Article information
La diabetes mellitus tipo 2 (DM2) es una enfermedad altamente prevalente, la cual ha mostrado un incremento acelerado en las últimas décadas, pues se ha duplicado el número de personas con esta enfermedad. Diversos estudios epidemiológicos revelan que el 70% de las muertes por diabetes son causadas por eventos cardiovasculares (enfermedad coronaria y accidente cerebrovascular). Recientemente se ha observado una expansión en el descubrimiento de medicamentos para el manejo de la DM2, los mismos que, para su introducción en el mercado, deben mostrar beneficios adicionales para el sistema cardiovascular. Este artículo tiene como propósito determinar el papel de los nuevos medicamentos hipoglicemiantes que actúan en el sistema de las incretinas y sus efectos en la prevención primaria de eventos cardiovasculares.
Palabras clave:
diabetes
enfermedades cardiovasculares
farmacología
inhibidores
Type 2 diabetes mellitus (T2DM) is a highly prevalent disease, which has shown a rapid increase in recent decades, doubling the number of people with this disease. Several epidemiological studies show that 70% of diabetes deaths are caused by cardiovascular events (coronary heart disease and stroke). Recently there has been an expansion in the discovery of drugs for the management of type 2 diabetes. These drugs must demonstrate additional cardiovascular system benefits before its introduction in the market. This paper aims to determine the role of new antidiabetic drugs that act on the incretin system and its effects on the primary prevention of cardiovascular events.
Keywords:
diabetes
cardiovascular disease
pharmacology
inhibitors
Full text is only aviable in PDF
Bibliografía
[1.]
G. Danaei, et al.
National, regional, and global trends in fasting plasma glucose and diabetes prevalence since 1980: systematic analysis of health examination surveys and epidemiological studies with 370 country-years and 2.7 million participants.
Lancet, 378 (2011), pp. 31-40
[2.]
Group of Diabetes Mellitus and Cardiovascular Disease of the Spanish Diabetes Society.
Diabetes mellitus and cardiovascular risk. Recommendations of the working group of Diabetes Mellitus and Cardiovascular Disease of the Spanish Diabetes Society 2009.
Clin Invest Arterioscl, 22 (2010), pp. 115-121
[3.]
S.E. Nissen, K. Wolski.
Effect of rosiglitazone on the risk of myocardial infarction and death from cardiovascular causes.
N Engl J Med, 356 (2007), pp. 2457-2471
[4.]
M.N. Feinglos, M.A. Bethel.
Therapy of type 2 diabetes cardiovascular death the UGDP.
Am Heart J, 138 (1999), pp. 346-352
[5.]
D.J. Margolis, O. Hoffstad, B.L. Strom.
Association between serious ischemic cardiac outcomes and medications used to treat diabetes.
Pharmacoepidemiol Drug Saf, 17 (2008), pp. 753-759
[6.]
J.E. Shaw, R.A. Sicree, P.Z. Zimmet.
Global estimates of the prevalence of diabetes for 2010 and 2030.
Diabetes Res Clin Pract, (2010), pp. 874-914
[7.]
O. Pinhas-Hamiel, P. Zeitler.
The global spread of type 2 diabetes mellitus in children and adolescents.
J. Pediatr, 146 (2005), pp. 693-700
[8.]
A.D. Liese, et al.
The burden of diabetes mellitus among US youth: prevalence estimates from the SEARCH for Diabetes in Youth Study.
Pediatrics, 118 (2006), pp. 1510-1518
[9.]
P. López-Jaramillo, J.J. Rey, D. Gómez-Arbeláez, et al.
Combatir la epidemia de diabetes mellitus tipo 2 en Latinoamérica: características especiales que demandan acciones innovadoras.
Clin Invest Arterioscl, 23 (2011), pp. 90-99
[10.]
P. López-Jaramillo, V. Lahera, J. López-López.
Epidemic of cardiometabolic diseases: a Latin American point of view.
Ther Adv Cardiovasc Dis, 5 (2011), pp. 119-131
[11.]
