We studied the wall motion characteristics of the ascending aorta by velocity vector imaging (VVI) in primary hypertension patients. The ascending aortas both in 30 patients with primary hypertension and 30 normal controls were examined by Acuson sequoia 512 equiped with VVI. The maximum velocity (Vs, Ve) of every point on the anterior wall of ascending aorta both in systole and diastole was measured. The aortic diameter was wider in the hypertension patients than that in the healthy subjects (P<0.05). The movement amplitude of the anterior wall of the ascending aorta in long axis view in the hypertension patients was lower than that in the healthy subjects (P<0.05). The motion and time to peak in systole of each point of the ascending aorta in the healthy subjects had no significant difference (P>0.05). The velocity curves of the anterior wall of ascending aorta both in the hypertension and healthy subjects were regular, and the curve in systole was named S wave and that in diastole named E wave. The velocity of S wave and E wave was slower in the hypertension patients than that in the healthy subjects (P<0.05). The time to peak of S wave on the anterior wall of ascending aorta in systole was shorter in the hypertension patients than in the healthy subjects (P<0.05). VVI could be used to accurately and directly observe the movement character of the ascending aorta walls, which would help us understand the elasticity of great arteries in patients with hypertension.
Aorta/pathology ; Aorta/*physiopathology ; Aorta/ultrasonography ; Blood Flow Velocity ; Case-Control Studies ; Echocardiography/*methods ; Elasticity ; Hypertension/pathology ; Hypertension/*physiopathology ; Vectorcardiography/*methods ; Ventricular Dysfunction, Left/physiopathology ; Young Adult

The effects of angiotensin II receptor antagonist losartan on elastic properties of aorta in patients with mild to moderate essential hypertension were assessed. The ascending aortic distensibility in 26 patients (48 +/- 3 years) with mild to moderate essential hypertension before and after 12 weeks of treatment with losartan (50 mg/day) was evaluated by using two-dimensional echocardiography. M-mode measurements of aortic systolic (Ds) and diastolic diameter (Dd) were taken at a level approximately 3 cm above the aortic valve. Simultaneously, cuff brachial artery systolic (SBP) and diastolic (DBP) pressures were measured. Aortic pressure-strain elastic modulus (Ep) was calculated as Dd x (SBP-DBP)/(Ds-Dd) x 1333 and stiffness index beta (beta) was defined as Dd x Ln (SBP/DBP)/(Ds-Dd). Blood pressure significantly decreased from 148 +/- 13/95 +/- 9 mmHg to 138 +/- 12/88 +/- 8 mmHg (systolic blood pressure, P = 0.001; diastolic blood pressure, P = 0.003). There was no significant difference in pulse pressure before and after treatment with losartan (53 +/- 10 mmHg vs 50 +/- 7 mmHg). The distensibility of ascending aorta increased significantly as showed by the significant decrease in pressure-strain elastic modulus from 4.42 +/- 5.79 x 10(6) dynes/cm2 to 1.99 +/- 1.49 x 10(6) dynes/cm2 (P = 0.02) and stiffness index beta from 27.4 +/- 32.9 to 13.3 +/- 9.9 (P = 0.02). Although there was a weak correlation between the percent changes in pressure-strain elastic modulus and stiffness index beta and that in diastolic blood pressure after losartan treatment (r = 0.40, P = 0.04 and r = 0.55, P = 0.004, respectively), no correlation was found between the percent changes in pressure-strain elastic modulus and stiffness index beta and that in systolic blood pressure (r = 0.04, P = 0.8 and r = 0.24, P = 0.2, respectively). Our study demonstrated that angiotensin II receptor antagonist losartan has a beneficial effect on aortic distensibility in patients with mild to moderate essential hypertension and this effect is partly independent of blood pressure reduction.
Aorta/*physiopathology ; Aorta/ultrasonography ; Echocardiography ; Elasticity ; Hypertension/*drug therapy ; Hypertension/*physiopathology ; Hypertension/ultrasonography ; Losartan/*therapeutic use ; Receptors, Angiotensin/*antagonists & inhibitors

