Relevant bibliographies by topics / Cardiac metabolic syndrome

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Cardiac metabolic syndrome'

Author: Grafiati
Published: 6 September 2023

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Journal articles on the topic "Cardiac metabolic syndrome"

1

Cheng, Tsung O. "Cardiac syndrome X versus metabolic syndrome X." International Journal of Cardiology 119, no. 2 (July 2007): 137–38. http://dx.doi.org/10.1016/j.ijcard.2006.06.062.

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Chiavelli, H., M. Lachaux, V. Tardif, A. Dumesnil, L. Nicol, G. Riou, D. Godefroy, et al. "Cardiac lymphatics in metabolic-syndrome related cardiac dysfunstion." Archives of Cardiovascular Diseases Supplements 12, no. 2-4 (October 2020): 239. http://dx.doi.org/10.1016/j.acvdsp.2020.03.095.

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Bugger, Heiko, and E. Dale Abel. "The Metabolic Syndrome and Cardiac Function." Advances in Pulmonary Hypertension 7, no. 3 (August 1, 2008): 332–36. http://dx.doi.org/10.21693/1933-088x-7.3.332.

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Yavelov, I. S. "SUDDEN CARDIAC DEATH AND METABOLIC SYNDROME." Journal of Clinical Practice 5, no. 4 (December 15, 2014): 53–59. http://dx.doi.org/10.17816/clinpract5453-59.

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In the review epidemiologic data regarding sudden cardiac death in patients with metabolic syndrome are presented. Suspected pathophysiologic mechanisms and approaches to primary prevention of this event are considered.
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Chahine, Mohamed. "Cardiac Metabolic State and Brugada Syndrome." Circulation Research 105, no. 8 (October 9, 2009): 721–23. http://dx.doi.org/10.1161/circresaha.109.208405.

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Fitchett, David, and Kim A. Connelly. "Impaired Cardiac Function in Metabolic Syndrome." Canadian Journal of Cardiology 30, no. 3 (March 2014): 270–71. http://dx.doi.org/10.1016/j.cjca.2014.01.012.

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Lavie, Carl J., and Richard V. Milani. "Metabolic Syndrome, Hostility, and Cardiac Rehabilitation." American Journal of Cardiology 96, no. 11 (December 2005): 1615. http://dx.doi.org/10.1016/j.amjcard.2005.08.001.

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Haq, M. Maksumul, and ZA Latif. "'Angry Fat' and Metabolic Syndrome." Ibrahim Cardiac Medical Journal 1, no. 2 (January 30, 2013): 5–6. http://dx.doi.org/10.3329/icmj.v1i2.13543.

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Yang, Yijun, Justin Kurian, Giana Schena, Jaslyn Johnson, Hajime Kubo, Joshua G. Travers, Chunya Kang, et al. "Cardiac Remodeling During Pregnancy With Metabolic Syndrome." Circulation 143, no. 7 (February 16, 2021): 699–712. http://dx.doi.org/10.1161/circulationaha.120.051264.

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Background: The heart undergoes physiological hypertrophy during pregnancy in healthy individuals. Metabolic syndrome (MetS) is now prevalent in women of child-bearing age and might add risks of adverse cardiovascular events during pregnancy. The present study asks if cardiac remodeling during pregnancy in obese individuals with MetS is abnormal and whether this predisposes them to a higher risk for cardiovascular disorders. Methods: The idea that MetS induces pathological cardiac remodeling during pregnancy was studied in a long-term (15 weeks) Western diet–feeding animal model that recapitulated features of human MetS. Pregnant female mice with Western diet (45% kcal fat)–induced MetS were compared with pregnant and nonpregnant females fed a control diet (10% kcal fat). Results: Pregnant mice fed a Western diet had increased heart mass and exhibited key features of pathological hypertrophy, including fibrosis and upregulation of fetal genes associated with pathological hypertrophy. Hearts from pregnant animals with WD-induced MetS had a distinct gene expression profile that could underlie their pathological remodeling. Concurrently, pregnant female mice with MetS showed more severe cardiac hypertrophy and exacerbated cardiac dysfunction when challenged with angiotensin II/phenylephrine infusion after delivery. Conclusions: These results suggest that preexisting MetS could disrupt physiological hypertrophy during pregnancy to produce pathological cardiac remodeling that could predispose the heart to chronic disorders.
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Asrih, Mohamed, François Mach, Alessio Nencioni, Franco Dallegri, Alessandra Quercioli, and Fabrizio Montecucco. "Role of Mitogen-Activated Protein Kinase Pathways in Multifactorial Adverse Cardiac Remodeling Associated with Metabolic Syndrome." Mediators of Inflammation 2013 (2013): 1–11. http://dx.doi.org/10.1155/2013/367245.

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Metabolic syndrome has been widely associated with an increased risk for acute cardiovascular events. Emerging evidence supports metabolic syndrome as a condition favoring an adverse cardiac remodeling, which might evolve towards heart dysfunction and failure. This pathological remodeling has been described to result from the cardiac adaptive response to clinical mechanical conditions (such as hypertension, dyslipidemia, and hyperglycemia), soluble inflammatory molecules (such as cytokines and chemokines), as well as hormones (such as insulin), characterizing the pathophysiology of metabolic syndrome. Moreover, these cardiac processes (resulting in cardiac hypertrophy and fibrosis) are also associated with the modulation of intracellular signalling pathways within cardiomyocytes. Amongst the different intracellular kinases, mitogen-activated protein kinases (MAPKs) were shown to be involved in heart damage in metabolic syndrome. However, their role remains controversial. In this paper, we will discuss and update evidence on MAPK-mediated mechanisms underlying cardiac adverse remodeling associated with metabolic syndrome.
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Dissertations / Theses on the topic "Cardiac metabolic syndrome"

1

Zibadi, Sherma. "Metabolic Syndrome-Induced Cardiac Fibrosis." Diss., The University of Arizona, 2009. http://hdl.handle.net/10150/195321.

