MiocardiopatÃa Diabética, lo que hoy conocemos
Resumen
La diabetes mellitus es un factor de riesgo bien conocido para desarrollo de insuficiencia cardÃaca. Varios mecanismos moleculares vinculan la diabetes a la inflamación del miocardio. Se sabe que en sujetos con sÃndrome metabólico y diabetes tipo 2, los altos niveles de glucosa y la dislipidemia inducen directamente la regulación positiva y secreción de citoquinas, quimiocinas y moléculas de adhesión en células cardÃacas mediante la modulación de múltiples vÃas de señalización que convergen hacia factor nuclear kappa-cadena ligera-potenciador de células B activadas. La activación del sistema renina-angiotensina-aldosterona, acumulación de productos finales de glicación avanzada y las moléculas del patrón molecular asociado al daño también representan mecanismos importantes que median la inflamación del corazón diabético, principalmente al actuar sobre los receptores Toll-like . Una expresión elevada de mediadores de inflamación del corazón diabético  promueve directamente los trastornos cardÃacos a través de la modulación de múltiples mecanismos. De hecho, se sabe que se modulan vÃas de señalización intracelular en el corazón que promueven la hipertrofia de los cardiomiocitos, la muerte, fibrosis y la insuficiencia cardÃaca.
La comprensión de la fisiopatologÃa y la patogénesis en pacientes con miocardiopatÃa diabética ha proporcionado mejores opciones de manejo. Esto incluye, modificaciones del estilo de vida, control diabético mejorado, la gestión de hipertensión coexistente y enfermedad de las arterias coronarias si está presente, terapias reductoras de lÃpidos y el manejo de la falla del corazón.
Palabras clave
Referencias
Bibliografia.
Wang ZV, Hill JA. Diabetic cardiomyopathy: catabolism driving metabolism. Circulation 2015;131:771-773.
Pappachan JM, Varughese GI, Sriraman R, Arunagiri¬nathan G. Diabetic cardiomyopathy: pathophysiology, diagnostic evaluation and management. World J Diabetes 2013;4:177-189.
Elliott P, Andersson B, Arbustini E, et al. Classification of the cardiomyopathies: a position statement from the European Society of Cardiology Working Group on Myocardial and Pericardial Diseases. Eur Heart J 2008;29:270-276.
Trachanas K, Sideris S, Aggeli C, et al. Diabetic cardiomy¬opathy: from pathophysiology to treatment. Hellenic J Cardiol 2014;55:411-421.
Finck BN, Lehman JJ, Leone TC, et al. The cardiac pheno¬type induced by PPARalpha overexpression mimics that caused by diabetes mellitus. J Clin Invest 2002;109:121- 130.
Aneja A, Tang WH, Bansilal S, Garcia MJ, Farkouh ME. Diabetic cardiomyopathy: insights into pathogenesis, diagnostic challenges, and therapeutic options. Am J Med 2008;121:748-757.
Kannel WB, McGee DL. Diabetes and cardiovascular dis¬ease: the Framingham study. JAMA 1979;241:2035-2038.
Wong AK, AlZadjali MA, Choy AM, Lang CC. Insulin re¬sistance: a potential new target for therapy in patients with heart failure. Cardiovasc Ther 2008;26:203-213.
Maisch B, Alter P, Pankuweit S. Diabetic cardiomyopathy: fact or fiction? Herz 2011;36:102-115.
Witteles RM, Fowler MB. Insulin-resistant cardiomyop¬athy clinical evidence, mechanisms, and treatment op¬tions. J Am Coll Cardiol 2008;51:93-102.
Jia G, DeMarco VG, Sowers JR. Insulin resistance and hyperinsulinaemia in diabetic cardiomyopathy. Nat Rev
Endocrinol 2016;12:144-153.
Grundy SM. Metabolic syndrome update. Trends Cardiovasc Med 2016;26:364–373.
Frieler RA, Mortensen RM. Immune cell and other noncardiomyocyte regulation of cardiac hypertrophy and remodeling. Circulation 2015;131:1019–1030.
Prabhu SD, Frangogiannis NG. The biological basis for cardiac repair after myocardial infarction. Circ Res 2016;119:91–112.
