scholarly journals Cardiac Remodeling in Obesity

2008 ◽  
Vol 88 (2) ◽  
pp. 389-419 ◽  
Author(s):  
E. Dale Abel ◽  
Sheldon E. Litwin ◽  
Gary Sweeney

The dramatic increase in the prevalence of obesity and its strong association with cardiovascular disease have resulted in unprecedented interest in understanding the effects of obesity on the cardiovascular system. A consistent, but puzzling clinical observation is that obesity confers an increased susceptibility to the development of cardiac disease, while at the same time affording protection against subsequent mortality (termed the obesity paradox). In this review we focus on evidence available from human and animal model studies and summarize the ways in which obesity can influence structure and function of the heart. We also review current hypotheses regarding mechanisms linking obesity and various aspects of cardiac remodeling. There is currently great interest in the role of adipokines, factors secreted from adipose tissue, and their role in the numerous cardiovascular complications of obesity. Here we focus on the role of leptin and the emerging promise of adiponectin as a cardioprotective agent. The challenge of understanding the association between obesity and heart failure is complicated by the multifaceted interplay between various hemodynamic, metabolic, and other physiological factors that ultimately impact the myocardium. Furthermore, the end result of obesity-associated changes in the myocardial structure and function may vary at distinct stages in the progression of remodeling, may depend on the individual pathophysiology of heart failure, and may even remain undetected for decades before clinical manifestation. Here we summarize our current knowledge of this complex yet intriguing topic.

2017 ◽  
Vol 61 (6) ◽  
pp. 721-732 ◽  
Author(s):  
Jeanne Mialet-Perez ◽  
Cécile Vindis

Autophagy is a highly conserved mechanism of lysosome-mediated protein and organelle degradation that plays a crucial role in maintaining cellular homeostasis. In the last few years, specific functions for autophagy have been identified in many tissues and organs. In the cardiovascular system, autophagy appears to be essential to heart and vessel homeostasis and function; however defective or excessive autophagy activity seems to contribute to major cardiovascular disorders including heart failure (HF) or atherosclerosis. Here, we review the current knowledge on the role of cardiovascular autophagy in physiological and pathophysiological conditions.


Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Amy Sarma ◽  
Samantha Paniagua ◽  
Elizabeth Liu ◽  
Emily Lau ◽  
Martin Larson ◽  
...  

Introduction: Greater parity has been associated with increased risk of cardiovascular disease, though effects on cardiac remodeling and heart failure risk remain unclear. Hypothesis: We hypothesized that multiple prior live births are associated with (1) structural and functional cardiac remodeling and (2) risk of future heart failure. Methods: We examined the association of number of live births and echocardiographic measures of cardiac structure and function in women participants of the Framingham Heart Study (FHS) using multivariable linear regression. We next examined the association of parity with incident heart failure (HFpEF, HFrEF) using Cox models in a pooled analysis of n=10,431 participants of FHS, the Cardiovascular Health Study, and the Multi-Ethnic Study of Atherosclerosis. Results: Among n=3931 FHS participants (mean age 48 ± 13 years), higher number of live births was associated with worse LV fractional shortening (multivariable β -1.11 (0.31), p= 0.0005 in ≥ 5 live births vs nulliparous women, p trend= 0.02, Figure ). In addition, greater parity was associated with worse cardiac mechanics including global circumferential strain and longitudinal and radial dyssynchrony (p< 0.01 for all comparing ≥ 5 live births vs nulliparity). Over a mean follow-up of 11.7 ± 3.2 years, 298 HFpEF and 225 HFrEF events occurred. Women with ≥5 live births were at higher risk of developing future HFrEF compared with nulliparous women (HR 1.93, 95% CI 1.19-3.12, p=0.008); by contrast, a lower risk of HFpEF was observed (HR 0.58, 95% CI 0.37-0.91, p=0.02, p trend= 0.04). Conclusions: Greater number of live births are associated with worse cardiac structure and function, as well as increased risk of incident HFrEF. Further studies are needed to better understand mechanisms by which repeated pregnancies portend adverse cardiovascular risk.


2021 ◽  
Vol 8 ◽  
Author(s):  
Myriam Carpenito ◽  
Diego Fanti ◽  
Simona Mega ◽  
Giovanni Benfari ◽  
Maria Caterina Bono ◽  
...  

In past cardiovascular medicine, the attention to the left ventricle-identified as the only indicator and determinant of healthy or unhealthy cardiac conditions- has systematically hidden the role of the left atrium (LA). The recent advances in cardiovascular imaging have provided a better understanding of LA anatomy, physiology, and pathology, making us realize that this functional structure is far from being an innocent spectator. We now know that the LA's mechanical and neuro-hormonal properties play a relevant part in several cardiovascular diseases, including atrial fibrillation, ischemic heart disease, valvular heart disease, and heart failure. The present review aims to describe the role of LA in the specific setting of heart failure. We provide currently available information on LA structure and function and summarize its role as a determinant of symptoms, prognosis, and potential therapeutic target in heart failure patients.


