CEREBRO-VISCERAL MALFUNCTIONS IN ACUTE STROKE PATIENTS WITH METABOLIC SYNDROME

Authors

  • Наталия Юрьевна Басанцова St. Petersburg State University, 7–9, Universitetskaya nab., St. Petersburg, 199034, Russian Federation
  • Александр Николаевич Шишкин St. Petersburg State University, 7–9, Universitetskaya nab., St. Petersburg, 199034, Russian Federation
  • Людмила Михайловна Тибекина St. Petersburg State University, 7–9, Universitetskaya nab., St. Petersburg, 199034, Russian Federation
  • Антон Олегович Иванов St. Petersburg State University, 7–9, Universitetskaya nab., St. Petersburg, 199034, Russian Federation

DOI:

https://doi.org/10.21638/11701/spbu11.2017.309

Abstract

This review examines clinical and pathophysiological aspects of internal organ diseases; in particular, poststroke heart and renal disturbances are discussed. Progression of cerebral-cardiac syndrome can be described as the emergence of ischemic and arrhythmic changes because of autonomic imbalance and catecholamine cytotoxicity in previously intact myocardium. Change in renal functional state can be explained with activation of proinflammatory cytokines, the sympathetic nervous system, and also
hypothalamic-pituitary disturbances through the interaction of the nervous, endocrine, and autacoid system. The article argues for the principal role of microangiopathy as a systemic process, taking place in metabolic syndrome and resulting in polyorganic insufficiency with major dysfunction of the brain, heart and kidney. Diagnostics of microangiopathy in one of these organs can predict stroke and other vascular diseases. Refs 44. Table 1.

Keywords:

Stroke, cerebral-cardiac syndrome, renal insufficiency, microangiopathy, metabolic syndrome

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References

Литература

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Trachanas K., Sideris S., Aggeli C. Diabetic cardiomyopathy: From pathophysiology to treatment //Hellenic J. Cardiol. 2014. Vol. 55. P. 411–421.


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Agre P., King L. S, Yasui M., Guggino W. B., Ottersen O. P., Fujiyoshi Y., Engel A., Nielsen S.

Aquaporins water channels — from atomic structure to clinical medicine. J. Physiol., 2002, vol. 542,pp. 3–6.

Nedvetsky P. I., Tamma G., Beulshausen S., Valenti G., Rosenthal W., Klussmann E. Regulation of aquaporin-2 trafficking. Handb. Exp. Pharmacol., 2009, vol. 190, pp. 133–157.

Baranchuk A., Nault M., Morillo C. The central nervous system and sudden cardiac death: What should we know? Cardiology J., 2009, vol. 16, no. 2, pp. 105–112.

Critchley H., Taggart P., Sutton P. M., Holdright D. R., Batchvarov V., Hnatkova K., Malik M.,Dolan R. J. Mental stress and sudden cardiac death: asymmetric midbrain activity as a linking mechanism.Brain, 2005, vol. 128, pp. 75–85.

De Morree H., Szabó B., Rutten G., Kop W. Central nervous system involvement in the autonomic responses to psychological distress. Neth. Heart J., 2012, vol. 21, no. 2, pp. 64–69.

Gregory T., Smith M. Cardiovascular complications of brain injury. Continuing Education in Anaesthesia, Critical Care & Pain, 2011, vol. 45, pp. 245–267.

Algra A., Gates P., Fox J., Hachinski V., Barnett H. Side of brain infarction and long-term risk of sudden death in patients with symptomatic carotid disease. Stroke, 2003, vol. 34, pp. 287–2875.

Chinda J., Nakagawa N., Kabara M., Matsuki M., Endo H., Saito T., Sawada J., Katayama T., Sato N.,Hasebe N. Impact of decreased estimated glomerular filtration rate on Japanese acute stroke and its subtype.Intern. Med., 2012, vol. 51, pp. 1661–1666.

Mlodawska E., Tomaszuk-Kazberuk A., Lopatowska P., Bachorzewska-Gajewska H., Malyszko J.,Dobrzycki S., Jerzy Musial W. Is there association between changes in eGFR Value and the risk of permanent type of atrial fibrillation? — Analysis of valvular and non-valvular atrial fibrillation population. Kidney Blood Press Res., 2014, vol. 39, pp. 600–608.

