Endothelial dysfunction, platelet activation, thrombogenesis and fibrinolysis in patients with hypertensive crisis

Born, Bert‐Jan H. van den; Löwenberg, Ester C.; Hoeven, Niels V. van der; Laat, Bas de; Meijers, Joost C. M.; Levi, Marcel; Montfrans, Gert A. van

doi:10.1097/hjh.0b013e328345023d

Cited by 57 publications

(36 citation statements)

References 19 publications

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“…An important function of VWF is to mediate platelet-platelet interactions and platelet adhesion to sub-endothelial collagen and is associated with platelet consumption and thrombocytopenia [13–15]. The median platelet count in patients with melioidosis was 189 × 10 9 /l compared to 299 × 10 9 /l in controls ( p = 0.0001, Fig 1A).…”

Section: Resultsmentioning

confidence: 99%

“…The plasma was stored at –70°C pending assay in The Netherlands. VWF antigen (Dako, Glostrup, Denmark) and VWF propeptide (Sanquin, Amsterdam, The Netherlands) were assayed by enzyme-linked immunoassay as described previously [15]. ADAMTS13 levels and prothrombin time (PT) were measured on an automated blood coagulation analyzer (BCS XP, Siemens Healthcare Diagnostics, Marburg, Germany) [26, 27].…”

Section: Methodsmentioning

confidence: 99%

“…VWF excess is therefore associated with platelet consumption and thrombocytopenia [13–15]. VWF is constitutively expressed by endothelial cells and stored in Weibel-Palade bodies, but can also be released following stimulation by endotoxin, cytokines or thrombin and is consequently detectable in its native, ultralarge isoform (ulVWF).…”

Section: Introductionmentioning

confidence: 99%

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Increased Von Willebrand factor, decreased ADAMTS13 and thrombocytopenia in melioidosis

et al. 2017

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BackgroundMelioidosis, caused by bioterror treat agent Burkholderia pseudomallei, is an important cause of community-acquired Gram-negative sepsis in Southeast Asia and Northern Australia. New insights into the pathogenesis of melioidosis may help improve treatment and decrease mortality rates from this dreadful disease. We hypothesized that changes in Von Willebrand factor (VWF) function should occur in melioidosis, based on the presence of endothelial stimulation by endotoxin, pro-inflammatory cytokines and thrombin in melioidosis, and investigated whether this impacted on outcome.Methods/Principal findingsWe recruited 52 controls and 34 culture-confirmed melioidosis patients at Sappasithiprasong Hospital in Ubon Ratchathani, Thailand. All subjects were diabetic. Platelet counts in melioidosis patients were lower compared to controls (p = 0.0001) and correlated with mortality (p = 0.02). VWF antigen levels were higher in patients (geometric mean, 478 U/dl) compared to controls (166 U/dL, p<0.0001). The high levels of VWF in melioidosis appeared to be due to increased endothelial stimulation (VWF propeptide levels were elevated, p<0.0001) and reduced clearance (ADAMTS13 reduction, p<0.0001). However, VWF antigen levels did not correlate with platelet counts implying that thrombocytopenia in acute melioidosis has an alternative cause.Conclusions/SignificanceThrombocytopenia is a key feature of melioidosis and is correlated with mortality. Additionally, excess VWF and ADAMTS13 deficiency are features of acute melioidosis, but are not the primary drivers of thrombocytopenia in melioidosis. Further studies on the role of thrombocytopenia in B. pseudomallei infection are needed.

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Section: Resultsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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Increased Von Willebrand factor, decreased ADAMTS13 and thrombocytopenia in melioidosis

et al. 2017

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“…In one study, serum aldosterone levels were found to be higher in MHT patients with TMA versus those without TMA [21]. In addition, hypertensive crises are known to be prothrombotic, leading to platelet aggregation, thrombin generation, and fibrinolysis [51]. …”

Section: Discussionmentioning

confidence: 99%

Atypical hemolytic uremic syndrome in the setting of complement-amplifying conditions: case reports and a review of the evidence for treatment with eculizumab

2016

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Atypical hemolytic uremic syndrome (aHUS) is a rare, genetic, progressive, life-threatening form of thrombotic microangiopathy (TMA) predominantly caused by dysregulation of the alternative pathway of the complement system. Complement-amplifying conditions (CACs), including pregnancy complications [preeclampsia, HELLP (hemolysis, elevated liver enzymes, low platelet count) syndrome], malignant hypertension, autoimmune diseases, transplantation, and others, are associated with the onset of TMA in up to 69 % of cases of aHUS. CACs activate the alternative pathway of complement and may be comorbid with aHUS or may unmask a previously undiagnosed case. In this review, three case reports are presented illustrating the onset and diagnosis of aHUS in the setting of different CACs (pregnancy complications, malignant hypertension, renal transplantation). The report also reviews the evidence for a variety of CACs, including those mentioned above as well as infections and drug-induced TMA, and the overlap with aHUS. Finally, we introduce an algorithm for diagnosis and treatment of aHUS in the setting of CACs. If TMA persists despite initial management for the specific CAC, aHUS should be considered. The terminal complement inhibitor eculizumab should be initiated for all patients with confirmed diagnosis of aHUS, with or without a comorbid CAC.

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“…Besides these mechanisms, a prothrombotic state may play a key role in hypertensive crisis; a recent, albeit small, study showed that sP-selectin was significantly higher in patients with hypertensive crisis compared with normotensive controls regardless of the presence of retinopathy, which suggests that platelet activation is a relatively early finding in the pathophysiologic sequelae of hypertensive crisis (11) (Figure 1). …”

Section: Pathophysiologymentioning

confidence: 99%

Cardiovascular Hypertensive Crisis: Recent Evidence and Review of the Literature

Varounis

Katsi

Nihoyannopoulos³

et al. 2017

Front. Cardiovasc. Med.

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Despite the high prevalence of hypertension (HTN), only a small proportion of the hypertensive patients will ultimately develop hypertensive crisis. In fact, some patients with hypertensive crisis do not report a history of HTN or previous use of antihypertensive medication. The majority of the patients with hypertensive crisis often report non-specific symptoms, whereas heart-related symptoms (dyspnea, chest pain, arrhythmias, and syncope) are less common. Hypertensive crises can be divided into hypertensive emergencies or hypertensive urgencies according to the presence or absence of acute target organ damage, respectively. This differentiation is an extremely useful classification in clinical practice since a different management is needed, which in turn has a significant effect on the morbidity and mortality of these patients. Therefore, it is very crucial for the physician in the emergency department to identify the hypertensive emergencies and to manage them through blood pressure lowering medications in order to avoid further target organ damage or deterioration. The aim of this narrative review is to summarize the recent evidence in an effort to improve the awareness, recognition, risk stratification, and treatment of hypertensive crisis in patients referred to the emergency department.

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Endothelial dysfunction, platelet activation, thrombogenesis and fibrinolysis in patients with hypertensive crisis

Cited by 57 publications

References 19 publications

Increased Von Willebrand factor, decreased ADAMTS13 and thrombocytopenia in melioidosis

Increased Von Willebrand factor, decreased ADAMTS13 and thrombocytopenia in melioidosis

Atypical hemolytic uremic syndrome in the setting of complement-amplifying conditions: case reports and a review of the evidence for treatment with eculizumab

Cardiovascular Hypertensive Crisis: Recent Evidence and Review of the Literature

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