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MEDICIÓN Y MONITORIZACIÓN DE LA PRESIÓN ARTERIAL
Journal of Hypertension 41(12):1874-2071
Difundido en siicsalud: 16 dic 2024

EL SISTEMA RENINA-ANGIOTENSINA-ALDOSTERONA Y EL ESTADO PROTROMBOTICO

(especial para SIIC © Derechos reservados)
Las anomalías de la hemostasia desempeñarían un papel en las complicaciones trombóticas de la hipertensión. Estas alteraciones pueden inducirse por la activación del sistema renina-angiotensina-aldosterona (SRAA). El potencial efecto antitrombótico de los inhibidores del SRAA podría contribuir a la preservación de la función cardiovascular.
remkova9_11211.gif Autor:
Anna Remkova
Columnista Experta de SIIC

Institución:
Slovak Medical University in Bratislava


Artículos publicados por Anna Remkova
Recepción del artículo
26 de Agosto, 2010
Aprobación
1 de Septiembre, 2010
Primera edición
30 de Enero, 2012
Segunda edición, ampliada y corregida
7 de Junio, 2021

Resumen
La hipertensión arterial se asocia con un incremento en el riesgo de eventos trombóticos oclusivos, como consecuencia de un estado protrombótico presente en los pacientes hipertensos. Una serie de anomalías de la hemostasia parecen desempeñar un papel en las complicaciones trombóticas de la hipertensión. Sistemáticamente se ha informado acerca de disfunción endotelial, incremento de la activación plaquetaria, aumento de la actividad del sistema de la coagulación y reducción de la función del sistema fibrinolítico en los pacientes hipertensos. Estas alteraciones pueden inducirse por la activación del sistema renina-angiotensina-aldosterona (SRAA) y contribuir a un mayor riesgo y gravedad del daño de los órganos blanco. El tratamiento antihipertensivo con antagonistas del SRAA podría revertir estas alteraciones protrombóticas. Dado que los inhibidores de la enzima convertidora de angiotensina (IECA) y los antagonistas del receptor de angiotensina II (ARA-II) tienen dos mecanismos diferentes de interrupción del SRAA, cada terapia podría tener repercusiones distintas sobre el estado protrombótico de los pacientes hipertensos. En algunos estudios se demostró un efecto beneficioso sobre el estado protrombótico de los IECA en particular y también de algunos ARA-II de forma parcial. El potencial efecto antitrombótico de los inhibidores del SRAA podría contribuir a la preservación de la función cardiovascular. Los datos disponibles pueden ofrecer una explicación adicional de la eficacia de los inhibidores del SRAA en la prevención de los eventos cardiovasculares en pacientes con enfermedad vascular aterosclerótica.

Palabras clave
hipertensión, endotelio, hemostasia, renina, angiotensina


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Abstract
Arterial hypertension is associated with increased risk of occlusive thrombotic events, reflecting a prothrombotic state that is present in hypertensive patients. A number of haemostatic abnormalities appear to play a role in the thrombotic complications of hypertension. Endothelial dysfunction, increased platelet activation, increased activity of the coagulation system, and the decreased function of the fibrinolytic system has been consistently reported in hypertensive patients. These abnormalities can be induced by the activated renin-angiotensin-aldosterone system (RAAS), and may contribute to the increased risk and severity of target organ damage. Antihypertensive treatment by RAAS inhibiting agents could result in a reversal of prothrombotic abnormalities. Since angiotensin converting enzyme (ACE) inhibitors and angiotensin II receptor blockers (ARBs) have two distinct mechanisms of RAAS interruption, each therapy might have different impact on the prothrombotic state in hypertensive patients. Some studies demonstrate a beneficial effect, mainly of ACE inhibitors and also partly of some ARBs on the prothrombotic state. The potentially antithrombotic effect of the RAAS inhibiting agents may in turn support the preservation of cardiovascular function. Available data may offer an additional explanation for the efficacy of the RAAS inhibiting agents in the prevention of cardiovascular events in patients with atherosclerotic vascular disease.

