Dynamic cerebral autoregulation is impaired during submaximal isometric handgrip in patients with heart failure

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Citações na Scopus
19
Tipo de produção
article
Data de publicação
2018
Título da Revista
ISSN da Revista
Título do Volume
Editora
AMER PHYSIOLOGICAL SOC
Citação
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY, v.315, n.2, p.H254-H261, 2018
Projetos de Pesquisa
Unidades Organizacionais
Fascículo
Resumo
The incidence of neurological complications, including stroke and cognitive dysfunction, is elevated in patients with heart failure (HF) with reduced ejection fraction. We hypothesized that the cerebrovascular response to isometric handgrip (iHG) is altered in patients with HF. Adults with HF and healthy volunteers were included. Cerebral blood velocity (CBV; transcranial Doppler, middle cerebral artery) and arterial blood pressure (BP; Finometer) were continuously recorded supine for 6 min, corresponding to 1 min of baseline and 3 min of iHG exercise, at 30% maximum voluntary contraction, followed by 2 min of recovery. The resistance-area product was calculated from the instantaneous BP-CBV relationship. Dynamic cerebral autoregulation (dCA) was assessed with the time-varying autoregulation index estimated from the CBV step response derived by an autoregressive moving-average time-domain model. Forty patients with HF and 23 BP-matched healthy volunteers were studied. Median left ventricular ejection fraction was 38.5% (inter-quartile range: 0.075%) in the HF group. Compared with control subjects. patients with HF exhibited lower time-varying autoregulation index during iHG, indicating impaired dCA (P < 0.025). During iHG, there were steep rises in CBV. BP, and heart rate in control subjects but with different temporal patterns in HF, which, together with the temporal evolution of resistance-area product, confirmed the disturbance in dCA in HF. Patients with HF were more likely to have impaired dCA during iHG compared with age-matched control subjects. Our results also suggest an impairment of myogenic, neurogenic. and metabolic control mechanisms in HF. The relationship between impaired dCA and neurological complications in patients with HF during exercise deserves further investigation. NEW & NOTEWORTHY Our findings provide the first direct evidence that cerebral blood flow regulatory mechanisms can be affected in patients with heart failure during isometric handgrip exercise. As a consequence, eventual blood pressure modulations are buffered less efficiently and metabolic demands may not be met during common daily activities. These deficits in cerebral autoregulation are compounded by limitations of the systemic response to isometric exercise, suggesting that patients with heart failure may be at greater risk for cerebral events during exercise.
Palavras-chave
cerebral blood flow, cerebral hemodynamics, exercise, transcranial Doppler ultrasound
Referências
  1. AASLID R, 1989, STROKE, V20, P45, DOI 10.1161/01.STR.20.1.45
  2. Bennett JA, 2002, HEART LUNG, V31, P262, DOI 10.1067/mhl.2002.124554
  3. Brassard P, 2016, CAN J CARDIOL, V32, P475, DOI 10.1016/j.cjca.2015.12.021
  4. Brys M, 2003, AM J PHYSIOL-HEART C, V285, pH1048, DOI 10.1152/ajpheart.00062.2003
  5. Caldas JR, 2017, AM J PHYSIOL-REG I, V312, pR108, DOI 10.1152/ajpregu.00361.2016
  6. Deegan BM, 2010, J APPL PHYSIOL, V109, P1424, DOI 10.1152/japplphysiol.01262.2009
  7. Deegan BM, 2011, STROKE, V42, P1988, DOI 10.1161/STROKEAHA.110.605618
  8. Dieberg G, 2015, J APPL PHYSIOL, V119, P726, DOI 10.1152/japplphysiol.00904.2014
  9. Dineen NE, 2010, J APPL PHYSIOL, V108, P604, DOI 10.1152/japplphysiol.01157.2009
  10. Erkelens CD, 2017, EUR J HEART FAIL, V19, P261, DOI 10.1002/ejhf.660
  11. Fadel PJ, 2003, J PHYSIOL-LONDON, V548, P983, DOI 10.1113/jphysiol.2003.039347
  12. Fisher JP, 2008, J APPL PHYSIOL, V105, P266, DOI 10.1152/japplphysiol.00118.2008
  13. Fontana J, 2015, NEUROCRIT CARE, V23, P355, DOI 10.1007/s12028-014-0104-7
