Left Ventricular Hypertrophy and Arterial Blood Pressure in Experimental Models of Hypertension

Author(s):  
A. F. Dominiczak ◽  
A. M. Devlin ◽  
M. J. Brosnan ◽  
N. H. Anderson ◽  
D. Graham ◽  
...  
1996 ◽  
Vol 14 (8) ◽  
pp. 1019???1024 ◽  
Author(s):  
Jos?? J.G. de Lima ◽  
Henry Abensur ◽  
Eduardo M. Krieger ◽  
F??lvio Pileggi

2021 ◽  
Author(s):  
Ruyi Cai ◽  
Lina Shao ◽  
Yifan Zhu ◽  
Jinshi Zhang ◽  
Yueming Liu ◽  
...  

Abstract Aims: In the general population, central arterial blood pressure has proved to be more closely related to left ventricular hypertrophy than brachial arterial blood pressure. We aimed to investigate whether this relationship was true in patients with chronic kidney disease. Methods: In this retrospective study, we reviewed the medical records of 289 adult patients with chronic kidney disease from the Zhejiang Provincial People’s Hospital in Zhejiang, China. Demographic, echocardiographic, and brachial and central blood pressure parameters were retrieved from medical records. Central blood pressure was measured using the SphygmoCor® CvMS (AtCor, Australia) device and its corresponding software. Multivariate logistic regression analyses were performed to identify independent predictors of left ventricular hypertrophy. Receiver operating characteristic curves were used to determine the ability of central and brachial blood pressure to predict left ventricular hypertrophy.Results: The left ventricular mass index was positively associated with both central and brachial blood pressures. However, multiple logistic regression analysis demonstrated that a central pulse pressure ≥ 58 mm Hg was an independent risk factor for left ventricular hypertrophy (OR=5.597, 95%CI 2.363-13.259, P <0.001). Brachial pulse pressure is not superior to central pulse pressure in predicting left ventricular hypertrophy (AUC = 0.695, 95%CI 0.634-0.756, P < 0.001 vs. AUC = 0.687, 95%CI: 0.626 to 0.748, P < 0.001, respectively; P = 0.4824).Conclusions: Our results suggested that, similarly to the general population, central pulse pressure is a better parameter for predicting the occurrence of left ventricular hypertrophy in patients with chronic kidney disease.


2011 ◽  
Vol 301 (3) ◽  
pp. H1153-H1165 ◽  
Author(s):  
M. Victoria Conde ◽  
M. Carmen Gonzalez ◽  
Begoña Quintana-Villamandos ◽  
Fatima Abderrahim ◽  
Ana M. Briones ◽  
...  

Liver growth factor (LGF) is an endogenous albumin-bilirubin complex with antihypertensive effects in spontaneously hypertensive rats (SHR). We assessed the actions of LGF treatment on SHR mesenteric resistance and intramyocardial arteries (MRA and IMA, respectively), heart, and vascular smooth muscle cells (VSMC). SHR and Wistar-Kyoto (WKY) rats treated with vehicle or LGF (4.5 μg LGF/rat, 4 ip injections over 12 days) were used. Intra-arterial blood pressure was measured in anesthetized rats. The heart was weighted and paraffin-embedded. Proliferation, ploidy, and fibronectin deposition were studied in carotid artery-derived VSMC by immunocytochemistry. In MRA, we assessed: 1) geometry and mechanics by pressure myography; 2) function by wire myography; 3) collagen by sirius red staining and polarized light microscopy, and 4) elastin, cell density, nitric oxide (NO), and superoxide anion by confocal microscopy. Heart sections were used to assess cell density and collagen content in IMA. Left ventricular hypertrophy (LVH) regression was assessed by echocardiography. LGF reduced blood pressure only in SHR. LGF in vitro or as treatment normalized the alterations in proliferation and fibronectin in SHR-derived VSMC with no effect on WKY cells. In MRA, LGF treatment normalized collagen, elastin, and VSMC content and passive mechanical properties. In addition, it improved NO availability through reduction of superoxide anion. In IMA, LGF treatment normalized perivascular collagen and VSMC density, improving the wall-to-lumen ratio. Paired experiments demonstrated a partial regression of SHR LVH by LGF treatment. The effective cardiovascular antifibrotic and regenerative actions of LGF support its potential in the treatment of hypertension and its complications.


2000 ◽  
Vol 41 (3) ◽  
pp. 339-348
Author(s):  
Sumino Hiroyuki ◽  
Nakamura Tetsuya ◽  
Kanda Tsugiyasu ◽  
Sakamaki Tetsuo ◽  
Sato Kunio ◽  
...  

Ultrasound ◽  
2021 ◽  
pp. 1742271X2098758
Author(s):  
Danfu Ma ◽  
Ahmed S Mandour ◽  
Tomohiko Yoshida ◽  
Katsuhiro Matsuura ◽  
Kazumi Shimada ◽  
...  

Introduction Intraventricular pressure gradient is regarded as a non-invasive indicator of diastolic function. Salvianolic acid B (Sal-B), a traditional Asian medicine, revealed its usefulness in myocardial infarction models; however, the hemodynamic effect of salvianolic acid B is still unknown. The present study aimed to investigate the intraventricular pressure gradient changes during the development of left ventricular hypertrophy with or without salvianolic acid B and a beta-blocker. Methods In total, 48 rats were divided into four groups; Sham, Non-treatment, salvianolic acid B, and Carvedilol. Aortic coarctation-induced left ventricular hypertrophy was done in three groups and the treatment was started from the third to the sixth week. Blood pressure, conventional echocardiography, and color M-mode echocardiography for measurement of intraventricular pressure gradient were carried out for six consecutive weeks. Results At 4.5 weeks, the LV mass was elevated in the coarctation groups but the blood pressure was significantly lower in salvianolic acid B and Carvedilol groups ( P < 0.05). In the Non-treatment group, the total intraventricular pressure gradient was increased at 4.5 and 6 weeks (2.60 and 2.65, respectively). Meanwhile, the basal intraventricular pressure gradient was elevated at 3 and 6 weeks (1.67 and 1.75) compared with the Sham group. Salvianolic acid B and Carvedilol significantly reduced the basal intraventricular pressure gradient at six weeks compared with the Non-treatment group (1.52 and 1.51 vs 1.75, respectively). Conclusions Salvianolic acid B and Carvedilol promote cardiac function by decreasing the elevated basal intraventricular pressure gradient. The current preclinical results revealed the efficacy of salvianolic acid B as a potential therapy for left ventricular hypertrophy because of the non-blood pressure lowering effect.


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