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Plain film radiography, computed tomography (CT) and magnetic resonance imaging (MRI) of his foot excluded infection. Additional images (CT of chest, abdomen, and pelvis) revealed bilateral lung nodules. The patient underwent left fifth toe amputation, sharp dissection of the heel ulcer and wedge resection of a lung nodule that confirmed metastatic involvement. [Extracted from the article]

The article reports on the treatment of heparin-induced thrombocytopenia (HIT), an immune-mediated disorder caused by the use of unfractionated heparin and low molecular weight heparin. HIT, which can lead to pulmonary embolism and stroke when not properly treated, occurs within five to 14 days after exposure to heparin. To prevent thromboembolic events when HIT occurred, treatment should directly be performed including immunoassay, alternative anticoagulant, argatroban and lepirudin.

Atheromatous embolization is a multisystem disease complicating advanced atherosclerosis. It occurs most often as a complication of angiography, an endovascular procedure or cardiovascular surgery. Atheromatous embolization can present in a subtle manner where it is often under-recognized, or with catastrophic results including myocardial infarction, strake or acute renal failure. It may mimic other disease processes and often goes underdiagnosed and undertreated. A high clinical suspicion is the key to diagnosis. Atheromatous embolization results in significant morbidity and mortality; therefore, early recognition followed by aggressive management may help to prevent end-organ damage and improve overall clinical outcomes. Management strategies should include risk factor modification, prevention of further insults by discontinuing or avoiding predisposing factors, supportive treatment and interventional or surgical approaches to remove the atheroembolic source. Atheromatous embolization is expected to increase as our population ages and the epidemics of diabetes mellitus and obesity increase. [ABSTRACT FROM AUTHOR]

Thrombotic thrombocytopenic purpura (TTP) is classically highlighted by a pentad of features: fever, hemolytic anemia, thrombocytopenia purpura, transient or permanent central nervous system signs, and renal disease. The antemortem diagnosis is reliant upon the multisystem clinical signs and symptoms in conjunction with severe hemolytic anemia and thrombocytopenia. Relapse is common within the first six months after initial presentation. Laboratory findings have been generally nonspecific per se, and antemortem tissue biopsy findings are frequently unrewarding. Recently, however, unusually large multimers of the Factor VIII:Ag molecule (von Willebrand protein) have been identified in the plasma of patients with TTP who have recovered from an acute attack. This observation is very important because it may lead to essential information on the nature of the inciting event in this devastating illness. The differential diagnosis includes several multisystem disease processes such as the hemolytic uremic syndrome, toxemia of pregnancy, systemic lupus erythematosus, subacute bacterial endocarditis, nonbacterial thrombotic endocarditis, immune thrombocytopenic purpura, and the postpartum renal failure syndrome. The hemolytic uremic syndrome, toxemia of pregnancy, and TTP may resemble each other, exhibit many overlapping features, and are probably related. The cause of TTP remains unknown; the overwhelming majority of cases occur in otherwise healthy people without any recognizable underlying illness. Since 1965 45 to 70% of patients survive, a significant improvement in contrast to the early 1900s when the mortality rate was greater than 90%. The most dramatic advance has been observed in therapeutics, namely the utilization of some mode of plasma therapy (either infusion alone or plasmapheresis followed by plasma infusion). Corticosteroids remain very important in the management of patients with TTP. Vincristine may be very helpful, but additional studies are needed. The efficacy of vinca alkaloids, chronic immunosuppressive therapy, and sple. nectomy remains undefined. At present there is very little, if any, evidence that antiplatelet agents, aspirin, and prostacyclin are beneficial to patients with TTP. Prompt diagnosis and vigorous aggressive therapy is critical for successful management of TTP patients. [ABSTRACT FROM PUBLISHER]

Background: Patients with lymphedema and lipedema share physical exam findings that may lead to misdiagnosis. Poor mobility is common in patients with obesity and patients with lymphedema and lipedema. This may constitute a risk factor for venous thromboembolism (VTE). Our objective was to evaluate the association of VTE in obese patients with lymphedema and lipedema. Methods: The National Inpatient Sample (NIS) was searched from 2016 to 2020 to identify hospital admissions of obese female patients with lymphedema and lipedema. Patients were analyzed in the context of presence or absence of VTE while adjusting for complex cluster sampling techniques. Predictors of VTE were accessed by multivariable regression. Results: Lymphedema was identified in 189,985 patients and lipedema in 50,645 patients. VTE was observed in 3.12% (n = 374,210) of patients with obesity. In patients with obesity, VTE was more common in patients with lymphedema than without (2.6% vs 1.6%; p < 0.01). Similarly, VTE was more common in patients with lipedema than without (0.6% vs 0.4%; p < 0.01). After multivariable logistic regression, VTE events in obese patients with lymphedema were higher versus without (OR 1.6; CI 1.08–2.43; p = 0.02). Similarly, VTE events were more common in obese patients with lipedema versus obese patients without lipedema (OR 1.20; CI 1.03–1.41; p = 0.02). Conclusions: In this hypothesis-generating study, lymphedema and lipedema show a positive association with VTE after adjusting for baseline patient characteristics such as obesity, which is a known independent risk factor for VTE. Mechanisms whereby lymphedema and lipedema are associated with VTE should be investigated. [ABSTRACT FROM AUTHOR]