P. López-Jaramillo, L.P. Pradilla, V.R. Castillo, et al.
Socioeconomic pathology as a cause of regional differences in the prevalence of metabolic syndrome and pregnancy-induced hypertension.
Rev Esp Cardiol, 60 (2007), pp. 168-178
[12.]
M. Laakso.
Hyperglycemia and cardiovascular disease in type 2 diabetes.
Diabetes, 48 (1999), pp. 937-942
[13.]
S. Yamagishi.
Cardiovascular disease in recent onset diabetes mellitus.
J Cardiol, 57 (2011), pp. 257-262
[14.]
E. Selvin, S. Marinopoulos, G. Berkenblit, et al.
Meta-analysis: Glycosylated hemoglobin and cardiovascular disease in diabetes mellitus.
Ann Intern Med, 141 (2004), pp. 421-431
[15.]
S.M. Grundy, et al.
Implications of recent clinical trials for the 2 National Cholesterol Education Program Adult Treatment Panel III guidelines.
Circulation, 110 (2004), pp. 227-239
[16.]
N. Sarwar, P. Gao, S.R. Seshasai, et al.
Diabetes mellitus, fasting blood glucose concentration, and risk of vascular disease: a collaborative meta-analysis of 102 prospective studies.
Lancet, 375 (2010), pp. 2215-2222
[17.]
E. Selvin, M.W. Steffes, H. Zhu, et al.
Glycated hemoglobin, diabetes, and cardiovascular risk in nondiabetic adults.
N Engl J Med, 362 (2010), pp. 800-811
[18.]
J.G. Cleland, A. Torabi, N.K. Khan.
Epidemiology and management of heart failure and left ventricular systolic dysfunction in the aftermath of a myocardial infarction.
Heart, 91 (2005),
[19.]
K. Hogg, K. Swedberg, J. McMurray.
Heart failure with preserved left ventricular systolic function: epidemiology, clinical characteristics, and prognosis.
J Am Coll Cardiol, 43 (2004), pp. 317-327
[20.]
J.G. Cleland, T. McDonagh, A.S. Rigby, et al.
The national heart failure audit for England and Wales 2008-2009.
Heart, 97 (2011), pp. 876-886
[21.]
M. Fujita, H. Asanuma, J. Kim, et al.
Impaired glucose tolerance: a possible contributor to left ventricular hypertrophy diastolic dysfunction.
Int J.Cardiol, 118 (2007), pp. 76-80
[22.]
A.G. Bertoni, W.G. Hundley, M.W. Massing, et al.
Heart failure in diabetes mellitus.
Diabetes Care, 27 (2004), pp. 699-703
[23.]
S. Boudina, E.D. Abel.
Diabetic cardiomyopathy revisited.
Circulation, 115 (2007), pp. 3213-3223
[24.]
S.M. Grundy, I.V. Benjamin, G.L. Burke, et al.
Diabetes and cardiovascular disease: a statement for healthcare professionals from the American Heart Association.
Circulation, 100 (1999), pp. 1134-1146
[25.]
J. Stamler, O. Vaccaro, J.D. Naton, et al.
Diabetes, other risk factors, and 12-year cardiovascular mortality for men screened in the Multiple Risk Factor Intervention Trial (MRFIT).
Diabetes Care, 16 (1993), pp. 434-444
[26.]
L.H. Kuller, National Diabetes Data Group Stroke and diabetes.
Diabetes in America.
National Institutes of Health, National Institute of Diabetes and Digestive and Kidney Diseases, (1995), pp. 449-456
[27.]
M.J. O’Donnell, D. Xavier, L. Liu, et al.
INTERSTROKE investigators Risk factors for ischaemic and intracerebral haemorrhagic stroke in 22 countries (the INTERSTROKE study): a case-control study.
Lancet, 376 (2010), pp. 112-123
[28.]
M. Coutinho, H.C. Gerstein, Y. Wang, et al.
The relationship between glucose and incident cardiovascular events. A metaregression analysis of published data from 20 studies of 95,783 individuals followed for 12.4 years.
