Cardiac steatosis in patients with dilated cardiomyopathy

Granér, Marit; Pentikäinen, Markku O.; Nyman, Kristofer; Sirén, Reijo; Lundbom, Jesper; Hakkarainen, Antti; Lauerma, Kirsi; Lundbom, Nina; Nieminen, Markku S.; Petzold, Max; Taskinen, Marja‐Riitta

doi:10.1136/heartjnl-2013-304961

Cited by 27 publications

(24 citation statements)

References 29 publications

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“…However, reducing cardiac TG content does not always improve cardiac function . Moreover, although increased myocardial TG content was found in patients with ischemic cardiomyopathy, patients with hypertrophic cardiomyopathy , as well as those with dilated cardiomyopathy , showed decreased myocardial TG content.…”

Section: Spectroscopy Of Cardiac Metabolismmentioning

confidence: 94%

MRS: a noninvasive window into cardiac metabolism

et al. 2015

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A well-functioning heart requires a constant supply of a balanced mixture of nutrients to be used for the production of adequate amounts of adenosine triphosphate, which is the main energy source for most cellular functions. Defects in cardiac energy metabolism are linked to several myocardial disorders. MRS can be used to study in vivo changes in cardiac metabolism noninvasively. MR techniques allow repeated measurements, so that disease progression and the response to treatment or to a lifestyle intervention can be monitored. It has also been shown that MRS can predict clinical heart failure and death. This article focuses on in vivo MRS to assess cardiac metabolism in humans and experimental animals, as experimental animals are often used to investigate the mechanisms underlying the development of metabolic diseases. Various MR techniques, such as cardiac (31) P-MRS, (1) H-MRS, hyperpolarized (13) C-MRS and Dixon MRI, are described. A short overview of current and emerging applications is given. Cardiac MRS is a promising technique for the investigation of the relationship between cardiac metabolism and cardiac disease. However, further optimization of scan time and signal-to-noise ratio is required before broad clinical application. In this respect, the ongoing development of advanced shimming algorithms, radiofrequency pulses, pulse sequences, (multichannel) detection coils, the use of hyperpolarized nuclei and scanning at higher magnetic field strengths offer future perspective for clinical applications of MRS.

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Section: Spectroscopy Of Cardiac Metabolismmentioning

confidence: 94%

MRS: a noninvasive window into cardiac metabolism

et al. 2015

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“…Both visceral obesity and ectopic fat accumulation in non-adipose tissues, including the heart, have been related to cardiac structure abnormalities and increased cardiometabolic risk (Britton & Fox 2011). Cardiac steatosis has been found in subjects with dilated cardiomyopathy (Graner et al 2014), and pericardial fat accumulation is independently correlated with left ventricular (LV) mass and is inversely correlated with LV mid-wall stress abnormalities in morbidly obese patients (Graner et al 2014). As an endocrine organ, adipose tissue produces and secretes a wide range of bioactive factors known as adipokines, which take part in the network of communication between adipose tissue and peripheral organs, including the heart (Kershaw & Flier 2004).…”

Section: Obesity As a Risk Factor For Heart Failurementioning

confidence: 99%

Role of the fatty acid-binding protein 4 in heart failure and cardiovascular disease

Rodríguez-Calvo¹,

Girona²,

Alegret

et al. 2017

Journal of Endocrinology

100

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Obesity and ectopic fat accumulation in non-adipose tissues are major contributors to heart failure (HF) and cardiovascular disease (CVD). Adipocytes act as endocrine organs by releasing a large number of bioactive molecules into the bloodstream, which participate in a communication network between white adipose tissue and other organs, including the heart. Among these molecules, fatty acid-binding protein 4 (FABP4) has recently been shown to increase cardiometabolic risk. Both clinical and experimental evidence have identified FABP4 as a relevant player in atherosclerosis and coronary artery disease, and it has been directly related to cardiac alterations such as left ventricular hypertrophy (LVH) and both systolic and diastolic cardiac dysfunction. The available interventional studies preclude the establishment of a direct causal role of this molecule in CVD and HF and propose FABP4 as a biomarker rather than as an aetiological factor. However, several experimental reports have suggested that FABP4 may act as a direct contributor to cardiac metabolism and physiopathology, and the pharmacological targeting of FABP4 may restore some of the metabolic alterations that are conducive to CVD and HF. Here, we review the current knowledge regarding FABP4 in the context of HF and CVD as well as the molecular basis by which this protein participates in the regulation of cardiac function.

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“…Adipose tissue exerts powerful effects on both vascular and cardiac function . In particular, excess epicardial fat is associated with cardiac remodeling and cardiomyopathy . Epicardial fat is anatomically adjacent to the epicardium and is not separated by any fascial layer .…”

Section: Discussionmentioning

confidence: 99%

Cardioprotective Heme Oxygenase‐1‐PGC1α Signaling in Epicardial Fat Attenuates Cardiovascular Risk in Humans as in Obese Mice

Singh

McClung

Thompson

et al. 2019

Obesity

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Objective This study investigated whether levels of signaling pathways and inflammatory adipokines in epicardial fat regulate cardiovascular risks in humans and mice. Methods Epicardial fat was obtained from the hearts of patients with heart failure requiring coronary artery bypass surgery, and signaling pathways were compared with visceral fat. The genetic profile of epicardial and visceral fat from humans was also compared with genetic profiles of epicardial and visceral fat in obese mice. Left ventricular (LV) fractional shortening was measured in obese mice before and after treatment with inducers of mitochondrial signaling heme oxygenase 1 (HO‐1)‐peroxisome proliferator‐activated receptor gamma coactivator 1‐alpha (PGC1α). An RNA array/heat map on 88 genes that regulate adipose tissue function was used to identify a target gene network. Results Human epicardial fat gene profiling showed decreased levels of mitochondrial signaling of HO‐1‐PGC1α and increased levels of the inflammatory adipokine CCN family member 3. Similar observations were seen in epicardial and visceral fat of obese mice. Improvement in LV function was linked to the increase in mitochondrial signaling in epicardial fat of obese mice. Conclusions There is a link between cardiac ectopic fat deposition and cardiac function in humans that is similar to that which is described in obese mice. An increase of mitochondrial signaling pathway gene expression in epicardial fat attenuates cardiometabolic dysfunction and LV fractional shortening in obese mice.

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Cardiac steatosis in patients with dilated cardiomyopathy

Cited by 27 publications

References 29 publications

MRS: a noninvasive window into cardiac metabolism

MRS: a noninvasive window into cardiac metabolism

Role of the fatty acid-binding protein 4 in heart failure and cardiovascular disease

Cardioprotective Heme Oxygenase‐1‐PGC1α Signaling in Epicardial Fat Attenuates Cardiovascular Risk in Humans as in Obese Mice

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