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Recent studies support the association between metabolic syndrome (MetS), a cluster of cardiovascular risk factors, and diastolic dysfunction. Disproportionate collagen accumulation, particularly cross-linking of collagen, plays a key role in translating interstitial fibrosis into mechanical chamber stiffness and diastolic dysfunction. Characteristic changes in the expression and activity of myocardial lysyl oxidase (LOX), a matrix modifying enzyme that catalyzes cross-linked collagen, are unclear in MetS. We established a diet-induced MetS model to study diastolic dysfunction by treating male C57BL/6 mice a high-fat high-simple carbohydrate (HFHSC) diet for 6 months. Despite blunted gene expression of LOX isoforms, MetS mice demonstrated significant increase in the ratio of protein expression of mature to proenzyme LOX, enhanced LOX activity, and increased cardiac cross-linked collagen compared with controls. This fibrotic response coincided with marked increase in left ventricular end-diastolic pressure and stiffness and impaired diastolic filling pattern. Our data demonstrate that diet-induced MetS alters the remodeling enzyme LOX, thereby increasing the amount of crosslinking and inducing diastolic dysfunction.Furthermore we examined the role of T-lymphocytes in myocardial LOX regulation in diet-induced fibrotic hearts. Female SCID mice which are devoid of functional T-lymphocytes and C57BL/6 mice were treated with HFHSC diet for 12 months. Similar to male C67BL/6, female HFHSC-fed C57BL/6 mice demonstrated significant increase in maturation and catalytic activity of myocardial LOX, cross-linking, ventricular stiffness and diastolic dysfunction. Whereas induction of LOX protein was minimal in SCID mice compared with wild-type counterparts. Correspondingly fibrillar cross-linked collagen formation and diastolic dysfunction were less prominent in SCID mice. Our results suggest a potential role of T-lymphocytes in induction of myocardial stiffness and diastolic dysfunction through modulation of LOX-dependent collagen maturation.Moreover we studied the role of leptin, an adipokine over-produced in MetS with fibrotic effects in non-cardiac tissues, as a key mediator of profibrogenic responses in the heart by administrating leptin to C57BL/6 and leptin-deficient ob/ob mice. With exogenous leptin administration ob/ob mice displayed passive diastolic filling dysfunction that coincided with increase in myocardial collagen compared with ob/ob controls. Our findings suggest profibrotic effects of leptin in the heart, primarily through predominance of collagen synthesis over degradation.
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Zullo, Melissa D. "Cardiovascular Disease Management and Functional Capacity in Patients With Metabolic Syndrome." Case Western Reserve University School of Graduate Studies / OhioLINK, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=case1232721609.

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NAGATA, KOHZO, TOYOAKI MUROHARA, SHOGO WATANABE, YUURI TAKESHITA, SAE OHURA, TAMAYO MURASE, TAKUYA HATTORI, MIWA TAKATSU, and KEIJI TAKAHASHI. "Premature Cardiac Senescence in DahlS.Z-Lepr fa/Lepr fa Rats as a New Animal Model of Metabolic Syndrome." Nagoya University School of Medicine, 2014. http://hdl.handle.net/2237/19482.

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Donner, Daniel Giordano. "Therapeutic Effects of Selective Androgen Receptor Modulation in the Treatment of Cardiac, Metabolic and Bone Pathologies Associated with Androgen Decline and Obesity." Thesis, Griffith University, 2015. http://hdl.handle.net/10072/367789.

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In males, the widespread prevalence of both obesity-related metabolic syndrome (MetS) and testosterone deficiency (TD) is further exacerbating the socio-economic and health burdens already elicited by the rapidly ageing global population. The strong reciprocal relationship between the MetS and TD in males often results in their shared pathologies presenting together in the clinical setting. Clinical and epidemiological studies have provided convincing evidence that the MetS and TD are highly comorbid [1, 2] and share mutual abnormalities, including visceral obesity, dyslipidaemia and insulin resistance. One or more of these changes associated with the MetS and TD contribute to life-threatening conditions such as cardiovascular disease and increased osteoporotic bone fragility, particularly in the ageing male. Due to limitations of traditional androgen replacement therapy with testosterone (TEST), which is readily converted to active metabolites by enzymes, the therapeutic potential of trenbolone (TREN), a selective androgen receptor modulator (SARM), remains an attractive alternative to TEST. However, TREN’s efficacy has not been investigated in appropriate models representative of obese and TEST-deficient males, especially within the context of cardiometabolic disease and obesity-related osteoporosis/bone strength.
Thesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Medical Science
Griffith Health
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Wachowiak, Paul Stephen. "Relationships among Cynical Hostility, Metabolic Syndrome, and Cardiac Structure and Function in Multi-Ethnic Post-Myocardial Infarction Patients: A Structural Modeling Approach." Scholarly Repository, 2009. http://scholarlyrepository.miami.edu/oa_dissertations/291.

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BACKGROUND: Risk factors associated with Metabolic Syndrome (MetS) have been implicated in cardiovascular disease (CVD) development and outcomes. Few studies have investigated relationships between psychological variables, MetS factors, and indices of cardiac structure and function (CSF) among healthy individuals in a single conceptual model. No studies to date have analyzed such relationships in patients with CVD. METHODS: The present study examined associations between cynical hostility (CynHo), MetS factors, and CSF in 186 multi-ethnic post-myocardial infarction (MI) patients. Structural equation modeling was used to test a theory driven model of MetS that had good statistical fit. Primary MetS variables included waist circumference (WC), the homeostatic model of insulin resistance (HOMA-IR), glucose area under the curve (G-AUC), triglycerides (TRIG), high-density lipoprotein cholesterol (HDL-C), and diastolic blood pressures (DBP). Secondary MetS variables included plasminogen activator inhibitor-1 (PAI-1) and a latent inflammation variable comprised of CRP and IL-6. Cardiac function variables were fractional shortening (FS), E/A ratio, and rate-pressure product (RPP). A latent cardiac mass (CM) variable was also created. RESULTS: The final structural model had good model fit (Chi-Square(102)=100.65, p=0.52, CFI=1.00, RMSEA=0.00, and SRMR=0.04). Direct paths were supported between WC and CM and all MetS factors except TRIG and G-AUC. WC was indirectly associated with DBP via CM. The model supported positive direct paths between HOMA-IR and G-AUC, TRIG, and PAI-1, but not inflammation or HDL-C. HOMA-IR demonstrated a direct positive association with RPP and direct inverse associations with FS and E/A ratio. No direct paths were supported between other MetS variables except one between TRIG and HDL-C. CynHo demonstrated a direct positive relationship with HOMA-IR. CONCLUSIONS: Similar to findings in healthy individuals, central adiposity and IR play primary roles in CSF impairment in post-MI patients. Findings suggest that CynHo could promote the progression of metabolic dysfunction and cardiac disease via factors that influence the efficiency of glucose metabolism. Interventions for post-MI patients should take into account both direct and indirect effects of CynHo, central adiposity, and IR on the progression of CVD in this population to reduce adverse outcomes and improve quality of life.
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Vidlund, Mårten. "Glutamate for metabolic intervention in coronary surgery : with special reference to the GLUTAMICS-trial." Doctoral thesis, Örebro universitet, Hälsoakademin, 2011. http://urn.kb.se/resolve?urn=urn:nbn:se:oru:diva-19757.

