scholarly journals Pharmacological and Nutritional Modulation of Vascular Calcification

Nutrients ◽  
2019 ◽  
Vol 12 (1) ◽  
pp. 100 ◽  
Author(s):  
Liv M. Vossen ◽  
Abraham A. Kroon ◽  
Leon J. Schurgers ◽  
Peter W. de Leeuw
Keyword(s):  
Cardiovascular Disease ◽  
Drug Therapy ◽  
Vascular Calcification ◽  
Vitamin K ◽  
Vascular Function ◽  
Clinical Importance ◽  
Arterial Calcification ◽  
Channel Blockers ◽  
Cardiovascular Morbidity And Mortality ◽  
Prevention And Treatment

Vascular calcification is an independent predictor of cardiovascular disease, and therefore, inhibition or regression of this processes is of clinical importance. The standard care regarding prevention and treatment of cardiovascular disease at this moment mainly depends on drug therapy. In animal and preclinical studies, various forms of cardiovascular drug therapy seem to have a positive effect on vascular calcification. In particular, calcium channel blockers and inhibitors of the renin–angiotensin–aldosteron system slowed down arterial calcification in experimental animals. In humans, the results of trials with these drugs are far less pronounced and often contradictory. There is limited evidence that the development of new atherosclerotic lesions may be retarded in patients with coronary artery disease, but existing lesions can hardly be influenced. Although statin therapy has a proven role in the prevention and treatment of cardiovascular morbidity and mortality, it is associated with both regression and acceleration of the vascular calcification process. Recently, nutritional supplements have been recognized as a potential tool to reduce calcification. This is particularly true for vitamin K, which acts as an inhibitor of vascular calcification. In addition to vitamin K, other dietary supplements may also modulate vascular function. In this narrative review, we discuss the current state of knowledge regarding the pharmacological and nutritional possibilities to prevent the development and progression of vascular calcification.

scholarly journals Vitamin K Supplementation for the Prevention of Cardiovascular Disease: Where Is the Evidence? A Systematic Review of Controlled Trials

Nutrients ◽  
2020 ◽  
Vol 12 (10) ◽  
pp. 2909
Author(s):  
Caitlyn Vlasschaert ◽  
Chloe J. Goss ◽  
Nathan G. Pilkey ◽  
Sandra McKeown ◽  
Rachel M. Holden
Keyword(s):  
Systematic Review ◽  
Cardiovascular Disease ◽  
Vascular Calcification ◽  
Vitamin K ◽  
Cochrane Collaboration ◽  
Matrix Gla Protein ◽  
Arterial Calcification ◽  
Current Evidence ◽  
Controlled Trials ◽  
Cochrane Central Register

Matrix gla protein (MGP) is an important vitamin K-dependent inhibitor of vascular calcification. High levels of uncarboxylated, dephosphorylated MGP have been associated with vascular calcification and are responsive to vitamin K treatment. In this systematic review, we summarize the available evidence examining whether vitamin K supplementation improves surrogate measures of cardiovascular disease including artery and valve calcification, atherosclerosis and artery stiffening. Data from controlled trials of adults were obtained by searching Ovid MEDLINE, Embase, the Cochrane Central Register of Controlled Trials and the Web of Science Core Collection. We identified nine randomized controlled trials for review, including trials of vitamin K1 or vitamin K2 supplementation, that assessed a surrogate measure of cardiovascular disease including arterial calcification, atherosclerosis or arterial stiffening. For each trial, the risk of bias was assessed applying Cochrane Collaboration methodology. The findings indicate that vitamin K does not consistently prevent progression of calcification, atherosclerosis or arterial stiffness. There may be some benefit in people with calcification at study entry. Studies were heterogenous, with relatively short follow-up and outcome measures were varied. While vitamin K supplementation clearly improves the carboxylation of dephosphoylated MGP, its role in mitigating vascular calcification is uncertain, based on current evidence.

