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L/Left – B-mode visualization of right common carotid artery; P/Right – echo-tracking computed curve of dynamic diameter carotid artery. Lower – arterial stiffness parameters: β – beta; Ep – epsilon; AC – arterial compliance ; PWVβ – one-point pulse wave velocity; AI – augmentation index
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Background:
Left ventricular hypertrophy (LVH) and geometry patterns vary in different hemodynamic profiles The concentric hypertrophy (CH) pattern has been proved to have the worst prognosis.
Objectives:
The aim of the study was to test the hypothesis that carotid artery stiffness, as a marker of vascular damage, is associated with CH, independ...
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Background
Increased head and neck cancer (HNC) survival requires attention to long-term treatment sequelae. Irradiated HNC survivors have a higher ischemic stroke risk. However, the pathophysiology of radiation-induced vasculopathy is unclear. Arterial stiffness could be a biomarker. This study examined alterations in intima-media thickness (IMT)...
Citations
... Central AIx (carotid or aortic) was associated with LVMi (standardized beta coefficient [β]: 0.05 [95% CI, 0.01 to 0.10]; Figure 1A) [25][26][27][28][29][30][31][32][33][34][35][36][37] ; when studies that used other indices than BSA to calculate LVMi were excluded significant association was also found (β: 0.08 [95% CI, 0.02 to 0.13]; Figure S2A) 25,26,28,29,[31][32][33][34][35][36][37] ; when studies that did not adjust (at least for) for age, sex and blood pressure were excluded marginal association was found (β: 0.04 [95% CI, 0.00 to 0.09]; Figure S3A) 27,28,31,32,35 ; when studies that did not adjust (at least for) for age, sex, blood pressure and heart rate were excluded no association was found (β: 0.00 [95% CI, −0.03 to 0.04]; Figure S4A) 27,28,32,35 ; when studies with only high CVD risk populations were included significant association was found (β: 0.07 [95% CI, 0.01 to 0.13]; Figure S5A). 26,[29][30][31][32][34][35][36][37] Carotid AIx-analyzed separately from aortic AIxwas significantly associated with LVMi (β: 0.14 [95% CI, 0.07 to 0.21]; Figure 1B) 26,[31][32][33][34][35][36] ; all studies used BSA for anthropometric correction of LVM; when studies that did not adjust (at least for) for age, sex and blood pressure were excluded similar results were found (β: 0.09 [95% CI, 0.03 to 0.16]; Figure S3B) 31,32,34,35 ; when studies that did not adjust (at least for) for age, sex, blood pressure and heart rate were excluded marginally non-significant association was found (β: 0.01 [95% CI, −0.01 to 0.03]; Figure S4B) 32,35 ; when studies with only high CVD risk populations were included significant association was found (β: 0.11 [95% CI, 0.04 to 0.18]; Figure S5B) 26,31,32,[34][35][36] ; when studies that provided data separately for male population where analyzed a marginal association was found (β: 0.16 [95% CI, 0.00 to 0.32]; Figure S7A). ...
... Central AIx (carotid or aortic) was associated with LVMi (standardized beta coefficient [β]: 0.05 [95% CI, 0.01 to 0.10]; Figure 1A) [25][26][27][28][29][30][31][32][33][34][35][36][37] ; when studies that used other indices than BSA to calculate LVMi were excluded significant association was also found (β: 0.08 [95% CI, 0.02 to 0.13]; Figure S2A) 25,26,28,29,[31][32][33][34][35][36][37] ; when studies that did not adjust (at least for) for age, sex and blood pressure were excluded marginal association was found (β: 0.04 [95% CI, 0.00 to 0.09]; Figure S3A) 27,28,31,32,35 ; when studies that did not adjust (at least for) for age, sex, blood pressure and heart rate were excluded no association was found (β: 0.00 [95% CI, −0.03 to 0.04]; Figure S4A) 27,28,32,35 ; when studies with only high CVD risk populations were included significant association was found (β: 0.07 [95% CI, 0.01 to 0.13]; Figure S5A). 26,[29][30][31][32][34][35][36][37] Carotid AIx-analyzed separately from aortic AIxwas significantly associated with LVMi (β: 0.14 [95% CI, 0.07 to 0.21]; Figure 1B) 26,[31][32][33][34][35][36] ; all studies used BSA for anthropometric correction of LVM; when studies that did not adjust (at least for) for age, sex and blood pressure were excluded similar results were found (β: 0.09 [95% CI, 0.03 to 0.16]; Figure S3B) 31,32,34,35 ; when studies that did not adjust (at least for) for age, sex, blood pressure and heart rate were excluded marginally non-significant association was found (β: 0.01 [95% CI, −0.01 to 0.03]; Figure S4B) 32,35 ; when studies with only high CVD risk populations were included significant association was found (β: 0.11 [95% CI, 0.04 to 0.18]; Figure S5B) 26,31,32,[34][35][36] ; when studies that provided data separately for male population where analyzed a marginal association was found (β: 0.16 [95% CI, 0.00 to 0.32]; Figure S7A). ...
