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Myocardial Remodeling in Hypertension

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Myocardial Remodeling in Hypertension Journal of Human Hypertension (2015) 29,1–6 & 2015 Macmillan Publishers Limited All rights reserved 0950-9240/15 www.nature.com/jhh REVIEW Myocardial remodeling in hypertension W Nadruz Left ventricular (LV) hypertrophy and remodeling are frequently seen in hypertensive subjects and result from a complex interaction of several hemodynamic and non-hemodynamic variables. Although increased blood pressure is considered the major determinant of LV structural alterations, ethnicity, gender, environmental factors, such as salt intake, obesity and diabetes mellitus, as well as neurohumoral and genetic factors might influence LV mass and geometry. The conventional concept of hypertensive LV remodeling has been that hypertension leads to concentric hypertrophy, as an adaptive response to normalize wall stress, which is then followed by chamber dilation and heart failure. However, several lines of evidence have challenged this dogma. Concentric hypertrophy is not the most frequent geometric pattern and is less usually seen than eccentric hypertrophy in hypertensive subjects. In addition, data from recent studies suggested that transition from LV concentric hypertrophy to dilation and systolic dysfunction is not a common finding, especially in the absence of coronary heart disease. LV hypertrophy is also consistently associated with increased cardiovascular morbidity and mortality, raising doubts whether this phenotype is an adaptive response. Experimental evidence exists that a blunting of load-induced cardiomyocyte hypertrophy does not necessarily result in LV dysfunction or failure. Furthermore, the hypertrophic myocardium shows fibrosis, alterations in the coronary circulation and cardiomyocyte apoptosis, which may result in heart failure, myocardial ischemia and arrhythmias. Overall, this body of evidence suggests that LV hypertrophy is a complex phenotype that predicts adverse cardiovascular outcomes and may not be necessarily considered as an adaptive response to systemic hypertension. Journal of Human Hypertension (2015) 29, 1–6; doi:10.1038/jhh.2014.36; published online 8 May 2014 INTRODUCTION concentric LV remodeling (normal LV mass and increased relative 5 Cardiac remodeling is defined as alterations in size, geometry, wall thickness). shape, composition and function of the heart resulting from cardiac load or injury.1 Left ventricular (LV) remodeling is frequently seen in hypertensive subjects and has been CELLULAR AND HISTOPATHOLOGICAL FEATURES considered an adaptive response to hemodynamic overload Hypertrophic growth of cardiomyocytes is the main mechanism imposed by systemic hypertension. This compensatory response by which the heart reduces LV wall stress imposed by pressure is assumed to be explained by the Laplace law, T ¼ P Â r/2h, where overload. It involves stimulation of an intricate web of intracellular tension or stress in the LV wall (T) is directly related to LV pressure signaling cascades that activate gene expression and promote (P) and radius (r) and is inversely related to LV wall thickness (h) protein synthesis and stability, with consequent increases in (Figure 1).2 Sustained elevated blood pressure leads to increases in protein content, in the number of force-generating units LV wall stress, which is a major determinant of myocardial oxygen (sarcomeres) and in the size of individual cardiomyocytes. demand. In response to increased LV wall stress, LV wall thickens Concentric hypertrophy is characterized by an increase in the and LV mass increases, thus resulting in normalization of wall width of cardiomyocytes caused by the parallel addition of new stress and the development of a structural pattern known as sarcomeres, whereas in eccentric hypertrophy there is an increase concentric hypertrophy. Alternatively, increases in blood volume in cardiomyocyte length due to the addition of new sarcomeres in would lead to an increase in the chamber radius, resulting in series.2,6 Adult cardiomyocytes were traditionally considered to be eccentric hypertrophy. terminally differentiated cells unable to divide. However, the LV structure and mass are complex phenotypes that may be paradigm that the adult heart is a postmitotic organ has been influenced by several factors other than chronic hemodynamic challenged by reports that cardiomyocytes may be able to overload. It is extensively acknowledged that non-hemodynamic proliferate in rat hearts as well as in severely hypertrophic, post- variables, such as ethnicity, gender, neurohumoral, environmental infarcted and end-stage-failing human hearts. Thus, it has been and genetic factors, modulate the myocardial hypertrophic suggested that the increased cardiac mass in LV hypertrophy may response.3,4 