scholarly journals Physiological, Pathological and Pharmacological Interactions of Hydrogen Sulphide and Nitric Oxide in the Myocardium of Rats with Left Ventricular Hypertrophy

2022 ◽  
Vol 44 (1) ◽  
pp. 433-448
Author(s):  
Ashfaq Ahmad
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Left Ventricular Hypertrophy ◽  
Hydrogen Sulphide ◽  
Ventricular Hypertrophy ◽  
Combined Treatment ◽  
Left Ventricular ◽  
Systemic Hemodynamic ◽  
Pharmacological Interactions

Left ventricular hypertrophy (LVH) is characterized by increased myocardium thickness due to increased oxidative stress and downregulation of cystathione γ lyase (CSE) endothelial nitric oxide synthase (eNOS). Upregulation of CSE by hydrogen sulphide (H2S) and ENOS by L-arginine can arrest the progression of LVH individually. The present study explored the combined treatment of H2S and NO in the progression of LVH, and demonstrated that the response is due to H2S, NO or formation of either new molecule in physiological, pathological, and pharmacological in vivo settings of LVH. Exogenous administration H2S+NO in LVH significantly reduced (all p < 0.05) systolic blood pressure (SBP) and mean arterial pressure (MAP), LV index, heart index and oxidative stress when compared to the LVH group. There was downregulation of CSE mRNA and eNOS in the heart, and exogenous administration of H2S+NO groups upregulated eNOS MRNA while CSE MRNA remained downregulated in the hearts of the LVH group. Similar trends were observed with concentrations of H2S and NO in the plasma and tissue. It can be concluded that combined treatment of LVH with H2S and NO significantly ameliorate the progression of LVH by attenuating systemic hemodynamic and physical indices, and by decreasing oxidative stress. Molecular expression data in the myocardium of LVH depicts that combined treatment upregulated eNOS/NO while it downregulated CSE/H2S pathways in in vivo settings, and it is always eNOS/NO pathways which play a major role.

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

2019 ◽  
Vol 40 (41) ◽  
pp. 3409-3417 ◽  
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.

RYR2 p.R169L mutation and left ventricular hypertrophy in a child with emotion-triggered sudden death

2020 ◽  
Vol 30 (7) ◽  
pp. 1039-1042
Author(s):  
Utkarsh Kohli ◽  
Lisa Kuntz ◽  
Hemal M. Nayak
Keyword(s):  
Ventricular Tachycardia ◽  
Left Ventricular Hypertrophy ◽  
Ventricular Hypertrophy ◽  
Left Ventricular ◽  
Catecholaminergic Polymorphic Ventricular Tachycardia ◽  
Polymorphic Ventricular Tachycardia ◽  
Exercise Induced ◽  
In Vivo Effects

AbstractCatecholaminergic polymorphic ventricular tachycardia is a rare (prevalence: 1/10,000) channelopathy characterised by exercise-induced or emotion-triggered ventricular arrhythmias. There is an overall paucity of genotype-phenotype correlation studies in patients with catecholaminergic polymorphic ventricular tachycardia, and in vitro and in vivo effects of individual mutations have not been well characterised. We report an 8-year-old child who carried a mutation in the coding exon 8 of RYR2 (p.R169L) and presented with emotion-triggered sudden cardiac death. He was also found to have left ventricular hypertrophy, a combination which has not been reported before. We discuss the association between genetic variation in RYR2, particularly mutations causing replacement of arginine at position 169 of RYR2 and structural cardiac abnormalities.

scholarly journals Spontaneous Development of Left Ventricular Hypertrophy and Diastolic Dysfunction in Mice Lacking All Nitric Oxide Synthases

2010 ◽  
Vol 74 (12) ◽  
pp. 2681-2692 ◽  
Author(s):  
Kiyoko Shibata ◽  
Yasuko Yatera ◽  
Yumi Furuno ◽  
Ken Sabanai ◽  
Naoya Morisada ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Left Ventricular Hypertrophy ◽  
Diastolic Dysfunction ◽  
Ventricular Hypertrophy ◽  
Nitric Oxide Synthases ◽  
Left Ventricular
Sign in / Sign up

Export Citation Format

Share Document