Vitamin K Influence on Cardiovascular Mortality in Chronic Hemodialysed Patients

2017 ◽  
Vol 68 (1) ◽  
pp. 52-54 ◽  
Author(s):  
Daniela Radulescu ◽  
Andra Elena Balcangiu Stroescu ◽  
Catalin Pricop ◽  
Bogdan Geavlete ◽  
Carolina Negrei ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Clinical Trials ◽  
Vascular Calcification ◽  
Vitamin K ◽  
Cardiovascular Mortality ◽  
Dietary Intervention ◽  
Vitamin K2

Cardiovascular disease causes increased mortality in chronic hemodialysed patients. The decrease of vascular calcification is one of the main targets in the management of these patients. According to several experimental and clinical trials, choosing the proper diet and prescribing vitamin K2 supplements help to improve prognosis and decrease mortality, but further larger researchers are required to advocate the importance of this dietary intervention in hemodialysed population.

scholarly journals Cardiovascular disease and osteoporosis: is there a link between lipids and bone?

2002 ◽  
Vol 39 (3) ◽  
pp. 203-210 ◽  
Author(s):  
John R Burnett ◽  
Samuel D Vasikaran
Keyword(s):  
Cardiovascular Disease ◽  
Bone Density ◽  
Vascular Calcification ◽  
Cholesterol Biosynthesis ◽  
Hormone Replacement ◽  
Plasma Lipid ◽  
Clinical Effects ◽  
Cardiovascular Morbidity And Mortality ◽  
The Relationship

Atherosclerotic heart disease and osteoporosis are both diseases of old age. Evidence is accumulating for a link between vascular and bone disease. Calcification is a common feature of atherosclerotic plaques, and osteoporosis is associated with both atherosclerosis and vascular calcification. However, the relationship of vascular calcification to the pathogenesis of atherosclerosis remains incompletely understood. Hormone replacement therapy has beneficial effects in the prevention of both atherosclerosis and osteoporosis. Bisphosphonates inhibit bone resorption and are used in the treatment of osteoporosis, whereas the statins inhibit cholesterol biosynthesis and are used for the treatment of atherosclerosis. We have reviewed recent advances in the knowledge of the actions of bisphosphonates and statins at the cellular, molecular and end-organ levels in order to examine the relationship between cardiovascular disease and osteoporosis and to explore the link between lipids and bones. These studies suggest that the mechanism of actions of these two classes of drugs at the cellular level may not be mutually exclusive. There are some early clinical data to complement these findings, suggesting that statins increase bone density and bisphosphonates may have a beneficial effect in vivo on plasma lipid levels and on the atherosclerotic process. Properly designed prospective studies that examine the effect of statins on bone density and fractures, as well as the effects of bisphosphonates on lipid profiles, atherosclerotic progression and cardiovascular morbidity and mortality are needed to define clearly the clinical effects and potential new roles for these agents.

Oral anticoagulant treatment: friend or foe in cardiovascular disease?

Blood ◽  
2004 ◽  
Vol 104 (10) ◽  
pp. 3231-3232 ◽  
Author(s):  
Leon J. Schurgers ◽  
Hermann Aebert ◽  
Cees Vermeer ◽  
Burkhard Bültmann ◽  
Jan Janzen
Keyword(s):  
Cardiovascular Disease ◽  
Vitamin K ◽  
Heart Valves ◽  
Vitamin K Antagonists ◽  
Oral Anticoagulants ◽  
Arterial Calcification ◽  
Adverse Side Effect ◽  
Oral Anticoagulant Treatment ◽  
Carboxyglutamic Acid

Abstract Calcification is a common complication in cardiovascular disease and may affect both arteries and heart valves. Matrix γ-carboxyglutamic acid (Gla) protein (MGP) is a potent inhibitor of vascular calcification, the activity of which is regulated by vitamin K. In animal models, vitamin K antagonists (oral anticoagulants [OACs]) were shown to induce arterial calcification. To investigate whether long-term OAC treatment may induce calcification in humans also, we have measured the grade of aortic valve calcification in patients with and without preoperative OAC treatment. OAC-treated subjects were matched with nontreated ones for age, sex, and disease. Calcifications in patients receiving preoperative OAC treatment were significantly (2-fold) larger than in nontreated patients. These observations suggest that OACs, which are widely used for antithrombotic therapy, may induce cardiovascular calcifications as an adverse side effect.

