Adverse effects of left ventricular hypertrophy in the reduction of endpoints in NIDDM with the angiotensin II

G Boner1, M E Cooper, K McCarroll

  • 1Department of Internal Medicine, Sackler Faculty of Medicine, University of Tel Aviv, Ramat Aviv, Tel Aviv, Israel. gboner1@barak-online.net

Diabetologia
|August 6, 2005
PubMed

Insights

Left ventricular hypertrophy (LVH) significantly increases cardiovascular and renal risks in type 2 diabetes patients. Losartan treatment effectively reduced these risks in patients with LVH, bringing them to levels comparable to those without LVH.

Area of Science:

  • Cardiology
  • Nephrology
  • Diabetology

Background:

  • Left ventricular hypertrophy (LVH) is a significant risk factor for cardiovascular and renal events in patients with type 2 diabetes and nephropathy.
  • The RENAAL trial investigated losartan's effects on renal disease progression and mortality in this population.

Purpose of the Study:

  • To investigate the impact of baseline LVH and losartan treatment on renal and cardiovascular (CV) events.
  • To assess the association between LVH and adverse outcomes in patients with type 2 diabetes and nephropathy.

Main Methods:

  • LVH assessed via ECG criteria (Cornell product, Sokolow-Lyon voltage).
  • Proportional hazards models used to determine risk of renal or CV events.
  • Baseline covariates included age, sex, blood pressure, proteinuria, and renal function markers.

Main Results:

  • 12% of patients had baseline LVH.
  • Losartan significantly reduced ECG measures of LVH.
  • LVH was associated with increased risk of composite renal endpoints (doubling of serum creatinine/end-stage renal disease) and CV events.
  • Losartan treatment in patients with LVH reduced both CV and renal risk to levels similar to those without LVH.

Conclusions:

  • LVH is a significant predictor of adverse renal and cardiovascular outcomes in type 2 diabetes with nephropathy.
  • Losartan effectively mitigates these risks in patients with LVH, normalizing outcomes to those without LVH.
Abstract

Related Concept Videos

Antihypertensive Drugs: Angiotensin-Converting Enzyme Inhibitors01:30

Antihypertensive Drugs: Angiotensin-Converting Enzyme Inhibitors

Angiotensin-converting enzyme (ACE), a vital component of the renin-angiotensin-aldosterone system, is abundant in lung endothelial cells. ACE converts the inactive decapeptide, angiotensin I, into the active octapeptide, angiotensin II. This potent vasoconstrictor narrows blood vessels, increasing resistance to blood flow and elevating blood pressure. Angiotensin II also stimulates aldosterone production, encouraging kidney cells to reabsorb more sodium and water from urine, thereby increasing...
Antihypertensive Drugs: Angiotensin II Receptor Blockers01:30

Antihypertensive Drugs: Angiotensin II Receptor Blockers

In the renin-angiotensin-aldosterone system, a hormone called angiotensin II plays a crucial role. It binds to the AT1 receptors in vascular smooth muscles coupled with Gq proteins. The activation of these receptors activates an enzyme called phospholipase C, which releases two molecules: inositol trisphosphate and diacylglycerol. These molecules cause a chain reaction that leads to the phosphorylation of myosin light chains and promotes interaction between actin and myosin, leading to smooth...
Antihypertensive Drugs: Direct Renin Inhibitors01:25

Antihypertensive Drugs: Direct Renin Inhibitors

The renin-angiotensin-aldosterone system (RAAS) is an intricate physiological pathway involving numerous enzymes and hormones, including renin, angiotensin-converting enzyme (ACE), angiotensin I and II, and aldosterone. Imbalances within this system increase the production of angiotensin II and aldosterone. Increased angiotensin II levels promote vasoconstriction and blood pressure elevation. Concurrently, higher aldosterone levels stimulate sodium and water reabsorption in the kidneys,...
Heart Failure Drugs: Diuretics01:22

Heart Failure Drugs: Diuretics

Heart failure and kidney perfusion are interconnected in a complex way. Reduced renal perfusion and venous congestion are two significant factors that contribute to renal dysfunction in heart failure. The kidneys, primarily responsible for fluid balance in the body, are adversely affected due to compromised cardiac output and increased venous pressure. In response to reduced renal perfusion, the kidneys activate neurohumoral mechanisms to restore balance. However, these mechanisms can be...
Heart Failure Drugs: Inhibitors of Renin-Angiotensin System01:26

Heart Failure Drugs: Inhibitors of Renin-Angiotensin System

The activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS) contributes to cardiac remodeling, and inhibiting the RAAS is a pharmacological target in heart failure management. As a result, neurohumoral modulation is a crucial treatment principle for managing heart failure. This approach involves using medications like ACE inhibitors (ACEIs), angiotensin receptor blockers (ARBs), β-blockers, mineralocorticoid receptor antagonists (MRAs), and neutral...
Heart Failure II: Pathophysiology01:29

Heart Failure II: Pathophysiology

Systolic Heart Failure and Compensatory MechanismsSystolic heart failure (also termed HFrEF, Heart Failure with Reduced Ejection Fraction) is the most prevalent type of heart filure. It results in a decreased volume of blood being pumped from the ventricle. The aortic arch and carotid sinuses have baroreceptors that detect reduced blood pressure, triggering the sympathetic nervous system (SNS) to release epinephrine and norepinephrine. Initially, this response aims to boost heart rate and...