... Central AIx (carotid or aortic) was associated with LVMi (standardized beta coefficient [β]: 0.05 [95% CI, 0.01 to 0.10]; Figure 1A) [25][26][27][28][29][30][31][32][33][34][35][36][37] ; when studies that used other indices than BSA to calculate LVMi were excluded significant association was also found (β: 0.08 [95% CI, 0.02 to 0.13]; Figure S2A) 25,26,28,29,[31][32][33][34][35][36][37] ; when studies that did not adjust (at least for) for age, sex and blood pressure were excluded marginal association was found (β: 0.04 [95% CI, 0.00 to 0.09]; Figure S3A) 27,28,31,32,35 ; when studies that did not adjust (at least for) for age, sex, blood pressure and heart rate were excluded no association was found (β: 0.00 [95% CI, −0.03 to 0.04]; Figure S4A) 27,28,32,35 ; when studies with only high CVD risk populations were included significant association was found (β: 0.07 [95% CI, 0.01 to 0.13]; Figure S5A). 26,[29][30][31][32][34][35][36][37] Carotid AIx-analyzed separately from aortic AIxwas significantly associated with LVMi (β: 0.14 [95% CI, 0.07 to 0.21]; Figure 1B) 26,[31][32][33][34][35][36] ; all studies used BSA for anthropometric correction of LVM; when studies that did not adjust (at least for) for age, sex and blood pressure were excluded similar results were found (β: 0.09 [95% CI, 0.03 to 0.16]; Figure S3B) 31,32,34,35 ; when studies that did not adjust (at least for) for age, sex, blood pressure and heart rate were excluded marginally non-significant association was found (β: 0.01 [95% CI, −0.01 to 0.03]; Figure S4B) 32,35 ; when studies with only high CVD risk populations were included significant association was found (β: 0.11 [95% CI, 0.04 to 0.18]; Figure S5B) 26,31,32,[34][35][36] ; when studies that provided data separately for male population where analyzed a marginal association was found (β: 0.16 [95% CI, 0.00 to 0.32]; Figure S7A). 31,33,35 Aortic AIx-analyzed separately from carotid AIx-was not associated with LVMi (β: −0.04 [95% CI, −0.09 to 0.02]; Figure 1C) 25,[27][28][29][30]37 ; when studies that used other than BSA to calculate LVMi were excluded similarly no association was found (β: −0.06 [95% CI, −0.15 to 0.03]; Figure S2B) 25,28,29,37 ; when studies that did not adjust (at least for) for age, sex, blood pressure and heart Figure S4C) 27,28 ; when studies with only high CVD risk populations were included non-significant association was found (β: −0.09 [95% CI, −0.24 to 0.05]; Figure S5C). ...
Background:
Pressure wave reflections (PWRs) within the circulation are assessed at various arterial sites by various noninvasive methods. We aimed at reviewing the conflicting data regarding the hypothesis that higher PWRs are associated with higher left ventricular mass and tested whether this association stands for all available indices of PWRs, all (proximal or distal to the heart) sites of assessment, and is modified by sex, age and heart rate.
Methods:
Based on a predefined protocol applying the MOOSE guidelines, we identified eligible for meta-analysis data regarding: augmentation index, augmentation pressure, backward pressure (Pb), reflection index, and their association with left ventricular mass index (19 studies, total population n=8686).
