Concentric versus eccentric remodeling

doi:10.1054/jcaf.2002.129250

Journal of Cardiac Failure

Volume 8, Issue 6, Part B, December 2002, Pages S258-S263

https://doi.org/10.1054/jcaf.2002.129250 Get rights and content

Abstract

Cardiac hypertrophy has long been recognized as one of the heart's mechanisms for compensating a pressure or volume overload. This compensation has often been viewed as a feedback loop in which the concentric hypertrophy, which develops in pressure overload, normalizes wall stress while the eccentric hypertrophy, which develops in volume overload, allows for an increase in total stroke volume to compensate that which is lost from regulation. While the concentric hypertrophy of pressure overload often is compensatory, many examples are noted where either too little hypertrophy occurs to normalize stress or in other cases, in which hypertrophy exceeds the amount needed for normalization. These observations invoke nonmechanical mechanisms which modulate the degree to which the mechanical signal of pressure overload is translated into an increase in myocardial mass. Hypertrophy develops when the rate of myocardial protein synthesis exceeds that of protein degradation. It now appears that in pressure overload this imbalance is created as synthesis rate increases while in volume overload hypertrophy appears to accrue because degradation rate decreases.

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Women pole dance athletes present morphofunctional left ventricular adaptations and greater physical fitness
2022, Science and Sports
Citation Excerpt :
It is known that an increased cardiac afterload results in new parallel sarcomeres, increasing the wall thickness (i.e., concentric hypertrophy). On the other hand, an increases cardiac preload led to the replication of sarcomeres in series, lengthening myocytes and increasing sphericity of the ventricular cavity (i.e., eccentric hypertrophy) [1]. Athletes commonly develop cardiac hypertrophy phenotypic called “athlete's heart” as an adaptive process to pressure overload (athletes trained in strength) and/or volume overload (athletes trained in resistance) [2].
This cross-section study evaluated physical fitness, heart rate variability (HRV) and, left ventricle (LV) morphology and function in pole dance (PD) athletes.
Control group (CG) was composed of 16 untrained women and the PD group (PG) was composed of 15 professional women. Physical fitness, echocardiographic, HRV and parameters were assessed.
A better physical performance was found in the PG compared to CG group, with significant differences for tests: handgrip strength test -left hand (P < 0.05) and right hand (P < 0.01), push-up (P < 0.001), curl-up (P < 0.001), and sit and reach (P < 0.001). Systolic function of LV did not differ statistically between CG and PG. The LV relative wall thickness was significantly high (P < 0.05, mean difference: 0.04) and the isovolumic relaxation time was significantly lower (P < 0.01, mean difference: −27 ms) in the PG. The HRV indices did not differ statistically between the groups.
The PD athletes have higher physical fitness without changes in HRV makers. Moreover, PD athletes had LV remodeling with an improved LV relaxation.
Cette étude transversale a évalué la condition physique, la variabilité de la fréquence cardiaque (VFC), la morphologie et la fonction du ventricule gauche (VG) chez les athlètes de pole dance (PD).
Le groupe témoin (CG) était composé de 16 femmes non entrainées en PD et le groupe PD (PG) était composé de 15 femmes professionnelles de cette discipline. La condition physique, l’échocardiographie, la VFC et les paramètres morphofonctionnels du VG ont été évalués et comparés entre les groupes.
Une meilleure performance physique a été retrouvée dans le groupe PG par rapport au groupe CG, avec des différences significatives pour les tests de force de préhension (main gauche (p < 0,05) et main droite (p < 0,01)), push-up (p < 0,001), curl-up (p < 0,001) et de flexibilité “seat and reach” (p < 0,001). La fonction systolique du VG ne différait pas statistiquement entre le groupe CG et le groupe PG. L’épaisseur relative de la paroi ventriculaire gauche était significativement plus élevée (p < 0,05, différence moyenne: 0,04) et le temps de relaxation isovolumique était significativement plus faible (p < 0,01, différence moyenne: -27 ms) dans le groupe PG, comparativement au groupe CG. Les indices de VHC ne différaient pas statistiquement entre les groupes.
Les athlètes de PD ont une meilleure forme physique sans modification des marqueurs de VFC. De plus, les athlètes du groupe PD présentaient un remodelage du VG avec une relaxation améliorée du VG.
A thermodynamic transient cross-bridge model for prediction of contractility and remodelling of the ventricle