This article discusses a case of Mondor's disease in a 55-year-old man with a history of renal transplantation and a stenosed upper-extremity arteriovenous fistula (AVF). The patient presented with chest pain, redness, and a palpable mass on the right chest wall. A venous Doppler ultrasound revealed acute superficial thrombophlebitis in the basilic vein and a superficial vein of the right chest. The diagnosis of Mondor's disease was made based on the history, clinical examination, and venous duplex. The patient was treated with anticoagulation and his symptoms resolved. Mondor's disease is a rare condition characterized by sclerosing superficial thrombophlebitis and can affect various veinous drainage systems. It is typically self-limiting and resolves within 6-8 weeks. [Extracted from the article]

Background: Desirudin, a bivalent direct thrombin inhibitor (DTI), is approved by the US Food and Drug Administration for the prevention of deep vein thrombosis, which may lead to pulmonary embolism, in patients undergoing elective hip replacement surgery. It became available in the United States in March 2010. Objective: The goal of the present article was to provide an overview of the rationale and design of the PREVENT-HIT study, a randomized, prospective, openlabel, active drug-controlled, exploratory trial comparing the clinical and economic utility of desirudin versus argatroban in patients with suspected heparin-induced thrombocytopenia (HIT), with or without thrombosis. Summary: The PREVENT-HIT study was designed to enroll ∼120 patients from 20 to 25 US centers. All eligible patients were required to be aged ≥18 years. Patients with suspected HIT with or without thrombosis were divided into 2 treatment arms and randomized to receive treatment with desirudin or argatroban in a 1:1 ratio using a block randomization method. Arm A comprised patients who were naive to DTI therapy; arm B included patients whose condition was previously stabilized with intravenous argatroban. Desirudin was administered as a fixed-dose injection (15 or 30 mg SC q12h in patients without or with thrombosis, respectively). Argatroban was administered by continuous intravenous infusion in accordance with approved prescribing information or institutional prescribing guidelines at each study site. The primary efficacy outcome measure included the occurrence of any of the following up to 30 days after study drug discontinuation: new-onset or worsening thrombosis requiring discontinuation of study drug; amputation; or all-cause mortality. Other outcomes that were assessed included platelet recovery, bleeding, and pharmacoeconomic parameters. In addition, adverse events and other safety parameters were evaluated. Study enrollment began in November 2008 and ended in December 2009 due to slow enrollment (N = 16). The study results will be published separately. Conclusion: The results from the PREVENT-HIT study should enhance understanding of the comparative clinical and economic utility of desirudin and argatroban in patients with HIT with or without thrombosis. [Copyright &y& Elsevier]

Background: Lipedema is a loose connective tissue disease predominantly in women identified by increased nodular and fibrotic adipose tissue on the buttocks, hips and limbs that develops at times of hormone, weight and shape change including puberty, pregnancy, and menopause. Lipedema tissue may be very painful and can severely impair mobility. Non-lipedema obesity, lymphedema, venous disease, and hypermobile joints are comorbidities. Lipedema tissue is difficult to reduce by diet, exercise, or bariatric surgery. Methods: This paper is a consensus guideline on lipedema written by a US committee following the Delphi Method. Consensus statements are rated for strength using the GRADE system. Results: Eighty-five consensus statements outline lipedema pathophysiology, and medical, surgical, vascular, and other therapeutic recommendations. Future research topics are suggested. Conclusion: These guidelines improve the understanding of the loose connective tissue disease, lipedema, to advance our understanding towards early diagnosis, treatments, and ultimately a cure for affected individuals. [ABSTRACT FROM AUTHOR]

