What Is The Left Ventricle’S Concentric Remodeling?

Left ventricular (LV) remodeling and hypertrophy are linked to the development of congestive heart failure (CHF) and an increased incidence of other major cardiovascular events, including sudden death. LV remodeling can be produced by increasing relative wall thickness, which alters myocardial geometry, resulting in reduced LV end. This process is triggered by insults to the myocardium, such as an infarction or viral disease, which may cause the ventricle to lose its function.

There are four basic patterns of left ventricular (LV) remodeling: wall thickening, wall thinning, and concentric remodeling. A normal left ventricular chamber size indicates a concentric or normal geometry, while differences in relative wall thickness distinguish concentric from normal. Concentric remodeling generally exhibits a trend toward higher LV mass than is seen with a truly normal geometry and appears to be an early response to LV hypertrophy.

In cardiology, ventricular remodeling refers to changes in the size, shape, structure, and function of the heart. Concentric remodeling, defined by the thickness of the septum or posterior wall divided by the left ventricular radius at end-diastole ≥0.45, is a frequent finding among patients with LV hypertrophy.

In summary, left ventricular remodeling and hypertrophy are significant pathophysiological processes in heart failure, with four basic patterns: wall thickening, wall thinning, and concentric remodeling. These processes can lead to increased cardiac afterload, chronic pressure, volume overload, and MI.

Is ventricular remodeling good or bad?

Ventricular remodeling is a harmful process that causes cellular and structural changes in the left ventricular myocardium, leading to dilation and reduced function. If unchecked, it can worsen LVEF and prognosis. ScienceDirect uses cookies and all rights are reserved, including those for text and data mining, AI training, and similar technologies. Open access content is licensed under Creative Commons terms.

What is the difference between concentric and eccentric cardiac remodeling?

Cardiac hypertrophy is a heart mechanism that compensates for pressure or volume overload. It is often seen as a feedback loop, with concentric hypertrophy normalizing wall stress and eccentric hypertrophy increasing stroke volume to compensate for lost regulation. However, there are instances where too little hypertrophy occurs to normalize stress or hypertrophy exceeds the amount needed for normalization. This suggests nonmechanical mechanisms that modulate the degree to which pressure overload signals an increase in myocardial mass.

Hypertrophy develops when the rate of myocardial protein synthesis exceeds that of protein degradation. In pressure overload, this imbalance is created as synthesis rate increases, while in volume overload, hypertrophy accumulates due to decreased degradation rate. This relationship between left ventricular geometry and hypertrophy is crucial in understanding the role of left ventricular function in valvular heart disease.

What is the meaning of left ventricular remodeling?

Ventricular remodeling, a maladaptive process affecting left ventricular (LV) geometry, mass, and volume, is a significant predictor of morbidity and mortality in patients with heart failure or myocardial infarction. Two classes of drugs, angiotensin-converting enzyme (ACE) inhibitors and beta-adrenergic blockers, have been found to inhibit LV remodeling. ACE inhibitors improve survival and prevent progressive remodeling, while beta-adrenergic blockers have a beneficial effect on both survival and remodeling.

The renin-angiotensin system and possibly the sympathetic nervous system play a role in this process. Therefore, ACE inhibitors and beta-blockers should be part of the pharmacologic regimen for treating patients with LV dysfunction to prevent progressive remodeling.

What causes concentric remodeling of the left ventricle?

Concentric left ventricular hypertrophy is an abnormal increase in left ventricular myocardial mass due to chronically increased workload on the heart, often resulting from pressure overload induced by arteriolar vasoconstriction. Eccentric left ventricular hypertrophy is induced by increased filling pressure of the left ventricle, known as diastolic overload. This mechanism can play a role in compensating for ischemic or infarcted myocardial tissue in patients with coronary artery disease.

The sustained increase in wall stress, cytokine and neuro-activation, stimulates the development of myocardial hypertrophy or increasing muscle thickness with the deposition of the extracellular matrix. This initially serves as a compensatory mechanism to maintain contractile forces and counteract increased ventricular wall stress. However, the benefits of increased wall thickness are offset by a significant increase in stiffness of the hypertrophied walls and increased diastolic ventricular pressures, which are transmitted back into the left atrium and pulmonary vasculature.

What causes ventricular Remodelling?

Heart remodeling can occur due to various heart diseases or cardiac damage, such as a heart attack. Initial remodelling occurs immediately after a heart attack to compensate for damage and pump enough blood to the body. If it persists for a long time, it can lead to heart failure. Physiological remodeling occurs during exercise and pregnancy, while pathological remodeling occurs due to heart problems causing pressure overload.

The extent of damage caused by ventricular remodeling can be measured using imaging studies like MRI scans and echocardiography, and left ventricular ejection fraction (LVEF) to measure the amount of blood pumped out of the left ventricle.

Can concentric left ventricular remodeling be reversed?

Medical therapies have been found to promote reverse remodeling, restoring a more normal ventricular shape, reducing LV volumes and mass, and improving LVEF. These changes are linked to reduced morbidity and mortality. Cookies are used by this site, and by continuing, you agree to the use of cookies. Copyright © 2024 Elsevier B. V., its licensors, and contributors. All rights reserved, including those for text and data mining, AI training, and similar technologies.