Diabetes care, 22 (1999), pp. 233-240
[29.]
C.M. Lawes, V. Parag, D.A. Bennett, et al.
Blood glucose and risk of cardiovascular disease in the Asia Pacific region.
Diabetes Care, 27 (2004), pp. 2836-2842
[30.]
E.J. Brunner, M.J. Shipley, D.R. Witte, et al.
Relation between blood glucose and coronary mortality over 33 years in the Whitehall Study.
Diabetes Care, 29 (2006), pp. 26-31
[31.]
M. Bartnik, L. Rydén, R. Ferrari, et al.
The prevalence of abnormal glucose regulation in patients with coronary artery disease across Europe The Euro Heart Survey on diabetes the heart.
Eur Heart J, 25 (2004), pp. 1880-1890
[32.]
S. Yamagishi.
Cardiovascular disease in recent onset diabetes mellitus.
J Cardiol, 57 (2011), pp. 257-262
[33.]
European, Diabetes Epidemiology Group.
Glucose tolerance and mortality: comparison of WHO and American Diabetes Association diagnostic criteria.
Lancet, 354 (1999), pp. 617-621
[34.]
M. Hanefeld, S. Fischer, U. Julius, et al.
Risk factors for myocardial infarction and death in newly detected NIDDM: the Diabetes Intervention Study, 11-year follow-up.
Diabetologia, 39 (1996), pp. 1577-1580
[35.]
UK Prospective Diabetes Study (UKPDS) Group.
Intensive blood-glucose control with sulphonylureas or insulin compared with conventional treatment and risk complications in patients with type 2 diabetes (UKPDS 33).
Lancet, 352 (1998), pp. 837-853
[36.]
R.R. Holman, S.K. Paul, M.A. Bethel, et al.
10-year follow-up of intensive glucose control in type 2 diabetes.
N Engl J Med, 359 (2008), pp. 1577-1580
[37.]
R.G. García, P. López-Jaramillo.
Cardiovascular prevention in high-risk patients with type 2 diabetes mellitus: when to start it?.
Eur Heart J, 29 (2008), pp. 2058-2059
[38.]
M. Brownlee.
Glycosylation products as toxic mediators of diabetic complications.
Annu Rev Med, 42 (1991), pp. 159-166
[39.]
S. Cellek, W. Qu, A.M. Schmidt, et al.
Synergistic action of advanced glycation end products and endogenous nitric oxide leads to neuronal apoptosis in vitro: a new insight into selective nitrergic neuropathy in diabetes.
Diabetologia, 47 (2004), pp. 331-339
[40.]
UK Prospective Diabetes Study (UKPDS) Effect of intensive blood-glucose control with metformin on complications in overweight patients with type 2 diabetes (UKPDS 34).) Group.
Lancet, 352 (1998), pp. 854-865
[41.]
R. Boussageon, I. Supper, T. Bejan-Angoulvant, et al.
Reappraisal of metformin efficacy in the treatment of type 2 diabetes: a meta-analysis of randomized controlled trials.
PLoS Med, 9 (2012),
[42.]
A. Wieczorek, P. Rys, I. Skrzekowska-Baran, et al.
The role of surrogate endpoints in the evaluation of efficacy and safety of therapeutic interventions in diabetes mellitus.
Rev Diabet Stud, 5 (2008), pp. 128-135
[43.]
M. Lehrke, N. Marx.
New antidiabetic therapies: innovative strategies for an old problem.
Curr Opin Lipidol, 23 (2012), pp. 1-7
[44.]
U.S. Department of Health and Human Services Food and Drug Administration Center for Drug Evaluation and Research (CDER) Guidance for Industry Diabetes Mellitus.
Evaluating Cardiovascular Risk in New Antidiabetic Therapies to Treat Type 2 Diabetes, (2008),
[45.]
H. Elrick, L. Stimmler, C.J. Hlad Jr., et al.
Plasma insulin response to oral and intravenous glucose administration.
J Clin Endocrinol Metab, 24 (1964), pp. 1076-1080
[46.]
M.A. Nauck, E. Homberger, E.G. Siegel, et al.
