Related Experiment Video
Updated: Aug 15, 2026

Scanning Electron Microscopy of Macerated Tissue to Visualize the Extracellular Matrix
Published on: June 14, 2016
Mechanisms of disease: pathologic structural remodeling is more than adaptive hypertrophy in hypertensive heart
Javier Díez1, Arantxa González, Begoña López
1Division of Cardiovascular Pathophysiology, Center for Applied Medical Research, University of Navarra, Pamplona, and Division of Cardiology, Donostia University Hospital, San Sebastián, Spain. jadimar@unav.es
Insights
Arterial hypertension causes cardiac fibrosis by disrupting collagen balance, increasing cardiac risk. This review explores mechanisms, consequences, diagnosis, and treatments for hypertensive ventricular fibrosis.
Area of Science:
- Cardiovascular Medicine
- Pathology
- Biochemistry
Background:
- Arterial hypertension induces cardiac tissue changes, leading to myocardial structural remodeling.
- This remodeling involves complex pathological processes in both cardiomyocyte and non-cardiomyocyte heart compartments.
- A key process is the imbalance in collagen type I and III synthesis and degradation, causing excessive fibrosis.
Purpose of the Study:
- To review the mechanisms driving hypertensive ventricular fibrosis.
- To examine the clinical consequences of this fibrosis, particularly in hypertensive heart disease.
- To discuss diagnostic methods and therapeutic strategies for reducing cardiac fibrosis.
Main Methods:
- Review of existing literature on hypertensive cardiomyopathy and cardiac fibrosis.
- Analysis of pathological pathways involving collagen metabolism.
- Evaluation of diagnostic techniques and therapeutic interventions.
Main Results:
- Hypertensive ventricular fibrosis results from disrupted collagen homeostasis.
- This fibrosis is linked to increased cardiac risk in patients with hypertensive heart disease.
- Noninvasive diagnostic methods and potential therapeutic targets are identified.
Conclusions:
- Understanding the mechanisms of hypertensive fibrosis is crucial for managing cardiac risk.
- Effective diagnosis and targeted therapies are needed to mitigate the effects of cardiac fibrosis.
- Further research into therapeutic strategies can improve outcomes for patients with hypertensive heart disease.
Abstract:
Changes in the composition of cardiac tissue develop in arterial hypertension and lead to structural remodeling of the myocardium. Structural remodeling is the consequence of a number of pathologic processes, mediated by mechanical, neurohormonal and cytokine routes, occurring in the cardiomyocyte and the noncardiomyocyte compartments of the heart. One of these processes is related to the disruption of the equilibrium between the synthesis and degradation of collagen type I and III molecules, which results in an excessive accumulation of collagen type I and III fibers in the interstitium and the perivascular regions of the myocardium. The clinical relevance of ventricular fibrosis is that it might contribute to the increased cardiac risk of patients with hypertensive heart disease. This review focuses on the mechanisms of hypertensive ventricular fibrosis and its clinical consequences. In addition, we discuss the noninvasive methods for the diagnosis of cardiac fibrosis and the therapeutic strategies aimed to promote its reduction.
Related Concept Videos
Heart Failure II: Pathophysiology
Pathophysiology of Heart Failure
Cellular Adaptation II: Hypertrophy
Hypertension II: Pathophysiology
Cardiomyopathy III: Hypertrophic Cardiomyopathy
Cellular Adaptation I: Introduction and Atrophy