What are the types of ventricular remodeling?

Ventricular remodeling, an aspect of cardiomyopathy, involves changes such as ventricular hypertrophy, ventricular dilation, and cardiomegaly. It is primarily influenced by the cardiac myocyte, with other cells such as fibroblasts, collagen, the interstitium, and coronary vessels playing a lesser role. Post-myocardial infarction, myocardial necrosis and disproportionate thinning of the heart can lead to dilatation of the chamber.

The initial remodeling phase may improve LV function and cardiac output, but over time, the heart becomes less elliptical and more spherical, leading to increased ventricular mass and volume, adversely affecting cardiac function.

Cardiac myocyte death can be triggered by necrosis, apoptosis, or autophagy, leading to thinning of the cardiac wall. Survivors of cardiac myocytes can either arrange parallel or in series, contributing to ventricular dilatation or hypertrophy. Reduced expression of V1 myosin and L-type calcium channels on cardiac myocytes is also thought to cause cardiac remodeling.

Fatty acid accounts for 60 to 90 percent of the heart’s energy supply. Post-MI, decreased fatty acid oxidation leads to reduced energy supply for cardiac myocytes, accumulation of fatty acids to toxic levels, and mitochondria dysfunction. This leads to increased oxidative stress on the heart, causing fibroblast proliferation, activation of metalloproteinases, and apoptosis. Inflammatory immune response also contributes to these changes.

How do you treat ventricular remodeling?

Therapeutic interventions in pathological ventricular remodeling include ACE inhibitors, ARBs, β-blockers, and MRAs, which reduce morbidity and mortality by reducing cell death, hypertrophy, and fibrosis. GLP-1 may be effective in treating metabolic derangements, while mechanical support using ventricular assist device therapy unloads the failing myocardium and limits ventricular dilation. ICDs and CRTs target electrophysiological remodeling events, and cell replacement therapy to replenish lost cardiomyocytes remains experimental.

ACE inhibitors and ARBs were initially used to treat hypertension but have shown substantial benefits in animal models of heart failure, including increased survival, by targeting adverse cardiac remodeling. Angiotensin receptor activation can induce cardiac remodeling independently of changes in blood pressure, and ACE inhibitors and ARBs both act to antagonize the effects of Ang II. Numerous clinical trials have demonstrated that ACE inhibitors and ARBs reduce heart failure morbidity and mortality.

Low-dose MRAs are recommended for treatment in select patients with moderately severe or severe heart failure symptoms, recent decompensation, or LV dysfunction early after myocardial infarction. The Eplerenone in Mild Patients Hospitalization And Survival Study in Heart Failure (EMPHASIS-HF) revealed that eplerenone reduces mortality and hospitalization in patients with systolic dysfunction and mild symptoms, expanding the role of MRAs to include asymptomatic patients.

What is the difference between eccentric and concentric left ventricular hypertrophy?

Concentric hypertrophy is linked to increased left ventricular wall thickness, while eccentric hypertrophy involves dilatation of the left ventricular chamber. Both conditions increase the overall size of cardiomyocytes. Studies have shown that atrial and ventricular function and structural adaptations of the heart in elite triathletes are assessed using cardiac MR imaging. Functional and metabolic evaluation of the athlete’s heart using magnetic resonance imaging and dobutamine stress magnetic resonance spectroscopy is also conducted.

What is the treatment for ventricular remodeling?

Therapeutic interventions in pathological ventricular remodeling include ACE inhibitors, ARBs, β-blockers, and MRAs, which reduce morbidity and mortality by reducing cell death, hypertrophy, and fibrosis. GLP-1 may be effective in treating metabolic derangements, while mechanical support using ventricular assist device therapy unloads the failing myocardium and limits ventricular dilation. ICDs and CRTs target electrophysiological remodeling events, and cell replacement therapy to replenish lost cardiomyocytes remains experimental.

ACE inhibitors and ARBs were initially used to treat hypertension but have shown substantial benefits in animal models of heart failure, including increased survival, by targeting adverse cardiac remodeling. Angiotensin receptor activation can induce cardiac remodeling independently of changes in blood pressure, and ACE inhibitors and ARBs both act to antagonize the effects of Ang II. Numerous clinical trials have demonstrated that ACE inhibitors and ARBs reduce heart failure morbidity and mortality.

Low-dose MRAs are recommended for treatment in select patients with moderately severe or severe heart failure symptoms, recent decompensation, or LV dysfunction early after myocardial infarction. The Eplerenone in Mild Patients Hospitalization And Survival Study in Heart Failure (EMPHASIS-HF) revealed that eplerenone reduces mortality and hospitalization in patients with systolic dysfunction and mild symptoms, expanding the role of MRAs to include asymptomatic patients.

Is concentric LVH curable?

The elevation of LDH levels may be attributable to an underlying cardiac pathology, which may be amenable to pharmacological and lifestyle modifications aimed at alleviating cardiac stress, contingent on the specific etiology.