Incretin effects of increasing glucose loads in man calculated from venous insulin and C-peptide responses.
J Clin Endocrinol Metab, 63 (1986), pp. 492-498
[47.]
M.A. Nauck, F. Stockmann, R. Ebert, et al.
Reduced incretin effect in type 2 (noninsulin dependent) diabetes.
Diabetologia, 29 (1986), pp. 46-52
[49.]
J. Dupre, S. Ross, D. Watson, et al.
Stimulation of insulin secretion by gastric inhibitory polypeptide in man.
J Clin Endocrinol Metab, 37 (1973), pp. 826-828
[50.]
G.I. Bell, R.F. Santerre, G.T. Mullenbach.
Hamster preproglucagon contains the sequence of glucagon and two related peptides.
Nature, 302 (1983), pp. 716-718
[51.]
B. Ahren.
Gut peptides and type 2 diabetes mellitus treatment.
Curr Diab Rep, 3 (2003), pp. 365-372
[52.]
J.W. White, G.F. Saunders.
Structure of the human glicagon gene.
Nucleic Acids Res, 14 (1986), pp. 4719-4720
[53.]
A. Kervran, P. Blache, D. Bataille.
Distribution of oxyntomodulin and glucagon in the gastrointestinal tract and the plasma of the rat.
Endocrinology, 121 (1987), pp. 704-713
[54.]
S. Dhanvantari, N.G. Seidah, P.L. Brubaker.
Role of prohormone convertases in the tissue-specific processing of proglucagon.
Mol Endocrinol, 10 (1996), pp. 342-355
[55.]
C. Orskov, S.S. Poulsen.
Glucagon like peptide-I-(7-36)-amide receptors only in islets of Langerhans.
Autoradiographic survey of extracerebral tissues in rats. Diabetes, 40 (1991), pp. 1292-1300
[56.]
F. Gribble.
RD Lawrence Lecture 2008: targeting GLP-1 release as a potential strategy for the therapy of type 2 diabetes.
Diabet Med, 25 (2008), pp. 889-894
[57.]
M.A. Nauck, D. Wollschlager, J. Werner, J.J. Holst, et al.
Effects of subcutaneous glucagon-like peptide 1 (GLP-1 [7-36 amide]) in patients with NIDDM.
Diabetologia, 39 (1996), pp. 1546-1550
[58.]
H. Larsson, J.J. Holst, B. Ahren.
Glucagon-like peptide-1 reduces hepatic glucose production indirectly through insulin and glucagon in humans.
Acta Physiol Scand, 160 (1997), pp. 413-422
[59.]
A. Flint, A. Raben, A. Astrup, et al.
Glucagon-like peptide 1 promotes satiety and suppresses energy intake in humans.
J Clin Invest, 101 (1998), pp. 515-520
[60.]
C.F. Deacon.
Circulation and degradation of GIP and GLP-1.
Horm Metab Res, 36 (2004), pp. 761-765
[61.]
C.F. Deacon, A.H. Johnsen, J.J. Holst.
Degradation of glucagon-like peptide-1 by human plasma in vitro yields an N-terminally truncated peptide that is a major endogenous metabolite in vivo.
J Clin Endocrinol Metab, 80 (1995), pp. 952-957
[62.]
D. Elahi, J. Egan, R. Shannon, et al.
GLP-1 (9-36) Amide Cleavage Product of GLP-1 (7-36) amide, is a glucoregulatory peptide. Obesity.
, 16 (2008), pp. 1501-1510
[63.]
J.J. Meier, A. Gethmann, M.A. Nauck, et al.
The glucagon-like peptide-1 metabolite GLP-1-(9-36) amide reduces postprandial glycemia independently of gastric emptying and insulin secretion in humans.
Am J Physiol Endocrinol Metab, 290 (2006), pp. 1118-1120
[64.]
A.K. Bose, M.M. Mocanu, R.D. Carr, et al.
Glucagon-like peptide 1 can directly protect the heart against ischemia/reperfusion injury.