Combination Drug Therapy: A Strategy for Aggressive Lipid Modification

2005 ◽  
Vol 40 (11) ◽  
pp. 954-962
Author(s):  
James M. Backes ◽  
Patricia A. Howard
Keyword(s):  
Cardiovascular Disease ◽  
Drug Therapy ◽  
Clinical Outcome ◽  
Combination Drug Therapy ◽  
Lipid Modification ◽  
Combination Drug ◽  
Cardiovascular Pharmacotherapy ◽  
The Us ◽  
Prevention And Treatment ◽  
Recent Developments

This continuing feature will update readers on recent developments in cardiovascular pharmacotherapy. Cardiovascular disease remains the number one killer in the US, and more clinical outcome trials have been conducted in cardiology than in any other field of medicine. Given this rapidly expanding knowledge base, pharmacists can have a significant impact on prevention and treatment — if they keep current with developments in drug therapy.

scholarly journals The effect of menaquinone-7 supplementation on vascular calcification in patients with diabetes: a randomized, double-blind, placebo-controlled trial

2019 ◽  
Vol 110 (4) ◽  
pp. 883-890 ◽  
Author(s):  
S R Zwakenberg ◽  
P A de Jong ◽  
J W Bartstra ◽  
R van Asperen ◽  
J Westerink ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Vascular Calcification ◽  
Vitamin K ◽  
Controlled Trial ◽  
Matrix Gla Protein ◽  
Arterial Calcification ◽  
Secondary Outcome ◽  
Double Blind

ABSTRACT Background Vitamin K occurs in the diet as phylloquinone and menaquinones. Observational studies have shown that both phylloquinone and menaquinone intake might reduce cardiovascular disease (CVD) risk. However, the effect of vitamin K on vascular calcification is unknown. Objectives The aim of this study was to assess if menaquinone supplementation, compared to placebo, decreases vascular calcification in people with type 2 diabetes and known CVD. Methods In this double-blind, randomized, placebo-controlled trial, we randomly assigned men and women with type 2 diabetes and CVD to 360 µg/d menaquinone-7 (MK-7) or placebo for 6 mo. Femoral arterial calcification at baseline and 6 mo was measured with 18sodium fluoride positron emission tomography (18F-NaF PET) scans as target-to-background ratios (TBRs), a promising technique to detect active calcification. Calcification mass on conventional computed tomography (CT) scan was measured as secondary outcome. Dephosphorylated–uncarboxylated matrix Gla protein (dp-ucMGP) concentrations were measured to assess compliance. Linear regression analyses were performed with either TBR or CT calcification at follow-up as the dependent variable, and treatment and baseline TBR or CT calcification as independent variables. Results We randomly assigned 35 patients to the MK-7 group (33 completed follow-up) and 33 to the placebo group (27 completed follow-up). After the 6-mo intervention, TBR tended to increase in the MK-7 group compared with placebo (0.25; 95% CI: −0.02, 0.51; P = 0.06), although this was not significant. Log-transformed CT calcification mass did not increase in the intervention group compared with placebo (0.50; 95% CI: −0.23, 1.36; P = 0.18). MK-7 supplementation significantly reduced dp-ucMGP compared with placebo (−205.6 pmol/L; 95% CI: −255.8, −155.3 pmol/L). No adverse events were reported. Conclusion MK-7 supplementation tended to increase active calcification measured with 18F-NaF PET activity compared with placebo, but no effect was found on conventional CT. Additional research investigating the interpretation of 18F-NaF PET activity is necessary. This trial was registered at clinicaltrials.gov as NCT02839044.

Amiodarone Prophylaxis: Impact on Atrial Fibrillation and Outcomes after Cardiac Surgery

2007 ◽  
Vol 42 (8) ◽  
pp. 680-685
Author(s):  
Patricia A. Howard ◽  
Brian J. Barnes
Keyword(s):  
United States ◽  
Atrial Fibrillation ◽  
Cardiovascular Disease ◽  
Cardiac Surgery ◽  
Drug Therapy ◽  
Clinical Outcome ◽  
The United States ◽  
Cardiovascular Pharmacotherapy ◽  
Prevention And Treatment ◽  
Recent Developments

This continuing feature will update readers on recent developments in cardiovascular pharmacotherapy. Cardiovascular disease remains the number one killer in the United States, and more clinical outcome trials have been conducted in cardiology than in any other field of medicine. Given this rapidly expanding knowledge base, pharmacists can have a significant impact on prevention and treatment—if they keep current with developments in drug therapy.

