P1833 Ultrasonic imaging of radial artery reactive response in patients with hypertension with and without left ventricular hypertrophy

Abstract Background Endothelium plays an important role in anti-inflammatory process and regulating vascular tone. It has been shown in numerous studies that increase of vessel dilation after several minutes hyperemia, was induced by mechanical transient flow stimulation of the endothelium. Most of the reported research experiments were conducted on the brachial artery. We proposed to measure the flow-mediated dilation in the radial artery (FMDr) in patients with hypertension (HT). In order to improve the axial resolution affecting the precision of FMDr determination, radial artery imaging was performed using a high frequency 20 MHz ultrasound. Aim The aim of the study was assessment of FMDr in patients with HT using 20 MHz probe. Methods: Our studies involved two groups group I consisted of 76 pts. 35 men and 41 women (71 ± 5.6 yr. old); with documented HT and group II consisted of 16 healthy volunteers, 12 men and 4 women (51.4 ± 9.4 yr. old). We divided patients with HT in to three subgroups: IA - 25 pts. with HT and left ventricular hypertrophy (VH), IB - 26 pts. with HT without VH, and IC patients with HT without VH but with coexisting coronary artery disease (CAD). Results Statistically significant differences in FMDr between the two groups were confirmed by a Wilcoxon-Mann-Whitney test. In group II FMDr was 11.9 ± 4.8%, and in group I FMDr was significantly less at 5.1% ± 4%. We have not observed any statistical differences in FMDr between groups: IA and IB ( 5.05%, 5.55%) respectively. We calculated FMDr for IC 4.21% (p = 0.018). Fig. 1. Conclusion The results confirm the usefulness of the proposed measurements of radial artery FMDr to differentiation of normal subjects from those with documented HT. There are no significant differences between males and females in all considered groups of subjects. We did not find the differences in FMDr between patients with and without VH. Patients with HT, without VH and with coexisting CAD had the lowest reactive response of FMDr. Abstract P1833 Figure. Fig. 1

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Is hypertensive left ventricular hypertrophy a cause of sustained ventricular arrhythmias in humans?

Journal of Human Hypertension ◽

10.1038/s41371-021-00503-w ◽

2021 ◽

Author(s):

R. Nadarajah ◽

P. A. Patel ◽

M. H. Tayebjee

Keyword(s):

Left Ventricular Hypertrophy ◽

Ventricular Arrhythmias ◽

Ventricular Hypertrophy ◽

Left Ventricular ◽

Systemic Hypertension ◽

Electrolyte Disturbance ◽

Electrocardiographic Monitoring ◽

Homogenous Distribution ◽

Artery Disease ◽

Asymptomatic Coronary Artery Disease

AbstractSudden cardiac death (SCD) is most commonly secondary to sustained ventricular arrhythmias (VAs). This review aimed to evaluate if left ventricular hypertrophy (LVH) secondary to systemic hypertension in humans is an isolated risk factor for ventricular arrhythmogenesis. Animal models of hypertensive LVH have shown changes in ion channel function and distribution, gap junction re-distribution and fibrotic deposition. Clinical data has consistently exhibited an increase in prevalence and complexity of non-sustained VAs on electrocardiographic monitoring. However, there is a dearth of trials suggesting progression to sustained VAs and SCD, with extrapolations being confounded by presence of co-existent asymptomatic coronary artery disease (CAD). Putatively, this lack of data may be due to the presence of more homogenous distribution of pathophysiological changes seen in those with hypertensive LVH versus known pro-arrhythmic conditions such as HCM and myocardial infarction. The overall impression is that sustained VAs in the context of hypertensive LVH are most likely to be precipitated by other causes such as CAD or electrolyte disturbance.

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Parathormone levels are independently associated with the presence of left ventricular hypertrophy in patients with coronary artery disease

The journal of nutrition health & aging ◽

10.1007/s12603-015-0649-y ◽

2015 ◽

Vol 20 (6) ◽

pp. 659-664 ◽

Cited By ~ 4

Author(s):

Á. Aceña ◽

A. M. Pello ◽

R. Carda ◽

Ó. Lorenzo ◽

M. L. Gonzalez-Casaus ◽

...