Results:
We found significant associations, independent from blood pressure level, for all indices of PWRs at all arterial sites (carotid augmentation index; odds ratio, 0.14 [95% CI, 0.07%-0.21%], per SD increase), radial augmentation index (0.21; 0.11-0.31), central augmentation pressure (0.15; 0.03-0.27), central Pb (0.23; 0.05-0.42), and central reflection index (0.14; 0.06-0.22), expect for aortic augmentation index as estimated by generalized transfer functions. Meta-regression analysis showed that the association between carotid augmentation index and left ventricular mass was higher among populations with higher heart rate (P=0.036, beta: 0.017 [CI, 0.001-0.033]) and tended to be higher in middle-aged (P=0.07, -0.001; -0.021 to 0.001).
Conclusions:
A clinically meaningful association between PWRs and left ventricular mass, assessed in either central or peripheral arterial sites by most available methods was shown, suggesting that PWR reduction strategies might be useful. Based on the present evidence, such trials should target middle-aged populations with high normal heart rate.
... и точное измерение показателей ссэ (таких как среднее, максимальное и периферическое изменения ссэ) в клинике было бы весьма желательным, эта цель ещё не достигнута в первую очередь из-за ограничений разрешения текущих методов визуализации [18]. измерение ссэ может помочь в выявлении атеросклеротических бляшек повышенного риска, а также в оценке эффективности различных фармакологических вмешательств [19]. эндотелий становится органом-мишенью при многих заболеваниях, поэтому максимально раннее выявление изменений его структуры и\или функции крайне актуально в диагностике атеросклероза. ...
... в качестве хорошо зарекомендовавшего себя «окна наблюдения» за структурой и функцией эндотелия всего сосудистого русла выступает эндотелий оса. оценка ссэ оса может отражать общее гемодинамическое состояние сосудов всего артериального русла [18,19,20,21]. одним из основных механизмов повреждения органов-мишеней при гб является хроническое повреждение эндотелия [22]. ...
... более высокое местное пульсовое давление может влиять на структурные и функциональные изменения внутричерепных сосудов и толщину стенки сонной артерии, способствовать развитию бляшек и стенозов, а также разрыву нестабильных бляшек, что может объяснить учащение цереброваскулярных событий у этих пациентов [33]. Jaroch et al. показали, что концентрическая гипертрофия миокарда лж при артериальной гипертензии тесно связана с жёсткостью сонных артерий и снижением параметров ссэ в оса [19]. низкое локальное напряжение сдвига и большое количество бляшек в сонных артериях у пациентов с болью в груди -значимые предикторы ибс. ...
Objective : to study the interconditionality of changes in the fluid shear stress on the endothelium (FSE) of the common carotid artery (CCA) wall which is intact from atherosclerosis with the value of the Cardiac Calcium Score (CCS) among patients with e arterial hypertension (AH).
Materials and methods : the study included 99 patients with AH, 52 of them had atherosclerotic lesions of the brachiocephalic arteries (BCA). The ultrasound investigation of the carotid arteries with the determination of FSE in the intact area of the CCA, multispiral computed tomography of the coronary arteries with the determination of CCS were performed to all patients.
Results : the prevalence of BCA atherosclerotic lesion in the study was 53%. The mean value of FSE for patients with AH and BCA atherosclerosis (group 1) were 660.7 (185.6) c-1, for patients with AH without its (group 2) — 735.8 (149.8) c-1, p = 0.009. The parameters of the lipid spectrum in patients of both groups were comparable. Мedian value of CCS in patients with atherosclerotic lesions of the BCA were statistically significantly higher (15.00 (0.00; 178.00),) compared with patients of the group 2 (0.00 (0.00; 171.00), at p = 0.001. The chances of detecting coronary artery calcification among patients of group 1 are in 2 times higher (OR = 2.25, 95% CI: 1.58-8.33) than among patients of group 2. Low FSE values correlated with male gender (rs = 0.40 (95% CI: 0.22; 0.55) p <0.001) and increasing of CCS (rs = -0.23 (95% CI: -0.41; -0.04) p = 0.022).