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Myocardial ischemia is a major cause of postoperative heart failure and adverse outcome in coronary artery bypass graft surgery (CABG). Conventional treatment of postoperative heart failure with inotropic drugs may aggravate underlying ischemic injury. Glutamate has been claimed to increase myocardial tolerance to ischemia and promote metabolic and hemodynamic recovery after ischemia. The aim of this work was to investigate if intravenous glutamate infusion given in association with CABG for acute coronary syndrome can reduce mortality and prevent or mitigate myocardial injury and postoperative heart failure. We also wanted to assess neurological safety issues, as a concern with the use of glutamate is that it may act as an excitotoxin under certain conditions.A metabolic strategy for perioperative care was assessed in an observational study on 104 consecutive patients with severe left ventricular dysfunction undergoing CABG. Based on encouraging clinical results, unsurpassed in the literature, the GLUTAMICS-trial was initiated. 861 patients undergoing CABG for acute coronary syndrome were randomly allocated to blinded intravenous infusion of L-glutamicacid solution or saline. The primary endpoint was a composite of postoperative mortality (≤30 days), perioperative myocardial infarction and left ventric ular heart failure in association with weaning from cardiopulmonary bypass. Secondary endpoints included neurological safety issues, degree of myocardial injury,postoperative hemodynamic state, use of circulatory support and cardiac mortality.The event rate was lower than anticipated and the primary endpoint did not differ significantly between the groups. Regarding secondary endpoints there were significant differences compatible with a beneficial effect of glutamate on post-ischemic myocardial recovery. The putative effect of glutamate infusion was seen in more ischemic patients (CCS class IV) and in patients with evident or anticipated LV-failure on weaning from CPB. No evidence for increased incidence of clinical or subclinical neurological injury was found. In conclusion, intravenous glutamate infusion is safe in the dosages employed and could provide a novel and important way of promoting myocardial recovery after ischemic injury.
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Maarman, Gerald Jerome. "The effect of CPT-1 inhibition on myocardial function and resistance to ischemia/reperfusion injury in a rodent model of the metabolic syndrome." Thesis, Stellenbosch : University of Stellenbosch, 2010. http://hdl.handle.net/10019.1/5354.