Coronavirus disease 2019 (COVID-19) caused by SARS-CoV-2 is an ongoing viral pandemic marked by increased risk of thrombotic events. However, the role of platelets in the elevated observed thrombotic risk in COVID-19 and utility of antiplatelet agents in attenuating thrombosis is unknown. We aimed to determine if the antiplatelet effect of aspirin may mitigate risk of myocardial infarction, cerebrovascular accident, and venous thromboembolism in COVID-19. We evaluated 22,072 symptomatic patients tested for COVID-19. Propensity-matched analyses were performed to determine if treatment with aspirin or nonsteroidal anti-inflammatory drugs (NSAIDs) affected thrombotic outcomes in COVID-19. Neither aspirin nor NSAIDs affected mortality in COVID-19. Thus, aspirin does not appear to prevent thrombosis and death in COVID-19. The mechanisms of thrombosis in COVID-19, therefore, appear distinct and the role of platelets as direct mediators of SARS-CoV-2-mediated thrombosis warrants further investigation. [ABSTRACT FROM AUTHOR]

Objectives: The aim of this study was a comparison of risk-adjusted outcomes of 3 approaches to carotid revascularization in the open heart surgery (OHS) population. Background: Without randomized clinical trials, the best approach to managing coexisting severe carotid and coronary disease remains uncertain. Staged carotid endarterectomy (CEA) followed by OHS or combined CEA and OHS are commonly used. A recent alternative is carotid artery stenting (CAS). Methods: From 1997 to 2009, 350 patients underwent carotid revascularization within 90 days before OHS at a tertiary center: 45 staged CEA-OHS, 195 combined CEA-OHS, and 110 staged CAS-OHS. The primary composite endpoint was all-cause death, stroke, and myocardial infarction (MI). Staged CAS-OHS patients had higher prevalence of previous stroke (p = 0.03) and underwent more complex OHS. Therefore, the propensity score adjusted multiphase hazard function models with modulated renewal to account for staging, and competing risks were used. Results: Using propensity analysis, staged CAS-OHS and combined CEA-OHS had similar early hazard phase composite outcomes, whereas staged CEA-OHS incurred the highest risk driven by interstage MI. Subsequently, staged CAS-OHS patients experienced significantly fewer late hazard phase events compared with both staged CEA-OHS (adjusted hazard ratio: 0.33; 95% confidence interval: 0.15 to 0.77; p = 0.01) and combined CEA-OHS (adjusted hazard ratio: 0.35; 95% confidence interval: 0.18 to 0.70; p = 0.003). Conclusions: Staged CAS-OHS and combined CEA-OHS are associated with a similar risk of death, stroke, or MI in the short term, with both being better than staged CEA-OHS. However, the outcomes significantly favor staged CAS-OHS after the first year. [Copyright &y& Elsevier]

Peripheral arterial disease predicts future cardiovascular events and all-cause mortality. Conventional methods of assessment might underestimate its true prevalence. We sought to determine whether a postexercise ankle-brachial index (ABI), not only improved peripheral arterial disease detection, but also independently predicted death. This was an observational study of consecutive patients referred for ABI measurement before and after the fixed-grade treadmill or symptom-limited exercise component to a noninvasive vascular laboratory from January 1990 to December 2000. The subjects were classified into 2 groups. Group 1 included patients with an ABI of ≥0.85 before and after exercise, and group 2 included patients with a normal ABI at rest but <0.85 after exercise. A total of 6,292 patients underwent ABI measurements with exercise during the study period. Propensity score matching of the groups was performed to minimize observational bias. Overall mortality, as determined using the United States Social Security death index, was the end point. The 10-year mortality rate of groups 1 and 2 was 32.7% and 41.2%, respectively. An abnormal postexercise ABI result independently predicted mortality (hazard ratio 1.3, 95% confidence interval 1.07 to 1.58, p = 0.008). Additional independent predictors of mortality were age, male gender, diabetes, and hypertension. After the exclusion of patients with a history of cardiovascular events, the predictive value of an abnormal postexercise ABI remained statistically significant (hazard ratio 1.67, 95% confidence interval 1.29 to 2.17, p <0.0001). In conclusion, our results have shown that the postexercise ABI is a powerful independent predictor of all-cause mortality and provides additional risk stratification beyond the ABI at rest. [Copyright &y& Elsevier]