Cardiac autophagy dramatically increases in heart failure induced by sustained pressure overload. However, it has not yet been addressed if enhanced autophagy plays a role in protecting myocardium or mediating progression from compensative hypertrophy to heart failure. The aim of the present study was to detect autophagic flux of cardiomyocytes from 20-week transverse abdominal aortic constriction (TAC) rats. Fasting rats were used as the positive control for detecting cardiac autophagy. Echocardiography was applied to find the changes of cardiac structure and function. Immunofluorescent histochemistry and Western blot were used to analyze the related biomolecular indexes reflecting cardiac autophagic flux. After the previous methods for detecting cardiac autophagy were confirmed, the autophagic flux in cardiomyocytes of rats subjected to 20-week TAC was examined. The results showed that fasting had no obvious influence on parameters of cardiac structure in rats, including interventricular septal wall thickness and left ventricle posterior wall thickness, but heart rate, diastolic left ventricle internal dimension, fractional shortening of left ventricle dimension, ejection fraction and mitral inflow velocity decreased in rats after fasting for 3 d. Meanwhile, positively stained particles of LC3 and cathepsin D, but not ubiquitin and complement 9, distributed within cardiomyocytes of 3-day fasting rats, indicating augmented autophagic flux. Compared with sham rats, 20-week TAC rats did not show any changes of LC3, cathepsin D, ubiquitin and complement 9 in myocardium detected by immunofluorescent histochemistry. In addition, protein levels of LC3, cathepsin D and p62 in myocardium of TAC rats did not changed. These results reveal the unchanged autophagic flux in cardiomyocytes at middle or late phase of cardiac hypertrophy in TAC rats, implying a balance between inhibition of hypertrophy and activation of pressure load stress on autophagy.
Animals ; Aorta ; pathology ; Autophagy ; Cardiomegaly ; physiopathology ; Constriction ; Heart ; physiopathology ; Myocardium ; pathology ; Myocytes, Cardiac ; cytology ; Rats

This study aims to explore the effect of aortic sinus diameter on aortic valve opening and closing performance in the case of no obvious disease of aortic valve and annulus and continuous dilation of aortic root. A total of 25 three-dimensional aortic root models with different aortic sinus and root diameters were constructed according to the size of clinical surgical guidance. The valve sinus diameter S is set to 32, 36, 40, 44 and 48 mm, respectively, and the aortic root diameter is set to 26, 27, 28, 29 and 30 mm, respectively. Through the structural mechanics calculation with the finite element software, the maximum stress, valve orifice area, contact force and other parameters of the model are analyzed to evaluate the valve opening and closing performance under the dilated state. The study found that aortic valve stenosis occurs when the = 32 mm, = 26, 27 mm and = 36 mm, = 26 mm. Aortic regurgitation occurs when the = 32, 36 and 40 mm, = 30 mm and = 44, 48 mm, = 29, 30 mm. The other 15 models had normal valve movement. The results showed that the size of the aortic sinus affected the opening and closing performance of the aortic valve. The smaller sinus diameter adapted with the larger root diameter and the larger sinus diameter adapted with the smaller root diameter. When the sinus diameter is 40 mm, the mechanical performance of the valve are good and it can well adapt with the relatively large range of aortic root dilation.
Aorta ; anatomy & histology ; Aortic Valve ; physiology ; Aortic Valve Insufficiency ; physiopathology ; Aortic Valve Stenosis ; physiopathology ; Humans

OBJECTIVETo investigate the aortic elastic properties and its clinical significance in intracranial aneurysms (IAs).

METHODSOne hundred and seven IAs patients (57 with hypertension) and 108 healthy subjects were recruited. The internal aortic diameters in systole and diastole were measured by the M-mode echocardiography, the aortic elasticity indexes were calculated and compared.

RESULTSThe aortic distensibility (DIS) was lower and the aortic stiffness index (SI) was higher in IAs patients than those in controls (both P <0.001). DIS was lower and SI was higher in IAs patients with hypertension (IAs-HP) than those in IAs with no hypertension (P <0.001). Similar results were obtained when the aortic elasticity index were adjusted for body surface area and body mass index.