Diabetes, 54 (2005), pp. 146-151
[65.]
B. Thorens.
Expression cloning of the pancreatic beta cell receptor for the glucoincretin hormone glucagon-like peptide 1.
Proc Natl Acad Sci USA, 89 (1992), pp. 8641-8645
[66.]
Y. Wei, S. Mojsov.
Tissue-specific expression of the human receptor for glucagonlike peptide-I: brain, heart and pancreatic forms have the same deduced amino acid sequences.
FEBS Lett, 358 (1995), pp. 219-224
[67.]
B.D. Green, K.V. Hand, J.E. Dougan, et al.
GLP-1 and related peptides cause concentration dependent relaxation of rat aorta through a pathway involving KATP and cAMP.
Arch Biochem Biophys, 478 (2008), pp. 136-142
[68.]
S.M. Kanse, B. Kreymann, M.A. Ghatei, et al.
Identification and characterization of glucagon-like peptide-1 7-36 amide binding sites in the rat brain and lung.
FEBS Lett, 241 (1988), pp. 209-212
[69.]
L.O. Uttenthal, E. Blazquez.
Characterization of high-affinity receptors for truncated glucagon-like peptide-1 in rat gastric glands.
FEBS Lett, 262 (1990), pp. 139-141
[70.]
C. Syme, L. Zhang, A. Bisello.
Caveolin regulates cellular trafficking and function of the glucagon-like peptide 1 receptor.
Mol Endocrinol, 20 (2006), pp. 3400-3410
[71.]
I. Shimizu, M. Hirota, C. Ohboshi, et al.
Identification and localization of glucagonlike peptide-1 and its receptor in rat brain.
Endocrinology, 121 (1987), pp. 1076-1080
[72.]
M. Stoffel, R. Espinosa III, M.M. Le Beau, et al.
Human glucagon-like peptide-1 receptor gene Localization to chromosome band 6p21 by fluorescence in situ hybridization and linkage of a highly polymorphic simple tandem repeat DNA polymorphism to other markers on chromosome 6.
Diabetes, 42 (1993), pp. 1215-1220
[73.]
K. Ohnuma, M. Uchiyama, T. Yamochi, et al.
Caveolin-1 triggers T-cell activation via CD26 in association with CARMA1.
J Biol Chem, (2007), pp. 10117-11013
[74.]
P. MacDonald, W. El-Kholy, M. Riedel, et al.
The multiple actions of GLp-1 on the process of glucose-stimulated insulin secretion.
Diabetes, 51 (2002), pp. 434-442
[75.]
K. Ban, M. Noyan-Ashraf, J. Hoefer, et al.
Cardioprotective and vasodilatory actions of glucagon-like peptide 1 receptor are mediated through both glucagon-like peptide 1 receptor-dependent and –independent pathways.
Circulation, 117 (2008), pp. 2340-2350
[76.]
A. Alcántara, M. Moralesa, E. Delgado, et al.
Exendin-4 agonist and exendin(9-39) amide antagonist of the GLP-1(7-36)amide effects in liver and muscle.
Arch Biochem Biophys, 341 (1997), pp. 1-7
[77.]
T. Nystrom, M.K. Gutniak, Q. Zhang, et al.
Effects of glucagon-like peptide-1 on endothelial function in type 2 diabetes patients with stable coronary artery disease.
Am J Physiol Endocrinol Metab, 287 (2004), pp. E1209-E1215
[78.]
L.A. Nikolaidis, S. Mankad, C.C. Sokos, et al.
Effects of glucagon-like peptide-1 in patients with acute myocardial infarction and left ventricular dysfunction after successful reperfusion.
Circulation, 109 (2004), pp. 962-965
[79.]
G.G. Sokos, L.A. Nikolaidis, S.D. Mankad, et al.
Glucagon-like peptide-1 infusion improves left ventricular ejection fraction and functional status in patients with chronic heart failure.
J Car Fail, 12 (2006), pp. 694-699
[80.]
J.P. Courre‘ges, T. Vilsbøll, M. Zdravkovic, et al.
