Cardiovascular Effects of Metformin on Left Ventricular Hypertrophy in Nondiabetic Patients with Coronary Artery Disease
type: CreativeWork
description: Left ventricular hypertrophy (LVH) is highly prevalent in patients with coronary artery disease (CAD) irrespective, of blood pressure (BP) and is associated with an increased risk of all-cause mortality and cardiovascular events including myocardial infarction, heart failure, stroke and arrhythmias. Previous studies of mainly antihypertensive therapies have shown LVH to be a reversible risk factor. However, controlling BP is only partially effective as LVH persists in 20% of hypertensive patients who attain target BP. Therefore, novel ways of regressing LVH, independent of BP, in patients with CAD could reduce cardiovascular events and mortality in this patient group. Apart from uncontrolled BP, insulin resistance (IR) and central obesity are implicated in the development of LVH. Metformin - an anti-diabetic drug, has been shown to reduce body weight and to improve insulin sensitivity, thus reducing IR. These properties of metformin may have the potential of regressing LVH. Additionally, metformin has complex multiple modes of actions involving both AMP-activated protein kinase (AMPK)-dependent and AMPK-independent mechanisms that is implicated in cardiac hypertrophy. Indeed, metformin has been shown to reduce cardiac hypertrophy in different animal models of hypertrophy. However, there has never been a clinical study to show that metformin is capable of regressing LVH. In my PhD, I tested the hypothesis that metformin may regress LVH in patients who have CAD with insulin resistance and/or pre-diabetes. The MET-REMODEL trial was a randomized, double-blinded, placebo controlled study of 68 patients without diabetes who had well controlled blood pressure and have CAD, LVH and IR and/or prediabetes. Study subjects were assigned to receive either metformin (2000mg/day) or placebo therapy, over a 12 month follow up period. LV mass was measured at baseline and 12 months using cardiac magnetic resonance imaging (CMR). Primary endpoint of this study was change in left ventr…
abstract: Left ventricular hypertrophy (LVH) is highly prevalent in patients with coronary artery disease (CAD) irrespective, of blood pressure (BP) and is associated with an increased risk of all-cause mortality and cardiovascular events including myocardial infarction, heart failure, stroke and arrhythmias. Previous studies of mainly antihypertensive therapies have shown LVH to be a reversible risk factor. However, controlling BP is only partially effective as LVH persists in 20% of hypertensive patients who attain target BP. Therefore, novel ways of regressing LVH, independent of BP, in patients with CAD could reduce cardiovascular events and mortality in this patient group. Apart from uncontrolled BP, insulin resistance (IR) and central obesity are implicated in the development of LVH. Metformin - an anti-diabetic drug, has been shown to reduce body weight and to improve insulin sensitivity, thus reducing IR. These properties of metformin may have the potential of regressing LVH. Additionally, metformin has complex multiple modes of actions involving both AMP-activated protein kinase (AMPK)-dependent and AMPK-independent mechanisms that is implicated in cardiac hypertrophy. Indeed, metformin has been shown to reduce cardiac hypertrophy in different animal models of hypertrophy. However, there has never been a clinical study to show that metformin is capable of regressing LVH. In my PhD, I tested the hypothesis that metformin may regress LVH in patients who have CAD with insulin resistance and/or pre-diabetes. The MET-REMODEL trial was a randomized, double-blinded, placebo controlled study of 68 patients without diabetes who had well controlled blood pressure and have CAD, LVH and IR and/or prediabetes. Study subjects were assigned to receive either metformin (2000mg/day) or placebo therapy, over a 12 month follow up period. LV mass was measured at baseline and 12 months using cardiac magnetic resonance imaging (CMR). Primary endpoint of this study was change in left ventr…
author: Mohan, Mohapradeep
language: eng
keywords: Left Ventricular Hypertrophy, Metformin, Insulin resistance, Prediabetes, Coronary Artery Disease
date published: 2019
date modified: 2026-07-24T02:08:46Z
provider: University of Dundee
publisher: Networked Digital Library of Theses and Dissertations
type: WebPage
source organization: University of Dundee