Diagnosis and Management of Cardiovascular Disease in Advanced and End‐Stage Renal Disease

Bhatti, Navdeep; Galougahi, Keyvan Karimi; Paz, Yehuda; Nazif, Tamim; Moses, Jeffrey W.; Leon, Martin B.; Stone, Gregg W.; Kirtane, Ajay J.; Karmpaliotis, Dimitri; Bokhari, Sabahat; Hardy, Mark A.; Dube, Geoffrey K.; Mohan, Sumit; Ratner, Lloyd E.; Cohen, David J.; Ali, Ziad A.

doi:10.1161/jaha.116.003648

Cited by 69 publications

(33 citation statements)

References 137 publications

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“…This is a relevant target population because even without atrial fibrillation, patients on hemodialysis are at risk of cardiovascular events and such events are responsible for at least 50% of the mortality. 61 Therefore, FXI-directed strategies may provide an effective and safe method for reducing major adverse cardiovascular events in these high-risk patients.…”

Section: Potential Indications For Fxi-directed Therapiesmentioning

confidence: 99%

2017 Scientific Sessions Sol Sherry Distinguished Lecture in Thrombosis

Weitz

Fredenburgh

2018

ATVB

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Abstract-The goal of anticoagulant therapy is to attenuate thrombosis without compromising hemostasis. Although the direct oral anticoagulants are associated with less intracranial hemorrhage than vitamin K antagonists, bleeding remains their major side effect. Factor XI has emerged as a promising target for anticoagulants that may be safer than those currently available. The focus on factor XI stems from epidemiological evidence of its role in thrombosis, the observation of attenuated thrombosis in factor XI-deficient mice, identification of novel activators, and the fact that factor XI deficiency is associated with only a mild bleeding diathesis. Proof-of-concept comes from the demonstration that compared with enoxaparin, factor XI knockdown reduces venous thromboembolism without increasing bleeding after elective knee arthroplasty. This article rationalizes the selection of factor XI as a target for new anticoagulants, reviews the agents under development, and outlines a potential path forward for their development. Visual Overview-An online visual overview is available for this article. (Arterioscler Thromb Vasc Biol. 2018;38: 304-310.

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Section: Potential Indications For Fxi-directed Therapiesmentioning

confidence: 99%

2017 Scientific Sessions Sol Sherry Distinguished Lecture in Thrombosis

Weitz

Fredenburgh

2018

ATVB

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“…The prevalence of cardiovascular diseases is high among patients with chronic kidney disease (CKD), which increases morbidity and mortality in this population and represents a significant financial burden for both the patients and the healthcare systems. Compared to patients with preserved renal function, CKD patients with a glomerular filtration rate (GFR) <45 mL/min/1.73 m 2 have higher risk for cardiovascular disease .…”

Section: Introductionmentioning

confidence: 99%

Role of vascular calcification inhibitors in preventing vascular dysfunction and mortality in hemodialysis patients

Güngör

Koçyiğit

Yılmaz

et al. 2017

Seminars in Dialysis

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Cardiovascular events make up the primary cause of death in hemodialysis patients, and the risk for cardiovascular mortality is significantly increased by vascular calcification, a condition observed frequently in this patient population. The mechanisms underlying the pathogenesis of vascular calcification are complex, and many factors facilitate or hinder the development of calcification. In this review, we first summarize the main factors contributing to the pathogenesis of vascular calcification in patients with end-stage renal disease. We then explore the role of calcification inhibitors in the calcification process, as well as their effect on vascular dysfunction and mortality in hemodialysis patients. | INTRODUCTIONThe prevalence of cardiovascular diseases is high among patients with chronic kidney disease (CKD), 1 which increases morbidity and mortality in this population and represents a significant financial burden for both the patients and the healthcare systems. where it may occur in the intima and media layers of the blood vessels and in the cardiac valves. 12 The prevalence of coronary artery calcification is high among dialysis patients; specifically, some degree of coronary artery calcification is observed in 54%-100% of patients, well above the prevalence in the general population. 13Older age, male sex, long duration of dialysis, diabetes, hypertension, smoking, alcohol consumption, hyperphosphatemia, hypercalcemia,

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“…Cardiovascular diseases (CV) represent a leading cause of mortality in patients with end-stage kidney disease (ESKD), accounting for nearly 50% of all deaths [1]. The severity of cardiovascular injury in these patients is the consequence of a complex and multifactorial vascular health impairment, in which several factors are involved.…”

Section: Introductionmentioning

confidence: 99%

Consequences of Supraphysiological Dialysate Magnesium on Arterial Stiffness, Hemodynamic Profile, and Endothelial Function in Hemodialysis: A Randomized Crossover Study Followed by a Non-Controlled Follow-Up Phase

et al. 2020

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Introduction: Increasing dialysate magnesium (D-Mg 2?) appears to be an intriguing strategy to obtain cardiovascular benefits in subjects with end-stage kidney disease (ESKD) on hemodialysis. To date, however, hemodialysis guidelines do not suggest to increase D-Mg 2? routinely set at 0.50 mmol/L. Methods: A randomized 4-week crossover study aimed at investigating the consequences of increasing D-Mg 2? from 0.50 to 0.75 mmol/L on arterial stiffness, hemodynamic profile, and endothelial function in subjects undergoing hemodialysis. The long-term effect of higher D-Mg 2? on mineral metabolism markers was investigated in a 6-month follow-up. Data were analyzed by linear mixed models for repeated measures. Results: Data of 39 patients were analyzed. Pulse wave velocity and pulse pressure significantly decreased on the higher D-Mg 2? compared with the standard one by-0.91 m/s (95% confidence interval-1.52 to-0.29; p = 0.01) and-9.61 mmHg (-18.89 to-0.33, p = 0.04), respectively. A significant reduction in systolic blood pressure of-12.96 mmHg (-24.71 to-1.22, p = 0.03) was also observed. No period or carryover effects were observed. During the long-term follow-up phase the higher D-Mg 2? significantly increased ionized and total serum Mg (respectively from 0.54 to 0.64 and from 0.84 to 1.07 mmol/L; mean percentage change from baseline to follow-up ? 21% and ? 27%; p B 0.001), while parathormone (PTH) decreased significantly (from 36.6 to 34.4 pmol/ L; % change-11%, p = 0.03). Conclusions: Increasing dialysate magnesium improves vascular stiffness in subjects undergoing maintenance hemodialysis. The present findings merit a larger trial to evaluate the Rosaria Del Giorno and Soraya Lavorato Hadjeres are joint first authors.

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Diagnosis and Management of Cardiovascular Disease in Advanced and End‐Stage Renal Disease

Cited by 69 publications

References 137 publications

2017 Scientific Sessions Sol Sherry Distinguished Lecture in Thrombosis

2017 Scientific Sessions Sol Sherry Distinguished Lecture in Thrombosis

Role of vascular calcification inhibitors in preventing vascular dysfunction and mortality in hemodialysis patients

Consequences of Supraphysiological Dialysate Magnesium on Arterial Stiffness, Hemodynamic Profile, and Endothelial Function in Hemodialysis: A Randomized Crossover Study Followed by a Non-Controlled Follow-Up Phase

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