Conclusions : the prevalence of atherosclerotic lesions of the BCA among patients with AH without a history of symptomatic diseases associated with atherosclerosis was 53%. In the group of patients with AH and atherosclerotic lesions of the BCA, median values of CCS were significantly higher, and coronary artery lesions were detected significantly more often (OR = 2.25, 95% CI: 1.58-8.33) than among patients with AH and intact BCA. The mean value of FSE for patients with AH and BCA atherosclerosis were statistically significantly lower than for patients with AH without it and amounted to 660.7 (185.6) c-1 and 735.8 (149.8) c-1, respectively, p = 0.009. Low FSE values correlated with male gender and increasing of CCS
... Several physiological markers of arterial stiffness (e.g., stiffness β, pulse wave velocity, and cardio-ankle vascular index) have been used in clinical settings. A number of clinical reports have shown the usefulness of these physiological markers as risk factors of CVD in patients with hypertension [9][10][11]. Recently, researchers also investigated a method for calculating the arterial pressure-volume index (API), which indicates arterial stiffness, using oscillometric blood pressure measurements [12]. ...
Background:
The arterial pressure-volume index (API), which is obtained by conventional blood pressure measurement, is a new marker for arterial stiffness. The aim of this study was to clarify the relationships between the API and various clinical parameters, including cardiovascular disease (CVD) biomarkers, in patients with hypertension for the prevention of CVD.
Methods:
This cross-sectional study enrolled 288 patients with hypertension receiving pharmacological treatment, without a history of CVD (males/females: 115/173; age: 63 ± 11 years (mean ± standard deviation)). The API was automatically calculated using a commercial device.
Results:
The API was significantly correlated with important CVD biomarkers, such as the concentration of urinary albumin (r = 0.42, P < 0.001), high-sensitivity troponin T (r = 0.39, P < 0.001), and skin autofluorescence (marker of advanced glycation end products in tissues) (r = 0.41, P < 0.001). Multiple regression analyses demonstrated that when the API was used as a subordinate factor, these biomarkers were independent variables. According to the receiver operating characteristic curve analysis, an API of > 26 is the optimal cut-off point for determining albuminuria as ≥ 30 mg/g Cr, high high-sensitivity cardiac troponin T concentration as ≥ 0.014 ng/mL, or high skin autofluorescence as ≥ 3.0 arbitrary unit (area under the curve = 0.703, 0.702, and 0.704; and P < 0.001, respectively).
Conclusion:
This investigation demonstrates that API had an independent relationship with relevant CVD biomarkers, such as urinary albumin, high-sensitivity troponin T, and skin autofluorescence. Additionally, the outcomes of receiver operating characteristic curve analysis are presented as values that an API > 26 defines for these biomarkers linked with the formation of CVD.
... Therefore, an increase in arterial stiffness is a part of the development of hypertension, ischemic heart disease and heart failure. 15,16 Both aging and diseases such as essential hypertension, diabetes and CKD contribute to the increase in arterial stiffness. [17][18][19] High-resolution echo-tracking is a direct and noninvasive method of the evaluation of local arterial stiffness. ...
Background:
Patients with kidney disease suffer from high cardiovascular risk due to classic and disease-specific risk factors. Arterial stiffness is a novel cardiovascular risk factor whose role is yet to be established. High-resolution echo-tracking is a developing method for the assessment of local arterial stiffness.
Objectives:
To assess carotid stiffness in patients on long-term hemodialysis (HD) using high-resolution echo-tracking and to analyze the impact of arterial stiffness on mortality in the mid-term follow-up.
Material and methods:
Fifty-eight HD patients (28 female (F), 30 male (M)) underwent clinical examination, laboratory tests and carotid stiffness assessment. Local arterial stiffness parameters such as beta stiffness index (β), Young's modulus (Ep), arterial compliance (AC), and one-point pulse wave velocity (PWVβ) were measured both before and after HD, allowing to calculate their change (Δ). The survival of patients was analyzed up to 48 months. The multivariate analysis of survival with the use of Cox proportional hazard stepwise regression was performed to determine the factors significantly correlated with the survival.