Hormone Replacement Therapy and Cardiovascular Risk

2002 ◽  
Vol 37 (12) ◽  
pp. 1269-1281
Author(s):  
Patricia A. Howard
Keyword(s):  
Cardiovascular Disease ◽  
Cardiovascular Risk ◽  
Hormone Replacement Therapy ◽  
Drug Therapy ◽  
Clinical Outcome ◽  
Hormone Replacement ◽  
Cardiovascular Pharmacotherapy ◽  
The Us ◽  
Prevention And Treatment ◽  
Recent Developments

This continuing feature will update readers on recent developments in cardiovascular pharmacotherapy. Cardiovascular disease remains the number one killer in the US, and more clinical outcome trials have been conducted in cardiology than in any other field of medicine. Given this rapidly expanding knowledge base, pharmacists can have a significant impact on the prevention and treatment of cardiovascular disease—if they keep current with developments in drug therapy.

The A-HeFT Trial: More Questions than Answers

2005 ◽  
Vol 40 (6) ◽  
pp. 483-489
Author(s):  
Patricia A. Howard
Keyword(s):  
Cardiovascular Disease ◽  
Drug Therapy ◽  
Clinical Outcome ◽  
Knowledge Base ◽  
Cardiovascular Pharmacotherapy ◽  
The Us ◽  
Prevention And Treatment ◽  
Recent Developments

This continuing feature will update readers on recent developments in cardiovascular pharmacotherapy. Cardiovascular disease remains the number one killer in the US, and more clinical outcome trials have been conducted in cardiology than in any other field of medicine. Given this rapidly expanding knowledge base, pharmacists can have a significant impact on prevention and treatment — if they keep current with developments in drug therapy.

Vascular calcification in chronic kidney disease

2010 ◽  
Vol 119 (3) ◽  
pp. 111-121 ◽  
Author(s):  
Adrian Covic ◽  
Mehmet Kanbay ◽  
Luminita Voroneanu ◽  
Faruk Turgut ◽  
Dragomir N. Serban ◽  
...  
Keyword(s):  
Risk Factors ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Arterial Stiffness ◽  
Vascular Calcification ◽  
Mineral Metabolism ◽  
Left Ventricular ◽  
Arterial Calcification ◽  
Pathophysiological Mechanism ◽  
Cardiovascular Morbidity And Mortality

VC (vascular calcification) is highly prevalent in patients with CKD (chronic kidney disease), but its mechanism is multifactorial and incompletely understood. In addition to increased traditional risk factors, CKD patients also have a number of non-traditional cardiovascular risk factors, which may play a prominent role in the pathogenesis of arterial calcification, such as duration of dialysis and disorders of mineral metabolism. The transformation of vascular smooth muscle cells into chondrocytes or osteoblast-like cells seems to be a key element in VC pathogenesis, in the context of passive calcium and phosphate deposition due to abnormal bone metabolism and impaired renal excretion. The process may be favoured by the low levels of circulating and locally produced VC inhibitors. VC determines increased arterial stiffness, left ventricular hypertrophy, a decrease in coronary artery perfusion, myocardial ischaemia and increased cardiovascular morbidity and mortality. Although current therapeutic strategies focus on the correction of phosphate, calcium, parathyroid hormone or vitamin D, a better understanding of the mechanisms of abnormal tissue calcification may lead to development of new therapeutic agents, which could reduce VC and improve cardiovascular outcome in CKD patients. The present review summarizes the following aspects: (i) the pathophysiological mechanism responsible for VC and its promoters and inhibitors, (ii) the methods for detection of VC in patients with CKD, including evaluation of arterial stiffness, and (iii) the management of VC in CKD patients.

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