We retrospectively evaluated argatroban dosing patterns, clinical outcomes, and the effects of heart failure and multiple organ system failure on dosing requirements in 65 adult, intensive care patients administered argatroban anticoagulation for clinically suspected heparin-induced thrombocytopenia (n = 56) or history of heparin-induced thrombocytopenia (n = 9). Argatroban was initiated then titrated to achieve target activated partial thromboplastin times 1.5 to 3 times normal control (ie, 42-84 seconds). Overall, argatroban was initiated at 1.14 ± 0.62 μg/kg/min (mean ± SD) and administered for 11.4 ± 9.5 days, with comparable dosing patterns between patients with suspected, versus previous, heparin-induced thrombocytopenia. Sixty-four (98.5%) patients achieved target activated partial thromboplastin times, typically following no or one dose adjustment. Therapeutic doses were lower in patients with, versus without, heart failure (0.58 ± 0.28 vs 0.97 ± 0.6 μg/kg/min, P = .042) and decreased as the number of failed organ systems increased from 1 to 2 to =3 (1.10 ± 0.67 vs 0.87 ± 0.47 vs 0.58 ± 0.47 μg/kg/min, P = .008). From argatroban initiation until patient discharge or death, 11 (16.9%) patients (3 off argatroban) developed thromboembolic complications; 14 (21.5%) died (11 off argatroban, 7 from multiple organ system failure); and 1 (1.5%) required amputation. Nine patients (13.8%) experienced bleeding, none fatal. This experience suggests that argatroban administered at approximately 1 μg/kg/min provides adequate levels of anticoagulation in many intensive care unit patients with suspected or previous heparin-induced thrombocytopenia. Reduced doses are needed when heart failure or multiple organ system failure is present. [ABSTRACT FROM AUTHOR]

Lymphedema and lipedema are chronic debilitating disorders that most commonly affect the upper and lower extremities. Although they can appear similar, they differ in important ways, which the authors of this article review and contrast., (Copyright © 2024 The Cleveland Clinic Foundation. All Rights Reserved.)

Competing Interests: Declaration of conflicting interestsThe authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Objective: There is a paucity of data on how race affects the clinical presentation and short-term outcome among hospitalized patients with SARS-CoV-2, the 2019 coronavirus (COVID-19)., Methods: Hospitalized patients ≥ 18 years, testing positive for COVID-19 from March 13, 2020 to May 13, 2020 in a United States (U.S.) integrated healthcare system with multiple facilities in two states were evaluated. We documented racial differences in clinical presentation, disposition, and in-hospital outcomes for hospitalized patients with COIVD-19. Multivariable regression analysis was utilized to evaluate independent predictors of outcomes by race., Results: During the study period, 3678 patients tested positive for COVID-19, among which 866 were hospitalized (55.4% self-identified as Caucasian, 29.5% as Black, 3.3% as Hispanics, and 4.7% as other racial groups). Hospitalization rates were highest for Black patients (36.6%), followed by other (28.3%), Caucasian patients (24.4%), then Hispanic patients (10.7%) (p &lt; 0.001). Caucasian patients were older, and with more comorbidities. Absolute lymphocyte count was lowest among Caucasian patients. Multivariable regression analysis revealed that compared to Caucasians, there was no significant difference in in-hospital mortality among Black patients (adjusted odds ratio [OR] 0.53; 95% confidence interval [CI] 0.26-1.09; p = 0.08) or other races (adjusted OR 1.62; 95% CI 0.80-3.27; p = 0.18). Black and Hispanic patients were admitted less frequently to the intensive care unit (ICU), and Black patients were less likely to require pressor support or hemodialysis (HD) compared with Caucasians., Conclusions: This observational analysis of a large integrated healthcare system early in the pandemic revealed that patients with COVID-19 did exhibit some racial variations in clinical presentation, laboratory data, and requirements for advanced monitoring and cardiopulmonary support, but these nuances did not dramatically alter in-hospital outcomes., (© 2021. W. Montague Cobb-NMA Health Institute.)

Background Certain echocardiographic parameters may serve as early predictors of adverse events in patients with hemodynamically compromising pulmonary embolism (PE). Methods and Results An observational analysis was conducted for patients with acute pulmonary embolism evaluated by a Pulmonary Embolism Response Team (PERT) between 2014 and 2020. The performance of clinical prediction algorithms including the Pulmonary Embolism Severity Index and Carl Bova score were compared using a ratio of right ventricle and left ventricle hemodynamics by dividing the pulmonary artery systolic pressure by the left ventricle stroke volume. The primary outcome of in-hospital mortality, cardiac arrest, and the need for advanced therapies was evaluated by univariate and multivariable analyses. Of the 343 patients meeting the inclusion criteria, 215 had complete data. Pulmonary artery systolic pressure/left ventricle stroke volume was a clear predictor of the primary end point (odds ratio [OR], 2.31; P =0.005), performing as well or better than the Pulmonary Embolism Severity Index (OR, 1.43; P =0.06) or the Bova score (OR, 1.28; P =0.01). Conclusions This study is the first study to demonstrate the utility of early pulmonary artery systolic pressure/left ventricle stroke volume in predicting adverse clinical events in patients with acute pulmonary embolism. Pulmonary artery systolic pressure/left ventricle stroke volume may be a surrogate marker of ventricular asynchrony in high-risk pulmonary embolism and should be prognostically evaluated.

