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Left Atrial Stenosis Induced Pulmonary Venous Arterialization and Group 2 Pulmonary Hypertension in Rat
Published on: November 18, 2018
[Arterial hypertension and heart failure]
1Dipartimento di Malattie Cardiovascolari, Azienda Ospedaliera San Giovanni-Addolorata, Rome. gfmureddu@hsangiovanni.roma.it
Insights
Systemic hypertension can lead to heart failure (HF) through left ventricular hypertrophy (LVH). Early detection of myocardial growth and dysfunction markers can identify at-risk patients for timely intervention.
Area of Science:
- Cardiology
- Pathophysiology
- Biomedical Engineering
Context:
- Systemic hypertension is a prevalent condition preceding heart failure (HF).
- Left ventricular hypertrophy (LVH) is a significant risk factor for developing HF.
- A linear relationship exists between LV mass and congestive HF risk.
Purpose:
- To highlight the role of LVH in HF development.
- To explain the mechanisms of 'load dependent myocyte dysfunction'.
- To emphasize early detection strategies for HF.
Summary:
- Cardiomyocyte and endothelial cell hypertrophy/hyperplasia reduce coronary reserve, leading to cell death (apoptosis/necrosis).
- This 'load dependent myocyte dysfunction' involves structural and functional alterations, detectable via mid-wall shortening.
- Detecting significant myocardial growth and 'load geometrical adaptation' markers aids early HF diagnosis.
Impact:
- Early identification of patients at risk for symptomatic LV dysfunction.
- Enables intensive treatment and specialized follow-up for high-risk individuals.
- Potential to improve patient outcomes by intervening before symptomatic HF onset.
Abstract:
Systemic hypertension is a condition that frequently occurs before the onset of heart failure; furthermore, left ventricular hypertrophy (LVH) is an important risk factor for the development of heart failure (HF). Many studies have demonstrated that a linear relationship exists between increasing values of LV mass and the relative risk of the development of congestive HF. Hypertrophy-hyperplasy of cardiomyocytes and endothelial cells leads to a reduction in coronary reserve and to cell death due to apoptosis or focal necrosis. This characteristic has been defined as 'load dependent myocyte dysfunction' and it is characterized both by structural dysfunctions with cell death and by functional alterations that are detectable early with the evaluation of myocardial function measuring the mid-wall shortening. The detection of extremely high myocardial growth is another factor that could help to make an early diagnosis of HF. The presence of 'load geometrical adaptation' markers, together with an early detection of systolic function anomalies that are often accompanied by diastolic modifications, could help to identify, in an early phase, patients who will develop symptomatic LV dysfunction; therefore, these patients can be intensively treated and undergo a specific follow-up.
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