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Myocardial Stress and Hypertrophy: a Complex Interface Between Biophysics and Cardiac Remodeling

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Myocardial Stress and Hypertrophy: a Complex Interface Between Biophysics and Cardiac Remodeling Myocardial stress and hypertrophy: a complex interface between biophysics and cardiac remodeling William Grossman, Walter J. Paulus J Clin Invest. 2013;123(9):3701-3703. https://doi.org/10.1172/JCI69830. Hindsight Pressure and volume overload results in concentric and eccentric hypertrophy of cardiac ventricular chambers with, respectively, parallel and series replication of sarcomeres. These divergent patterns of hypertrophy were related 40 years ago to disparate wall stresses in both conditions, with systolic wall stress eliciting parallel replication of sarcomeres and diastolic wall stress, series replication. These observations are relevant to clinical practice, as they relate to the excessive hypertrophy and contractile dysfunction regularly observed in patients with aortic stenosis. Stress-sensing mechanisms in cardiomyocytes and activation of cardiomyocyte death by elevated wall stress continue to intrigue cardiovascular scientists. Find the latest version: https://jci.me/69830/pdf Hindsight Myocardial stress and hypertrophy: a complex interface between biophysics and cardiac remodeling William Grossman and Walter J. Paulus Center for Prevention of Heart and Vascular Disease, UCSF, San Francisco, California, USA. Institute for Cardiovascular Research, VU University Medical Center, Amsterdam, The Netherlands. Pressure and volume overload results in concentric and eccentric hypertro- catheters (1). This allowed matching of phy of cardiac ventricular chambers with, respectively, parallel and series instantaneous LV pressure, radius, and wall replication of sarcomeres. These divergent patterns of hypertrophy were thickness throughout the cardiac cycle, related 40 years ago to disparate wall stresses in both conditions, with sys- something not possible using only imag- tolic wall stress eliciting parallel replication of sarcomeres and diastolic wall ing and measured blood pressure (4, 5). stress, series replication. These observations are relevant to clinical practice, The ability to match these measurements as they relate to the excessive hypertrophy and contractile dysfunction reg- turns out to be important because of the ularly observed in patients with aortic stenosis. Stress-sensing mechanisms wide variation in the LV pressure contour, in cardiomyocytes and activation of cardiomyocyte death by elevated wall in which the rate of rise, the duration of stress continue to intrigue cardiovascular scientists. peak (spiky or broad), and the rate of fall have enormous influence on calculated Pattern recognition in left ventricular wall stress suggested that maladaptive stress or the presumed force at the level of hypertrophy hypertrophy develops insidiously during individual myocytes. Pressure and volume overload result in volume overload. divergent patterns of LV hypertrophy. Based on the development of concen- Cardiac remodeling and disease The presence of LV hypertrophy implies tric hypertrophy in pressure overload and In concentric LV remodeling, the contri- a higher-than-normal myocardial mass. eccentric hypertrophy in volume overload, bution of LV hypertrophy to the prevailing Pressure overload usually elicits con- peak systolic wall stress was proposed as a LV wall stress remains clinically relevant. centric hypertrophy, with a high ratio stimulus for parallel replication of sarcom- It is still debated whether asymptomatic of LV wall thickness to radius (h/R). In eres in concentric hypertrophy and end-di- patients with extensive LV hypertrophy contrast, volume overload triggers eccen- astolic wall stress as a stimulus for series should undergo aortic valve replacement tric hypertrophy with a normal h/R ratio replication of cardiomyocytes in eccentric to prevent progression of LV hypertrophy (Figure 1). Nearly 40 years ago, an article hypertrophy (1). A reflection of LV remod- or whether they should be managed con- in these pages related the divergent pat- eling in cardiomyocyte remodeling was servatively until symptoms develop (6, 7). terns of LV hypertrophy to disparate LV confirmed more than two decades later Knowledge of LV wall stress helps to solve wall stresses in both conditions (1). In by detailed histomorphometric measure- this clinical dilemma. When LV wall stress patients with aortic stenosis, both sys- ments in concentric and eccentric human is lower than normal, LV hypertrophy tolic and diastolic LV wall stresses were or animal LV hypertrophy (2). In concen- is excessive. This probably results from normal because concentric hypertrophy tric LV hypertrophy, cardiomyocytes only comorbidities such as diabetes mellitus had succeeded in nicely counter balancing grow in a transverse