Mann DL. The emerging role of innate immunity in the heart and vascular system: for whom the cell tolls. Circ Res 2011;108:1133–1145.
Yan SF, Ramasamy R, Naka Y, Schmidt AM. Glycation, inflammation, and RAGE: a scaffold for the macrovascular complications of diabetes and beyond. Circ Res 2003;93:1159–1169.
Boudina S, Abel ED. Diabetic cardiomyopathy revisited. Circulation, 2007;115: 3213–3223.
Sciarretta S, Ferrucci A, Ciavarella GM, De Paolis P, Venturelli V, Tocci G, De Biase L, Rubattu S, Volpe M. Markers of inflammation and fibrosis are related to cardiovascular damage in hypertensive patients with metabolic syndrome. Am J Hypertens 2007;20:784–791.
Bahrami H, Bluemke DA, Kronmal R, Bertoni AG, Lloyd-Jones DM, Shahar E, Szklo M, Lima JA. Novel metabolic risk factors for incident heart failure and their relationship with obesity: the MESA (Multi-Ethnic Study of Atherosclerosis) study. J Am CollCardiol 2008;51:1775–1783.
Suzuki T, Katz R, Jenny NS, Zakai NA, LeWinter MM, Barzilay JI, Cushman M. Metabolic syndrome, inflammation, and incident heart failure in the elderly: the cardiovascular health study. Circ Heart Fail 2008;1:242–248.
MacDonald MR, Petrie MC, Varyani F, Ostergren J, Michelson EL, Young JB, Solomon SD, Granger CB, Swedberg K, Yusuf S, Pfeffer MA, McMurray JJ. Impact of diabetes on outcomes in patients with low and preserved ejection fraction heart failure: an analysis of the Candesartan in Heart failure: assessment of reduction in mortality and morbidity (CHARM) programme. Eur Heart J 2008;29:1377–1385.
Kannel WB, Hjortland M, Castelli WP. Role of diabetes in congestive heart failure: the Framingham study. Am J Cardiol 1974;34:29–34.
Holscher ME, Bode C, Bugger H. Diabetic cardiomyopathy: does the type of diabetes matter? Int J Mol Sci 2016;17(12):pii:E2136.
Palmieri V, Bella JN, Arnett DK, Liu JE, Oberman A, Schuck MY, Kitzman DW, Hopkins PN, Morgan D, Rao DC, Devereux RB. Effect of type 2 diabetes mellitus on left ventricular geometry and systolic function in hypertensive subjects: Hypertension Genetic Epidemiology Network (HyperGEN) study. Circulation2001;103:102–107.
Zarich SW, Arbuckle BE, Cohen LR, Roberts M, Nesto RW. Diastolic abnormalities in young asymptomatic diabetic patients assessed by pulsed Doppler echocardiography. J Am Coll Cardiol 1988;12:114–120.
Baker RG, Hayden MS, Ghosh S. NF-kappaB, inflammation, and metabolic disease. Cell Metab 2011;13:11–22.
Gordon JW, Shaw JA, Kirshenbaum LA. Multiple facets of NF-kappaB in the heart: to be or not to NF-kappaB. Circ Res 2011;108:1122–1132.
Shah MS, Brownlee M. Molecular and cellular mechanisms of cardiovascular disorders in diabetes. Circ Res 2016;118:1808–1829.
Thomas CM, Yong QC, Rosa RM, Seqqat R, Gopal S, Casarini DE, Jones WK, Gupta S, Baker KM, Kumar R. Cardiac-specific suppression of NF-kappaB signaling prevents diabetic cardiomyopathy via inhibition of the renin-angiotensin system. AmJ Physiol Heart Circ Physiol 2014;307:H1036–1045.
Mariappan N, Elks CM, Sriramula S, Guggilam A, Liu Z, Borkhsenious O, Francis J. NF-kappaB-induced oxidative stress contributes to mitochondrial and cardiac dysfunction in type II diabetes. Cardiovasc Res 2010;85:473–483.
