Zusammenfassung
Der Energiestoffwechsel des Herzens ist obligatorisch aerob, um den hohen Adenosintriphosphat(ATP)-Bedarf bei geringer ATP-Reserve zu decken. Je nach Verfügbarkeit greift der Herzmuskel auf die verschiedenen Substrate wie Fettsäuren, Glucose und Lactat zurück, sodass ein Substratmangel praktisch ausgeschlossen ist. Eine hocheffiziente Vorwärtskopplung von Stoffwechsel und Durchblutung an die Herzarbeit gewährleistet unter physiologischen Bedingungen die kontinuierliche Anpassung an den ATP-Bedarf. Einschränkungen in der Energieversorgung können aber auftreten, wenn die Koronardurchblutung fällt (Flussstopp) oder Diffusionsstrecken für Sauerstoff zunehmen (Myokardhypertrophie). Hier kommt der Substratwahl eine wichtige Bedeutung für die Aufrechterhaltung des Energiestoffwechsels zu. Zwar ist der Energiegehalt von Fettsäuren hoch, ihre Energieeffizienz ist jedoch deutlich niedriger als diejenige von Kohlenhydraten. Die Kombination von Fasten, Stress, Flussstopp und Heparingabe im Rahmen kardiochirurgischer Eingriffe stellt eine ungünstige Konstellation für einen effizienten Energiestoffwechsel dar, da hier die Fettsäurespiegel typischerweise hoch sind. Stoffwechselinterventionen zielen auf eine Reduktion der Fettsäureplasmaspiegel bei Steigerung der myokardialen Glucoseaufnahme, z. B. durch normoglykämische Insulin-Glucose-Infusion. Ziel ist die Optimierung des Energiestoffwechsels, um die perioperative Mortalität bzw. die notwendige Dauer der Intensivtherapie kardiochirurgischer Patienten weiter zu reduzieren.
Abstract
The heart requires aerobic energy metabolism to cover the high adenosine triphosphate (ATP) demands when ATP energy reserves are low. Depending on the circulatory supply, heart muscle can switch between the use of various substrates, such as fatty acids, glucose and lactate, hence avoiding substrate deprivation. A highly efficient feed forward control of metabolism and coronary blood flow guarantees the continuous supply with energy under physiological conditions; however, impairment of the energy supply can result from decreased perfusion (flow stop) or increased myocardial diffusion distances (myocardial hypertrophy). Under such conditions the choice of substrate gains importance for maintenance of cardiac energy metabolism. While the energy content of fatty acids is high, the energy efficiency is much lower than that of carbohydrates. The combination of fasting, stress, flow stop, and heparin supplementation during cardiac surgery creates an unfortunate condition for efficient myocardial energy metabolism, because plasma levels of fatty acids are typically enhanced. Metabolic interventions aim to lower fatty acid concentrations in plasma and to increase myocardial glucose uptake, e. g. by normoglycemic insulin-glucose infusion. The aim is the optimization of energy metabolism to decrease perioperative mortality and the duration of intensive care treatment of patients undergoing cardiac surgery.
Literatur
Berne RM (1963) Cardiac nucleotides in hypoxia: possible role in regulation of coronary blood flow. Am J Physiol 204:317–322
Cappola TP, Kass DA, Nelson GS, Berger RD, Rosas GO, Kobeissi ZA, Marban E, Hare JM (2001) Allopurinol improves myocardial efficiency in patients with idiopathic dilated cardiomyopathy. Circulation 104:2407–2411
Caputo M, Ascione R, Angelini GD, Suleiman MS, Bryan AJ (1998) The end of the cold era: from intermittend cold to intermittend warm blood cardioplegia. Eur J Cardiothorac Surg 14:467–475
Carley AN, Taegtmeyer H, Lewandowski ED (2014) Matrix revisited. Mechanisms linking energy substrate metabolism to the function of the heart. Circ Res 114:717–729
Carvalho G, Pelletier P, Albacker T, Lachapelle K, Joanisse DR, Hatzakorzian R, Lattermann R, Sato H, Marette A, Schricker T (2011) Cardioprotective effects of glucose and insulin administration while maintaining normoglycemia (GIN therapy) in patient undergoing coronary artery bypass grafting. J Clin Endocrinol Metab 96:1469–1477
Deussen A, Borst M, Kroll K, Schrader J (1988) Formation of S‑Adenosylhomocysteine in the heart. II: a sensitive index for regional myocardial underperfusion. Circ Res 63:250–261
