ascorbic-acid has been researched along with Aortic-Valve-Stenosis* in 3 studies
1 trial(s) available for ascorbic-acid and Aortic-Valve-Stenosis
Article | Year |
---|---|
Impact of vitamin E and C supplementation on serum adhesion molecules in chronic degenerative aortic stenosis: a randomized controlled trial.
An inflammatory component has been identified in degenerative aortic stenosis (AS). The combination of vitamins E and C has been shown to have anti-inflammatory properties. The aim of this study was to determine the impact of the combination of vitamins C and E or vitamin C only on serum levels of cell adhesion molecules and C-reactive protein in patients with chronic degenerative AS, with or without concomitant coronary artery disease.. One hundred patients with asymptomatic or mildly symptomatic moderate AS were randomized in 2:2:1 format in an open-label trial. Forty-one patients received vitamin E (400 IU) and vitamin C (1000 mg) daily, 39 patients received vitamin C (1000 mg) only, and 20 patients were followed as controls. Serum intracellular adhesion molecule (ICAM-1), E selectin, P selectin, vascular-cellular adhesion molecule (VCAM-1), C-reactive protein, and alpha-tocopherol (vitamin E) were measured by enzyme-linked immunosorbent assay at baseline and 6 months postsupplementation. Half of the patients from each of the 2 active groups were followed for further 6 months to determine any changes after cessation of therapy. In the vitamin E and C, group there was reduction in serum ICAM-1 (298 +/- 12 to 272 +/- 12 ng/mL at 6 months, P = .0015) with a return to base line 6 months after cessation of therapy. In the vitamin C only group, there was a reduction in serum P selectin (134 +/- 10 to 118 +/- 10 ng/mL at 6 months, P = .033). All the inflammatory markers were unchanged in control group over 6 months of follow-up.. Vitamin E and C supplementation had modest anti-inflammatory effect in chronic degenerative AS. The clinical relevance of this would require further clarification. Topics: Aged; Anti-Inflammatory Agents, Non-Steroidal; Antioxidants; Aortic Valve Stenosis; Ascorbic Acid; C-Reactive Protein; Cell Adhesion Molecules; Drug Therapy, Combination; E-Selectin; Female; Humans; Inflammation; Intercellular Adhesion Molecule-1; Male; Middle Aged; P-Selectin; Treatment Outcome; Vascular Cell Adhesion Molecule-1; Vitamin E | 2005 |
2 other study(ies) available for ascorbic-acid and Aortic-Valve-Stenosis
Article | Year |
---|---|
Cellular Mechanisms of Aortic Valve Calcification.
Comparative in vitro study examined the osteogenic potential of interstitial cells of aortic valve obtained from the patients with aortic stenosis and from control recipients of orthotopic heart transplantation with intact aortic valve. The osteogenic inductors augmented mineralization of aortic valve interstitial cells (AVIC) in patients with aortic stenosis in comparison with the control level. Native AVIC culture of aortic stenosis patients demonstrated overexpression of osteopontin gene (OPN) and underexpression of osteoprotegerin gene (OPG) in comparison with control levels. In both groups, AVIC differentiation was associated with overexpression of RUNX2 and SPRY1 genes. In AVIC of aortic stenosis patients, expression of BMP2 gene was significantly greater than the control level. The study revealed an enhanced sensitivity of AVIC to osteogenic inductors in aortic stenosis patients, which indicates probable implication of OPN, OPG, and BMP2 genes in pathogenesis of aortic valve calcification. Topics: Aged; Aortic Valve; Aortic Valve Stenosis; Ascorbic Acid; Bone Morphogenetic Protein 2; Calcinosis; Cell Differentiation; Core Binding Factor Alpha 1 Subunit; Dexamethasone; Female; Gene Expression Regulation; Glycerophosphates; Heart Transplantation; Humans; Male; Membrane Proteins; Middle Aged; Osteoblasts; Osteogenesis; Osteopontin; Osteoprotegerin; Phosphoproteins; Primary Cell Culture; Stromal Cells; Tricuspid Valve | 2018 |
Vitamin C and quinapril abrogate LVH and endothelial dysfunction in aortic-banded guinea pigs.
Left ventricular hypertrophy (LVH) is a cardiovascular risk factor. A possible role for endothelial dysfunction in this condition was investigated in a Dunkin-Hartley guinea pig aortic-banded pressure overload-induced model of LVH. Aortic banding produced significant elevation of fore- and hindlimb blood pressure (BP), heart-to-body weight ratios, plasma angiotensin II (ANG II), endothelin-1 (ET-1), tumor necrosis factor-alpha (TNF-alpha) levels, and coronary microvascular endothelial cell (CMEC) NAD(P)H-dependent superoxide (O) production, and a significant decrease in basal and stimulated CMEC cGMP levels. Treatment of aortic-banded animals with the angiotensin-converting enzyme inhibitor quinapril and the antioxidant vitamin C, either alone or in combination, did not affect BP but caused a significant inhibition of the increases in the heart-to-body weight ratio, ANG II, ET-1, and TNF-alpha levels, and O production and restored cGMP responses to levels comparable with sham-operated animals. These data suggest that quinapril and vitamin C are capable of inhibiting LVH development due to pressure overload via mechanisms that involve the inhibition of oxidative stress, an improvement in coronary endothelial function, and increased nitric oxide bioavailability. Topics: Animals; Aortic Valve Stenosis; Ascorbic Acid; Blood Pressure; Coronary Vessels; Endothelium, Vascular; Guinea Pigs; Hypertension; Hypertrophy, Left Ventricular; Isoquinolines; Male; NAD; NADP; Quinapril; Superoxides; Tetrahydroisoquinolines | 2001 |