Sciarretta S, Paneni F, Palano F, Chin D, Tocci G, Rubattu S, Volpe M. Role of the renin-angiotensin-aldosterone system and inflammatory processes in the development and progression of diastolic dysfunction. Clin Sci (Lond) 2009;116:467–477.
Cameron AR, Morrison VL, Levin D, Mohan M, Forteath C, Beall C, McNeilly AD, Balfour DJ, Savinko T, Wong AK, Viollet B, Sakamoto K, Fagerholm SC, Foretz M, Lang CC, Rena G. Anti-inflammatory effects of metformin irrespective of diabetes status. Circ Res 2016;119:652–665.
Zhang J, Cheng Y, Gu J, Wang S, Zhou S, Wang Y, Tan Y, Feng W, Fu Y, Mellen N, Cheng R, Ma J, Zhang C, Li Z, Cai L. Fenofibrate increases cardiac autophagy via FGF21/SIRT1 and prevents fibrosis and inflammation in the hearts of Type 1 diabetic
mice. Clin Sci (Lond) 2016;130:625–641.
Kumar R, Kerins DM, Walther T. Cardiovascular safety of anti-diabetic drugs. Eur Heart J Cardiovasc Pharmacother 2016;2:32–43.
Sola S, Mir MQ, Lerakis S, Tandon N, Khan BV. Atorvastatin improves left ventricular systolic function and serum markers of inflammation in nonischemic heart failure. J Am Coll Cardiol 2006;47:332–337.
Levine B, Kroemer G. Autophagy in the pathogenesis of disease. Cell 2008;132:27–42.
Sciarretta S, Zhai P, Volpe M, Sadoshima J. Pharmacological modulation of autophagy during cardiac stress. J Cardiovasc Pharmacol, 2012;60(3):235–241.
Sciarretta S, Boppana VS, Umapathi M, Frati G, Sadoshima J. Boosting autophagy in the diabetic heart: a translational perspective. Cardiovasc Diagn Ther 2015;5:394–402.
Sciarretta S, Zhai P, Shao D, Maejima Y, Robbins J, Volpe M, Condorelli G, Sadoshima J. Rheb is a critical regulator of autophagy during myocardial ischemia: pathophysiological implications in obesity and metabolic syndrome. Circulation 2012;125:1134–1146.
Fang ZY, Prins JB, Marwick TH. Diabetic cardiomyopa¬thy: evidence, mechanisms, and therapeutic implications. Endocr Rev 2004;25:543-567.
Khouri SJ, Maly GT, Suh DD, Walsh TE. A practical ap¬proach to the echocardiographic evaluation of diastolic function. J Am Soc Echocardiogr 2004;17:290-297.
Yu CM, Sanderson JE, Marwick TH, Oh JK. Tissue Dop¬pler imaging a new prognosticator for cardiovascular diseases. J Am Coll Cardiol 2007;49:1903-1914.
Miki T, Yuda S, Kouzu H, Miura T. Diabetic cardiomyopa¬thy: pathophysiology and clinical features. Heart Fail Rev 2013;18:149-166.
Gottlieb I, Macedo R, Bluemke DA, Lima JA. Magnetic resonance imaging in the evaluation of non-ischemic cardiomyopathies: current applications and future per¬spectives. Heart Fail Rev 2006;11:313-323.
Rijzewijk LJ, van der Meer RW, Smit JW, et al. Myocardial steatosis is an independent predictor of diastolic dys¬function in type 2 diabetes mellitus. J Am Coll Cardiol 2008;52:1793-1799.
Paulus WJ, Tschope C, Sanderson JE, et al. How to diag¬nose diastolic heart failure: a consensus statement on the diagnosis of heart failure with normal left ventricular ejection fraction by the Heart Failure and Echocardiogra¬phy Associations of the European Society of Cardiology. Eur Heart J 2007;28:2539-2550.
Dinh W, Bansemir L, Futh R, et al. Increased levels of laminin and collagen type VI may reflect early remod¬elling in patients with acute myocardial infarction. Acta Cardiol 2009;64:329-334.
D’Souza A, Howarth FC, Yanni J, et al. Left ventricle struc¬tural remodelling in the prediabetic Goto-Kakizaki rat. Exp Physiol 2011;96:875-888.