Key words
hypertension, endothelium, haemostasis, renin, angiotensin


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Especialidades
Principal: Cardiología, Hematología
Relacionadas: Bioquímica, Cuidados Intensivos, Diagnóstico por Laboratorio, Educación Médica, Geriatría, Medicina Interna, Nefrología y Medio Interno



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Enviar correspondencia a:
Anna Remkova, Slovak Medical University Department of Internal Medicine, 833 03, Limbova 12, Bratislava, Eslovaquia
Patrocinio y reconocimiento:
El trabajo fue financiado por una beca del Ministerio de Educación de Eslovaquia (VEGA grant No 1/0084/10).
Bibliografía del artículo
1. Nadar S, Lip GY. The prothrombotic state in hypertension and the effects of antihypertensive treatment. Curr Pharm Des 9:1715 32, 2003.
2. Varughese GI, Lip GY. Is hypertension a prothrombotic state? Curr Hypertens Rep 7:168-73, 2005.
3. Kakar P, Lip GY. Hypertension: endothelial dysfunction, the prothrombotic state and antithrombotic therapy. Expert Rev Cardiovasc Ther 5:441-50, 2007.
4. Sechi LA, Zingaro L, Catena C, Casaccio D, De Marchi S. Relationship of fibrinogen levels and hemostatic abnormalities with organ damage in hypertension. Hypertension 36:978-85, 2000.
5. Nadar SK, Blann AD, Kamath S, Beevers DG, Lip GY. Platelet indexes in relation to target organ damage in high-risk hypertensive patients: a substudy of the Anglo-Scandinavian Cardiac Outcomes Trial (ASCOT). J Am Coll Cardiol 44:415-22, 2004.
6. Spencer CGC, Martin SC, Felmden DC, Blann AD, Beevers GD, Lip GYH. Relationship of homocysteine to markers of platelet and endothelial activation in "high risk" hypertensives: a substudy of the Anglo-Scandinavian Cardiac Outcomes Trial. Internat J Cardiol 94:293-300, 2004.
7. Sechi LA, Novello M, Volussi GL et al. Relationship of plasma renin with a prothrombotic state in hypertension: relevance for organ damage. Am J Hypertens 21:1347-53, 2008.
8. Tay KH, Lip GYH: What "drives" the link between the renin-angiotensin-aldosterone system and the prothrombotic state in hypertension? Am J Hypertens 22:1278-79, 2008.
9. Lip GYH, Blann AD, Edmunds E, Beevers DG. Baseline abnormalities of endothelial function and thrombogenesis in relation to prognosis in essential hypertension. Blood Coag Fibrinolys 13:35-41, 2002.
10. Varughese GI, Patel JV, Tomson J, Blann AD, Hughes EA, Lip GY. Prognostic value of plasma soluble P-selectin and von Willebrand factor as indices of platelet activation and endothelial damage/dysfunction in high-risk patients with hypertension: a sub-study of the Anglo-Scandinavian Cardiac Outcomes Trial. J Intern Med 261:384-91, 2007.
11. Gkaliagkousi E, Passacquale G, Douma S, Zamboulis C, Ferro A. Platelet activation in essential hypertension: implications for antiplatelet treatment. Am J Hypertens 23:229-36, 2010.
12. Verhamme P, Hoylaerts MF. Hemostasis and inflammation: two of a kind? Thrombosis J 7:15, 2009.
13. Remkova A, Kratochvilova H. Effect of the new centrally acting antihypertensive agent rilmenidine on endothelial and platelet function in essential hypertension. J Hum Hypertens 16:549-55, 2002.
14. Remková A, Kratochvíová H, Kurina J. Impact of the therapy by renin-angiotensin system targeting antihypertensive agents perindopril versus telmisartan on prothrombotic state in essential hypertension. J Hum Hypertens 22:338-45, 2008.
15. Blann AD, Naqvi T, Waite M, McCollum CN. Von Willebrand factor and endothelial damage in essential hypertension. J Hum Hypertens 7:107-11, 1993.