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Thesis (MScMedSc (Dept. of Biomedical Sciences. Medical Physiology))University of Stellenbosch, 2010.
ENGLISH ABSTRACT: Background: Obesity is associated with dyslipidemia, insulin resistance and glucose intolerance and together these components characterise the metabolic syndrome (Dandona et al. 2005). In the state of obesity, there are high levels of circulating free fatty acids and increased rates of fatty oxidation which inhibit glucose oxidation. This: (i) reduce the heart‘s contractile ability, (ii) exacerbates ischemic/reperfusion injury and (iii) decreases cardiac mechanical function during reperfusion (Kantor et al. 2000; Liu et al. 2002; Taegtmeyer, 2000). Aim: The aim of our study was to investigate the effect of inhibiting fatty acid oxidation, with oxfenicine (4-Hydroxy-L-phenylglycine), on (i) cardiac mechanical function, (ii) mitochondrial respiration, (iii) myocardial tolerance to ischemia/reperfusion injury, (iv) CPT-I expression, MCAD expression, IRS-1 activation, total GLUT- 4 expression and (v) the RISK pathway (ERK42/44 and PKB/Akt). Methods: Male Wistar rats were fed a control rat chow diet or a high calorie diet (HCD) for 16 weeks. The HCD caused diet induced obesity (DIO). The animals were randomly divided into 4 groups [Control, DIO, Control + oxfen and DIO + oxfen]. The drug was administered for the last 8 weeks of feeding (200mg/kg/day). Animals were sacrificed and the hearts were perfused on the Langendorff perfusion system. After being subjected to regional ischemia and two hours of reperfusion, infarct size was determined. A separate series of animals were fed and/or treated and hearts were collected after 25 minutes global ischemia followed by 30 min reperfusion for determination of GLUT- 4, CPT-1, IRS -1, MCAD, ERK (42/44) and PKB/Akt expression/phosphorylation using Western blot analysis. A third series of hearts were excised and used for the isolation of mitochondria. Results: In the DIO rats, chronic oxfenicine treatment improved cardiac mechanical function by improving mitochondrial respiration. Oxfenicine inhibited CPT-1 expression but had no effect on MCAD or GLUT- 4 expression. Oxfenicine decreased IRS-1 iv expression, but not IRS-1 activation. Oxfenicine also improved myocardial tolerance to ischemia/reperfusion without activation of the RISK pathway (ERK & PKB). In the control rats, chronic oxfenicine treatment worsened cardiac mechanical function by adversely affecting mitochondrial respiration. Oxfenicine also worsened myocardial tolerance to ischemia/reperfusion in the control rats without changes in the RISK pathway (ERK & PKB). Oxfenicine had no effect on CPT-1, MCAD or GLUT- 4 expression. Oxfenicine increased IRS-1 expression, but not IRS-1 activity. Conclusion: Chronic oxfenicine treatment improved cardiac mechanical function and myocardial resistance to ischemia/reperfusion injury in obese animals, but worsened it in control animals. The improved cardiac mechanical function and tolerance to ischemia/reperfusion injury may be due to improvement in mitochondrial respiration.
AFRIKAANSE OPSOMMING: Agtergrond: Vetsug word geassosieer met dislipidemie, insulien weerstandigheid en glukose intoleransie, wat saam die metaboliese sindroom karakteriseer (Dandona et al. 2005). Met vetsug is daar ‗n hoë sirkulasie van vetsure, sowel as verhoogde vertsuur oksidasie wat gevolglik glukose oksidasie onderdruk. Dit: (i) verlaag die hart se vermoë om saam te trek, (ii) vererger isgemiese/herperfusie skade en (iv) verlaag kardiale effektiwiteit gedurende herperfusie (Kantor et al. 2000; Liu et al. 2002; Taegtmeyer, 2000). Doel: Die doel van die studie was om die effekte van vetsuur onderdrukking m.b.v. oksfenisien (4-Hidroksie-L-fenielglisien) op (i) meganiese hart funksie, (ii) mitokondriale respirasie, (iii) miokardiale toleransie teen isgemiese/herperfusie skade, (iv) CPT-I uitdrukking, MCAD uitdrukking, IRS-1 aktiwiteit, totale GLUT-4 uitdrukking en (v) die RISK pad (ERK42/44 en PKB/Akt) te ondersoek. Metodes: Manlike Wistar rotte was gevoer met ‗n kontrole rot dieet of ‗n hoë kalorie dieet (HKD) vir 16 weke. Die HKD lei tot dieet-geïnduseerde vetsug (DGV). Die diere was lukraak verdeel in 4 groepe [kontrole, DGV, kontrole + oksfen en DGV + oksfen]. Die behandeling met die middel was toegedien vir die laaste 8 weke van die voeding protokol (200mg/kg/dag). Die diere was geslag en die harte was geperfuseer op die Langendorff perfusie sisteem. Na blootstelling aan streeks- of globale isgemie en 2 ure herperfusie was infark groottes bepaal. ‗n Aparte reeks diere was gevoer en/of behandel en die harte was versamel na 25 minute globale isgemie gevolg deur 30 minute herperfusie vir die bepaling van GLUT-4, CPT 1, IRS -1, MCAD, ERK (42/44) en PKB/Akt uitdrukking/aktivering d.m.v. Western blot analise. ‗n Derde reeks diere was gebruik vir die isolasie van mitokondria. Resultate: In die DGV diere, het kroniese oksfenisien behandeling meganiese hart funksie verbeter d.m.v. die verbetering van mitokondriale respirasie. Oksfenisien het CPT-1 uitdrukking verlaag terwyl GLUT- 4 en MCAD uitdrukking nie geaffekteer was vi nie. Oksfenisien het IRS-1 uitdrukking verlaag, maar nie IRS-1 aktiwiteit nie. Oksfenisien het ook miokardiale weerstand teen isgemiese/herperfusie verbeter met sonder aktivering van die RISK pad (ERK & PKB). In die kontrole diere, het kroniese oksfenisien behandeling die meganiese hart funksie versleg d.m.v. negatiewe effekte op mitokondriale respirasie. Oksfenisien het die miokardiale weerstand teen isgemiese/herperfusie van die kontrole rotte versleg sonder veranderinge in die RISK pad (ERK & PKB). Oksfenisien het geen effek gehad op CPT-1, MCAD en GLUT-4 uitdrukking nie. Oksfenisien het IRS-1 uitdrukking verhoog, maar nie IRS-1 aktiwiteit nie. Samevatting: Kroniese oksfenisien behandeling het die meganiese hart funksie en miokardiale weerstand teen isgemiese/herperfusie skade in die vet diere verbeter, maar versleg in die kontrole diere. Hierdie verbetering van meganiese hart funksie en weerstand teen isgemiese/herperfusie skade kon dalk wees a.g.v. ‗n verbetering in mitokondriale respirasie.
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Smith, Wayne. "A pathologic role for angiotensin II and endothelin-1 in cardiac remodelling and ischaemia and reperfusion injury in a rat model of the metabolic syndrome." Thesis, Link to the online version, 2006. http://hdl.handle.net/10019/1217.

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Mittoux, Aurélia. "Évaluation de la mortalité chez les patients schizophrènes traités par des antipsychotiques dans des conditions normales de prescription en Europe et en Asie." Thesis, Lyon 1, 2011. http://www.theses.fr/2011LYO10268.

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Fatica, Erica Marie. "Investigating Cardiac Metabolism in Barth Syndrome Using Induced Pluripotent Stem Cell-Derived Cardiomyocytes." Cleveland State University / OhioLINK, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=csu1556630870935279.

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Books on the topic "Cardiac metabolic syndrome"

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Casaer, Michael P., and Greet Van den Berghe. Nutrition support in acute cardiac care. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0032.

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Malnutrition in cardiac and critical illness is associated with a compromised clinical outcome. The aim of nutrition therapy is to prevent these complications and particularly to attenuate lean tissue wasting and the loss of muscle force and of physical function. During the last decade, several well-powered randomized controlled nutrition trials have been performed. Their results challenge the existing nutrition practices in critically ill patients. Enhancing the nutritional intake and the administration of specialized formulations failed to evoke clinical benefit. Some interventions even provoked an increased mortality or a delayed recovery. These unexpected new findings might be, in part, caused by an important leap forward in the methodological quality in the recent trials. Perhaps reversing early catabolism in the critically ill patient by nutrition or anabolic interventions is impossible or even inappropriate. Nutrients effectively suppress the catabolic intracellular autophagy pathway. But autophagy is crucial for cellular integrity and function during metabolic stress, and consequently its inhibition early in critical illness might be deleterious. Evidence from large nutrition trials, particularly in acute cardiac illness, is scarce. Nutrition therapy is therefore focused on avoiding iatrogenic harm. Some enteral nutrition is administered if possible and eventually temporary hypocaloric feeding is tolerated. Above all, the refeeding syndrome and other nutrition-related complications should be prevented. There is no indication for early parenteral nutrition, increased protein doses, specific amino acids, or modified lipids in critical illness.
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Casaer, Michael P., and Greet Van den Berghe. Nutrition support in acute cardiac care. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199687039.003.0032_update_001.