The manuscript discusses the application of CT pulmonary angiography, ventilation-perfusion scan, and magnetic resonance angiography to detect acute pulmonary embolism and to plan endovascular therapy. CT pulmonary angiography offers high accuracy, speed of acquisition, and widespread availability when applied to acute pulmonary embolism detection. This imaging modality also aids the planning of endovascular therapy by visualizing the number and distribution of emboli, determining ideal intra-procedural catheter position for treatment, and signs of right heart strain. Ventilation-perfusion scan and magnetic resonance angiography with and without contrast enhancement can also aid in the detection and pre-procedural planning of endovascular therapy in patients who are not candidates for CT pulmonary angiography.

The optimal management of a submassive or massive pulmonary embolism (PE) during pregnancy is unclear because of a lack of large clinical trials. Evaluation of the patient who may be a candidate for more aggressive therapy includes the use of biomarkers and echocardiogram for risk stratification. PE Response teams (PERTs) have gained increasing acceptance by the medical community and are being implemented in hospitals in the United States and worldwide. PERTs bring together a team of specialists from different disciplines to enhance decision-making in the patient with acute submassive and massive PE., Competing Interests: Disclosure The author have nothing to disclose., (Copyright © 2020 Elsevier Inc. All rights reserved.)

Treatment strategies for complex patients with pulmonary embolism (PE) are often debated given patient heterogeneity, multitude of available treatment modalities, and lack of consensus guidelines. Although multidisciplinary Pulmonary Embolism Response Teams (PERT) are emerging to address this lack of consensus, their impact on patient outcomes is not entirely clear. This analysis was conducted to compare outcomes of all patients with PE before and after PERT availability. We analyzed all adult patients admitted with acute PE diagnosed on computed tomography scans in the 18 months before and after the institution of PERT at a large tertiary care hospital. Among 769 consecutive inpatients with PE, PERT era patients had lower rates of major or clinically relevant nonmajor bleeding (17.0% vs 8.3%, p = 0.002), shorter time-to-therapeutic anticoagulation (16.3 hour vs 12.6 hour, p = 0.009) and decreased use of inferior vena cava filters (22.2% vs 16.4%, p = 0.004). There was an increase in the use of thrombolytics/catheter-based strategies, however, this did not achieve statistical significance (p = 0.07). There was a significant decrease in 30-day/inpatient mortality (8.5% vs 4.7%, p = 0.03). These differences in outcomes were more pronounced in intermediate and high-risk patients (mortality 10.0% vs 5.3%, p = 0.02). The availability of multidisciplinary PERT was associated with improved outcomes including 30-day mortality. Patients with higher severity of PE seemed to derive most benefit from PERT availability., (Copyright © 2019 Elsevier Inc. All rights reserved.)

Management of intermediate and high risk acute pulmonary embolism (PE) is challenging. The role of multidisciplinary teams for the care of these patients is emerging. Herein, we report our experience with a pulmonary embolism response team (PERT). We conducted a retrospective chart review on all patients admitted to the Cleveland Clinic main campus who required activation of the (PERT) from October 1, 2014 to September 1, 2016. We extracted data pertaining to clinical presentation, bleeding complications, and pre- and post-discharge imaging. Patients were classified as low, intermediate or high risk PE. Descriptive and continuous variables were collected and analyzed. There were 134 PERT activations. PE was confirmed by CT-PA in 118 patients. Fifteen (13%) patients were classified as low risk, 80 (68%) intermediate risk PE and 23 (19%) high risk PE. Fourteen (12%) patients were treated with catheter directed rtPA, 6 (5%) received full dose (100 mg rtPA), 16 (13%) received systemic half-dose (50 mg rtPA), 6 (5%) underwent a surgical embolectomy and 4 (3%) underwent mechanical thrombectomy. 65 (55%) patients received anticoagulation only, and 8 (7%) patients were managed conservatively without any anticoagulation or advanced therapy. 11 (9%) patients died while during the hospitalization. Fourteen patients had major bleeding events. There were no bleeding events among patients who received systemic low dose or full dose rtPA. A multidisciplinary approach to cases of intermediate risk and high risk PE can be implemented successfully. We saw a relatively low rate of bleeding events with use of rtPA.