16. Lee KW, Blann AD, Lip GYH. High pulse pressure and nondipping circadian blood pressure in patients with coronary artery disease: Relationship to thrombogenesis and endothelial damage/dysfunction. Am J Hypertens 18:104-15, 2005.
17. Vischer UM. Von Willebrand factor, endothelial dysfunction and cardiovascular disease. J Thromb Haemost 4:1186-93, 2006.
18. Ceconi C, Fox KM, Remme WJ et al. on behalf of the EUROPA and the PERTINENT Investigators. ACE inhibition with perindopril and endothelial dysfunction. Results of a substudy of the EUROPA study: PERTINENT. Cardiovasc Res 73:237-46, 2007.
19. Okrucká A, Pechá J, Kratochvíová H. Effects of the angiotensin-converting enzyme (ACE) inhibitor perindopril on endothelial and platelet functions in essential hypertension. Platelets 9:63-7, 1998.
20. Remkova A, Kovacova E, Prikazska M, Kratochvilova H. Thrombomodulin as a marker of endothelium damage in some clinical conditions. Eur J Int Med 11:79-84, 2000.
21. Blann AD, Nadar SK, Lip GYH. The adhesion molecule P-selectin and cardiovascular disease. Eur Heart J 24:2166-79, 2003.
22. Riondino S, Pignatell P, Pulcinelli FM et al. Platelet hyperactivity in hypertensive older patients is controlled by lowering blood pressure. J Am Geriatr Soc 47:943-47, 1999.
23. Nadar SK, Blann AD, Lip GY. Platelet morphology and plasma indices of platelet activation in essential hypertension: effects of amlodipine-based antihypertensive therapy. Ann Med 36:552-7, 2004.
24. Nadar SK, Blann AD, Lip GY. Platelet morphology, soluble P selectin and platelet P-selectin in acute ischaemic stroke. The West Birmingham Stroke Project. Thromb Haemost 92:1342-8, 2004.
25. Blann AD, Lanza F, Galajda P et al. Increased platelet glycoprotein V levels in patients with coronary and peripheral atherosclerosis - the influence of aspirin and cigarette smoking. Thromb Haemost 86:777-83, 2001.
26. Wolff V, Aleil B, Giroud M et al. Soluble platelet glycoprotein V is a marker of thrombosis in patients with ischemic stroke. Stroke 36:e17-e19, 2005.
27. Jastrzebskal M, Widecka K, Naruszewicz M et al. Effects of perindopril treatment on hemostatic function in patients with essential hypertension in relation to angiotensin converting enzyme (ACE) and plasminogen activator inhibitor-1 (PAI-1) gene polymorphisms. Nutr Metab Cardiovasc Dis 14:259-69, 2004.
28. Saposnik B, Reny JL, Gaussem P, Emmerich J, Aiach M, Gandrille S. A haplotype of the EPCR gene is associated with increased plasma levels of sEPCR and is candidate risk factor for thrombosis. Blood 103:1311-18, 2004.
29. Tomiyama H, Kimura Y, Mitsuhashi H et al. Relationship between endothelial function and fibrinolysis in early hypertension. Hypertension 31:321-7, 1998.
30. Aso Y, Wakabayashi S, Yamamoto R, Matsutomo R, Takebayashi K, Inukai T. Metabolic syndrome accompanied by hypercholesterolemia is strongly associated with proinflammatory state and impairment of fibrinolysis in patients with type 2 diabetes. Diabetes Care 28:2211-6, 2005.
31. Poli KA, Tofler GH, Larson MG et al. Association of blood pressure with fibrinolytic potential in the Framingham Offspring Study. Circulation 101:264-9, 2000.
32. Sakata K, Pawlak R, Urano T, Takada A. Effects of a long-term pharmacological interruption of the renin-angiotensin system on the fibrinolytic system in essential hypertension. Pathophysiol Haemost Thromb 32:67-75, 2002.
33. Koh KK, Chung WJ, Ahn JY et al. Angiotensin II type receptor blockers reduce tissue factor activity and plasminogen activator inhibitor type-1 antigen in hypertensive patients: a randomized, double - blind, placebo controlled study. Atherosclerosis 177:155-60, 2004.