Results:
After 48 months, 33 patients were alive (16 F, 17 M) and 25 patients (12 F, 13 M) died. The deceased group was significantly older (66.5 ±12.3 years compared to 56.6 ±17.8 years), had more pronounced coronary artery disease (percutaneous coronary intervention (PCI) 36% compared to 9%, p < 0.05, respectively). Deceased patients had significantly higher ΔAC than survivors. The results showed that age, history of PCI, left ventricular ejection fraction (LVEF), ΔAC, fasting glucose, serum total protein, sodium level after HD, and potassium level before HD were significantly associated with mortality.
Conclusions:
Echo-tracking-based arterial stiffness assessment in patients with chronic kidney disease (CKD) yields the clinical information regarding mid-term mortality risk. A paradoxical increase in AC is among independent risk factors for mid-term mortality in patients undergoing maintenance HD. The proper estimation of the correlations among vascular, hemodynamic and sympathetic-dependent changes in a given patient with kidney failure is complex.
... Arterial stiffness has a close association with the progression of DM complications (namely nephropathy, retinopathy and neuropathy), involving multiple organs and systems. Large-artery stiffness will increase the left ventricular afterload [39,40] and effectuate left ventricular hypertrophy [41] and coronary perfusion damage. Further, arterial stiffness has been demonstrated to be significantly correlated with the development of diabetic retinopathy (DR) [42], neuropathy in T2DM patients [43], production of proteinuria in diabetic patients, a decreased glomerular filtration rate (GFR) [44] and degenerative cognitive status [45]. ...
Vascular aging is defined as organic and functional changes in blood vessels, in which decline in autophagy levels, DNA damage, MicroRNA (miRNA), oxidative stress, sirtuin, and apoptosis signal-regulated kinase 1 (ASK1) are integral thereto. With regard to vascular morphology, the increase in arterial stiffness, atherosclerosis, vascular calcification and high amyloid beta levels are closely related to vascular aging. Further closely related thereto, at the cellular level, is the aging of vascular endothelial cells (ECs) and vascular smooth muscle cells (VSMCs). Vascular aging seriously affects the health, economy and life of patients, but can be delayed by SGLT2 inhibitors through the improvement of vascular function. In the present article, a review is conducted of recent domestic and international progress in research on SGLT2 inhibitors,vascular aging and diseases related thereto, thereby providing theoretical support and guidance for further revealing the relationship between SGLT2 inhibitors and diseases related to vascular aging.
... Carotid elasticity and distensibility are two important parameters that can be easily evaluated by ultrasonography and show subclinical atherosclerosis. The role of both elasticity and distensibility in predicting cardiovascular adverse events has been demonstrated in previous studies [5][6][7] . ...
Amaç: Yüksek kan basıncının karotis arterler üzerinde istenmeyen etkilere yol açtığı iyi bilinmesine ragmen bu etkinin hangi değerden itibaren başladığı net değildir. Bu çalışmanın amacı bunu değerlendirmektir.
Yöntem: Çalışma kesitsel planlandı ve toplam 308 birey dahil edildi. Sistolik kan basıncı (SKB) <120 mmHg ve diyastolik kan basıncı (DKB) <90 mmHg olan (optimal) bireyler 1.Gruba, SKB 120-129 mmHg ve/veya DKB 80-84 mmHg olan (normal) bireyler 2.Gruba, SKB 130-139 mmHg ve/veya DKB 85-89 mmHg olan (yüksek-normal) bireyler 3.Gruba, SKB 140-159 mmHg ve/veya DKB 90-99 mmHg olan bireyler 4.Gruba, SKB 160-179 mmHg ve/veya DKB 100-109 mmHg olan bireyler 5.Gruba ve SKB≥180 mmHg ve/veya DKB≥110 mmHg olan bireyler 6.Gruba alındı. Tüm gruplarda karotis distensibilitesi ve elastisitesi ölçülerek gruplar arasında fark olup olmadığı ve eğer fark var ise hangi kan basıncı değerinden itibaren bu farkın oluşmaya başladığı değerlendirildi.
