Hypertension‐induced remodelling: on the interactions of cardiac risk factors. (30th March 2017)

• Record Type: Journal Article
• Authors: Tomek, Jakub; Bub, Gil
• Is Part Of: Journal of physiology. Volume 595:Number 12(2017)
• Page Start: 4027
• Page End: 4036
• Publication Date: 2017-03-30
• Subjects: arrhythmia -- extracellular matrix -- heart failure -- hypertension; Physiology -- Periodicals; 612.005
• DOI: 10.1113/JP273043
• Languages: English
• ISSNs: 0022-3751

Abstract

Abstract : Hypertension and myocardial infarction trigger tissue remodelling, where different outcomes of the remodelling processes interact with each other and their subtle balance may decide the ultimate cardiac disease. Collagen deposition and crosslinking may be the deciding factor between systolic and diastolic heart failure, while sympathetic stimulation may balance the risk of ventricular fibrillation with the risk of pulseless electrical activity. Abstract: Hypertension induces considerable cardiac remodelling, such as hypertrophy, interstitial fibrosis, and abnormal activity of the cardiac sympathetic nervous system, which are established risk factors in several highly dangerous heart diseases, such as ventricular fibrillation and congestive heart failure. All these risk factors and heart diseases are studied extensively in isolation, but to our knowledge, there is no comprehensive review of their interactions. At the same time, there is growing evidence suggesting that such interactions are numerous and that a successful therapy against a particular condition may have unexpectedly weak effects on mortality, as treated patients may die of a different cause exacerbated by the therapy. In this article, we present a multiscale review of the literature focusing on the relationships between the above‐mentioned risk factors and heart diseases, and introduce a framework that gives insight into their possible interactions. We use this framework to demonstrate that conditions such as fibrosis and elevated activity of the sympathetic nervous system may be compensatory, rather than purely pathological, mechanisms in certain contexts. Finally, we show why the described mechanisms are relevant not only in hypertension, but also in the case of healed myocardial infarction.