Faculty Opinions recommendation of Markers of endothelial dysfunction, coagulation and tissue fibrosis independently predict venous thromboembolism in HIV.

Author(s):  
Andrew Badley ◽  
Nathan Cummins
AIDS ◽  
2011 ◽  
Vol 25 (6) ◽  
pp. 787-795 ◽  
Author(s):  
Laura W Musselwhite ◽  
Virginia Sheikh ◽  
Thomas D Norton ◽  
Adam Rupert ◽  
Brian O Porter ◽  
...  

2016 ◽  
Vol 139 ◽  
pp. 17-21 ◽  
Author(s):  
Megha Prasad ◽  
Robert McBane ◽  
Martin Reriani ◽  
Lilach O. Lerman ◽  
Amir Lerman

Author(s):  
Hooman D. Poor ◽  
Corey E. Ventetuolo ◽  
Thomas Tolbert ◽  
Glen Chun ◽  
Gregory Serrao ◽  
...  

AbstractCritically ill COVID-19 patients have relatively well-preserved lung mechanics despite severe gas exchange abnormalities, a feature not consistent with classical ARDS but more consistent with pulmonary vascular disease. Patients with severe COVID-19 also demonstrate markedly abnormal coagulation, with elevated D-dimers and higher rates of venous thromboembolism. We present four cases of patients with severe COVID-19 pneumonia with severe respiratory failure and shock who demonstrated immediate improvements in gas exchange and/or hemodynamics with systemic tPA.Subject category4.6 ICU Management and Outcome


Blood ◽  
2021 ◽  
Vol 138 (Supplement 1) ◽  
pp. 4266-4266
Author(s):  
Alberto D. Lopez ◽  
Kanisha Patel ◽  
Vincent P. Diego ◽  
Marcio A. Almeida ◽  
John Blangero ◽  
...  

Abstract Background: Hemostasis variables represent well-known pathogenic determinants of venous-thromboembolism and are hypothesized to influence risk for cardiometabolic outcomes (CMOs) by effecting susceptibility to vascular inflammation and/or endothelial dysfunction. Methods: We investigated in Mexican American (MA)-participants of the San Antonio Family Study the effects of 20 measured hemostasis variables on CMOs including type-2 diabetes (T2D), impaired-fasting glucose (IFG), insulin resistance (IR), hypertension, obesity based on sex-specific waist circumference (OBWC), low high-density lipoprotein (Low-HDL)-cholesterol, hypertriglyceridemia, and a heart distress (HD) variable comprised of history of heart attack and/or heart surgery. The hemostasis variables included PT, aPTT, TFPI, aPC-ratio, fibrinogen, von Willebrand Factor (VWF), ADAMST-13, D-dimer, fPS, tPS, plasminogen, and factor (F)II, FV, FVII, FVIII, FX, FXI, and FXII of the coagulation system. We used a backward stepwise-regression selection approach to identify the preliminary sets of hemostasis predictors. Results: Our final regression models consisted of the final set of hemostasis variables while accounting for age and sex as covariates. For the T2D, IFG, and HD outcomes, VWF was the only significant hemostasis predictor (p<0.05). In each case, VWF was positively associated with the outcome. The hemostasis variable fibrinogen was a significant positive predictor for the IR, OBWC, and Low-HDL-cholesterol outcomes (p<0.05). For OBWC, FV was an additional significant positive predictor (p<0.05). Finally, no hemostasis variables significantly predicted hypertension or hypertriglyceridemia. Conclusions: Our results demonstrate that, among the MA-population, all measured CMOs-except hypertension and hypertriglyceridemia-are significantly influenced by individual-variability in several hemostasis parameters with most important predictors being VWF and fibrinogen. Keywords: Hemostasis; Venous-thromboembolism; Cardiovascular diseases/disorders; Metabolic syndrome; Inflammation; Endothelial dysfunction; Mexican American; Coagulation factors; von Willebrand Factor; and Fibrinogen Disclosures No relevant conflicts of interest to declare.