Bulgular: Tüm gruplar arasında karotis distensibilitesi ve elastisitesi yönünden istatistiksel anlamlı fark vardı (p<0.001, her iki değer için). Grup 2 ve 1 arasında anlamlı fark saptanmadı (p>0.05) ancak grup 3 ile 1 arasında anlamlı fark vardı (p<0.05). SKB>135,5 mmHg olmasının%78,2 sensitivite, %74,6 spesifite, DKB>86,5 mmHg olmasının %79,3 sensitivite ve %71,6 spesifite ile karotis distensibilitesini etkilemeye başladığı bulundu. Benzer olarak SKB>137,5 mmHg olmasının %80,4 sensitivite, %73,1 spesifite, DKB>88,5 mmHg olmasının ise %79,1 sensitivite ve %73,8spesifite ile karotis elastisitesini etkilemeye başladığı gösterildi.
Sonuç: Karotis distensibilitesi ve elastisitesi kan basıncının artışı ile azalmaktadır. Yüksek-normal kan basıncına sahip bireylerde belirli bir kan basıncı değerinden sonra karotis hasarı başlıyor olabilir.
... Although effective medical treatment, including smoking cessation and the reduction of blood pressure and lipid levels, could significantly reduce cardiovascular mortality in patients with atherosclerosis, a large proportion of people still have adverse outcomes, and the early identification of cardiac dysfunction has the potential to prevent further cardiovascular disease in these patients. Previous studies have indicated a possible association between the presence of carotid atherosclerosis, left ventricular (LV) morphology and high prevalence of coronary artery disease [6,7], which might account for the increased risk of cardiovascular events in such patients. However, the relationship between cardiac function and atherosclerosis may have been underestimated in patients with carotid stenosis, and this might be responsible for the high incidence of premature death in these individuals [8]. ...
The relationship between subclinical left ventricular (LV) dysfunction and atherosclerosis may have been underestimated in the past, which might be responsible for the high incidence of premature death in individuals with carotid stenosis. We sought to evaluate the underlying myocardial dysfunction in asymptomatic carotid stenosis patients using speckle tracking echocardiography (STE). Fifty patients with carotid stenosis ≥ 50% and a preserved LV ejection fraction (LVEF), and 45 controls without carotid stenosis who were matched in terms of vascular comorbidities were enrolled. All participants underwent carotid ultrasound and echocardiographic examination. The global LV longitudinal strain (GLS) was measured using STE. Compared with the control group, the e’ of the mitral annular velocity and GLS were decreased in asymptomatic carotid stenosis patients (p < 0.05), however, the LVEF was well preserved. Based on a predefined cutoff for subclinical LV systolic dysfunction that was defined at a GLS < − 18%, this dysfunction was detected in 22 patients with carotid stenosis (44%) and in 10 patients in the control group (22%) (p < 0.05). The GLS was negatively correlated with the levels of low-density lipoprotein cholesterol (r = − 0.356, p < 0.05) and triglyceride (r = − 0.396, p < 0.05). In conclusion, LV diastolic and systolic functioning were significantly decreased in patients with asymptomatic carotid stenosis, and dyslipidemia likely contributed to the subclinical LV dysfunction in these patients. Our findings indicated the importance of detecting LV subclinical dysfunction and early intervention in this patient population.
... [2][3][4]9 Hypertension is multifactorial, but has been related to vascular wall thickness and stiffness, and leads to atherosclerosis. 10 However, in most of these studies, hypertension was more strongly related to fibroid cases that led to hysterectomy rather than fibroid cases detected before needing surgical intervention. 4,8,9 We aimed to study the association between fibroids and CVD using markers of subclinical disease to further elucidate possible common pathways: (1) wall thickness and vascular stiffness using markers of carotid intima media thickness (CIMT) and left ventricular (LV) mass and (2) plaque formation using coronary artery calcification (CAC). ...
Background:
Uterine fibroids, the most common reproductive tract tumor in women, have been associated with hypertension and atherosclerotic cardiovascular disease (CVD). Prior studies of fibroids and CVD have examined the subset of women with symptomatic fibroids who undergo hysterectomy, itself a risk factor for CVD. We aimed to study the risk of subclinical CVD, as determined by coronary artery calcification (CAC), carotid intima media thickness (CIMT), and left ventricular (LV) mass, in women with ultrasound-diagnosed uterine fibroids.