Ito S. Cardiorenal syndrome. An evolutionary point of view. Hypertension, 2012, vol. 60, pp. 589–595.

Makin S. D. J., Cook F. A. B., Dennis M. S., Wardlaw J. M. Cerebral small vessel disease and renal function: Systematic review and meta-analysis. Cerebrovasc Dis., 2015, vol. 39, pp. 39–52.

Xiao L., Lan W., Sun W., Dai Q., Xiong Y., Li l. Zhou Y., Zheng p., Fan W. Ma N., Guo Z., Chen X.,Xie X., Xu L., Zhu W., Xu G., Liu X. Chronic kidney disease in patients with lacunar stroke association with enlarged perivascular spaces and total magnetic resonance imaging burden of cerebral small vessel disease. Stroke, 2015, vol. 46, pp. 2081–2086.

Bugnicourt J.-M., Godefroy O., Chillon J.-M., Choukroun G., Massy Z. A. Cognitive disorders and

dementia in CKD: The neglected kidney-brain axis. J. Am. Soc. Nephrol., 2013, vol. 24, pp. 353–363.

Lau W. L., Huisa B. N., Fisher M. The Cerebrovascular-Chronic Kidney Disease Connection: Perspectives and Mechanisms. Transl. Stroke Res., 2017, vol. 8, pp. 67–76.

Mogi M., Horiuchi M. Clinical Interaction between Brain and Kidney in Small Vessel Disease. Cardiology Research and Practice, 2011: 306189, pp. 1–5.

Corson M. A., James N. L., Latta S. E., Nerem R. M., Berk B. C., Harrison D. G. Phosphorylation of

endotelial nitric oxide synthase in response to fluid shear stress. Cir. Res., 1996, vol. 79, pp. 984–991.

Gallis B., Corthals G. L., Goodlett D. R., Ueba H., Kim F., Presnell S. P., Figeys D., Harrison D. G.,

Berk B. C., Aebersold R., Corson M. A. Identification of flow-dependent endotelial nitric-oxide synthase phosphorylation sites by mass spectrometry and regulation of phosphorylation and nitric oxide production by phosphatidylinositol 3-kinase inhibitor LY294002. J. Biol. Chem., 1999, vol. 274, pp. 30101–30108.

Pluta R. Delayed cerebral vasospasm and nitric oxide: review, new hypothesis and proposed treatment Pharmacol. Ther., 2005, vol. 105, pp. 23–56.

Hudetz A. G., Wood J. D., Kampine J. P. Nitric oxide syntase inhibitor augments post-ischemic leucocyte adhesion in the cerebral microcirulation in vivo. Neurol. Res., 1999, vol. 21, pp. 378–384.

Lavara G., Pueyo M. E., Philippe M., Mandet C., Savoie F., Henrion D., Michel J. B. Chronic blokade of NO syntase activity induces: A proinflammatory phenotype in the arterial wall: prevention by angiotensin II antagonism. Arterioscler. Thromb. Vasc. Biol., 1998, vol. 18, pp. 1408–1416.

Galea E., Issertial O., Seylas J., Pelligrino D. A., Pinard E. Chronic nitric oxide synthase inhibition

does not induce cerebrovascular inflammation. Soc. Neurosci. Abstr., 2000, vol. 26, p. 644.

Boudina S., Abel E. Diabetic cardiomyopathy, causes and effects. Rev. Endocr. Metab. Disord., 2010,vol. 11, no. 1, pp. 31–39.

Trachanas K., Sideris S., Aggeli C. Diabetic Cardiomyopathy: From Pathophysiology to Treatment.Hellenic J. Cardiol., 2014, vol. 55, pp. 411–421.

Published

2017-09-01

How to Cite

Басанцова, Н. Ю., Шишкин, А. Н., Тибекина, Л. М., & Иванов, А. О. (2017). CEREBRO-VISCERAL MALFUNCTIONS IN ACUTE STROKE PATIENTS WITH METABOLIC SYNDROME. Vestnik of Saint Petersburg University. Medicine, 12(3), 289–301. https://doi.org/10.21638/11701/spbu11.2017.309

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Section

Neurology. Neurosurgery. Psychiatry

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