Fatty acids and the risk of death during acute myocardial ischaemia

Oliver, M.F.

doi:10.1042/cs20140404

Cited by 23 publications

(22 citation statements)

References 52 publications

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“…Elevated free fatty acids impair insulin signaling and cause subclinical inflammation with subsequent pancreatic beta-cell dysfunction. 107,115,116 Free fatty acid elevation may also be involved in terminal arrhythmias 117 and induction of a prothrombotic state. 118 The CETP inhibitor torcetrapib raises HDL-cholesterol concentration but also improves hyperglycemia.…”

Section: Mechanisms Of Increased Ascvd Risk and Mortality In Type 2 Dmentioning

confidence: 99%

Clinical Update: Cardiovascular Disease in Diabetes Mellitus

et al. 2016

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Cardiovascular disease remains the principal cause of death and disability among patients with diabetes mellitus. Diabetes exacerbates mechanisms underlying atherosclerosis and heart failure. Unfortunately, these mechanisms are not adequately modulated by therapeutic strategies focusing solely on optimal glycemic control with currently available drugs or approaches. In the setting of multi-factorial risk reduction with statins and other lipid lowering agents, anti-hypertensive therapies, and anti-hyperglycemic treatment strategies, cardiovascular complication rates are falling, yet remain higher for patients with diabetes than for those without. This review considers the mechanisms, history, controversies, new pharmacologic agents, and recent evidence for current guidelines for cardiovascular management in the patient with diabetes mellitus to support evidence-based care in the patient with diabetes and heart disease outside of the acute care setting.

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Section: Mechanisms Of Increased Ascvd Risk and Mortality In Type 2 Dmentioning

confidence: 99%

Clinical Update: Cardiovascular Disease in Diabetes Mellitus

et al. 2016

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“…It has been proposed that for the ischemic cardiomyocyte, glucose metabolism is more beneficial, and FA metabolism is deleterious [114] . However, FA availability is much greater: catecholamines induce lipolysis in adipose tissue, abruptly rising circulating FA levels [115] , and inhibit insulin signaling, reducing glucose entry into the myocardium [116] . Likewise, FA can inhibit glucose oxidation and potentiate oxygen consumption in ischemic myocardial areas, leading to a preferential utilization of FA over glucose during ischemia [117] .…”

Section: Resultsmentioning

confidence: 99%

Energetic metabolism in cardiomyocytes: molecular basis of heart ischemia and arrhythmogenesis

Martínez¹,

Machado²,

Luzardo³

et al. 2017

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Cardiac muscle contraction is a strictly regulated process which conjugates a series of electrophysiological, biochemical and mechanic events, resulting in the pumping of blood to all bodily tissues. These phenomena require a very high energetic demand both for generating the necessary mechanical force, and for maintaining cellular homeostasis during the process. In the myocardium, fatty acids (FA) represent the main energy substrate, although other secondary substrates, such as glucose and ketone bodies, may also be used. Nevertheless, under certain conditions such as heart failure or myocardial ischemia, FA metabolism may become deleterious via mechanisms such as oxidative stress and arrhythmogenesis. In an ischemic milieu, various metabolic changes occur as a consequence of hypoxia, favoring cell necrosis, ventricular arrhythmias, and death. Major events in this context include an increase in extracellular K + , a decrease in pH, and accumulation of intracellular calcium. This review includes a detailed description of the molecular basis underlying myocardial contraction and energetic metabolism in cardiomyocytes, aiming to promote an integral understanding of the pathophysiology of heart ischemia. This in turn may aid in the development of future, more satisfactory alternative treatments in the management of acute coronary ischemia episodes.

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“…Indeed, both IMA and level of free FAs increase within minutes from the onset of ischemia (including balloon-induced myocardial ischemia during percutaneous coronary intervention) [31, 53], remain elevated for 6–12 hours, and then return to normal within 24 hours [27, 40]. This relationship also supports the concept of “FA occupation.”…”

Section: Evidence In Support Of “Fa Occupation Of Albumin”mentioning

confidence: 84%

“…Patients with acutely ischemic myocardium exhibit a rapid increase in serum levels of free FAs, which can exceed normal average values at the time of admission by a factor of 3–10 [22–27]. Measurement of serum levels of free FAs in the diagnosis of acute myocardial ischemia has been the subject of a number of patent applications [28–30].…”

Section: Fatty Acid As a Marker Of Myocardial Ischemiamentioning

confidence: 99%

Ischemia-Modified Albumin as a Marker of Acute Coronary Syndrome: The Case for Revising the Concept of “N-Terminal Modification” to “Fatty Acid Occupation” of Albumin

Oran

2017

Disease Markers

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Ischemia-modified albumin (IMA) is assumed “N-terminal modified” albumin which is generated immediately following myocardial ischemia. The diagnosis of IMA is based on reduced cobalt binding affinity to albumin which is attributed mainly to incapability of cobalt to bind at albumin's modified N-terminus. Although the albumin cobalt binding test was accepted as a potentially powerful marker for discriminating acute coronary syndrome from nonischemic chest pain, its usefulness has been brought into question in recent years. Patients with acutely ischemic myocardium exhibit a rapid increase in serum levels of fatty acids (FAs). Almost all released FAs are strongly bound to albumin which create conformational changes in the protein with resultant reduced cobalt binding affinity. There is a clear metabolic and temporal relationship between IMA measured via albumin cobalt binding testing and serum levels of FAs. In line with what has been suggested recently in the literature, we conclude that a shift from the concept of “N-terminal modified” to “FA-occupied” albumin is required, as this better describes IMA in patients with acute coronary syndrome. We also offer “oxidation modified albumin, OMA,” which is conceptually different from the “FA-occupied” IMA, to describe modification of albumin in chronic disease associated with increased oxidative stress.

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Fatty acids and the risk of death during acute myocardial ischaemia

Cited by 23 publications

References 52 publications

Clinical Update: Cardiovascular Disease in Diabetes Mellitus

Clinical Update: Cardiovascular Disease in Diabetes Mellitus

Energetic metabolism in cardiomyocytes: molecular basis of heart ischemia and arrhythmogenesis

Ischemia-Modified Albumin as a Marker of Acute Coronary Syndrome: The Case for Revising the Concept of “N-Terminal Modification” to “Fatty Acid Occupation” of Albumin

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