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Malnutrition in cardiac and critical illness is associated with a compromised clinical outcome. The aim of nutrition therapy is to prevent these complications and particularly to attenuate lean tissue wasting and the loss of muscle force and of physical function. During the last decade, several well-powered randomized controlled nutrition trials have been performed. Their results challenge the existing nutrition practices in critically ill patients. Enhancing the nutritional intake and the administration of specialized formulations failed to evoke clinical benefit. Some interventions even provoked an increased mortality or a delayed recovery. These unexpected new findings might be, in part, caused by an important leap forward in the methodological quality in the recent trials. Perhaps reversing early catabolism in the critically ill patient by nutrition or anabolic interventions is impossible or even inappropriate. Nutrients effectively suppress the catabolic intracellular autophagy pathway. But autophagy is crucial for cellular integrity and function during metabolic stress, and consequently its inhibition early in critical illness might be deleterious. Evidence from large nutrition trials, particularly in acute cardiac illness, is scarce. Nutrition therapy is therefore focused on avoiding iatrogenic harm. Some enteral nutrition is administered if possible and eventually temporary hypocaloric feeding is tolerated. Above all, the refeeding syndrome and other nutrition-related complications should be prevented. There is no indication for early parenteral nutrition, increased protein doses, specific amino acids, or modified lipids in critical illness.
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Casaer, Michael P., and Greet Van den Berghe. Nutrition support in acute cardiac care. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199687039.003.0032_update_002.

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Malnutrition in cardiac and critical illness is associated with a compromised clinical outcome. The aim of nutrition therapy is to prevent these complications and particularly to attenuate lean tissue wasting and the loss of muscle force and of physical function. During the last decade, several well-powered randomized controlled nutrition trials have been performed. Their results challenge the existing nutrition practices in critically ill patients. Enhancing the nutritional intake and the administration of specialized formulations failed to evoke clinical benefit. Some interventions even provoked an increased mortality or a delayed recovery. These unexpected new findings might be, in part, caused by an important leap forward in the methodological quality in the recent trials. Perhaps reversing early catabolism in the critically ill patient by nutrition or anabolic interventions is impossible or even inappropriate. Nutrients effectively suppress the catabolic intracellular autophagy pathway. But autophagy is crucial for cellular integrity and function during metabolic stress, and consequently its inhibition early in critical illness might be deleterious. Evidence from large nutrition trials, particularly in acute cardiac illness, is scarce. Nutrition therapy is therefore focused on avoiding iatrogenic harm. Some enteral nutrition is administered if possible and eventually temporary hypocaloric feeding is tolerated. Above all, the refeeding syndrome and other nutrition-related complications should be prevented. There is no indication for early parenteral nutrition, increased protein doses, specific amino acids, or modified lipids in critical illness.
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Schmid, Jean-Paul, and Hugo Saner. Ambulatory preventive care: outpatient clinics and primary care. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199656653.003.0023.

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Cardiac rehabilitation (CR) services aim to restore the physical, psychosocial, and vocational status of cardiac patients. The role of these services has evolved due to the progress of interventional cardiology with its prompt and effective treatment of acute coronary syndromes. The focus has moved from the restoration of a patient’s health following an acute event towards a more pronounced long-term targeted secondary prevention intervention. As a consequence, CR services have also expanded their indication in order to include not only patients after myocardial infarction or surgery but also a variety of ’non-acuteʼ cardiovascular disease (CVD) states like stable coronary heart disease and peripheral obstructive artery disease as well as asymptomatic patients with no history of CVD but with a constellation of cardiovascular risk factors, especially metabolic syndrome or diabetes mellitus. This chapter provides a wide-ranging summary of the issues concerning outpatients and primary care.
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Schmid, Jean-Paul, Hugo Saner, Paul Dendale, and Ines Frederix. Ambulatory preventive care: outpatient clinics and primary care. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199656653.003.0023_update_001.

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Cardiac rehabilitation (CR) services aim to restore the physical, psychosocial, and vocational status of cardiac patients. The role of these services has evolved due to the progress of interventional cardiology with its prompt and effective treatment of acute coronary syndromes. The focus has moved from the restoration of a patient’s health following an acute event towards a more pronounced long-term targeted secondary prevention intervention. As a consequence, CR services have also expanded their indication in order to include not only patients after myocardial infarction or surgery but also a variety of ’non-acuteʼ cardiovascular disease (CVD) states like stable coronary heart disease and peripheral obstructive artery disease as well as asymptomatic patients with no history of CVD but with a constellation of cardiovascular risk factors, especially metabolic syndrome or diabetes mellitus. This chapter provides a wide-ranging summary of the issues concerning outpatients and primary care.
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Karon, Barry L., and Naveen L. Pereira. Heart Failure and Cardiomyopathies. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780199755691.003.0046.

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Heart failure is a clinical syndrome characterized by the inability of the heart to maintain adequate cardiac output to meet the metabolic demands of the body while still maintaining normal or near-normal ventricular filling pressures. Heart failure may be present at rest, but often it is present only during exertion as a result of the dynamic nature of cardiac demands. For correct treatment of heart failure, the mechanism, underlying cause, and any reversible precipitating factors must be identified. Typical manifestations of heart failure are dyspnea and fatigue that limit activity tolerance and fluid retention leading to pulmonary or peripheral edema. The most recent proposed categorization divided the cardiomyopathies into primary and secondary cardiomyopathies, and the primary disorders are further subdivided as genetic, acquired, or mixed. Although this proposal takes into account our progressive understanding of this heterogeneous group of disorders, the previous phenotypic classification of dilated, hypertrophic, and restrictive diseases still provides utility in day-to-day understanding and management of these disorders.
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Gluckman, Sir Peter, Mark Hanson, Chong Yap Seng, and Anne Bardsley. Magnesium in pregnancy and breastfeeding. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780198722700.003.0021.

