 0.82 and 1.16 mg/l in drinking water for 7 days decreased the thrombotic rate and increased the death rate, dose-dependently. Therefore in the following study, 0.80 mg/l of WF was used. After 2 days of WF-treatment, 1.5, 14 and 145 mg/kg of K2 was administered for 5 days. The blood coagulation time was markedly prolonged by WF treatment for 7 days and this effect was completely inhibited by all doses of K2. WF treatment significantly decreased the cumulative thrombotic rate for 5 days. Administration of 1.5 and 14 mg/kg of K2 did not influence the WF effect on thrombosis. The thrombotic rate in the 145 mg/kg K2 group was lower than that in the WF-control group, but similar to that in the WF-untreated group. These findings suggest that high dose of K2 reduces the effect of WF on thrombosis but does not enhance the occurrence of thrombosis more than that without WF treatment.

Topics: Animals; Aortic Diseases; Drug Interactions; Male; Rats; Rats, Sprague-Dawley; Thrombosis; Vitamin K; Warfarin

We sought to determine the influence of plaque morphology and warfarin anticoagulation on the risk of recurrent emboli in patients with mobile aortic atheroma.. An epidemiologic link between aortic atheroma and systemic emboli has been described both in pathologic and transesophageal studies. Likewise, a few studies have found an increased incidence of recurrent emboli in these patients. The therapeutic implications of these findings has not been studied.. Thirty-one patients presenting with a systemic embolic event and found to have mobile aortic atheroma were studied. The height, width and area of both immobile and mobile portions of atheroma were quantitated. The dimensions of the mobile component was used to define three groups: small, intermediate and large mobile atheroma. The patients were followed up by means of telephone interview and clinical records, with emphasis on anticoagulant use and recurrent embolic or vascular events.. Patients not receiving warfarin had a higher incidence of vascular events (45% vs. 5%, p = 0.006). Stroke occurred in 27% of these patients and in none of those treated with warfarin. The annual incidence of stroke in patients not taking warfarin was 0.32. Myocardial infarction occurred in 18% of patients also in this group. Taken together, the risk of myocardial infarction or stroke was significantly increased in this group (p = 0.001). Forty-seven percent of patients with small, mobile atheroma did not receive warfarin. Recurrent stroke occurred in 38% of these patients, representing an annual incidence of 0.61. There were no strokes in patients with small, mobile atheroma treated with warfarin (p = 0.04). Likewise, none of the patients with intermediate or large mobile atheroma had a stroke during follow-up. Only three of these patients had not been taking warfarin.. Patients presenting with systemic emboli and found to have mobile aortic atheroma on transesophageal echocardiography have a high incidence of recurrent vascular events. Warfarin is efficacious in preventing stroke in this population. The dimension of the mobile component of atheroma should not be used to determine the need for anticoagulation.

Topics: Aged; Anticoagulants; Aortic Diseases; Arteriosclerosis; Cerebrovascular Disorders; Coronary Thrombosis; Echocardiography, Transesophageal; Female; Humans; Male; Middle Aged; Recurrence; Treatment Outcome; Warfarin

Topics: Aged; Anticoagulants; Aortic Diseases; Fatal Outcome; Female; Humans; Hypereosinophilic Syndrome; Thrombosis; Warfarin

Topics: Acute Disease; Aged; Aorta, Abdominal; Aortic Diseases; Fatal Outcome; Female; Humans; Thrombosis; Warfarin

Topics: Aorta, Thoracic; Aortic Diseases; Arteriosclerosis; Blue Toe Syndrome; Cohort Studies; Embolism, Cholesterol; Heparin; Humans; Ischemic Attack, Transient; Warfarin

A 41-year-old woman with systemic lupus erythematosus and lupus anticoagulant developed aortic thrombosis. The patient was receiving low dose aspirin. Aortography showed a complete obliteration of the infrarenal aorta. Computed tomography and magnetic resonance imaging showed no evidence of aortitis. The patient improved with medical treatment. Six other published cases are reviewed.

Topics: Adult; Antiphospholipid Syndrome; Aorta, Abdominal; Aortic Diseases; Aortography; Calcium Channel Blockers; Drug Therapy, Combination; Female; Humans; Lupus Erythematosus, Systemic; Thrombosis; Tomography, X-Ray Computed; Warfarin

Two cases of acute aortic thrombosis, a previously unreported complication of antithrombin III deficiency, are reported. Both patients had abnormally low antithrombin III levels, which improved to normal levels with warfarin ;sodium therapy. The possibility of antithrombin III deficiency should be considered in young patients with acute arterial thrombosis.

Topics: Acute Disease; Adult; Antithrombin III; Antithrombin III Deficiency; Aorta, Abdominal; Aortic Diseases; Female; Humans; Infarction; Intermittent Claudication; Kidney; Male; Thrombosis; Warfarin

Arterial emboli were extracted from 79 patients between 1955 and 1963 with polyethylene catheter suction systems and/or retrograde flushing and from 149 patients between 1963 and 1973 with Fogarty catheters. The Fogarty-era patients were older, had a greater incidence of ischemic heart disease, and presented with a greater degree of preoperative peripheral ischemia. The limb salvage rate of 87 percent after Fogarty catheter embolectomy was not statistically different from the salvage rate of 79 percent after suction catheter embolectomy, but the number of limbs with distal pulses postoperatively was significantly greater after Fogarty treatment, 64 vs. 42 percent. Delay in treatment and the presence of prior occlusive vascular disease adversely affected results in both eras. The in-hospital embolic recurrences occurred in 9 percent of the patients anticoagulated postoperatively and in 31 percent of those not anticoagulated. Heparin and warfarin were equally effective in preventing recurrences, but wound complications were seen in 33 percent of the heparinized patients, compared with 7 percent of those receiving warfarin and 4 percent of those not anticoagulated.

Topics: Aged; Aortic Diseases; Arm; Catheterization; Embolism; Femoral Artery; Follow-Up Studies; Gangrene; Heparin; Humans; Iliac Artery; Ischemia; Leg; Popliteal Artery; Postoperative Care; Recurrence; Warfarin

A 56-year-old male patient diagnosed as a case of procainamide-induced systemic lupus erythematosus (SLE) was found to have a lymphoproliferative disorder at postmortem examination.Contrary to other immune disorders, the association of SLE with neoplasia is a rare occurrence. The present case raises the question of whether a relationship exists between the lupus diathesis and lymphoreticular neoplasia. The study of the incidence of neoplasia in families of patients with SLE may prove helpful in establishing this relationship.

Topics: Aortic Diseases; Autopsy; Blindness; Bone Marrow; Digoxin; Drug Therapy, Combination; Heart Diseases; Heparin; Humans; Immunologic Deficiency Syndromes; Kidney; Lupus Erythematosus, Systemic; Lymph Nodes; Lymphoma; Male; Middle Aged; Procainamide; Quinidine; Retinal Artery; Spleen; Thromboembolism; Warfarin