34. Dielis AWJH, Smid M, Spronk HMH et al. Changes in fibrinolytic activity after angiotensin II receptor blockade in therapy-resistant hypertensive patients. J Thromb Haemost 5:1509-15, 2007.
35. Ruiz Ortega M, Esteban V, Egido J. The regulation of the inflammatory response through nuclear factor-kappab pathway by angiotensin IV extends the role of the renin angiotensin system in cardiovascular diseases. Trends Cardiovasc Med 17:19-25, 2007.
36. Vyssoulis G, Karpanou E, Kyvelou SM et al. Associations between plasma homocysteine levels, aortic stiffness and wave reflection in patients with arterial hypertension, isolated office hypertension and normotensive controls. J Hum Hypertens 24:183-9, 2010.
37. Sawathiparnich P, Murphey LJ, Kumar S, Vaughan DE, Brown NJ. Effect of combined AT1 receptor and aldosterone receptor and aldosterone receptor antagonism on plasminogen activator inhibitor-1. J Clin Endocrinol Metab 88:3867-73, 2003.
38. Brown NJ, Kim KS, Chen YQ et al. Synergistic effect of adrenal steroids and angiotensin II on plasminogen activator inhibitor 1 production. J Clin Endocrinol Metab 85:336 44, 2000.
39. Sawathiparnich P, Kumar S, Vaughan DE, Brown NJ. Spironolactone abolishes the relationship between aldosterone and plasminogen activator inhibitor 1 in humans. J Clin Endocrinol Metab 87:448 52, 2002.
40. Mancia G, Giannattasio C, Seravalle G, Quarti-Serano F, Grassi G. Protective effects of renin-angiotensin blockade beyond blood pressure control. J Jum Hypertens 23:570-7, 2009.
41. Brown NJ, Agirbasli MA, Williams GH, Litchfield WR, Vaughan DE. Effect of activation and inhibition of the renin angiotensin system on plasma PAI 1. Hypertension 32:965 71, 1998.
42. Brown NJ, Agirbasli MA, Vaughan DE. Comparative effect of angiotensin converting enzyme inhibition and angiotensin II type 1 receptor antagonism on plasma fibrinolytic balance in humans. Hypertension 34:285 90, 1999.
43. Brown NJ, Kumar S, Painter CA, Vaughan DE. ACE inhibition versus angiotensin type 1 receptor antagonism: differential effects on PAI 1 over time. Hypertension 40:859 65, 2002.
44. Ma J, Albornoz F, Yu C, Byrne DW, Vaughan DE, Brown NJ. Differing effects of mineralocorticoid receptor dependent and independent potassium sparing diuretics on fibrinolytic balance. Hypertension 46:313 20, 2005.
45. Ghiadoni L, Magagna A, Versari D et al. Different effect of antihypertensive drugs on conduit artery endothelial function. Hypertension 41:1281-6, 2003.
46. Taddei S, Virdis A, Ghiadoni L, Sudano I, Salvetti A. Effects of antihypertensive drugs on endothelial dysfunction - Clinical implications. Drugs 62:265-84, 2002.
47. Matsumoto T, Minai K, Horie H et al. Angiotensin-converting enzyme inhibition but not angiotensin II type 1 receptor antagonism augments coronary release of tissue plasminogen activator in hypertensive patients. J Am Coll Cardiol 41:1373-9, 2003.
48. Ferrari R, Arbustini E, Blann A et al. PERTINENT. Perindopril - Thrombosis, Inflammation, Endothelial dysfunction and Neurohormonal activation Trial: A sub-study of the EUROPA study. Cardiovasc Drug Ther 17:83-91, 2003.
49. Fox KM and the EUROPA Investigators. Efficacy of perindopril in reduction of cardiovascular events among patients with stable coronary artery disease: randomised, double-blind, placebo-controlled, multicentre trial (the EUROPA study). Lancet 362:782-8, 2003.
50. Poduri A, Kaur J, Thakur JS, Kumari S, Jain S, Khullar M. Effect of ACE inhibitors and ? blockers on homocysteine levels in essential hypertension. J Hum Hypertens 22:289 94, 2008.
51. Kishi Y, Ohta S, Kasuya N, Sakita S, Ashikaga T, Isobe M. Perindopril augments ecto-ATP diphosphohydrolase activity and enhances endothelial anti-platelet function in human umbilical vein endothelial cells. J Hypertens 21:1347-53, 2003.