In the article, "Update on the management of venous thromboembolism" (Bartholomew JR, Cleve Clin J Med 2017; 84[suppl 3]:39-46), 2 sentences in the text regarding dose reduction for body weight have errors. The corrected sentences follow: On page 42, left column, the last 5 lines should read: "The recommended dose should be reduced to 2.5 mg twice daily in patients that meet 2 of the following criteria: age 80 or older; body weight of 60 kg or less; or with a serum creatinine 1.5 mg/dL or greater." And on page 42, right column, the sentence 10 lines from the top should read: "Edoxaban is given orally at 60 mg once daily but reduced to 30 mg once daily if the CrCL is 30 mL/min to 50 mL/min, if body weight is 60 kg or less, or with use of certain P-glycoprotein inhibitors."

Pulmonary embolism (PE) is a common thrombotic event that is variable in its presentation. Depending on the patients' risk for mortality, guidelines provide several treatment strategies including thrombolysis, catheter-directed therapies, pulmonary embolectomy, anticoagulation, and inferior vena cava filters. However, there is considerable disagreement between guidelines regarding the optimal treatment strategy for patients, particularly for those with intermediate-risk PE. In order to provide rapid and individualized care, PE response teams (PERT) have been developed. These teams consist of members from different specialties with a particular interest in PE, varying technical skills, and clinical experience, thereby allowing for a multidisciplinary approach. PERT allows for consensus decision making, and for rapid intervention in patients whose conditions worsen. In this review, we provide an overview of treatment guidelines for PE, and of results from recent clinical trials involving patients with submassive PE. In addition, we discuss an outline of our approach and use of PERT.

Objectives: The purpose of this study was to investigate the effect of post-exercise ankle-brachial index (ABI) on the incidence of lower extremity (LE) revascularization, cardiovascular outcomes, and all-cause mortality in patients with normal and abnormal resting ABI., Background: The clinical and prognostic value of post-exercise ABI in the setting of normal or abnormal resting ABI remains uncertain., Methods: A total of 2,791 consecutive patients with ABI testing between September 2005 and January 2010 were classified into group 1: normal resting (NR)/normal post-exercise (NE); group 2: NR/abnormal post-exercise (AE); group 3: abnormal resting (AR)/NE; and group 4: AR/AE. Abnormal post-exercise ABI was defined as a drop of >20% from resting ABI as per the American College of Cardiology/American Heart Association guidelines. The primary endpoint was incidence of LE revascularization. Secondary endpoints were major adverse cardiovascular events (MACE) and all-cause mortality. Associations between post-exercise ABI and outcomes were adjusted using multivariable Cox proportional hazard and propensity analyses., Results: Compared with group 1 (NR/NE), group 2 (NR/AE) had increased LE revascularization (propensity-matched adjusted hazard ratio [HR]: 6.63, 95% confidence interval [CI]: 3.13 to 14.04; p < 0.001) but no differences in MACE or all-cause mortality. When resting ABI was abnormal, group 4 (AR/AE) compared with group 3 (AR/NE), abnormal post-exercise ABI was still associated with increased LE revascularization (adjusted HR: 1.59, 95% CI: 1.11 to 2.28; p = 0.01), which persisted after propensity matching (adjusted HR: 2.32, 95% CI: 1.52 to 3.54; p < 0.001). Compared with group 1 (NR/NE) and after propensity matching, group 4 (AR/AE) had a significant increase in MACE (adjusted HR: 1.44, 95% CI: 1.09 to 1.90; p = 0.009) and a trend toward increased all-cause mortality (adjusted HR: 1.37, 95% CI: 0.99 to 1.88; p = 0.052); however, group 3 (AR/NE) did not., Conclusions: Post-exercise ABI appears to offer both clinical (lower extremity revascularization) and prognostic information in those with normal and abnormal resting ABI., (Copyright © 2015 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.)

Unfractionated heparin (UFH) and the low molecular weight heparin (LMWH) preparations are two of the most commonly prescribed medications in the hospital, and indications for their use are increasing. An increasingly recognized untoward effect of either UFH or LMWH is heparin-induced thrombocytopenia (HIT), a transient, prothrombotic condition that may result in venous or arterial thrombosis and amputation or death. This immune-mediated process generally develops within 4 to 14 days of administration, although it may occur more rapidly if there has been a recent exposure; it may even occur days to weeks after UFH or LMWH has been discontinued. Although once considered necessary for the diagnosis of HIT, thrombocytopenia is no longer essential. A 50% reduction in the platelet count from pre-heparin treatment levels is now considered a more specific finding. Prompt recognition, discontinuation of the offending agent, and initiation of an alternative anticoagulant are essential for prevention and/or treatment of these potentially devastating complications.