Chavali V, Tyagi SC, Mishra PK. Predictors and preven¬tion of diabetic cardiomyopathy. Diabetes Metab Syndr Obes 2013;6:151-160.
Quilliot D, Alla F, Bohme P, et al. Myocardial collagen turnover in normotensive obese patients: relation to in¬sulin resistance. Int J Obes (Lond) 2005;29:1321-1328.
Stolen TO, Hoydal MA, Kemi OJ, et al. Interval training normalizes cardiomyocyte function, diastolic Ca2+ con¬trol, and SR Ca2+ release synchronicity in a mouse model of diabetic cardiomyopathy. Circ Res 2009;105:527-536.
Epp RA, Susser SE, Morissette MP, Kehler DS, Jassal DS, Duhamel TA. Exercise training prevents the development of cardiac dysfunction in the low-dose streptozotocin diabetic rats fed a high-fat diet. Can J Physiol Pharmacol 2013;91:80-89.
Epshteyn V, Morrison K, Krishnaswamy P, et al. Utility of B-type natriuretic peptide (BNP) as a screen for left ven¬tricular dysfunction in patients with diabetes. Diabetes Care 2003;26:2081-2087.
Russell NE, Higgins MF, Amaruso M, Foley M, McAu¬liffe FM. Troponin T and pro-B-type natriuretic peptide in fetuses of type 1 diabetic mothers. Diabetes Care 2009;32:2050-2055.
Feng B, Chen S, George B, Feng Q, Chakrabarti S. miR133a regulates cardiomyocyte hypertrophy in diabetes. Diabe¬tes Metab Res Rev 2010;26:40-49.
Rijzewijk LJ, Jonker JT, van der Meer RW, et al. Effects of hepatic triglyceride content on myocardial metabolism in type 2 diabetes. J Am Coll Cardiol 2010;56:225-233.
Rijzewijk LJ, van der Meer RW, Lamb HJ, et al. Altered myocardial substrate metabolism and decreased diastolic function in nonischemic human diabetic cardiomyopa¬thy: studies with cardiac positron emission tomography and magnetic resonance imaging. J Am Coll Cardiol 2009;54:1524-1532.
DeMarco VG, Aroor AR, Sowers JR. The pathophysiology of hypertension in patients with obesity. Nat Rev Endo¬crinol 2014;10:364-376.
Voulgari C, Papadogiannis D, Tentolouris N. Diabetic cardiomyopathy: from the pathophysiology of the cardiac myocytes to current diagnosis and management strate¬gies. Vasc Health Risk Manag 2010;6:883-903.
Kodama S, Tanaka S, Heianza Y, et al. Association be¬tween physical activity and risk of all-cause mortality and cardiovascular disease in patients with diabetes: a me¬ta-analysis. Diabetes Care 2013;36:471-479.
Sharma AK, Srinivasan BP. Triple verses glimepiride plus metformin therapy on cardiovascular risk biomarkers and diabetic cardiomyopathy in insulin resistance type 2 diabetes mellitus rats. Eur J Pharm Sci 2009;38:433-444.
Aboukhoudir F, Rekik S. Left ventricular systolic function deterioration during dobutamine stress echocardiogra¬phy as an early manifestation of diabetic cardiomyopathy and reversal by optimized therapeutic approach. Int J Cardiovasc Imaging 2012;28:1329-1339.
Chung J, Abraszewski P, Yu X, et al. Paradoxical increase in ventricular torsion and systolic torsion rate in type I diabetic patients under tight glycemic control. J Am Coll Cardiol 2006;47:384-390.
Zib I, Jacob AN, Lingvay I, et al. Effect of pioglitazone therapy on myocardial and hepatic steatosis in insu¬lin-treated patients with type 2 diabetes. J Investig Med 2007;55:230-236.
von Bibra H, St John Sutton M. Impact of diabetes on postinfarction heart failure and left ventricular remodel¬ing. Curr Heart Fail Rep 2011;8:242-251.
Wong AK, Symon R, AlZadjali MA, et al. The effect of met¬formin on insulin resistance and exercise parameters in patients with heart failure. Eur J Heart Fail 2012;14:1303- 1310.
