Related Experiment Video

Updated: Jul 16, 2026

Studying Left Ventricular Reverse Remodeling by Aortic Debanding in Rodents
07:26

Studying Left Ventricular Reverse Remodeling by Aortic Debanding in Rodents

Published on: July 14, 2021

Regression of left ventricular hypertrophy by a candesartan-based regimen in clinical practice. The VIPE study

Vivencio Barrios1, Carlos Escobar, Alberto Calderón

  • 1Department of Cardiology, Hospital Ramón y Cajal, Ctra. Colmenar km. 9.100, Madrid 28034, Spain. vbarriosa@meditex.es

Journal of the Renin-Angiotensin-Aldosterone System : JRAAS
|February 24, 2007
PubMed

Insights

A six-month candesartan regimen significantly reduced left ventricular hypertrophy (LVH) in hypertensive patients. This treatment effectively lowered blood pressure and improved echocardiographic measures of LVH, with good tolerability.

Area of Science:

  • Cardiology
  • Hypertension Management
  • Pharmacology

Background:

  • Hypertension is a major risk factor for cardiovascular disease.
  • Left ventricular hypertrophy (LVH) is a common complication of uncontrolled hypertension.
  • Effective antihypertensive therapies are crucial for preventing cardiovascular events.

Purpose of the Study:

  • To evaluate the efficacy of a candesartan-based regimen in reducing left ventricular hypertrophy (LVH) in hypertensive patients.
  • To assess the impact of the treatment on blood pressure and echocardiographic parameters.
  • To determine the tolerability and safety of the candesartan-based regimen.

Main Methods:

  • Prospective, open-label clinical evaluation of 97 hypertensive patients with echocardiographic LVH.
  • Treatment with a candesartan-based regimen for six months, including hydrochlorothiazide (HCTZ) and additional antihypertensives as needed.
  • Monitoring of blood pressure (BP) and echocardiographic parameters, including left ventricular mass index (LVMI).

Main Results:

  • Significant reduction in systolic and diastolic BP by 19.3 +/- 8 mmHg and 9.4 +/- 5 mmHg, respectively (p<0.001).
  • Significant decrease in LVMI by 17.01 g/m2 (p<0.001), with 28% of patients achieving target LVMI.
  • No significant changes in ejection fraction, shortening fraction, or LV diastolic function were observed.

Conclusions:

  • A six-month candesartan-based regimen effectively reduces echocardiographic LVH in hypertensive patients.
  • The treatment demonstrates significant BP-lowering effects and improves cardiac remodeling.
  • The regimen was well-tolerated with no serious adverse events reported, suggesting a favorable safety profile.

Related Concept Videos

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...
Aortic Regurgitation III: Medical Management01:25

Aortic Regurgitation III: Medical Management

Aortic regurgitation (AR) is when the aortic valve does not close or seal properly, leading to backward blood circulation from the aorta into the left ventricle during diastole. Common causes of AR include rheumatic heart disease, congenital valve defects, and aortic root dilation. Managing AR requires a multifaceted approach to alleviate symptoms, preserve left ventricular function, and address the underlying cause of the regurgitation. Patients with symptomatic AR or significant left...
Heart Failure V: Medical Management01:30

Heart Failure V: Medical Management

Medical Management of Acute Decompensated Heart Failure (ADHF)The primary goals of therapy for patients hospitalized with acute decompensated heart failure (ADHF) include:Relieving symptomsOptimizing volume statusSupporting oxygenation and ventilationMaintaining cardiac output (CO) and end-organ perfusionIdentifying and addressing the cause of ADHFPreventing complicationsProviding patient education on factors precipitating HF exacerbationPlanning for dischargeOngoing monitoring and assessment...
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: 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: 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,...