Background: Venous thromboembolism (VTE) is a concerning problem for hospitalized heart failure (HF) patients. Current recommendations are that all hospitalized New York Heart Association Class III or IV HF patients should receive VTE prophylaxis. Our purpose was to describe the rate of use and the characteristics of patients receiving VTE prophylaxis in the Acute Decompensated Heart Failure National Registry (ADHERE)., Methods and Results: HF hospitalization episodes in ADHERE were analyzed. Patients were excluded from analysis if they were receiving Coumadin or intravenous heparin, had elevated troponin levels, underwent cardiac catheterization or dialysis before or during hospitalization, or were initially admitted to the intensive care unit. VTE prophylaxis was defined as low-molecular-weight or subcutaneous unfractionated heparin administered at any time during hospitalization and intravenous vasoactive therapy was defined as any inotrope, inodilator, or vasodilator. Chi-square, analysis of variance, and Wilcoxon tests were used for univariate and multivariate analyses. Logistic regression was used to evaluate outcomes. A total of 155,073 entries were evaluated, with 71,376 eligible for VTE prophylaxis; 21,847 (31%) received VTE prophylaxis. VTE prophylaxis patients were more often African American (28% versus 21%) or admitted from the emergency department (84% versus 79%), compared with those who did not receive VTE prophylaxis (both P < .0001). Medical history and initial presentation characteristics were similar, except edema, which was more likely in VTE prophylaxis patients (71% versus 66%, P < .0001). Patients receiving VTE prophylaxis more often received an intravenous vasoactive agent (23% versus 18%), angiotensin-converting enzyme inhibitor (61% versus 54%), or beta-blocker (63% versus 58%) during their hospitalization and were more likely discharged on an angiotensin-converting enzyme inhibitor (53% versus 49%) or beta-blocker (57% versus 54%) than non-VTE prophylaxis patients, all P < .0001. VTE prophylaxis patients were more often admitted to the intensive care unit (4.8% versus 2.5%, P < .0001) and had longer median hospital stays (4.2 versus 3.8 days, P < .0001). Mortality was similar between cohorts (3.0% versus 2.9%, P = .69)., Conclusions: Despite recommendations that all hospitalized New York Heart Association III and IV CHF patients receive venous thromboembolic disease prophylaxis, less than one third of eligible patients receive this guideline recommended therapy.

Background: Argatroban, a direct thrombin inhibitor that has reduced clearance in elderly versus younger volunteers, is used for thromboprophylaxis or treatment in heparin-induced thrombocytopenia (HIT)., Objective: To evaluate the effect of aging on argatroban therapy, including dosage, anticoagulant responses, clinical outcomes and factors influencing those responses, in elderly patients with HIT or a history of HIT., Methods: This was a retrospective multicentre database analysis of 118 inpatients treated with argatroban at six medical centres between August 2001 and January 2005. Sixty-two adults aged >/=65 years were administered argatroban for clinically diagnosed HIT (n = 54) or a history of HIT (n = 8). Argatroban infusion was adjusted to achieve activated partial thromboplastin times (aPTTs) 1.5-3 times baseline. All study measures and analyses were prospectively defined. Argatroban dosage patterns, aPTTs and platelet count responses, and 37-day outcomes (death, amputation, new thrombosis, major bleeding) were summarised for patients stratified by age (65-74 years [n = 31]; 75-84 years [n = 26]; >/=85 years [n = 5]) to identify possible age-related trends. Regression analyses explored relationships between dose and patient age, liver function and renal function. Cox proportional hazards models evaluated the effect of age, dose, gender, aPTT and platelet count on the risk of new thrombosis., Results: In each age group, the median argatroban dosage was initially 1.0 microg/kg/min and was generally maintained at or near that dose during therapy (median, 5-7 days). Therapeutic aPTTs occurred within 11.5 hours; the median aPTT during therapy was 54.7 seconds, without obvious trend by age. By regression analysis, the initial and mean argatroban dosages decreased 0.08-0.09 microg/kg/min with each 0.2 mg/dL increase in serum creatinine, but no association was detected between dose and patient age, serum total bilirubin, calculated creatinine clearance or blood urea nitrogen. Platelet counts recovered within 6-7 days of initiating therapy, without apparent trend by age. No patient experienced amputation or major bleeding, and no patient in the oldest group died or had new thrombosis. Overall, 13 (21%) patients died (9 in the 65-74 years group; 1 receiving argatroban) and 5 (8%) had new thrombosis (4 in the 65-74 years group; 2 receiving argatroban), comparing favourably with previously reported rates, irrespective of patient age. By univariate (but not multivariate) analysis, the risk of new thrombosis decreased with increasing argatroban dose (hazard ratio 0.020; 95% CI 0.001, 0.757; p = 0.035). No effect of age or the other covariates considered on thrombotic risk was detected., Conclusion: Argatroban at a median initial dosage of 1.0 microg/kg/min, adjusted to achieve median aPTTs of 54.7 seconds during therapy, generally provided safe, adequate anticoagulation across a wide age range in elderly patients with HIT or a history of HIT. In these elderly patients, age was not a significant determinant of argatroban dosage or thrombotic risk. Prospective evaluation of this initial dose of argatroban in the elderly is warranted.