Mamas MA, Deaton C, Rutter MK, et al. Impaired glucose tolerance and insulin resistance in heart failure: under¬recognized and undertreated? J Card Fail 2010;16:761-768.
Sacca L, Napoli R. Insulin resistance in chronic heart failure: a difficult bull to take by the horns. Nutr Metab Cardiovasc Dis 2009;19:303-305.
Caglayan E, Stauber B, Collins AR, et al. Differential roles of cardiomyocyte and macrophage peroxisome prolifer¬ator-activated receptor gamma in cardiac fibrosis. Diabe¬tes 2008;57:2470-2479.
Younce CW, Burmeister MA, Ayala JE. Exendin-4 at¬tenuates high glucose-induced cardiomyocyte apop¬tosis via inhibition of endoplasmic reticulum stress and activation of SERCA2a. Am J Physiol Cell Physiol 2013;304:C508-C518.
Doehner W, Frenneaux M, Anker SD. Metabolic impair¬ment in heart failure: the myocardial and systemic per¬spective. J Am Coll Cardiol 2014;64:1388-1400.
Witteles RM, Keu KV, Quon A, Tavana H, Fowler MB. Dipeptidyl peptidase 4 inhibition increases myocardial glucose uptake in nonischemic cardiomyopathy. J Card Fail 2012;18:804-809.
Bostick B, Habibi J, Ma L, et al. Dipeptidyl peptidase inhibition prevents diastolic dysfunction and reduces myocardial fibrosis in a mouse model of Western diet in¬duced obesity. Metabolism 2014;63:1000-1011.
Adeghate E, Kalasz H. Amylin analogues in the treatment of diabetes mellitus: medicinal chemistry and structural basis of its function. Open Med Chem J 2011;5:78-81.
Inzucchi SE, Zinman B, Wanner C, et al. SGLT-2 inhib¬itors and cardiovascular risk: proposed pathways and review of ongoing outcome trials. Diab Vasc Dis Res 2015;12:90-100
Thomas CM, Yong QC, Seqqat R, et al. Direct renin inhi¬bition prevents cardiac dysfunction in a diabetic mouse model: comparison with an angiotensin receptor antag¬onist and angiotensin-converting enzyme inhibitor. Clin Sci (Lond) 2013;124:529-541.
Machackova J, Liu X, Lukas A, Dhalla NS. Renin-angioten¬sin blockade attenuates cardiac myofibrillar remodelling in chronic diabetes. Mol Cell Biochem 2004;261:271-278.
Symeonides P, Koulouris S, Vratsista E, et al. Both rami¬pril and telmisartan reverse indices of early diabetic cardiomyopathy: a comparative study. Eur J Echocardiogr 2007;8:480-486.
Sharma V, McNeill JH. Parallel effects of β-adrenoceptor blockade on cardiac function and fatty acid oxidation in the diabetic heart: confronting the maze. World J Cardiol 2011;3:281-302.
Mohamad HE, Askar ME, Hafez MM. Management of cardiac fibrosis in diabetic rats: the role of peroxisome proliferator activated receptor gamma (PPAR-gamma) and calcium channel blockers (CCBs). Diabetol Metab Syndr 2011;3:4.
Giannetta E, Isidori AM, Galea N, et al. Chronic inhibi¬tion of cGMP phosphodiesterase 5A improves diabetic cardiomyopathy: a randomized, controlled clinical trial using magnetic resonance imaging with myocardial tag¬ging. Circulation 2012;125:2323-2333.
Seferovic et al. Lancet Diabetes Endocrinol. 2017 [Epub] doi:10.1016/S2213-8587(17)30087-6
Giamouzis & Butler. Lancet Diabetes Endocrinol. 2017 [Epub] doi:10.1016/S2213-8587(17)30089-X
Yasonuri et al. The impact of an inverse correlation between plama B-type natriuretic peptide levels and insulin resisstance on the diabetic condition in patients with HF.Division of Cardiology, Department of Internal Medicine, The Jikei University School of Medicine, 3-25-8 Nishi-shimbashi, Minato-ku, Tokyo105-8461, Japan
Chen YH, Feng B, Chen ZW. Statins for primary pre¬vention of cardiovascular and cerebrovascular events in diabetic patients without established cardiovascular diseases: a meta-analysis. Exp Clin Endocrinol Diabetes 2012;120:116-120.