Keyword(s):

Coronary Artery Disease ◽

Coronary Artery ◽

Left Ventricular Hypertrophy ◽

Ventricular Hypertrophy ◽

Left Ventricular ◽

Artery Disease

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A randomized controlled trial of metformin on left ventricular hypertrophy in patients with coronary artery disease without diabetes: the MET-REMODEL trial

European Heart Journal ◽

10.1093/eurheartj/ehz203 ◽

2019 ◽

Vol 40 (41) ◽

pp. 3409-3417 ◽

Cited By ~ 27

Author(s):

Mohapradeep Mohan ◽

Shaween Al-Talabany ◽

Angela McKinnie ◽

Ify R Mordi ◽

Jagdeep S S Singh ◽

...

Keyword(s):

Oxidative Stress ◽

Coronary Artery Disease ◽

Body Weight ◽

Coronary Artery ◽

Left Ventricular Hypertrophy ◽

Ventricular Hypertrophy ◽

Left Ventricular ◽

Haemoglobin A1c ◽

Metformin Treatment ◽

Artery Disease

Abstract Aim We tested the hypothesis that metformin may regress left ventricular hypertrophy (LVH) in patients who have coronary artery disease (CAD), with insulin resistance (IR) and/or pre-diabetes. Methods and results We randomly assigned 68 patients (mean age 65 ± 8 years) without diabetes who have CAD with IR and/or pre-diabetes to receive either metformin XL (2000 mg daily dose) or placebo for 12 months. Primary endpoint was change in left ventricular mass indexed to height1.7 (LVMI), assessed by magnetic resonance imaging. In the modified intention-to-treat analysis (n = 63), metformin treatment significantly reduced LVMI compared with placebo group (absolute mean difference −1.37 (95% confidence interval: −2.63 to −0.12, P = 0.033). Metformin also significantly reduced other secondary study endpoints such as: LVM (P = 0.032), body weight (P = 0.001), subcutaneous adipose tissue (P = 0.024), office systolic blood pressure (BP, P = 0.022) and concentration of thiobarbituric acid reactive substances, a biomarker for oxidative stress (P = 0.04). The glycated haemoglobin A1C concentration and fasting IR index did not differ between study groups at the end of the study. Conclusion Metformin treatment significantly reduced LVMI, LVM, office systolic BP, body weight, and oxidative stress. Although LVH is a good surrogate marker of cardiovascular (CV) outcome, conclusive evidence for the cardio-protective role of metformin is required from large CV outcomes trials.

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Association of renal artery stenosis with left ventricular remodeling in patients coexisting with renovascular and coronary artery disease

Vascular ◽

10.1177/1708538118819676 ◽

2018 ◽

Vol 27 (2) ◽

pp. 190-198

Author(s):

Haojian Dong ◽

Yanqiu Ou ◽

Zhiqiang Nie ◽

Wenhui Huang ◽

Yuan Liu ◽

...

Keyword(s):

Coronary Artery Disease ◽

Coronary Artery ◽

Left Ventricular Hypertrophy ◽

Renal Artery ◽

Renal Artery Stenosis ◽

Ventricular Hypertrophy ◽

Left Ventricular ◽

Artery Stenosis ◽

Bilateral Renal Artery Stenosis ◽

Artery Disease

Objective Data about renal artery stenosis association with left ventricular remodeling in patients coexisting with coronary artery disease are scanty. Methods Patients with suspected both coronary artery disease and renal artery stenosis undergoing coronary and renal arteriography between October 2013 and December 2015 were prospectively enrolled. Left ventricular remodeling patterns were compared among different severity of renal artery stenosis group. Logistic regression was done to investigate the determinants of the left ventricular morphology. Results The overall prevalence of left ventricular hypertrophy was 40.5%, the highest in bilateral renal artery stenosis group compared to unilateral or normal ones (65.4% versus 41.8% versus 34.8%, p = 0.012). Significantly lower estimated glomerular filtration rate and higher cystatin C level were found in bilateral renal artery stenosis group than that in other two groups. Multivariate regression analysis showed that bilateral renal artery stenosis was associated with increased left ventricular hypertrophy and concentric hypertrophy with statistical significance (adjusted odds ratio = 2.909 (95%CI: 1.063–7.961), and 3.021 (95%CI: 1.136–8.033)). In addition, estimated glomerular filtration rate level was also related to left ventricular hypertrophy, while there was no significant interaction between renal artery stenosis and coronary artery disease on left ventricular hypertrophy/concentric hypertrophy occurrence. Conclusions Bilateral renal artery stenosis is significantly associated with increased left ventricular hypertrophy/concentric hypertrophy in patients with suspected concomitant coronary and renal artery disease, while no synergic effect could be found in coronary artery disease.

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