Peripheral arterial disease (PAD) is a systemic atherosclerotic process for which the major risk factors are similar to those for atherosclerosis in the carotid, coronary, and other vascular beds. Among the traditional risk factors for PAD, those with the strongest associations are advanced age, smoking, and diabetes mellitus. More recently, a number of nontraditional risk factors for PAD have also been recognized. This article briefly reviews the pathophysiology of PAD and the evidence supporting established and emerging risk factors for its development.

Background: Heparin-induced thrombocytopenia (HIT) can lead to catastrophic thromboembolic complications and requires treatment with an alternative, rapidly active anticoagulant, such as a direct thrombin inhibitor (DTI), either to prevent or treat these complications. Switching to oral warfarin after initial treatment with a DTI is necessary in most patients. Most references related to warfarin suggest that an increased risk for bleeding will occur with elevated international normalized ratios (INRs) > 4.6. In patients receiving argatroban, it is not uncommon to achieve an INR > 4 during this transition. Because the clinical outcomes in patients achieving an INR > 4 during combined argatroban/warfarin therapies for HIT are not well described, we evaluated the clinical outcomes of 111 patients with this phenomenon., Methods: We identified patients from the prospective studies of argatroban anticoagulation, Argatroban-911 and Argatroban-915. Data collected from these studies included death from all causes, amputation, new thrombosis, major bleeding, INR values, argatroban doses, aPTT values, platelet counts, and duration of therapy., Results: Patients were on argatroban monotherapy for a median of 2.8 (0.1-8.1) days, and on cotherapy for a median of 3.7 (0.9-12.8) days. The median platelet count was 70.9 (18-325) x 10(9)/L at the time of HIT diagnosis and increased to 94 (30-324) x 10(9)/L by the time warfarin was initiated. At a median argatroban dose of 1.4 (0.2-2.0) mcg/kg/min, the maximum INR ranged from 4.1 to 21.2 (median 6.4, n = 111) and the corresponding aPTT ranged from 48.1 to 105 (median 71, n = 93) seconds. After argatroban cessation, the first recorded INR within 4 to 24 hours ranged from 1.5 to 12.5 (median 2.9, n = 58). Adverse clinical outcomes occurred in 9 (8.1%) patients during cotherapy and in 12 (10.8%) patients after argatroban anticoagulation was discontinued. Adverse clinical outcomes included 7 cases of new thrombosis, 3 amputations, 12 deaths and 1 major bleed. Eleven of 12 (91.7%) patients died due to causes other than thrombosis, and most deaths (83%) occurred following cotherapy. Five (4.5%) patients developed new thrombosis during argatroban/warfarin cotherapy despite an INR > 4. In contrast only 1 (0.9%) patient experienced major bleeding., Conclusion: In patients receiving argatroban/warfarin cotherapy and with an elevated INR > 4, the risk for thrombosis exceeds the risk of bleeding. Traditional paradigms concerning elevated INRs and warfarin may need to be redesigned for the patient population on cotherapy with direct thrombin inhibitors.Abbreviated Abstract. The clinical outcomes of 111 patients with INRs > 4 while on combined argatroban (dose < or = 2 mcg/kg/min) and warfarin were evaluated. Adverse clinical outcomes (7 new thrombosis, 3 amputations, 12 deaths and 1 major bleed) occurred in 21 patients. Eleven deaths were due to causes other than thrombosis. Five patients developed new thrombosis while only 1 had major bleeding. The risk for thrombosis exceeds the risk of bleeding in patients with HIT despite an INR > 4.

Varicose veins are not only a cosmetic annoyance: they can lead to complications that result in lost time from work and lost wages. Treatment has improved with the use of minimally invasive techniques that reduce recovery time and complications and offer better long-term results--encouraging news, considering that the problem affects 10% to 20% of adult men and 25% to 33% of adult women.

Heparin-induced thrombocytopenia (HIT) is a potentially devastating complication of therapy with either unfractionated or low-molecular-weight heparin. Thrombocytopenia is no longer essential for the diagnosis of HIT, since a 50% drop in the platelet count may be a more specific indicator. Once HIT is clinically suspected, heparin should be stopped immediately and direct thrombin inhibitor therapy started; waiting for laboratory confirmation may be catastrophic.