Beneficial effects of once-daily liraglutide, a human glucagon-like peptide-1 analogue, on cardiovascular risk biomarkers in patients with type 2 diabetes.
Diabetic Medicine, 2005 (2008), pp. 1129-1130
[81.]
R.M. Bergenstal, C. Wysham, L. MacConell, et al.
Efficacy and safety of exenatide once weekly versus sitagliptin or pioglitazone as an adjunct to metformin for treatment of type 2 diabetes (DURATION-2): a randomised trial.
Lancet, 376 (2010), pp. 9739
[82.]
S.M. Nicholl, E. Roztocil, M.G. Davies.
Plasminogen activator system and vascular disease.
Curr Vasc Pharmacol, 4 (2006), pp. 101-116
[83.]
J. Plutzky, A.J. Garber, A. Falahati, et al.
The once daily human GLP-1-analogue liraglutide significantly reduces markers of cardiovascular risk in type 2 diabetes: a metaanalysis of six clinical trials.
Eur Heart J, 30 (2009), pp. 917-919
[84.]
M.H. Davidson.
Cardiovascular effects of glucagonlike peptide-1 agonists.
Am J Cardiol, 108 (2011), pp. 33B-41B
[85.]
J. Jendle, M.A. Nauck, D.R. Matthews, et al.
Weight loss with liraglutide, a oncedaily human glucagon-like peptide- 1 analogue for type 2 diabetes treatment as monotherapy or added to metformin, is primarily as a result of a reduction in fat tissue.
Diabetes Obes Metab, 11 (2009), pp. 1163-1170
[86.]
M.C. Bunck, M. Diamant, B. Eliasson, et al.
Exenatide affects circulating cardiovascular risk biomarkers independently of changes in body composition.
Diabetes Care, 33 (2010), pp. 1734-1740
[87.]
D.D. Mafong, R.R. Henry.
The role of incretins in cardiovascular control.
Curr Hypertens Rep, 11 (2009), pp. 18-22
[88.]
A.H. Barnett, J. Burger, D. Johns, et al.
Tolerability and efficacy of exenatide and titrated insulin glargine in adult patients with type 2 diabetes previously uncontrolled with metformin or a sulfonylurea: a multinational, randomized, open-label, two-period, crossover noninferiority trial.
Clin Ther, 29 (2007), pp. 2333-2340
[89.]
G. Xu, D.A. Stoffers, J.F. Habener, et al.
Exendin-4 stimulates both beta-cell replication and neogenesis, resulting in increased beta-cell mass and improved glucose tolerance in diabetic rats.
Diabetes, 48 (1999), pp. 2270-2276
[90.]
M.S. Fineman, T.A. Bicsak, L.Z. Shen, et al.
Effect on glycemic control of exenatide (synthetic exendin-4) additive to existing metformin and/or sulfonylurea treatment in patients with type 2 diabetes.
Diabetes Care, 26 (2003), pp. 2370-2380
[91.]
S. Bregenholt, A. Moldrup, N. Blume, et al.
The long-acting glucagon-like peptide-1 analogue, liraglutide, inhibits beta-cell apoptosis in vitro.
Biochem Biophys Res Commun, 330 (2005), pp. 577-584
[92.]
FDA. Exenatide FDA. 2009. Disponible en: http://www.accessdata.fda.gov/drugsatfda_docs/label/2009/021773s9s11s18s22s25lbl.pdf. Fecha de consulta: 08/10/2012.
[93.]
A. Crespel, F. De Boisvilliers, L. Gros, et al.
Effects of glucagon and glucagonlike peptide-1-(7-36) amide on C cells from rat thyroid and medullary thyroid carcinoma CA-77 cell line.
Endocrinology, 137 (1996), pp. 3674-3680
[94.]
K. Augustyns, G. Bal, G. Thonus, et al.
The unique properties of dipeptidyl peptidase IV (DPP IV/CD26) and the therapeutic potential of DPP IV inhibitors.
Curr Med Chem, 6 (2009), pp. 311-327
[95.]
D.J. Drucker.