Cholesterol Treatment Trialists’ (CTT) Collaborators, Kearney PM, Blackwell L, et al. Efficacy of cholester¬ol-lowering therapy in 18,686 people with diabetes in 14 randomised trials of statins: a meta-analysis. Lancet 2008;371:117-125.
Van Linthout S, Riad A, Dhayat N, et al. Anti-inflammato¬ry effects of atorvastatin improve left ventricular function in experimental diabetic cardiomyopathy. Diabetologia 2007;50:1977-1986.
Dai QM, Lu J, Liu NF. Fluvastatin attenuates myocardial interstitial fibrosis and cardiac dysfunction in diabetic rats by inhibiting over-expression of connective tissue growth factor. Chin Med J (Engl) 2011;124:89-94.
Nickel A, Loffler J, Maack C. Myocardial energetics in heart failure. Basic Res Cardiol 2013;108:358.
Gao D, Ning N, Niu X, Hao G, Meng Z. Trimetazidine: a meta-analysis of randomised controlled trials in heart failure. Heart 2011;97:278-286.
Zhao P, Zhang J, Yin XG, et al. The effect of trimetazidine on cardiac function in diabetic patients with idiopathic dilated cardiomyopathy. Life Sci 2013;92:633-638.
Maier LS, Layug B, Karwatowska-Prokopczuk E, et al. RAnoLazIne for the treatment of diastolic heart failure in patients with preserved ejection fraction: the RALI-DHF proof-of-concept study. JACC Heart Fail 2013;1:115-122.
Senanayake EL, Howell NJ, Ranasinghe AM, et al. Multi¬centre double-blind randomized controlled trial of per¬hexiline as a metabolic modulator to augment myocardi¬al protection in patients with left ventricular hypertrophy
undergoing cardiac surgery. Eur J Cardiothorac Surg 2015;48:354-362.
Li CJ, Lv L, Li H, Yu DM. Cardiac fibrosis and dysfunction in experimental diabetic cardiomyopathy are ameliorated by alpha-lipoic acid. Cardiovasc Diabetol 2012;11:73.
Delucchi F, Berni R, Frati C, et al. Resveratrol treatment reduces cardiac progenitor cell dysfunction and prevents morpho-functional ventricular remodeling in type-1 dia¬betic rats. PLoS One 2012;7:e39836.
Wang G, Li W, Lu X, Bao P, Zhao X. Luteolin ameliorates cardiac failure in type I diabetic cardiomyopathy. J Dia¬betes Complications 2012;26:259-265.
Wang G, Li W, Lu X, Zhao X. Riboflavin alleviates cardi¬ac failure in type I diabetic cardiomyopathy. Heart Int 2011;6:e21.
Xu X, Xiao H, Zhao J, Zhao T. Cardioprotective effect of sodium ferulate in diabetic rats. Int J Med Sci 2012;9:291- 300.
Sulaiman M, Matta MJ, Sunderesan NR, Gupta MP, Periasamy M, Gupta M. Resveratrol, an activator of SIRT1, upregulates sarcoplasmic calcium ATPase and improves cardiac function in diabetic cardiomyopathy. Am J Physi¬ol Heart Circ Physiol 2010;298:H833-H843.
Rabassa M, Zamora-Ros R, Urpi-Sarda M, Andres-Lac¬ueva C. Resveratrol metabolite profiling in clinical nu¬trition research: from diet to uncovering disease risk biomarkers: epidemiological evidence. Ann N Y Acad Sci 2015;1348:107-115.
Enlaces refback
- No hay ningún enlace refback.
Copyright (c) 2018 Nelson Campos Vera, Eduardo Rivas Estany, Mirna Andrade Ruiz
![Licencia de Creative Commons](https://i.creativecommons.org/l/by-nc/4.0/88x31.png)
Esta obra está bajo una licencia de Creative Commons Reconocimiento-NoComercial 4.0 Internacional.