Left Ventricular Reverse Remodeling: What Is It?

Increased left ventricular dilation and reduced systolic function are consistently associated with poor prognosis and worse clinical outcomes. This review discusses the pathophysiological mechanisms behind these issues and discusses the use of medical therapies to promote reverse remodeling, which involves restoration of a more normal ventricular shape, reduction in left ventricular volumes and mass, and an improvement in left ventricular efficiency (LVEF). The term “left ventricular remodeling” gained popularity in the mid-1980s after studies by Pfeffer and colleagues documented progressive left ventricular dysfunction.

LV reverse remodeling (LVRR) is characterized by a decrease in chamber volume and normalization of shape, associated with improvement in both systolic and diastolic function. It occurs progressively in untreated patients after large myocardial infarction and those with dilated forms of left ventricular stress and injury. LVRR can target biological pathways that aberrate ventricular loading conditions and cause cavity enlargement and distortion.

The rationale behind LVRR is to restore a normal ratio between wall thickness and the radius of the left ventricle to normalize systolic wall stress. Reverse remodeling in cardiology implies an improvement in ventricular mechanics and function following a remote injury or pathological process. This pathological process is responsible for the onset and progression of heart failure, causing hypertrophy, dilatation, and other complications.

A reduction in LVESV of 10 signifies clinically relevant reverse remodeling, which is a strong predictor of lower long-term mortality and heart failure events.

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 does LV remodelling mean?

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 is the left ventricular adverse remodeling?

Adverse remodeling in left ventricular (LV) is a complex biological process that begins early after myocardial infarction (MI) and can lead to long-term poor cardiovascular outcomes. Cardiac Magnetic Resonance (CMR) is the best tool to define adverse remodeling due to its ability to accurately measure LV end-diastolic and end-systolic volumes and their variation over time. CMR is the gold standard method to assess in vivo myocardial infarction extension and detect microvascular obstruction and intramyocardial hemorrhage, both associated with adverse remodeling.

New CMR quantitative biomarkers, such as T1 mapping, myocardial strain, and 4D flow, have emerged as predictive of post-ischemic adverse remodeling. T1 mapping imaging can depict infarcted tissue and assess diffuse myocardial fibrosis using surrogate markers like extracellular volume fraction, which may predict functional recovery or risk stratification of remodeling. The 4D flow CMR technique has been shown to be useful as early predictors of remodeling.

What is reverse transformation?

Reverse transformations are used to ensure that the model’s information is expressed in a format similar to the data used to train it. These transformations are reversed in model details and scoring results. Some attributes used by the model correspond to columns in the build data, but due to algorithmic logic, nested data, and transformations, some attributes do not correspond to columns. For example, a nested column in training data is not interpreted as an attribute by the model.

Is LV remodeling reversible?

Cardiac remodeling, which involves changes in ventricular volume and the thickness and shape of the myocardial wall, is an adaptive mechanism in heart failure syndrome. This remodeling can lead to an increase in neurohormonal activity, which initially aims to maintain compensation but intensifies clinical manifestations and myocardial damage when it remains high. Cardiac remodeling can be reversed with optimized treatment, resulting in gradual improvement in cardiac function and improved prognosis. The study highlights the importance of understanding and managing cardiac remodeling in heart failure and stroke volume management.

What is left ventricular remodeling pathophysiology?

Pathological ventricular remodeling is a complex process influenced by various factors, including ischemia/reperfusion, excessive mechanical load, and cellular processes. These processes include cardiomyocyte loss through cell death pathways, hypertrophic cardiomyocytes, accumulation of excess extracellular matrix, metabolic derangements, insulin resistance, lipotoxicity, and structural changes leading to a pro-arrhythmic phenotype.

Current therapies, such as angiotensin converting enzyme inhibitors, angiotensin receptor blockers, aldosterone antagonists, and β-blockers, have shown significant efficacy in reducing morbidity and mortality in patients with chronic systolic heart failure. However, disease progression continues unabated, and less is known about the proportion of disease where systolic performance of the left ventricular ejection fraction (LV) is preserved.

The majority of current therapies target HFrEF, previously termed systolic heart failure, but it is estimated that 50 of heart failure patients have a preserved left ventricular ejection fraction (HFpEF). Initial studies attributed HFpEF to dysfunction of the myocardium during the filling phase of the cardiac cycle, but it is clear that in some cases, the left ventricular myocardium is an innocent bystander, manifesting dysfunctional filling due to volume overload, insufficiency of perfusion, or inadequate filling times. In many cases, a combination of perturbed diastolic relaxation and excessive volume due to extrinsic factors may combine to perturb ventricular filling.

What is reverse remodeling of the left ventricle?

Adverse remodeling, a hallmark of heart failure (HF) development and progression, is characterized by changes in the size, shape, and function of the myocardium. While cardiac remodelling may be compensatory in the short term, further neurohumoral activation and haemodynamic overload drive this deleterious process that is associated with impaired prognosis. In some patients, the changes may be reversed, such as left ventricular reverse remodelling (LVRR), which is characterized by a decrease in chamber volume and normalization of shape associated with improvement in both systolic and diastolic function.

