Key result
Myocardial interstitial fibrosis drives maladaptive structural remodeling in hypertensive heart disease.
Why the study?
Diffuse myocardial interstitial fibrosis contributes critically to maladaptive remodeling, altered cardiac function, electrical activity, and perfusion, resulting in poor outcomes in hypertensive heart disease.
This review highlights the critical role of diffuse myocardial interstitial fibrosis in hypertensive heart disease, emphasizing the need for noninvasive diagnostic tools and effective therapeutic strategies to prevent or regress its development.
May warrant antifibrotic strategies in hypertensive heart disease; leaves open validation of noninvasive fibrosis assessment.
Hypertensive heart disease (HHD) can no longer be considered as the beneficial adaptive result of the hypertrophy of cardiomyocytes in response to pressure overload leading to the development of left ventricular hypertrophy. The current evidence indicates that in patients with HHD, pathological lesions in the myocardium lead to maladaptive structural remodeling and subsequent alterations in cardiac function, electrical activity, and perfusion, all contributing to poor outcomes. Diffuse myocardial interstitial fibrosis is probably the most critically involved lesion in these disorders. Therefore, in this review, we will focus on the histological characteristics, the mechanisms, and the clinical consequences of myocardial interstitial fibrosis in patients with HHD. In addition, we will consider the most useful tools for the noninvasive diagnosis of myocardial interstitial fibrosis in patients with HHD, as well as the most effective available therapeutic strategies to prevent its development or facilitate its regression in this patient population. Finally, we will issue a call to action for the need for more fundamental and clinical research on myocardial interstitial fibrosis in HHD.
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González et al. (2023) conducted a review in Hypertensive heart disease. Myocardial interstitial fibrosis in hypertensive heart disease drives maladaptive structural remodeling, necessitating improved noninvasive diagnostic tools and targeted therapeutic strategies.
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