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Magnesium in important for a wide variety of physiological processes; prominent among them is the control of muscle contractions, cardiac function, and carbohydrate metabolism. In pregnancy, low magnesium status is associated with hypertension, pre-eclampsia, gestational diabetes, leg cramping, and preterm labour. Magnesium has been used extensively in obstetrics to reduce uterine contractility in threatened preterm labour. Although current evidence does not support a requirement for magnesium supplementation for most pregnant women, those who are overweight, have risk factors for hypertensive or metabolic disorders or malabsorption syndromes, or who are carrying multiple fetuses, should pay particular attention to their diets and should be monitored for signs of magnesium deficiency. Consuming a magnesium-rich diet throughout pregnancy is recommended.
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Sever, Mehmet Şükrü, and Raymond Vanholder. Acute kidney injury in polytrauma and rhabdomyolysis. Edited by Norbert Lameire. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0252_update_001.

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The term ‘polytrauma’ refers to blunt (or crush) trauma that involves multiple body regions or cavities, and compromises physiology to potentially cause dysfunction of uninjured organs. Polytrauma frequently affects muscles resulting in rhabdomyolysis. In daily life, it mostly occurs after motor vehicle accidents, influencing a limited number of patients; after mass disasters, however, thousands of polytrauma victims may present at once with only surgical features or with additional medical complications (crush syndrome). Among the medical complications, acute kidney injury (AKI) deserves special mention, since it is frequent and has a substantial impact on the ultimate outcome.Several factors play a role in the pathogenesis of polytrauma (or crush)-induced AKI: (1) hypoperfusion of the kidneys, (2) myoglobin-induced direct nephrotoxicity, and intratubular obstruction, and also (3) several other mechanisms (i.e. iron and free radical-induced damage, disseminated intravascular coagulation, and ischaemia reperfusion injury). Crush-related AKI is prerenal at the beginning; however, acute tubular necrosis may develop eventually. In patients with crush syndrome, apart from findings of trauma, clinical features may include (but are not limited to) hypotension, oliguria, brownish discoloration of urine, and other symptoms and findings, such as sepsis, acute respiratory distress syndrome, disseminated intravascular coagulation, bleeding, cardiac failure, arrhythmias, electrolyte disturbances, and also psychological trauma.In the biochemical evaluation, life-threatening hyperkalaemia, retention of uraemic toxins, high anion gap metabolic acidosis, elevated serum levels of myoglobin, and muscle enzymes are noted; creatine phosphokinase is very useful for diagnosing rhabdomyolysis.Early fluid administration is vital to prevent crush-related AKI; the rate of initial fluid volume should be 1000 mL/hour. Overall, 3–6 L are administered within a 6-hour period considering environmental, demographic and clinical features, and urinary response to fluids. In disaster circumstances, the preferred fluid formulation is isotonic saline because of its ready availability. Alkaline (bicarbonate-added) hypotonic saline may be more useful, especially in isolated cases not related to disaster, as it may prevent intratubular myoglobin, and uric acid plugs, metabolic acidosis, and also life-threatening hyperkalaemia.In the case of established acute tubular necrosis, dialysis support is life-saving. Although all types of dialysis techniques may be used, intermittent haemodialysis is the preferred modality because of medical and logistic advantages. Close follow-up and appropriate treatment improve mortality rates, which may be as low as 15–20% even in disaster circumstances. Polytrauma victims after mass disasters deserve special mention, because crush syndrome is the second most frequent cause of death after trauma. Chaos, overwhelming number of patients, and logistical drawbacks often result in delayed, and sometimes incorrect treatment. Medical and logistical disaster preparedness is useful to improve the ultimate outcome of disaster victims.
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Schwitter, Juerg, and Jens Bremerich. Cardiac magnetic resonance in the intensive and cardiac care unit. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0023.

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Current applications of cardiac magnetic resonance offer a wide spectrum of indications in the setting of acute cardiac care. In particular, cardiac magnetic resonance is helpful for the differential diagnosis of chest pain by the detection of ischaemia, myocardial stunning, myocarditis, and pericarditis. Also, Takotsubo cardiomyopathy and acute aortic diseases can be evaluated by cardiac magnetic resonance and are important differential diagnoses in patients with acute chest pain. In patients with restricted windows for echocardiography, according to guidelines, cardiac magnetic resonance is the method of choice to evaluate complications of an acute myocardial infarction. In an acute myocardial infarction, cardiac magnetic resonance allows for a unique characterization of myocardial damage by quantifying necrosis, microvascular obstruction, oedema (i.e. area at risk), and haemorrhage. These features will help us to understand better the pathophysiological events during infarction and will also allow us to assess new treatment strategies in acute myocardial infarction. To which extent the information on tissue damage will guide patient management is not yet clear, and further research, e.g. in the setting of the European Cardiovascular MR registry, is ongoing to address this issue. Recent studies also demonstrated the possiblity to reduce costs in the management of acute coronary syndromes when cardiac magnetic resonance is integrated into the routine work-up. In the near future, applications of cardiac magnetic resonance will continue to expand in the acute cardiac care units, as manufacturers are now strongly focusing on this aspect of user-friendliness. Finally, in the next decade or so, magnetic resonance imaging of other nuclei, such as fluorine and carbon, might become a reality in clinics, which would allow for metabolic and targeted molecular imaging with excellent sensitivity and specificity.
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Schwitter, Juerg, and Jens Bremerich. Cardiac magnetic resonance in the intensive and cardiac care unit. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199687039.003.0023_update_001.