2021, Journal of the Mechanical Behavior of Biomedical Materials
Citation Excerpt :
Heart failure (the inability to pump sufficient blood to the body) often results from cardiac hypertrophy. This is a medical condition whereby the cardiomyocytes in the tissue wall remodel in response to an alteration in the mechanical environment (Carabello, 2002; Grossman et al., 1975). Hypertrophy is typically categorised as concentric or eccentric.
Cardiac hypertrophy is an adaption of the heart to a change in cardiovascular loading conditions. The current understanding is that progression may be stress or strain driven, but the multi-scale nature of the cellular remodelling processes have yet to be uncovered. In this study, we develop a model of the contractile left ventricle, with the active cell tension described by a thermodynamically motivated cross-bridge cycling model. Simulation of the transient recruitment of myosin results in correct patterns of ventricular pressure predicted over a cardiac cycle. We investigate how changes in tissue loading and associated deviations in transient force generation can drive restructuring of cellular myofibrils in the heart wall. Our thermodynamic framework predicts in-series sarcomere addition (eccentric remodelling) in response to volume overload, and sarcomere addition in parallel (concentric remodelling) in response to valve and signalling disfunction. This framework provides a significant advance in the current understanding of the fundamental sub-sarcomere level biomechanisms underlying cardiac remodelling. Simulations reveal that pathological tissue loading conditions can significantly alter actin-myosin cross-bridge cycling over the course of the cardiac cycle. The resultant variation in sarcomere stress pushes an imbalance between the internal free energy of the myofibril and that of unbound contractile proteins, initiating remodelling. The link between cross-bridge thermodynamics and myofibril remodelling proposed in this study may significantly advance current understanding of cardiac disease onset.
Serum uric acid level and left ventricular hypertrophy in elderly male patients with nonvalvular atrial fibrillation
2016, Nutrition, Metabolism and Cardiovascular Diseases
Citation Excerpt :
A rat model of hyperuricemia has been reported to develop all the hemodynamic findings observed in essential hypertension, including prominent vasoconstriction of the afferent arteriole, with a reduction in renal blood flow and a relative preservation of the GFR [21,22]. Cardiac hypertrophy compensates the pressure overload seen in hypertension [23]. In this study, a medical history of hypertension was more prevalent in patients with hyperuricemia, but this finding was not statistically significant.
Recent studies have suggested that serum uric acid (SUA) induces oxidative stress and inflammation, which are involved in the mechanism of cardiac hypertrophy. In patients with atrial fibrillation (AF), comorbidity of left ventricular hypertrophy (LVH) exacerbates cardiac function. In this study, we investigated the association between SUA and cardiac hypertrophy in AF patients.
Initially, 1296 consecutive elderly patients (age >60) with nonvalvular AF were retrospectively selected from the inpatient clinic between January 2012 and April 2015. Demographic, clinical, and echocardiographic characteristics were carefully recorded. The final study population was 577 patients. The mean SUA level was significantly higher in patients with LVH than those without LVH. Compared with the non-LVH group, the LVH group was older, had a higher percentage of female patients, and had lower hemoglobin levels and estimated glomerular filtration rates. Patients in the LVH group also had a higher rate of coronary heart disease and fewer had history of radiofrequency ablation compared with the non-LVH group. In the hyperuricemia group, B-type natriuretic peptide levels, left atrial diameter, left ventricular mass index, and percentage of NYHA (New York Heart Association) class III/IV were significantly higher than the SUA normal group. Multivariate logistic regression analysis indicated the independent risk factors for LVH in elderly AF patients included SUA, age, male sex, the presence of coronary heart disease, and diuretic therapy. Subgroup analysis identified SUA as a significant risk factor associated with LVH in men.
SUA was independently associated with LVH in elderly male patients with nonvalvular AF.
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Session 1: Global Structural Ventricular RemodelingConcentric versus eccentric remodeling

Abstract

Session 1: Global Structural Ventricular Remodeling
Concentric versus eccentric remodeling