Materials and methods:
Participants were 972 women from the Coronary Artery Risk Development in Young Adults (CARDIA) study, a cohort recruited in 1985-1986. CARDIA screened black and white women aged 35-49 years by ultrasound for fibroids at 16 years of follow-up (2002-2004). Demographics and CVD risk factors were collected in 2000-2001 at 15 years of follow-up (baseline for this analysis). Women were tested at years 15, 20, and 25 for CAC, at year 20 for CIMT, and at year 25 for echocardiographic LV mass. Multivariable logistic regression was used to estimate the odds of CAC, CIMT, and LV mass.
Results:
Fifty-two percent of women had fibroids (61.7% in black, 38.3% in white women). Most CVD risk factors were more common in women with fibroids. Adjusted odds of subclinical CVD, such as elevated CIMT and elevated LV mass, were not different for women with fibroids compared with those without (CIMT odds ratio [OR] = 1.03; confidence interval [95% CI] 0.7-1.5 and LV mass OR = 1.14; 95% CI 0.77-1.68), when adjusted for confounders.
Conclusions:
Although women with fibroids had more CVD risk factors, presence of fibroids was not associated with subclinical CVD.
... However, there is often a situation when there is no correlation between the frequency and intensity of cephalalgia and increased blood pressure in a patient with arterial hypertension and, hence, taking antihypertensive drugs does not lead to relief headache [1,2,14]. In today's date, it has been scientifically substantiated and proved by clinical practice that the use of adequate, therapeutic hypotensive programs allows to improve significantly the effectiveness of treatment of patients, to reduce the incidence of cardiovascular complications of the disease and of the rates of disability and mortality [11,13,16,20]. ...
A comprehensive examination of 114 patients with stage I and II hypertension was carried out. The aim of the study was to develop a modern, pathogenetically substantiated, comprehensive non-medicamentous method of curative correction of early cerebral manifestations of hypertension. The main correction of the initial manifestations of hypertension was a special technique of curative gymnastics and respiratory gymnastics with elements of group psychotherapy. Group 1 (n=80) - patients who received complex non-drug treatment; Group 2 (n=34) - patients who received drug-induced antihypertensive therapy on the basis of monotherapy or low-dose combination therapy. Patients of the 1 st group reported a significant (p< 0.01) improvement after the end of treatment. Intergroup differences obtained before and after treatment, in patients of the 1 st and 2 nd groups it had a significant (p< 0.01) nature. The study of cerebral hemodynamics significantly (p< 0.01) indicated an increase in the majority of patients of the 1st group of blood flow along the vertebral arteries, the posterior cerebral arteries. In the state of vasomotor reactivity and autoregulation of cerebral blood flow, there was significant (p< 0.01) positive dynamics only in patients of the 1st group. Thus, the analysis of the results of our algorithm for treating patients with initial manifestations of hypertension, conducted with the use of non-drug methods, demonstrates the validity of the proposed pathogenetic approach to ongoing therapy.
Objective
To investigate the inter-relationships between left ventricular mass (LVM), left ventricular (LV) geometry and arterial stiffness parameters (aortic pulse wave velocity [Ao-PWV] and heart rate-corrected augmentation index [c-AIx]) in patients with chronic heart failure (CHF).
Methods
This study was a secondary analysis of existing data that were collected from patients with CHF New York Heart Association class I–III with reduced ejection fraction (HFrEF) or preserved ejection fraction (HFpEF). Transthoracic echocardiography was performed on all patients, along with measurement of arterial stiffness parameters (Ao-PWV and c-AIx) using sphygmocardiography.
Results
A total of 73 patients (58 males) with a mean ± SD age of 55.9 ± 11.6 years were enrolled in this study. Of these, 20 patients (27.4%) had systemic hypertension, 46 (63.0%) had type 2 diabetes mellitus. Ischaemic heart disease was the main aetiology of CHF (63 of 73 patients; 86.3%). In multiple linear regression, the left ventricular mass index (LVMI) was significantly associated with c-AIx (β = –1.59) and EF (β = –1.51). Comparison of Ao-PWV among the four LV geometric patterns revealed significant differences.
Conclusion
In this cohort of CHF patients, LVMI was predicted by c-AIx and EF. The corresponding values of Ao-PWV were parallel in different LV geometric patterns and confirmed their adverse prognostic values.