direction while keep- (8) or from a genetic predisposition such the effect on LV wall stress of elevated ing cell length constant, whereas in eccen- as the DD genotype of the ACE gene (9). In systolic and diastolic LV pressures. tric LV hypertrophy, cardiomyocytes grow both conditions, excessive LV hypertrophy Concentric hypertrophy was therefore proportionally in both longitudinal and is accompanied by prominent LV fibrosis labeled an adaptive mechanism, which transverse directions. The difference in car- (10), which predisposes patients to ventric- avoids afterload excess to hinder myo- diomyocyte remodeling is also reflected in ular arrhythmias or sudden death. Under cardial shortening. In contrast, eccentric distinct patterns of peptide growth factor these circumstances, early aortic valve hypertrophy, as observed in patients with induction in concentric and eccentric LV replacement, even in the absence of symp- mitral or aortic regurgitation, corrected hypertrophy (3). toms, could be the more favorable option. systolic LV wall stress but failed to nor- This 1975 assessment of cardiac remod- The appropriateness of LV hypertro- malize diastolic LV wall stress. Although eling continues to stand out because of phy to LV wall stress is also relevant in the eccentric hyper trophy resembled phys- its unique methodology: LV remodeling reverse situation in which patients with iological growth, its effect on diastolic of the human heart was assessed using an aortic stenosis present with higher-than- integrated, multimodality approach with normal LV wall stress (11, 12). Excessive simultaneous measurement of LV dimen- LV wall stress results from insufficient LV Conflict of interest: The authors have declared that no conflict of interest exists. sion, septal and posterior wall thickness hypertrophy with a low h/R ratio and is Citation for this article: J Clin Invest. 2013; by echocardiography, and LV pressures accompanied by depressed LV contractile 123(9):3701–3703. doi:10.1172/JCI69830. by high-fidelity micromanometer-tipped performance (11). In the majority of these The Journal of Clinical Investigation http://www.jci.org Volume 123 Number 9 September 2013 3701 hindsight Figure 1 Schematic overview of the development of concentric hypertrophy with the parallel addition of sarcomeres in pressure overload and of eccentric hypertrophy with a series addition of sarcomeres in volume overload. Chamber enlargement increases systolic wall stress in volume overload (dashed black arrow indicates positive feedback). Wall thick- ening induces concentric hypertrophy in pres- sure overload and contributes to eccentric hypertrophy in volume overload (blue arrow). Concentric hypertrophy reduces systolic wall stress in pressure overload, and eccentric hypertrophy reduces diastolic wall stress in volume overload (dashed red lines indicate negative feedback). patients, the depressed LV contractile per- from ubiquitin-related autophagy and induced pulmonary hypertension sup- formance merely reflects afterload mis- ischemic cell death or oncosis, i.e., swell- ports this explanation (14). When rats were match and does not jeopardize postopera- ing of cardiomyocytes. In patients with a given low-dose monocrotaline, they devel- tive outcome (12). Occasionally, however, greatly reduced LVEF (<30%), myocardial oped slow-onset pulmonary hypertension the depressed LV contractile performance degeneration was 32 times more frequent and adaptive RV hypertrophy, but when is worse than predicted by the high LV wall than in control myocardium, and all of rats were given high-dose monocrotaline, stress, and in these patients it heralds a these patients failed to improve postop- they developed rapid-onset pulmonary poor postoperative outcome (12, 13). eratively. Myocardial fibrosis increased hypertension accompanied by RV failure A histopathological study of patients concordantly with cardiomyocyte degener- and premature death. Fourteen days after with aortic stenosis and varying degrees of ation and resulted in replacement fibrosis monocrotaline administration, the extent LV systolic dysfunction nicely confirmed being superimposed on reactive interstitial of RV hypertrophy was still identical in the concept of insufficient LV hypertro- fibrosis, with a greater likelihood of reentry both groups, but microarray analysis of RV phy underlying depressed LV contractile arrhythmias and poor outcome. myocardium revealed that 63 of the 3,010 performance (13). In this study, markers The cause of cardiomyocyte degeneration cardiac genes screened were differentially of cardiomyocyte hypertrophy, such as an in aortic stenosis patients with a low EF is expressed between both groups. The dif- elevated cardiomyocyte cross-sectional area unclear. The severity of aortic stenosis does ferentially expressed genes included those and increased nuclear DNA content, were not seem to be involved
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