LVRR may occur spontaneously or more often in response to therapeutic interventions that remove the initial stressor or alleviate some of the mechanisms contributing to further deterioration of the failing heart.

The process of LVRR in patients with new-onset HF may take up to two years after initiating treatment, but there is a significant portion of patients who do not improve despite optimal therapy. This has serious clinical implications when considering treatment escalation towards more aggressive options. In patients that achieve delayed improvement in cardiac function and architecture, waiting might avoid untimely implantable cardioverter-defibrillator implantation. Therefore, prognostication of successful LVRR based on clinical, imaging, and biomarker predictors is of utmost importance.

Reverse remodelled hearts continue to have abnormal features, with most molecular, cellular, interstitial, and genome expression abnormalities remaining and a susceptibility to dysfunction redevelopment under biomechanical stress persisting in most patients. A distinction should be made between reverse remodelling and true myocardial recovery.

What is reverse remodelling?

Reverse remodeling is the process where the failing myocardium shows changes in chamber geometry and function, potentially correcting molecular and transcriptional abnormalities. Studies have shown that acute infarct dilation can have late effects on heart size, and progressive ventricular remodeling can occur in rats with myocardial infarction. Further research is needed to understand these processes.

What is left ventricular hypertrophy remodeling?

Left ventricular hypertrophy (LVH) is a compensatory process that develops over time in response to wall stress or significant hemodynamic pressure or volumetric burden. It initially serves as a compensatory mechanism to maintain contractile forces and counteract increased ventricular wall stress. However, the benefits of increased wall thickness offset the increased stiffness of the hypertrophied walls, which leads to increased diastolic ventricular pressures.

LVH is an abnormal increase in the myocardium of the left ventricle induced by chronically elevated workload on the heart muscle. Once pathologic LVH is developed, the patient is at significant risk for heart failure, dysrhythmias, and sudden death. The most common etiologic cause is the heart contracting against an elevated afterload, as seen in hypertension and valvar aortic stenosis. Another cause is increased filling of the left ventricle inducing diastolic overload, which is the underlying mechanism for eccentric LVH in patients with regurgitant valvular lesions.

Coronary artery disease plays a role in the pathogenesis of LVH, as the normal myocardium tries to compensate for tissue that has become ischemic or infarcted. One key pathophysiologic component in LVH is the concomitant development of myocardial fibrosis, which initially manifests as diastolic dysfunction but will also develop with progressive disease.

What is reverse remodeling of left ventricle?

Adverse remodeling, a hallmark of heart failure (HF) development and progression, is characterized by changes in the size, shape, and function of the myocardium. While cardiac remodelling may be compensatory in the short term, further neurohumoral activation and haemodynamic overload drive this deleterious process that is associated with impaired prognosis. In some patients, the changes may be reversed, such as left ventricular reverse remodelling (LVRR), which is characterized by a decrease in chamber volume and normalization of shape associated with improvement in both systolic and diastolic function.

LVRR may occur spontaneously or more often in response to therapeutic interventions that remove the initial stressor or alleviate some of the mechanisms contributing to further deterioration of the failing heart.

The process of LVRR in patients with new-onset HF may take up to two years after initiating treatment, but there is a significant portion of patients who do not improve despite optimal therapy. This has serious clinical implications when considering treatment escalation towards more aggressive options. In patients that achieve delayed improvement in cardiac function and architecture, waiting might avoid untimely implantable cardioverter-defibrillator implantation. Therefore, prognostication of successful LVRR based on clinical, imaging, and biomarker predictors is of utmost importance.

Reverse remodelled hearts continue to have abnormal features, with most molecular, cellular, interstitial, and genome expression abnormalities remaining and a susceptibility to dysfunction redevelopment under biomechanical stress persisting in most patients. A distinction should be made between reverse remodelling and true myocardial recovery.

What is reverse LV remodeling?

Adverse remodeling, a hallmark of heart failure (HF) development and progression, is characterized by changes in the size, shape, and function of the myocardium. While cardiac remodelling may be compensatory in the short term, further neurohumoral activation and haemodynamic overload drive this deleterious process that is associated with impaired prognosis. In some patients, the changes may be reversed, such as left ventricular reverse remodelling (LVRR), which is characterized by a decrease in chamber volume and normalization of shape associated with improvement in both systolic and diastolic function.

LVRR may occur spontaneously or more often in response to therapeutic interventions that remove the initial stressor or alleviate some of the mechanisms contributing to further deterioration of the failing heart.

The process of LVRR in patients with new-onset HF may take up to two years after initiating treatment, but there is a significant portion of patients who do not improve despite optimal therapy. This has serious clinical implications when considering treatment escalation towards more aggressive options. In patients that achieve delayed improvement in cardiac function and architecture, waiting might avoid untimely implantable cardioverter-defibrillator implantation. Therefore, prognostication of successful LVRR based on clinical, imaging, and biomarker predictors is of utmost importance.

Reverse remodelled hearts continue to have abnormal features, with most molecular, cellular, interstitial, and genome expression abnormalities remaining and a susceptibility to dysfunction redevelopment under biomechanical stress persisting in most patients. A distinction should be made between reverse remodelling and true myocardial recovery.