Therefore, distinct cardiac structural adaptations are be a result from a combination of hypertrophy and hyperplasia of seen in hypertensive subjects. LV geometry can be described both cardiomyocytes and non-cadiomyocytic cells.1,2 based on the LV mass (hypertrophy) and the relative wall Besides cardiomyocyte hypertrophy, several alterations of the thickness. Four LV geometric patterns have been identified: cardiomyocyte and the non-cardiomyocyte components (includ- normal LV geometry (normal LV mass and lower value of ing apoptosis, fibrosis and changes in the coronary circulation) are relative wall thickness), eccentric LV hypertrophy (increased LV also seen and seem to explain the increased risk of mass and lower value of relative wall thickness), concentric LV adverse cardiovascular outcomes related to LV hypertrophy.7 hypertrophy (increased LV mass and relative wall thickness) and Cardiomyocytes exhibit increased rates of cell death, especially Department of Internal Medicine, School of Medical Sciences, University of Campinas, Campinas, Brazil. Correspondence: Professor W Nadruz, Departamento de Clı´nica Me´dica, Faculdade de Cieˆncias Me´dicas, Universidade Estadual de Campinas, Cidade Universita´ria ‘Zeferino Vaz’, Campinas, Sa˜o Paulo 13081-970, Brazil. E-mail: [email protected] Received 16 January 2014; revised 25 March 2014; accepted 2 April 2014; published online 8 May 2014 Heart and hypertension W Nadruz 2 hypertrophy usually have the highest stroke volume and cardiac output and the lowest systemic vascular resistance levels compared with those with other geometric patterns. In such individuals, increased volemia seems to be a major determinant of wall stress and LV hypertrophy. On the other hand, hyper- tensive subjects with concentric remodeling usually have a lower cardiac output and intravascular volume.4 Differences in LV shape are also described among the LV geometric patterns. Noticeably, higher stroke volumes have been coupled with more spherical LV chambers. Therefore, subjects with eccentric hypertrophy usually exhibit the most spherical LV cavities, whereas those with concentric remodeling generally show the most elliptic shape.4 The notion that cardiomyocytes grow in response to hemody- namic load indicates that the mechanical stimulus is transduced into a biochemical event, thus modifying gene transcription. Attractive candidates for such a transducer are the components of the focal adhesion complex, through which the cytoskeleton of a cell connects to the extracellular matrix.13 Furthermore, Figure 1. The Laplace law and how it may explain the development mechanical stress may be coupled to intracellular signals that of concentric and eccentric LV hypertrophy in response to pressure are responsible for the hypertrophic response via phospholipases, and volume overload, respectively. T, tension or stress in the LV wall; P, LV pressure; r, radius of the chamber; h, LV wall thickness. ion channels and ion exchangers or may induce the release of growth-promoting factors (for example, angiotensin II, endothelin- 1 and transforming growth factor-beta), thus providing alternative pathways of growth induction.9,13 apoptosis, which may result in reduced contractile mass and affect In addition to raised blood pressure and variation in volemic contractility.1,6 Fibroblasts proliferate and there is exaggerated status, non-hemodynamic factors have been also implicated in the accumulation of collagen type I and type III fibers within the pathogenesis of hypertensive LV remodeling. For instance, interstitium and perivascular regions. These events induce the impaired suppression of the renin–angiotensin axis or increased development of fibrosis, which predisposes to diastolic and sensitivity to angiotensin II may act as stimuli for LV hypertrophy systolic LV dysfunction, diminished coronary flow reserve and in hypertensive patients. Likewise, increased plasma renin activity ventricular arrhythmias. Furthermore, there are changes in the levels have been related to hypertensive LV hypertrophy and data coronary circulation, such as hyperplasia and hypertrophy of derived from clinical trials suggested that agents targeting the intramyocardial arteries and a relative decrease in arteriolar and renin–angiotensin system may offer beneficial effects on LV mass capillary density, which predispose to inadequate myocardial beyond blood pressure reduction.10 In contrast, the role of the perfusion.6 Conversely, experimental evidence exists that a renin–angiotensin–aldosterone system in LV geometry is more blunting of cardiomyocyte hypertrophy does not necessarily controversial. Although some lines of evidence have suggested result in dysfunction or failure, even in the presence of pressure that low-renin states are coupled with eccentric hypertrophy and overload.8 These findings
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