Is The Remodeling Of The Left Ventricle Common?

Despite the use of various therapies, myocardial ischemia can lead to left ventricular remodeling, which changes cardiac geometry, dimension, and function and eventually progresses to heart failure (HF). These findings suggest that biological aging processes likely contribute to alterations in left ventricular structure. LV remodeling occurs spontaneously among patients with HCM in several ways: wall thickening, otherwise defined as positive remodeling; wall thinning. Acute in-hospital MI mortality has markedly decreased, and most MI survivors have preserved left ventricular (LV) systolic function and excellent 1-year survival rate. However, patients who undergo serial echocardiograms during the first year post-infarct often demonstrate LV remodeling and the process is biologically complex.

Cardiac remodeling is the process of structural and functional changes in the left ventricle in response to internal or external cardiovascular damage or influence. Ventricular remodeling, first described in animal models of left ventricular stress and injury, occurs progressively in untreated patients after large myocardial infarction and in patients with transmural anteroseptal myocardial infarction (MI). Clinical trial data from the thrombolytic era demonstrated that post-infarct LV remodeling, defined as increases in LV end-diastolic area on TTE, was common in both women and men visiting outpatient cardiology clinics.

Postinfarct ventricular remodeling represents a prevailing cause of heart failure (HF), occurring in almost 30 of patients with a previous anterior myocardial infarction. Late remodeling involves the left ventricle globally and is associated with time-dependent dilatation, the distortion of ventricular shape, and other cardiac-related changes. Cardiac remodeling refers to changes in the heart’s size and shape that occur in response to cardiac disease or damage.

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 causes LV remodeling?

Pathologic left ventricular remodeling is linked to the activation of neuroendocrine, paracrine, and autocrine factors, which are up-regulated after myocardial injury and in the context of increased LV wall stress and hemodynamic derangement. These factors are crucial for maintaining proper function and preventing complications. The use of cookies on this site is governed by copyright © 2024 Elsevier B. V., its licensors, and contributors.

Can the heart remodel itself?

Cardiac remodelling refers to changes in the heart’s size and shape due to cardiac disease or damage, typically affecting the left ventricle. Doctors can assess this and track its extent over time using imaging studies. Common tests for measuring remodelling are non-invasive and do not expose patients to radiation, allowing for repeated measurements as needed. These tests are often used to monitor the left ventricle’s size, shape, and function.

Can a person live with 40% heart function?

Congestive heart failure (CHF) is a chronic, progressive condition that affects the heart’s ability to pump blood around the body. A normal output is 55-70, and people with an ejection fraction (EF) under 40 may have a higher risk of dying from CHF. A 2017 study reported a poor 5-year life expectancy among all people admitted to the hospital with heart failure, with an estimated 5-year death rate of 75. 4. CHF does not mean the heart has completely failed, but untreated complications can be life-threatening.

How common is left ventricular hypertrophy?

Left ventricular hypertrophy affects approximately 15-20% of the general population, which equates to nearly 1 in 5 individuals. The following factors have been identified as contributing to an increased risk of developing this condition: elevated blood pressure, obesity, advanced age, and a person’s ethnicity. It is frequently a consequence of other cardiac disorders, thereby elevating the likelihood of significant complications. In the absence of treatment, LVH impairs the heart’s ability to pump blood efficiently, thereby increasing the risk of other cardiac complications.

How common is left ventricular dysfunction?

The study found that 31. 6 participants had LV systolic dysfunction, with moderate/severe systolic dysfunction occurring in 9. 0 participants. In 87. 4 participants, a degree of LV diastolic dysfunction was also present. LV diastolic dysfunction was found in 88. 3 participants, with two-thirds of these being graded as’mild’. The study focused on moderate or severe LV diastolic dysfunction, which has been shown to have prognostic importance. In total, just over half of all participants had LV systolic or isolated moderate/severe diastolic dysfunction.

Dyspnoea data were available in 73. 9 participants, but dyspnoea status could not be assigned in 98 participants due to uncertainty about whether dyspnoea limited activity due to other limiting conditions. Echocardiographically assessed LV function and pre-existing heart failure diagnoses were broadly comparable between those with and without dyspnoea status. Of those with significant LV dysfunction, 62. 1 (87/140) had limiting dyspnoea.

The proportion was similar among participants with systolic and isolated LV diastolic dysfunction. Overall, 20. 5 (57/278) participants had LV systolic dysfunction with limiting dyspnoea, and 10. 8 (30/278) had isolated moderate/severe LV diastolic dysfunction with limiting dyspnoea.

What causes 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.

How common is concentric remodeling of the LV?

The study reveals that ventricular remodeling is an adaptive response to aging and exposure to risk factors for cardiovascular disease and myocardial injury. A community study with 4492 participants showed that 64 had normal geometry, 18 had concentric remodeling, 13 had eccentric hypertrophy, and 5 had concentric hypertrophy. The data were similar to the population with normal geometry but different in remodeling standards, especially concerning concentric remodeling and eccentric hypertrophy.

The differences can be attributed to the greater number of hypertensive and diabetic patients. A study by Teh et al. found that there was an increased prevalence of eccentric remodeling in older individuals and those with more comorbidities. Aging is directly related to the progression of cardiac remodeling, likely due to exposure to multiple cardiovascular risk factors. This finding is present in both the study and the literature.

Can anxiety cause left ventricular hypertrophy?

Anxiety disorders can increase circulating catecholamines through the hypothalamic-pituitary-adrenal axis, leading to chronic hyperstimulation of the hypothalamic centers and activation of the sympathetic nervous system. This can increase cardiovascular workload and risk of LVH and serious dysrhythmias. Anxiety may promote LVH and increased TDR through chronic sympathetic hyperactivity in hypertensive patients.

Subgroup analyses were performed stratified by sex, age, BMI, and smoking. Interaction analyses found that the associations between anxiety and hypertensive LVH and between anxiety and TDR showed interactions with sex, but not with age, BMI, or smoking. The results showed that anxiety prevalence was significantly higher in men than in women, consistent with previous studies. Anxiety was associated with LVH and increased Tp-Te/QT ratio in men, but not in women. This discrepancy may be due to differences in biological stress responses to anxiety, such as higher salivary cortisol levels in men and greater perceived stress in men with anxiety.

However, the study had limitations, including being a single-center study limited to the native Chinese population, not performing serial HAM-A assessments, and calculating the sample size without considering subgroups, which limited the generalizability of the findings.

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.

Can you have left ventricular dysfunction without heart failure?

Asymptomatic left ventricular systolic dysfunction (ALVSD) is a condition characterized by a decline in left ventricular ejection fraction (LVEF) without the presence of heart failure symptoms. The underlying cause of this condition requires further evaluation and may necessitate treatment.