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Current applications of cardiac magnetic resonance offer a wide spectrum of indications in the setting of acute cardiac care. In particular, cardiac magnetic resonance is helpful for the differential diagnosis of chest pain by the detection of ischaemia, myocardial stunning, myocarditis, and pericarditis. Also, Takotsubo cardiomyopathy and acute aortic diseases can be evaluated by cardiac magnetic resonance and are important differential diagnoses in patients with acute chest pain. In patients with restricted windows for echocardiography, according to guidelines, cardiac magnetic resonance is the method of choice to evaluate complications of an acute myocardial infarction. In an acute myocardial infarction, cardiac magnetic resonance allows for a unique characterization of myocardial damage by quantifying necrosis, microvascular obstruction, oedema (i.e. area at risk), and haemorrhage. These features will help us to understand better the pathophysiological events during infarction and will also allow us to assess new treatment strategies in acute myocardial infarction. To which extent the information on tissue damage will guide patient management is not yet clear, and further research, e.g. in the setting of the European Cardiovascular MR registry, is ongoing to address this issue. Recent studies also demonstrated the possiblity to reduce costs in the management of acute coronary syndromes when cardiac magnetic resonance is integrated into the routine work-up. In the near future, applications of cardiac magnetic resonance will continue to expand in the acute cardiac care units, as manufacturers are now strongly focusing on this aspect of user-friendliness. Finally, in the next decade or so, magnetic resonance imaging of other nuclei, such as fluorine and carbon, might become a reality in clinics, which would allow for metabolic and targeted molecular imaging with excellent sensitivity and specificity.
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Book chapters on the topic "Cardiac metabolic syndrome"

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Alpert, Martin A. "Obesity and Cardiac Disease." In Metabolic Syndrome, 619–39. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-11251-0_35.

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Alpert, Martin A., and Brent M. Parker. "Obesity and Cardiac Disease." In Metabolic Syndrome, 1–24. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-12125-3_35-1.

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Steinberger, Julia, and Aaron S. Kelly. "Obesity, Metabolic Syndrome and Type 2 Diabetes." In Pediatric and Congenital Cardiology, Cardiac Surgery and Intensive Care, 499–507. London: Springer London, 2013. http://dx.doi.org/10.1007/978-1-4471-4619-3_53.

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Turan, Belma. "Role of Sodium-Glucose Co-transporters on Cardiac Function in Metabolic Syndrome Mammalians." In Biochemistry of Cardiovascular Dysfunction in Obesity, 125–44. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-47336-5_7.

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Heidari-Foroozan, Mahsa, and Nima Rezaei. "Metabolic Encephalomyopathic Crises, Recurrent with Rhabdomyolysis, Cardiac Arrhythmias, and Neurodegeneration (MECRCN)." In Genetic Syndromes, 1–4. Cham: Springer International Publishing, 2023. http://dx.doi.org/10.1007/978-3-319-66816-1_1765-1.

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Bagger, Jens Peder. "Myocardial Metabolism in Cardiac Syndrome X." In Developments in Cardiovascular Medicine, 81–89. Boston, MA: Springer US, 1999. http://dx.doi.org/10.1007/978-1-4615-5181-2_7.

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Sternick, Eduardo Back. "Inherited Metabolic Diseases: Emphasis on Myocardial Disease and Arrhythmogenesis." In Clinical Approach to Sudden Cardiac Death Syndromes, 233–58. London: Springer London, 2009. http://dx.doi.org/10.1007/978-1-84882-927-5_19.

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Chen, Wei. "Evolution of Metabolic Syndrome from Childhood." In Evolution of Cardio-Metabolic Risk from Birth to Middle Age:, 35–52. Dordrecht: Springer Netherlands, 2011. http://dx.doi.org/10.1007/978-94-007-1451-9_4.

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Jaquet, Kornelia, Andreas Mügge, and Nazha Hamdani. "Cardiac transcriptomic remodeling in metabolic syndrome." In Epigenetics in Cardiovascular Disease, 187–211. Elsevier, 2021. http://dx.doi.org/10.1016/b978-0-12-822258-4.00011-0.

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Yanger, Sheryl. "Sudden Infant Death Syndrome." In Pediatric Emergencies, 35–36. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780190073879.003.0004.

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Sudden infant death syndrome (SIDS) is the third leading cause of infant mortality in the United States. SIDS is defined as the sudden death of an infant younger than age 1 year that cannot be explained after a thorough investigation, including autopsy, scene investigation, and clinical history. Despite research and advances in understanding of SIDS, it remains a diagnosis of exclusion after ruling out accidental causes such as suffocation/strangulation and cardiac, infectious, metabolic, or traumatic etiologies. Although the exact pathogenesis is unknown, a working model of SIDS includes a combination of exogenous factors, such as overbundling, prone sleep position, and airway obstruction, and intrinsic factors such as immature cardiorespiratory or arousal systems.
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Conference papers on the topic "Cardiac metabolic syndrome"

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Stojanovska, Jadranka, El-Sayed Ibrahim, Slavica Nikolovska, and Thomas Chenevert. "Identifying cardiac magnetic resonance signatures of obesity phenotypes in metabolic syndrome using multi-echo DIXON imaging." In 2016 IEEE 13th International Symposium on Biomedical Imaging (ISBI 2016). IEEE, 2016. http://dx.doi.org/10.1109/isbi.2016.7493304.

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Albarado-Ibañez, Alondra, Marcia Hiriart, Alejandro Frank Hoeflich, and Julian Torres-Jacome. "Assessment the change on rhythm cardiac produces by the metabolic syndrome in rats: using nonlinear methods." In 6th International Conference on Nonlinear Science and Complexity. São José dos Campos, Brazil: INPE Instituto Nacional de Pesquisas Espaciais, 2016. http://dx.doi.org/10.20906/cps/nsc2016-0019.

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Galerneau, Louis-Marie, Jean-Louis Pépin, Anne-Laure Borel, Olivier Chabre, Marc Sapene, Bruno Stach, Janie Girey-Rannaud, Renaud Tamisier, and Philippe Caron. "Is IGF-1 a marker of cardio-metabolic risk in sleep apnea syndrome (SAS)?" In ERS International Congress 2016 abstracts. European Respiratory Society, 2016. http://dx.doi.org/10.1183/13993003.congress-2016.oa1802.