2015 ◽  
Vol 35 (suppl_1) ◽  
Author(s):  
Megha Prasad ◽  
Martin Reriani ◽  
Robert McBane ◽  
Lilach O Lerman ◽  
Amir Lerman

Introduction: Venous thromboembolism (VTE) is a cause of significant morbidity and mortality. The vascular endothelium may be involved in the pathogenesis of both VTE and arterial thrombosis, as endothelial injury and dysfunction may disrupt normal anticoagulation mechanisms. We aimed to test the hypothesis that coronary endothelial dysfunction (CED) is associated with development of VTE in prospective follow-up. Methods: Coronary vascular reactivity was evaluated in 502 patients with non-obstructive coronary artery disease by administration of intracoronary acetylcholine during diagnostic angiography. Microvascular CED was defined as ≤50% increase in coronary blood flow (CBF) from baseline in response to maximal dose of acetylcholine. After median follow-up of 6.3 years (IQR 3.5, 10.7), patients were assessed by standardized questionnaire, phone-call and review of medical records for development of VTE. Results: Median age of the population was 53 years (IQR 45, 62); 68% were females. Hypertension was prevalent in 40.8%, diabetes in 8.4%, and hyperlipidemia in 58.3% of patients. Of 502 patients, 279 had CED. There were no significant differences in baseline characteristics including cardiovascular and VTE risk factors between patients with and without CED (p>0.05). Eighty-nine percents of patients who developed VTE had CED. Patients who developed spontaneous or provoked VTE both had significantly lower % change in CBF than patients who did not develop VTE (p<0.05) (Figure 1). In univariate analysis, microvascular dysfunction was associated with increased risk of VTE (OR 6.55 (95% confidence interval (0.81, 52.79); p=0.04). Conclusion: We found a seven-fold increased risk of VTE with CED, suggesting a link between the two. Endothelial injury disrupting vascular homeostasis may predispose patients to VTE.


2017 ◽  
Vol 177 (5) ◽  
pp. 1248-1255 ◽  
Author(s):  
C. Huang ◽  
L. Liu ◽  
Z. You ◽  
Y. Zhao ◽  
J. Dong ◽  
...  

Author(s):  
Darae Ko ◽  
Sarah R. Preis ◽  
Andrew D. Johnson ◽  
Ramachandran S. Vasan ◽  
Emelia J. Benjamin ◽  
...  

Haematologica ◽  
2007 ◽  
Vol 92 (6) ◽  
pp. 812-818 ◽  
Author(s):  
R. Migliacci ◽  
C. Becattini ◽  
R. Pesavento ◽  
G. Davi ◽  
M. C. Vedovati ◽  
...  

2004 ◽  
Vol 71 ◽  
pp. 121-133 ◽  
Author(s):  
Ascan Warnholtz ◽  
Maria Wendt ◽  
Michael August ◽  
Thomas Münzel

Endothelial dysfunction in the setting of cardiovascular risk factors, such as hypercholesterolaemia, hypertension, diabetes mellitus and chronic smoking, as well as in the setting of heart failure, has been shown to be at least partly dependent on the production of reactive oxygen species in endothelial and/or smooth muscle cells and the adventitia, and the subsequent decrease in vascular bioavailability of NO. Superoxide-producing enzymes involved in increased oxidative stress within vascular tissue include NAD(P)H-oxidase, xanthine oxidase and endothelial nitric oxide synthase in an uncoupled state. Recent studies indicate that endothelial dysfunction of peripheral and coronary resistance and conductance vessels represents a strong and independent risk factor for future cardiovascular events. Ways to reduce endothelial dysfunction include risk-factor modification and treatment with substances that have been shown to reduce oxidative stress and, simultaneously, to stimulate endothelial NO production, such as inhibitors of angiotensin-converting enzyme or the statins. In contrast, in conditions where increased production of reactive oxygen species, such as superoxide, in vascular tissue is established, treatment with NO, e.g. via administration of nitroglycerin, results in a rapid development of endothelial dysfunction, which may worsen the prognosis in patients with established coronary artery disease.


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