  14. Fraser KS, 2015, JACC-HEART FAIL, V3, P168, DOI 10.1016/j.jchf.2014.07.017
  15. Gruhn N, 2001, STROKE, V32, P2530, DOI 10.1161/hs1101.098360
  16. Haeusler KG, 2011, STROKE, V42, P2977, DOI 10.1161/STROKEAHA.111.628479
  17. Havakuk O, 2017, J AM COLL CARDIOL, V69, P1609, DOI 10.1016/j.jacc.2017.01.022
  18. Haykowsky MJ, 2007, J AM COLL CARDIOL, V49, P2329, DOI 10.1016/j.jacc.2007.02.055
  19. Hellstrom G, 1996, J APPL PHYSIOL, V81, P413
  20. Katsogridakis E, 2011, ULTRASOUND MED BIOL, V37, P530, DOI 10.1016/j.ultrasmedbio.2010.12.015
  21. Kim MS, 2015, CIRC J, V79, P942, DOI 10.1253/circj.CJ-15-0360
  22. Kim YS, 2007, AM J PHYSIOL-HEART C, V293, pH467, DOI 10.1152/ajpheart.00045-2007
  23. Krzeminski K, 2012, EUR J APPL PHYSIOL, V112, P1315, DOI 10.1007/s00421-011-2069-y
  24. Low DA, 2009, AM J PHYSIOL-REG I, V296, pR1598, DOI 10.1152/ajpregu.90900.2008
  25. Mandic S, 2009, CLIN REHABIL, V23, P207, DOI 10.1177/0269215508095362
  26. Massaro AR, 2006, NEUROLOGY, V66, P124, DOI 10.1212/01.wnl.0000191397.57244.91
  27. Meng LZ, 2015, ANESTHESIOLOGY, V123, P1198, DOI 10.1097/ALN.0000000000000872
  28. Negrao CE, 2001, AM J PHYSIOL-HEART C, V280, pH1286
  29. Nogueira RC, 2013, PLOS ONE, V8, DOI 10.1371/journal.pone.0070821
  30. Ogoh S, 2005, AM J PHYSIOL-HEART C, V288, pH1461, DOI 10.1152/ajpheart.00948.2004
  31. Ogoh S, 2010, J APPL PHYSIOL, V108, P1701, DOI 10.1152/japplphysiol.01031.2009
  32. Ogoh S, 2009, EXERC SPORT SCI REV, V37, P123, DOI 10.1097/JES.0b013e3181aa64d7
  33. Panerai RB, 2010, J APPL PHYSIOL, V109, P1860, DOI 10.1152/japplphysiol.00857.2010
  34. Panerai RB, 2003, MED ENG PHYS, V25, P621, DOI 10.1016/S1350-4533(03)00027-4
  35. Panerai RB, 2005, J APPL PHYSIOL, V99, P2352, DOI 10.1152/japplphysiol.00631.2005
  36. Panerai RB, 1998, PHYSIOL MEAS, V19, P305, DOI 10.1088/0967-3334/19/3/001
  37. Panerai RB, 1998, STROKE, V29, P2341, DOI 10.1161/01.STR.29.11.2341
  38. Panerai RB, 2008, CARDIOVASC ENG, V8, P42, DOI 10.1007/s10558-007-9044-6
  39. Panerai RB, 2012, AM J PHYSIOL-REG I, V303, pR395, DOI 10.1152/ajpregu.00161.2012
  40. Panerai RB, 2009, CLIN AUTON RES, V19, P197, DOI 10.1007/s10286-009-0011-8
  41. Patel N, 2016, PHYSIOL MEAS, V37, P1485, DOI 10.1088/0967-3334/37/9/1485
  42. PAULSON OB, 1986, EUR J CLIN INVEST, V16, P124, DOI 10.1111/j.1365-2362.1986.tb01319.x
  43. Poole DC, 2018, J APPL PHYSIOL, V124, P208, DOI 10.1152/japplphysiol.00747.2017
  44. Prodel E, 2016, AM J PHYSIOL-HEART C, V310, pH1201, DOI 10.1152/ajpheart.00894.2015
  45. Ravits JM, 1997, MUSCLE NERVE, V20, P919, DOI 10.1002/(SICI)1097-4598(199708)20:8<919::AID-MUS1>3.0.CO;2-9
  46. Salinet ASM, 2015, J APPL PHYSIOL, V118, P170, DOI 10.1152/japplphysiol.00620.2014
  47. Salinet ASM, 2012, J NEUROSCI METH, V206, P143, DOI 10.1016/j.jneumeth.2012.02.011
  48. Schrier RW, 1999, NEW ENGL J MED, V341, P577, DOI 10.1056/NEJM199908193410806
  49. Silber DH, 1998, J APPL PHYSIOL, V84, P1551
  50. Smirl JD, 2014, HYPERTENSION, V64, P1314, DOI 10.1161/HYPERTENSIONAHA.114.04236
  51. Smirl JD, 2012, J HEART LUNG TRANSPL, V31, P906, DOI 10.1016/j.healun.2012.04.003
  52. TIECKS FP, 1995, STROKE, V26, P1014, DOI 10.1161/01.STR.26.6.1014
  53. Triposkiadis F, 2009, J AM COLL CARDIOL, V54, P1747, DOI 10.1016/j.jacc.2009.05.015
  54. Tzeng YC, 2012, AM J PHYSIOL-HEART C, V303, pH658, DOI 10.1152/ajpheart.00328.2012
  55. Tzeng YC, 2014, EUR J APPL PHYSIOL, V114, P545, DOI 10.1007/s00421-013-2667-y
  56. van Beek AHEA, 2008, J CEREBR BLOOD F MET, V28, P1071, DOI 10.1038/jcbfm.2008.13
  57. van der Velpen IF, 2017, CAN J CARDIOL, V33, P1587, DOI 10.1016/j.cjca.2017.07.008
  58. Verbree J, 2017, J CEREBR BLOOD F MET, V37, P2921, DOI 10.1177/0271678X16679419
  59. Vianna LC, 2015, AM J PHYSIOL-HEART C, V308, pH681, DOI 10.1152/ajpheart.00343.2014
  60. Vogels RLC, 2007, EUR J HEART FAIL, V9, P440, DOI 10.1016/j.ejheart.2006.11.001
  61. Willie CK, 2014, J PHYSIOL-LONDON, V592, P841, DOI 10.1113/jphysiol.2013.268953
  62. Yancy CW, 2013, J AM COLL CARDIOL, V62, pE147, DOI 10.1016/j.jacc.2013.05.019