Doenst T, Brugger H, Schwarzer M, Faerber G, Borger MA, Mohr FW (2008) Three good reasons for heart surgeons to understand cardiac metabolism. Eur J Cardiothorac Surg 33:862–871
Doenst T, Nguyen TD, Abel ED (2013) Cardiac metabolism in heart failure. Implications beyond ATP production. Circ Res 113:709–724
Dorn GW II, Maak C (2013) SR and mitochondria: calcium cross-talk between kissing cousins. J Mol Cell Cardiol 55:42–49
Gündüz D, Thom J, Hussain I, Lopez D, Härtel FV, Erdogan A, Grebe M, Sedding D, Piper HM, Tillmanns H, Noll T, Aslam M (2010) Insulin stabilizes microvascular endothelial barrier function via phosphatidylinositol 3‑kinase/Akt-mediated Rac1 activation. Arterioscler Thromb Vasc Biol 30:1237–1245
Heiss HW, Barmeyer J, Wink K, Hell G, Cerny FJ, Keul J, Reindell H (1976) Studies on the regulation of myocardial blood flow in man. Basic Res Cardiol 71:658–675
Hirsch GA, Bottomley PA, Gerstenblith G, Weiss RG (2012) Allopurinol acutely increases adenosine triphosphate energy delivery in failing human hearts. J Am Coll Cardiol 59:802–808
Huang JM, Xian H, Bacaner M (1992) Long-chain fatty acids activate calcium channels in ventricular myocytes. Proc Natl Acad Sci USA 89:6452–6456
Ingels C, Debaveye Y, Milants I, Buelens E, Peeraer A, Devriendt Y, Vanhoutte T, Van Damme A, Schetz M, Wouters PJ, Van den Berghe G (2006) Strict blood glucose control with insulin during intensive care after cardiac surgery: impact on 4‑years survival, dependency on medical care, and quality of life. Eur Heart J 27:2716–2724
Ingwall JS, Weiss RG (2004) Is the failing heart energy starved? On using chemical energy to support cardiac function. Circ Res 95:135–145
Lazar HL, Chipkin AR, Fitzgerald CA, Bao Y, Cabral H, Apstein CS (2004) Tight glycemic control in diabetic coronary artery bypass graft patients improves perioperative outcomes and decreases recurrent ischemic events. Circulation 109:1497–1502
Mallet RT, Bünger R (1994) Energetic modulation of cardiac inotropism and sarcoplasmic reticular Ca2+ uptake. Biochim Biophys Acta 1224:22–32
Mjos OD (1971) Effect of free fatty acids on myocardial function and oxygen consumption in intact dogs. J Clin Invest 50:1386–1389
Noll T, Koop A, Piper HM (1992) Mitochondrial ATP-synthase activity in cardiomyocytes after aerobic-anaerobic metabolic transition. Am J Physiol 262:C1297–C1303
Olivencia-Yurvati AH, Blair JL, Baig M, Mallet RT (2003) Pyruvate-enhanced cardioprotection during surgery with cardiopulmonary bypass. J Cardiothorac Vasc Anesth 6:715–720
Rauen U, De Groot H (2004) New insights into the cellular and molecular mechanism of cold storage injury. J Investig Med 52:299–309
Ryou MG, Flaherty DC, Hoxha B, Gurji H, Sun J, Hodge LM, Olivencia-Yurvati AH, Mallet RT (2010) Pyruvate-enriched cardioplegia suppresses cardiopulmonary bypass-induced myocardial inflammation. Ann Thorac Surg 90:1529–1535
Schröder C, Heintz A, Pexa A, Rauen U, Deussen A (2007) Preclinical evaluation of coronary vascular function after cardioplegia with HTK and different antioxidant additives. Eur J Cardiothorac Surg 31:822–827
Siddiqi N, Singh S, Beadle R, Dawson D, Frenneaux M (2013) Cardiac metabolism in hypertrophy and heart failure: implication for therapy. Heart Fail Rev 18:595–606
Simonsen S, Kjekshus JK (1978) The effect of free fatty acids on myocardial oxygen consumption during atrial pacing and catecholamine infusion in man. Circulation 58:484–491
Smolenski RT, Schrader J, De Groot H, Deussen A (1991) Oxygen partial pressure and free intracellular adenosine of isolated cardiomyocytes. Am J Physiol 260:C708–C714
Stanley WC, Recchia FA, Lopaschuk GD (2005) Myocardial substrate metabolism in the normal and failing heart. Physiol Rev 85:1093–1129
Yamazaki K, Miwa S, Toyokuni S, Nemoto S, Oriyanhan W, Takaba K, Saji Y, Marui A, Nishina T, Ikeda T, Komeda M (2009) Effect of edaravone, a novel free radical scavenger, supplemented to cardioplegia on myocardial function after cardioplegic arrest: in vitro study of isolated rat heart. Heart Vessels 24:228–235
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Deussen, A. Klinische Relevanz des Energiestoffwechsels im Herzen. Z Herz- Thorax- Gefäßchir 31, 357–363 (2017). https://doi.org/10.1007/s00398-017-0178-6
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DOI: https://doi.org/10.1007/s00398-017-0178-6