CONCLUSIONAbnormal aortic elasticity is a common finding in IAs patients and hypertension is closely related to the severity of aortic elasticity.

Adult ; Aged ; Aorta ; diagnostic imaging ; physiopathology ; Case-Control Studies ; Elasticity ; Female ; Humans ; Intracranial Aneurysm ; physiopathology ; Male ; Middle Aged ; Ultrasonography

Acidosis ; complications ; physiopathology ; Animals ; Aorta, Thoracic ; drug effects ; physiopathology ; Dopamine ; pharmacology ; In Vitro Techniques ; Male ; Rats ; Rats, Wistar ; Shock, Septic ; complications ; physiopathology ; Sympathomimetics ; pharmacology

OBJECTIVETo establish a mouse model of abdominal aorta stenosis and analyze the alterations in the arterial wall response to high and low shear stress.

METHODSTwenty mouse were randomized equally into 4 groups, including 3 test groups (1, 7 and 14 day groups) with surgically induced stenosis of the abdominal aorta, and a sham-operated group without stenosis. The hemodynamics and the internal diameter of the blood vessel were measured by color Doppler flow imaging. The wall shear stress was calculated by Poiseiulle hydrodynamics formula (τ(m)=η×4×V(m)/D). Pathological examination and immunohistochemistry were performed to observe the arterial morphological changes and the endothelial vascular cell adhesion molecule-1 (VCAM-1) expression. The intimal-media thickness of the aorta was measured and endothelial VCAM-1 expression analyzed quantitatively.

RESULTSRegions of low and high flow shear stress were created upstream from the stenosis and within the stenosis, respectively. Compared with the sham-operated group, the mice with aorta stenosis showed gradually increased vascular intimal-media thickness and VCAM-1 expression intensity in the upstream aorta, but not within the regions of the stenosis.

CONCLUSIONVascular remodeling may occur shortly after exposure to low shear stress, which plays a significant role in initiation and progression of the pathological process of atherosclerosis mediated by VCAM-1, whereas high shear stress may exert an anti-atherosclerotic effect.

Animals ; Aorta, Abdominal ; metabolism ; pathology ; physiopathology ; Aortic Valve Stenosis ; physiopathology ; Atherosclerosis ; physiopathology ; Constriction ; Hemodynamics ; Male ; Mice ; Shear Strength ; physiology ; Stress, Mechanical ; Vascular Cell Adhesion Molecule-1 ; metabolism

In the treatment of aortic arch dissections involving left subclavian artery (LSA), a double stent implantation is sometimes required to treat the disease of each branch. In this study, aortic arch and LSA were modeled by using Pro/engineer wildfire3. 0. Two deployed stents were inserted in the aortic arch and LSA. There are 3 kinds of model according to the stent struts protruding into the inlet of the collateral branch, and the healthy aortic arch model without any stent was provided as a reference case. We used computational fluid dynamics (CFD) to investigate the flows in the model stents and focused on the changes of blood speed and wall shear stress caused by the implanted stents of different models. The results showed that the stent strcuts protruding into the inlet of LSA induced the conspicuous decrease of blood speed and the emergence of large-scale low shear stress,which would cause thrombogenesis, neointimal hyperplasia and result in in-stent restenosis, so it would be judicious to use dedicated bifurcated stents for treatment of bifurcation lesions.
Aneurysm, Dissecting ; physiopathology ; surgery ; Aorta ; physiopathology ; Aortic Aneurysm ; physiopathology ; surgery ; Hemodynamics ; Humans ; Prosthesis Implantation ; methods ; Shear Strength ; Stents ; Stress, Mechanical ; Subclavian Artery ; surgery

OBJECTIVETo investigate the differentially expressed genes in rat in the process of regression of vascular calcification by using the suppression subtractive hybridization (SSH).

