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Therapeutic Effect and Mechanism of Action of Abnormal Savda Munziq in Development of Degenerative Atherosclerotic Aortic Valve Disease.

ABSTRACT: BACKGROUND The aim of this study was to investigate the therapeutic effect of abnormal Savda Munziq (ASMq) on the development of degenerative atherosclerotic aortic valve disease and its underlying mechanisms. MATERIAL AND METHODS We randomly divided 80 rabbits into 4 groups: a normal control group (group N, n=20); a high-fat diet group (group HC, n=20); a high-fat diet and Atorvastatin calcium intervention group (group AI, n=20); and a high-fat diet and ASMq intervention group (group MI, n=20). For evaluation of blood lipid profiles, blood samples were collected at week 0 and at the end of week 8. Aortic valve samples were taken at weeks 0, 2, 4, 6, and 8 for atomic force microscopy (AFM) examination of endothelial cell nanostructures, and at week 8 for pathological examinations. RESULTS Triglyceride (TG), cholesterol (TC), low-density lipoprotein (LDL), and high-density lipoprotein HDL levels of rabbits in group HC were significantly different from those in group N (P<0.01). TG, TC, LDL, and HDL values of rabbits in group MI were significantly different from rabbits in group HC (P<0.05). Pathological examination revealed that the aortic valves from rabbits in group MI were visibly clear, with strong endothelial cell continuity. No infiltration of macrophages or other inflammatory cells nor subendothelial calcium deposition was found when compared with rabbits in group HC. CONCLUSIONS ASMq therapy can delay the onset of degenerative calcific aortic valve disease, and its effects are similar to those of Atorvastatin.

SUBMITTER: Shabiti A

PROVIDER: S-EPMC5609653 | biostudies-literature | 2017 Sep

REPOSITORIES: biostudies-literature

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Therapeutic Effect and Mechanism of Action of Abnormal Savda Munziq in Development of Degenerative Atherosclerotic Aortic Valve Disease.

Shabiti Aisikaer A Aibibula Aili A Tuerxun Aikeremu A Wufuer Halmurat H

Medical science monitor : international medical journal of experimental and clinical research 20170914

BACKGROUND The aim of this study was to investigate the therapeutic effect of abnormal Savda Munziq (ASMq) on the development of degenerative atherosclerotic aortic valve disease and its underlying mechanisms. MATERIAL AND METHODS We randomly divided 80 rabbits into 4 groups: a normal control group (group N, n=20); a high-fat diet group (group HC, n=20); a high-fat diet and Atorvastatin calcium intervention group (group AI, n=20); and a high-fat diet and ASMq intervention group (group MI, n=20). ...[more]

PMID: 28910266

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Project description:AimsDonor heart shortage leads to increasing use of left ventricular assist device (LVAD) as bridge-to-transplant or destination therapy. Prolonged LVAD support is associated with aortic valve insufficiency, representing a relevant clinical problem in LVAD patients. Nevertheless, the impact of LVAD support on inflammation, remodelling, and chondro-osteogenic differentiation of the aortic valve is still not clearly understood. The aim of the study is to evaluate the impact of LVAD support on structural and molecular alterations of the aortic valve.Methods and resultsDuring heart transplantation, aortic valves of 63 heart failure patients without (n = 22) and with LVAD support (n = 41) were collected and used for analysis. Data on clinical course as well as echocardiographic data were analysed. Calcification and markers of remodelling, chondro-osteogenic differentiation, and inflammation were evaluated by computed tomography, by mRNA analysis and by histology and immunohistochemistry. Expression of inflammation markers of the LVAD group was analysed with regard to levels of C-reactive protein and driveline infections. Calcium accumulation and mRNA expression of determined markers were correlated with duration of LVAD support. Data were also analysed relating to aortic valve opening and aortic valve insufficiency. There was no difference in the frequency of cardiovascular risk factors or comorbidities between the patient groups. Expression of matrix metalloproteinase-9 (P = 0.007), alpha-smooth muscle actin (P = 0.045), and osteopontin (P = 0.003) were up-regulated in aortic valves of LVAD patients. Histological appearance of the aortic valve was similar in patients with or without LVAD, and computed tomography-based analysis not yet revealed significant difference in tissue calcification. Expression of interferon gamma (P = 0.004), interleukin-1 beta (P < 0.0001), and tumour necrosis factor alpha (P = 0.04) was up-regulated in aortic valves of LVAD patients without concomitant inflammatory cell infiltration and independent from unspecific inflammation. Expression of matrix metalloproteinase-2 (P = 0.038) and transforming growth factor beta (P = 0.0504) correlated negatively with duration of LVAD support. Presence of aortic valve insufficiency led to a significantly higher expression of interferon gamma (P = 0.007) in LVAD patients. There was no alteration in the determined markers in relation to aortic valve opening in LVAD patients.ConclusionsLeft ventricular assist device support leads to signs of early aortic valve degeneration independent of support duration. Thus, the aortic valve of patients with LVAD support should be closely monitored, particularly in patients receiving destination therapy as well as in the prospect of using aortic valves of LVAD patients as homografts in case of bridge-to-transplant therapy.

Project description:BackgroundThe effect of different expressions of aortic valve disease on 3D aortic hemodynamics is unclear.PurposeTo investigate changes in aortic hemodynamics in patients with dilated ascending aorta (AAo) but different severity of aortic valve stenosis (AS) and/or regurgitation (AR).Study typeRetrospective.PopulationA total of 111 subjects (86 patients with AAo diameter ≥ 40 mm and 25 healthy controls, all with trileaflet aortic valve [TAV]). Patients were further stratified by TAV dysfunction: n = 9 with combined moderate or severe AS and AR (ASR, 56 ± 13 years), n = 14 with moderate or severe AS (AS, 64 ± 14 years), n = 33 with moderate or severe AR (AR, 62 ± 14 years), n = 30 with neither AS nor AR (no AS/AR, 63 ± 9 years).Field strength/sequence4D flow MRI on 1.5/3T systems for the in vivo analysis of aortic blood flow dynamics.AssessmentData analysis included grading of 3D AAo vortex/helix flow and AAo flow eccentricity as well as quantification of systolic peak velocities and wall shear stress (WSS).Statistical testsContinuous variables were compared by one-way analysis of variance or Kruskal-Wallis, followed by a pairwise Tukey or Dunn test if there was a significant difference.ResultsAll patients demonstrated markedly elevated vortex and helix flow compared with controls (P < 0.05). Peak velocities were significantly elevated in ASR, AS, and AR patients compared with controls (P < 0.05). Increased flow eccentricity was observed in entire AAo for AR, at the mid and distal AAo for ASR and AS, and at the proximal AAo for no AS/AR. Compared with controls, WSS in the AAo was significantly elevated in ASR and AS patients (P < 0.05) and reduced in no AS/AR patients (P < 0.05).Data conclusionThe presence of TAV dysfunction is associated with aberrant hemodynamics and altered WSS, which may play a role in the development of aortopathy.Level of evidence3 Technical Efficacy Stage: 3 J. Magn. Reson. Imaging 2020;51:481-491.

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Therapeutic Effect and Mechanism of Action of Abnormal Savda Munziq in Development of Degenerative Atherosclerotic Aortic Valve Disease.

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Therapeutic Effect and Mechanism of Action of Abnormal Savda Munziq in Development of Degenerative Atherosclerotic Aortic Valve Disease.

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