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[Interstitial changes and ventricular hypertrophy in man]
1Cattedra di Cardiologia, Università degli Studi Federico II, Napoli.
Insights
Left ventricular hypertrophy in aortic stenosis involves abnormal collagen architecture, impacting myocardial stiffness. Post-surgery, hypertrophy and fibrosis normalize over years, restoring diastolic function.
Area of Science:
- Cardiovascular Medicine
- Cardiac Pathophysiology
- Biomedical Engineering
Context:
- Left ventricular hypertrophy (LVH) is a significant cardiac condition.
- Aortic stenosis frequently leads to secondary LVH.
- Collagen network remodeling plays a role in myocardial stiffness.
Purpose:
- To investigate the role of collagen network architecture in LVH secondary to aortic stenosis.
- To assess the influence of collagen on myocardial stiffness and ejection fraction.
- To examine the long-term effects of aortic valve replacement on LVH and interstitial fibrosis.
Summary:
- Collagen architecture abnormalities are present in 2/3 of aortic stenosis patients with LVH, more so than collagen concentration, affecting myocardial stiffness and ejection fraction.
- Myocardial relaxation and asynchrony are primarily influenced by the degree of hypertrophy, not the collagen network.
- Post-aortic valve replacement, LVH regression is a lengthy process, with normalization of diastolic stiffness and interstitial fibrosis observed 6-7 years after surgery.
Impact:
- Findings highlight the importance of collagen architecture over concentration in LVH-related stiffness.
- Reveals that hypertrophy degree, not collagen, dictates relaxation and asynchrony.
- Demonstrates long-term normalization of cardiac structure and function after aortic valve replacement, offering insights into myocardial recovery timelines.
Abstract:
Left ventricular hypertrophy is accompanied by the remodeling of the collagen network. We have studied collagen network in left ventricular hypertrophy secondary to aortic stenosis by cardiac catheterization and endomyocardial biopsies. We have demonstrated that collagen architecture is abnormal in 2/3 of patients with aortic stenosis and is more important than collagen concentration in influencing myocardial stiffness and ejection fraction. Furthermore, we observed that relaxation and asynchrony were influenced by the degree of hypertrophy instead of by the collagen network. The postoperative regression of left ventricular hypertrophy and the changes in interstitial tissue after valve replacement have been studied in a subgroup of patients. The major finding is that the regression of myocardial hypertrophy is a process that occurs over many years after correction of primary hemodynamic abnormality. Six to 7 years after valve replacement we observed, together with the normalization of diastolic stiffness, the complete normalization of interstitial fibrosis that was primarily increased (both pre and early postoperatively).