METHODS24 SD male rats which aged 6 weeks and specific pathogen free grade were selected and randomly divided into 3 groups (n = 8): control group, calcification group and regression group respectively. Vascular calcification model (vitamin D3 plus nicotine, VDN) were made from rats in calcification group and regression group, and rats in control group were intragastric administered with normal saline and lavaged with peanut oil. Rats were bred for 8 weeks in calcification group and control group, while rats in regression group were fed for 16 weeks. All rats were killed to measure concentration of calcium in the arterial tissue and examine the pathological lesion changes. Subtractive hybridization among vascular cDNA sequences from calcification group and regression group were established. The cDNA fragments which expressed higher or lower in regression group than those in calcification group were isolated. Differentially expressed genes with cDNA fragment were inserted into PMD18-T plasmid vector and transformed competent DH-5alpha, cDNA libraries of differentially expressed gene between calcification group and regression group were then constructed. Recombinant vectors were analyzed by colony PCR, positive genes were randomly selected for sequencing and analyzed by BLAST. 4 genes were randomly selected for RT-PCR certification combined with semi-quantitative analysis of DNA bands.

RESULTSVDN model of rats were successfully constructed. Concentration of tissue calcium in calcification group (15.34 mg/g +/- 2.51 mg/g) was significantly increased compared to that in control group (5.20 mg/g +/- 0.75 mg/g, P < 0.001), while in comparison with calcification group (15.34 mg/g +/- 2.51 mg/g), calcium in regression group was relatively lower (12.73 mg/g +/- 1.89 mg/g, P < 0.05). 28 up-regulated genes and 22 down-regulated genes were gained through sequencing and BLAST analysis among positive clones. RT-PCR validation indicated that 4 genes such as prdx3 and Ank2 had increasedly expressed in regression group than those in calcification group, the average fold change was 1.7.

CONCLUSIONRat vascular calcification tissue had characteristic of active regression. Genes in relation to pyrophosphoric acid synthesis, glutamate signal peptides, anti-oxidant and ant-apoptosis were up-regulated, at the same time many genes related to ossification and oxidation activity were down-regulated in the process of calcification regression. Increased expression of calcification suppressor genes accompanying decreased expression of calcification promoting genes might be the intrinsic mechanisms which initiated the active regression of calcified tissues.

Animals ; Aorta ; metabolism ; pathology ; Gene Expression Profiling ; Gene Expression Regulation ; Male ; Rats ; Rats, Sprague-Dawley ; Vascular Calcification ; genetics ; physiopathology

OBJECTIVETo investigate the differences in central hemodynamic indices between hypertensive and normotensive subjects and identify the blood pressure index that the most strongly correlate with arterial stiffness and vascular damage markers.

METHODSA cohort of 820 hypertensive patients and 820 normotensive individuals matched for age and gender were enrolled in this study. We measured carotid-femoral and carotid-radial pulse wave velocity (PWV), aortic augmentation index (AIx) and central blood pressures using pulse wave analysis and applanation tonometry. Plasma homocysteine (HCY), high-sensitivity C-reactive protein (hsCRP) and N-terminal pro-B-type natriuretic peptide (NT-proBNP) were also tested in these subjects.

RESULTSIn both hypertensive and normotensive subjects, the central systolic blood pressure (SBP) and pulse pressure (PP) were significantly lower than brachial SBP and PP; this PP amplification was significantly lower in the normotensives (9.85∓6.55 mmHg) than in the hypertensives (12.64∓6.69 mmHg), but the amplification ratios were comparable between the two groups. Blood pressure and age were closely related with aortic arterial stiffness. Compared with normotensive subjects, hypertensive subjects had higher carotid-femoral PWV and AIx, and showed significantly lowered PP amplification ratio with age. Central PP was more strongly related to arterial stiffness and vascular damage markers than the other pressure indices. Multivariate analyses revealed that carotid-femoral PWV and aortic AIx were strongly influenced by central PP but not by the mean blood pressure or brachial PP.

CONCLUSIONThe central PP is a more direct indicator of central arterial stiffness and a better marker of vascular aging than other blood pressure variables. These findings support the use of central blood pressure as a treatment target in future trials.

Aorta ; physiopathology ; Arterial Pressure ; Blood Pressure ; Case-Control Studies ; Hemodynamics ; Humans ; Hypertension ; Pulse Wave Analysis ; Vascular Stiffness