Dipeptidyl peptidase-4 inhibition and the treatment of type 2 diabetes Preclinical biology and mechanism of action.
Diabetes Care, 30 (2007), pp. 1335-1340
[96.]
B. Green, P. Flatt, C. Bailey.
Dipeptidyl peptidase IV (DPP IV) inhibitors: A newly emerging drug class for the treatment of type 2 diabetes.
Diabetes Vasc Dis Res, 3 (2006), pp. 159-165
[97.]
D. Dicker.
DPP-4 Inhibitors. Impact on glycemic control and cardiovascular risk factors.
Diabetes Care, 34 (2011), pp. S276-S278
[98.]
R.E. Amori, J. Lau, A.G. Pittas.
Efficacy and safety of incretin based therapy in type 2 diabetes; systematic review and meta-analysis.
JAMA, 298 (2007), pp. 194-206
[99.]
Instituto Nacional de Vigilancia de Medicamentos y Alimentos - INVIMA. ACTA Número. 22 DE 2011. Disponible en: http://web.invima.gov.co/portal/documents/portal/documents/root/SALAS%20ESPECIALIZADAS/2011_biologicos/ACTA%20No%2022%20DE%202011.pdf Fecha de consulta: 08/10/2012.
[100.]
S. Kalra, A.G. Unnikrishnan, N. Agrawal.
Linagliptin and newer DPP4 inhibitors: newer uses and newer indications.
Recent Pat Endocr Metab Immune Drug Discov, 5 (2011), pp. 202
[101.]
G.P. Fadini, A. Avogaro.
Cardiovascular effects of DPP-4 inhibition: Beyond GLP-1.
Vascul Pharmacol, 55 (2011), pp. 10-16
[102.]
G. Schernthaner, A.H. Barnett, A. Emser, et al.
Safety and tolerability of linagliptin: a pooled analysis of data from randomized controlled trials in 3572 patients with type 2 diabetes mellitus.
Diabetes Obes Metab, 14 (2012), pp. 470-478
[103.]
J. Doucet, A. Chacra, P. Maheux, et al.
Efficacy and safety of saxagliptin in older patients with type 2 diabetes mellitus.
Curr Med Res Opin, 27 (2011), pp. 863-869
[104.]
D. Williams-Herman, S.S. Engel, E. Round, et al.
Safety and tolerability of sitagliptin in clinical studies: a pooled analysis of data from 10.246 patients with type 2 diabetes.
BMC Endocr Disord, 10 (2011), pp. 17
[105.]
A. Schweizer, S. Dejager, J.E. Foley, et al.
Assessing the cardio-cerebrovascular safety of vildagliptin: meta-analysis of adjudicated events from a large phase III type 2 diabetes population.
Diabetes Obes Metab, 12 (2010), pp. 485-494
[106.]
M. Monami, I. Dicembrini, D. Martelli, et al.
Dipeptydil peptidase-4 inhibitors in type 2 diabetes: a meta-analysis of randomized clinical trials.
Nutr Metab Cardiovasc Dis, 20 (2010), pp. 224-235
[107.]
M. Monami, B. Ahren, I. Dicembrini, E. Mannucci.
Dipeptidyl peptidase-4 inhibitors and cardiovascular risk: a meta-analysis of randomized clinical trials.
Diabetes Obes Metab, 12 (2013), pp. 112-120
[108.]
J.H. Best, B.J. Hoogwerf, W.H. Herman, et al.
Risk of cardiovascular disease events in patients with type 2 diabetes prescribed the Glucagon-Like Peptide 1 (GLP-1) receptor agonist exenatide twice daily or other glucose-lowering therapies: a retrospective analysis of the lifelink database.
Diabetes Care, 34 (2011), pp. 90-95
[109.]
M. Monami, F. Cremasco, C. Lamanna, et al.
Glucagon like peptide-1 receptor agonists and cardiovascular events: a meta-analysis of randomized clnical trials.
Exp Diabetes Res, (2011),
Copyright © 2013. Sociedad Colombiana de Cardiología y Cirugía Cardiovascular