In cardiology, ventricular remodeling (or cardiac remodeling ) refers to changes in the size, shape, structure, and function of the heart. This can occur as a result of exercise (physiological remodeling) or after injury to the heart muscle (pathological remodeling). Injuries are usually due to acute myocardial infarction (usually a transmural segment elevation infarction or ST), but possibly from a number of causes resulting in increased pressure or volume, causing excessive pressure or excessive volume (tension forms) to the heart. Chronic hypertension, congenital heart disease with intracardiac shunt, and valvular heart disease can also cause remodeling. After the humiliation occurs, a series of histopathological and structural changes occur in the left ventricular myocardium leading to progressive decline in left ventricular performance. Ultimately, ventricular remodeling can result in reduced contractile function (systolic) and reduced stroke volume.
Physiological remodeling is reversible while pathological remodeling is largely irreversible. Remodeling the ventricles under the request of the left/right pressure makes an unavoidable mismatch. Incompatibility of pathological pressure between pulmonary circulation guidance and compensatory compensation of the left and right ventricle. The term "reverse remodeling" in cardiology implies an improvement in the mechanics and function of the ventricle after a long-range injury or pathological process.
Ventricular remodeling may include ventricular hypertrophy, ventricular dilation, cardiomegaly, and other changes. This is an aspect of cardiomyopathy, in which there are many types. Concentric hypertrophy is caused by excessive pressure, while eccentric hypertrophy is caused by excessive volume.
Video Ventricular remodeling
Pathophysiology
Myocyte heart is the main cell involved in remodeling. Fibroblasts, collagen, interstitium, and coronary vessels to the lower levels, also play a role. A common scenario for remodeling is after myocardial infarction. There is myocardial necrosis (cell death) and disproportionate heart depletion. This thin and weak area is unable to withstand the pressure and volume load on the heart in the same way as other healthy tissues. As a result, there is a dilatation of space arising from the infarct region. The initial remodeling phase after myocardial infarction results in the improvement of the necrotic area and myocardial scar tissue which may, to some extent, be considered beneficial as there is an increase or maintenance of LV function and cardiac output. Over time, however, when the heart undergoes an ongoing remodeling, it becomes less elliptical and more rounded. Ventricular mass and volume increase, which together adversely affect heart function. Finally, diastolic function, or the ability of the heart to relax between contractions may become impaired, leading to further decline.
After myocardial infarction (MI), cardiac myocyte death can be triggered by necrosis, apoptosis, or autophagy, leading to thinning of the heart wall. Successful cardiac myocytes either regulate in parallel or in series with each other, contributing to ventricular dilatation or ventricular hypertrophy, depending on stress loading on the ventricular wall. In addition, decreased expression of calcium channel V1 mysoin and L-type in cardiac myocytes is also considered to cause cardiac remodeling. Under normal body conditions, fatty acids contribute 60 to 90% of the heart's energy supply. Post-MI, because the oxidation of fatty acids decreases, it causes a decrease in energy supply for cardiac myocytes, accumulation of fatty acids to toxic levels, and mitochondrial dysfunction. This consequence also causes increased oxidative stress on the heart, leading to fibroblast proliferation, metalloproteinase activation, and apoptotic induction, which is described below. In addition, the inflammatory immune response after MI also contributes to the above changes.
In addition, cardiac interstitium consisting of Type I and Type III collagen fibers is also involved in cardiac remodeling. Cardiac collagen is synthesized by fibroblasts and degraded by metalloproteinases. Fibroblasts are activated post MI, leading to increased synthesis of collagen and cardiac fibrosis. Increased expression of MMP1 and MMP9 leads to collagen fibers degradation, and further dilatation of the heart. Some signal paths such as Angiotensin II, Transforming growth factor beta (TGF-beta), and Endothelin 1 are known to trigger the synthesis and degradation of collagen fibers in the heart.
Other factors such as high blood pressure, activation of sympathetic systems that release norepinephrine, activation of the renin-angiotensin system that releases renin and anti-diuretic hormone are important contributors of cardiac remodeling. However, atrial natriuretic peptides are considered cardio protectors.
Maps Ventricular remodeling
Evaluation
Cardiac remodeling is evaluated by performing an echocardiogram. The size and function of atria and ventricle may be characterized using this test.
Treatment
Many factors affect the time and rate of remodeling, including the severity of injuries, secondary events (ischemia or recurrent infarction), neurohormonal activation, genetic factors and gene expression, and treatment. Drugs can dilute remodeling. Angiotensin-converting enzyme (ACE) inhibitors have been consistently shown to decrease remodeling in animal models or transmural infarcts and excessive chronic stress. Clinical trials show that ACE inhibitor therapy after myocardial infarction leads to improved myocardial performance, better ejection fraction, and mortality reduction than patients treated with placebo. Likewise, inhibition of aldosterone, either directly or indirectly, leads to remodeling improvements. Carvedilol, the 3rd generation beta blocker, can actually reverse the remodeling process by reducing left ventricular volume and improving systolic function. Early correction of congenital heart defects, if appropriate, can prevent remodeling, as well as the treatment of chronic hypertension or valvular heart disease. Often, reversed remodeling, or improved left ventricular function, will also be seen.
See also
- Dor Procedure
References
Further reading
- "Left Ventricular Remodeling in Heart Failure: Current Concept in Discovery and Clinical Assessment". imaging.onlinejacc.org . Retrieved 2016-02-12 .
Source of the article : Wikipedia
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