52. Montón M, Jiménez A, Núñez A et al. Comparative effects of angiotensin II AT-1-type receptor antagonists in vitro on human platelet activation. J Cardiovasc Pharmacol 35:906-13, 2000.
53. Makris TK, Stavroulakis GA, Krespi PG et al. Fibrinolytic/ hemostatic variables in arterial hypertension: response to treatment with irbesartan or atenolol. Am J Hypertens 13:783-8, 2000.
54. Nagel JM, Tietz AB, Guke B, Parhofer KG. The effect of telmisartan on glucose and lipid metabolism in nondiabetic, insulin-resistant subjects. Metabolism 55:1149-54, 2006.
55. Fogari R, Zoppi A, Lazzari P et al. ACE inhibition but not angiotensin II antagonism reduces plasma fibrinogen and insulin resistance in overweight hypertensive patients. J Cardiovasc Pharmacol 32:616-20, 1998.
56. Li-Saw-Hee FL, Beevers DG, Lip GYH. Effect of antihypertensive therapy using enalapril or losartan on haemostatic markers in essential hypertension: a pilot prospective randomised double-blind parallel group trial. Internat J Cardiol 78:241-6, 2001.
57. Remková A, Kratochvíová H. Effect of the angiotensin-converting enzyme inhibitor perindopril on haemostasis in essential hypertension. Blood Coag Fibrinolys 7:641-4, 2000.
58. Fogari R, Zoppi A, Preti P, Fogari E, Malamani G, Mugellini A. Differential effects of ACE-inhibition and angiotensin II antagonism on fibrinolysis and insulin sensitivity in hypertensive postmenopausal women. Am J Hypertens 14:921-6, 2001.
59. Fogari R, Zoppi A, Malamani G et al. Effects of four angiotensin II-receptor antagonists on fibrinolysis in postmenopausal women in hypertension. Curr Ther Res Clin Exp 62:68-78, 2001.
60. Erlinger TP, Conlin PR, Macko RF et al. The impact of angiotensin II receptor blockade and the DASH diet on markers of endogenous fibrinolysis. J Hum Hypertens 16:391-7, 2002.
61. Erdem Y, Usalan C, Haznedaroglu IC et al. Effects of angiotensin-converting enzyme and angiotensin II receptor inhibition on impaired fibrinolysis in systemic hypertension. Am J Hypertens 12:1071-6, 1999.
62. Fogari R, Mugellini A, Zoppi A et al. Losartan and perindopril effects on plasma plasminogen activator inhibitor-1 and fibrinogen in hypertensive type 2 diabetic patients. Am J Hypertens 15:316-20, 2002.
63. Fogari R, Preti P, Lazzari P et al. Effect of benazepril amlodipine combination on fibrinolysis in hypertensive diabetic patients. Eur J Clin Pharmacol 59:271-5, 2003.
64. Fogari R, Zoppi A. Antihypertensive drugs and fibrinolytic function. Am J Hypertens 19:129-39, 2006.
65. Shao J, Nangaku M, Inagi R et al. Receptor-independent intracellular radical scavenging activity of an angiotensin II receptor blocker. J Hypertens 25:1643-9, 2007.
66. Bauersachs J, Heck M, Fraccarollo D et al. Addition of spironolactone to angiotensin-converting enzyme inhibition in heart failure improves endothelial vasomotor dysfunction: role of vascular superoxide anion formation and endothelial nitric oxide synthase suppression. J Am Coll Cardiol 39:351-8, 2002.
67. Schäfer A, Fraccarollo D, Hildemann S et al. Inhibition of platelet activation in congestive heart failure by aldosterone receptor antagonism and ACE inhibition. Thromb Haemost 89:1024-30, 2003.
68. Serebruany VL, Malinin A, Barsness G, Vahabi J, Atard D. Effects of aliskiren, a renin inhibitor, on biomarkers of platelet activity, coagulation and fibrinolysis in subjects with multiple risk factors for vascular disease. J Hum Hypertens 22:303-10, 2008.

 
 
 
 
 
 
 
 
 
 
 
 
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