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Assad, Nour, Clifford Qualls, Lewis J. Smith, Alexander Arynchyn, Bharat Thyagarajan, David Jacobs, and Akshay Sood. "BMI-Defined Obesity Is A Stronger Predictor Than Metabolic Syndrome For Future Asthma Risk In Women- The Longitudinal Cardia Study." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a6499.

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van Zeller, M., O. K. Basoglu, J. Verbraecken, C. Lombardi, W. T. Mcnicholas, J. L. Pepin, P. Steiropoulos, et al. "Sleep characteristics and cardio-metabolic comorbidities in the OSA-COPD overlap syndrome: Data from the European Sleep Apnea Database (ESADA)." In ERS International Congress 2022 abstracts. European Respiratory Society, 2022. http://dx.doi.org/10.1183/13993003.congress-2022.1459.

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Folts, J. D. "A MODEL OF ACUTE PLATELET THROMBUS FORMATION IN STENOSED CORONARY AND CAROTID ARTERIES." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643712.

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There is currently a great deal of interest in the diagnosis and treatment of unstable angina and silent ischemia.Many feel that these syndromes are due, in part, to periodic accumulation of platelet thrombi which subsequently embolize.In addition, anti-piatelet therapy is also considered necessary for patients after coronary artery bypass grafts (CABG'S), balloon angioplasty, and thrombolysis. Currently the two antiplatelet agents most commonly prescribed for the patient conditions mentioned above are aspirin (ASA), alone or in combination with dipyridamole (Dip). ASA reduces cardiac events in patients with unstable angina, and prolongs CABG graft patency. The addition of Dip to ASA therapy is very confusing since most studies done compared ASA + Dip to placebo. In several studies however,when an ASA group was compared to an ASA + Dip group there was no significant difference.We have developed and will describe ananimal model of coronary artery stenosis in the dog and the pig, or carotid arterystenosis in the monkey and the rabbit, with intimal damage, that simulates some ofthe conditions that exist in patients with coronary or carotid artery disease. The artery to be studied is dissected outand blood flow is continuously measured with an electromagnetic flowmeter probe. As acute platelet thrombus formation (APTF) developes in the stenosed lumen, the blood flow declines to low levels, producing ischemia until the thrombus emobolizesdistally resulting in abrupt restoration of blood flow. These cyclical flow reductions (CFR's), when they occur in the coronaries, produce ECG changes identical to those observed in patients with silent ischemia and unstable angina. They also produce significant transient regional dyskinesis of the ventricular wall, which resolves when blood flow is restored. Histologic examination of myocardial tissue in the bed distal to the stenosis shows focal areas of ischemic change presumably caused by the embolized platelet emboli.We have examined factors which exacerbate the size and frequency of these CFR"ssuch as; IV infusion of epinephrine (E) 0.4 μg/kg/min for 15 min, ventilating the animals with cigarette smoke, infusing nicotine IV, or placing chewing tobacco under the tongue.We have examined four groups of agentswhich prevent APTF in our model.1. Antiplatelet agents including ASA, indomethacin, ibuprofen and several other NSAI agentsas well as several experimental thromboxane synthetase inhibitors. These agents all block the production of TXA2and inhibit APTF in our model. Unfortunately the IV infusion of E reinstates APTtemporarily (by another biochemical pathway) until the E is metabolized. High (2-4 mg/kg) doses of Dip, alone or with sub threshold dose of ASA does nothing to I APTF.However,0.6mg/kg of chi orpromaz i ne abolishes APTF in all four species and protects agents renewal of APTF by E.2. Dietary Substances In our model, caffeine 10 mg/kg, or the extract from two garlic cloves, or enough ethanol to achieve a blood alcohol level of 0.07 mg% all significantly inhibit or abolish APTF in our model.3. Metabolic Inhibitors POCA, an oral hypoglycemic agent, which inhibits mitochondrial beta oxidation of fatty acids also inhibits APTF in our model possibly by reducing ATP production in the platelet.4. We have studied a monoclonal antibody(developed by Dr. Barry Coller) to the platelet I Ib�I I la glycoprotein receptor where fibrinogen binds platelets into aggregates and ultimately leads to APTF. This antibody 0.3 mg/kg/completely inhibits APTF, and also strongly inhibits in vitro platelet aggregation in response to either ADP or collagen given alone or each combined with E. This antibody is the most potent inhibitor of APTF that we have studied.
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Reports on the topic "Cardiac metabolic syndrome"

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Czerwaty, Katarzyna, Karolina Dżaman, Krystyna Maria Sobczyk, and Katarzyna Irmina Sikrorska. The Overlap Syndrome of Obstructive Sleep Apnea and Chronic Obstructive Pulmonary Disease: A Systematic Review. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, November 2022. http://dx.doi.org/10.37766/inplasy2022.11.0077.

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Review question / Objective: To provide the essential findings in the field of overlap syndrome of chronic obstructive pulmonary disease and obstructive sleep apnea, including prevalence, possible predictors, association with clinical outcomes, and severity compared to both chronic obstructive pulmonary disease and obstructive sleep apnea patients. Condition being studied: OSA is characterized by complete cessation (apnea) or significant decrease (hy-popnea) in airflow during sleep and recurrent episodes of upper airway collapse cause it during sleep leading to nocturnal oxyhemoglobin desaturations and arousals from rest. The recurrent arousals which occur in OSA lead to neurocognitive consequences, daytime sleepiness, and reduced quality of life. Because of apneas and hypopneas, patients are experiencing hypoxemia and hypercapnia, which result in increasing levels of catecholamine, oxidative stress, and low-grade inflammation that lead to the appearance of cardio-metabolic consequences of OSA. COPD is a chronic inflammatory lung disease defined by persistent, usually pro-gressive AFL (airflow limitation). Changes in lung mechanics lead to the main clini-cal manifestations of dyspnea, cough, and chronic expectoration. Furthermore, patients with COPD often suffer from anxiety and depression also, the risk of OSA and insomnia is higher than those hospitalized for other reasons. Although COPD is twice as rare as asthma but is the cause of death eight times more often.
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