2021 ◽  
Vol 93 (9) ◽  
pp. 1073-1077
Author(s):  
Sofia V. Miklishanskaya ◽  
Olga V. Stukalova ◽  
Lilia V. Solomasova ◽  
Nikolai A. Mazur

Currently, the world is constantly increasing the number of people with obesity. As was shown by the Framingham study, obesity is a risk factor for many cardiovascular diseases. The effect of obesity on the structure and function of the heart is manifested in the form of cardiac remodeling, the effect on energy metabolism in the heart and infiltration of both myocardium with lipids, and an increase in the accumulation of adipose tissue in the pericardium, imbalance of adipokines and activation of inflammatory markers. Cardiac remodeling occurs primarily due to thickening of the left ventricle (LV) walls and an increase in the LV myocardium mass. Systolic dysfunction of the heart is less common in obese individuals compared with diastolic dysfunction. However, more modern methods (tissue Doppler, visualization of the deformation of the chambers of the heart strain imaging) reveal a subclinical decrease in systolic function in people with obesity. It is not fully known whether obesity is associated with systolic dysfunction, regardless of other risk factors. In any case, it has been proven that heart failure in people with obesity can develop independently of other risk factors. As an illustration, we give an example when the presence of obesity and concomitant pathology (arterial hypertension, diabetes) led to the development of systolic dysfunction with a decrease in the LV ejection fraction to 35% (fat cardiopathy), which show the potential for the influence of both obesity itself and in combination with concomitant diseases to lead to severe systolic heart failure.


2017 ◽  
Vol 2017 ◽  
pp. 1-16 ◽  
Author(s):  
Jingyu Ni ◽  
Yang Shi ◽  
Lan Li ◽  
Jingrui Chen ◽  
Lingyan Li ◽  
...  

Objective. To explore the potential cardioprotective mechanism of Shenfu injection (SFI) against heart failure (HF) by attenuating myocardial fibrosis and cardiac remodeling.Methods and Results. Four weeks after myocardial infarction (MI), adult male Sprague Dawley rats were randomized for 4-week treatment with Valsartan, SFI, or vehicle. Echocardiography and hemodynamics were applied to evaluate cardiac functions. Myocardia of coronary artery ligated (CAD) rats were observed to investigate changes in cardiac structure and function. Our findings suggest that treatment with SFI could inhibit progression of myocardial fibrosis and attenuate cardiac remodeling. In addition, SFI decreased expression of Smad2 and Smad3, while increasing the expression of Smad7 through regulation of TGF-β/Smads signaling pathway.Conclusion. Treatment with SFI in Sprague Dawley rats improves ventricular structure and function and reduces cardiac fibrosis by ameliorating TGF-β/Smads signaling pathway after ventricular remodeling.


2013 ◽  
Vol 305 (11) ◽  
pp. R1201-R1214 ◽  
Author(s):  
Hiroko Nishimura ◽  
Yimu Yang

For terrestrial vertebrates, water economy is a prerequisite for survival, and the kidney is their major osmoregulatory organ. Birds are the only vertebrates other than mammals that can concentrate urine in adaptation to terrestrial environments. Aquaporin (AQP) and glyceroporin (GLP) are phylogenetically old molecules and have been found in plants, microbial organisms, invertebrates, and vertebrates. Currently, 13 AQPs/aquaGLPs and isoforms are known to be present in mammals. AQPs 1, 2, 3, 4, 6, 7, 8, and 11 are expressed in the kidney; of these, AQPs 1, 2, 3, 4, and 7 are shown to be involved in fluid homeostasis. In avian kidneys, AQPs 1, 2, 3, and 4 have been identified and characterized. Also, gene and/or amino acid sequences of AQP5, AQP7, AQP8, AQP9, AQP11, and AQP12 have been reported in birds. AQPs 2 and 3 are expressed along cortical and medullary collecting ducts (CDs) and are responsible, respectively, for the water inflow and outflow of CD epithelial cells. While AQP4 plays an important role in water exit in the CD of mammalian kidneys, it is unlikely to participate in water outflow in avian CDs. This review summarizes current knowledge on structure and function of avian AQPs and compares them to those in mammalian and nonmammalian vertebrates. Also, we aim to provide input into, and perspectives on, the role of renal AQPs in body water homeostasis during ontogenic and phylogenetic advancement.


The Oxford Handbook of the Auditory Brainstem provides an in-depth reference to the organization and function of ascending and descending auditory pathways in the mammalian brainstem. Individual chapters are organized along the auditory pathway, beginning with the cochlea and ending with the auditory midbrain. Each chapter provides an introduction to the respective area and summarizes our current knowledge before discussing the disputes and challenges that the field currently faces.The handbook emphasizes the numerous forms of plasticity that are increasingly observed in many areas of the auditory brainstem. Several chapters focus on neuronal modulation of function and plasticity on the synaptic, neuronal, and circuit level, especially during development, aging, and following peripheral hearing loss. In addition, the book addresses the role of trauma-induced maladaptive plasticity with respect to its contribution in generating central hearing dysfunction, such as hyperacusis and tinnitus.The book is intended for students and postdoctoral fellows starting in the auditory field and for researchers of related fields who wish to get an authoritative and up-to-date summary of the current state of auditory brainstem research. For clinical practitioners in audiology, otolaryngology, and neurology, the book is a valuable resource of information about the neuronal mechanisms that are currently discussed as major candidates for the generation of central hearing dysfunction.


2020 ◽  
Vol 118 (3) ◽  
pp. 258a
Author(s):  
Laszlo Csernoch ◽  
Mónika Gönczi ◽  
Zsolt Ráduly ◽  
László Szabó ◽  
Nóra Dobrosi ◽  
...  

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