Acute Hypertensive Response and Stroke

Figure 68.1. Algorithm for treatment of acute hypertensive response among patients with stroke and stroke subtypes. Based on the NINDS rtPA prethrombolytic protocol for patients with acute ischemic stroke, for short-term BP management by Emergency Medical Services without delaying early diagnosis and differentiation. The Emergency Medical Services BP management practices vary considerably in the absence of distinction between ischemic stroke and ICH. Based on recommendations of the ASA, Stroke Council, and/or European Stroke Initiative. The recommended BP treatment threshold is similar to the existing ASA and European Stroke Initiative recommendations for patients with ICH. Based on recommendations of JNC 7 and the ACCESS protocol.

IV = intravenous; SBP = systolic blood pressure; DBP = diastolic blood pressure; CPP = cerebral perfusion pressure.

The most common pathological findings of the hypertensive microangiopathy are: microatheroma, lipohyalinosis, fibrinoid necrosis, and microaneurysm. These vascular lesions are the subtract for the most common parenchymal brain lesions found in patient with long standing arterial hypertension: lacunar infarcts [95], subcortical leukoencephalopathy [96], leukoaraiosis [97], and small deep intraparenchymal hemorrhage. The cumulative long term consequences of these lesions in the brain are mainly related to a stepwise cognitive decline defined as subcortical vascular dementia. Adequate treatment of the arterial hypertension can diminish these devastating cerebral complications. In a patient with chronic hypertension who suffers from an acute ischemic stroke, it is recommended the cautious use of antihypertensive medication in order to prevent hypotension with consequently worsening of the ischemic penumbra. The decision to continue or discontinue antihypertensive agents must be made on a case-by-case basis with the intent to avoid hypotension, excessive hypertension, and myocardial ischemia. Reduction of the dose of the current agent or a change to a short-acting intravenous antihypertensive agent may be considered. Another issue is the timing of initiation or aggressive titration of oral antihypertensive treatment in patients with stroke who have chronic hypertension or undetected hypertension. In the California Acute Stroke Prototype Registry, great variability in practices between hospitals and considerable room for improvement was noted among two thirds of patients with acute ischemic cerebrovascular events discharged from the hospital that were given 1 or more antihypertensive medications [98]. The heterogeneity in practice despite the definitive benefit demonstrated in clinical trials is concerning [99-101].

Theoretically, oral hypertensive agents can be initiated at 24 to 48 hours after symptom onset, because most of the acute processes, such as ischemic penumbra and hematoma expansion, are uncommon after the first 24 hours. In the ACCESS trial treatment was started with daily candesartan or placebo on day 1. On day 2, the dosage was increased 2- or 4-fold if BP was higher than 160/100 mmHg. If patients in the candesartan group showed a hypertensive profile on day 7 (mean daytime BP equal or higher than 135/85 mmHg), candesartan was increased or an additional antihypertensive drug was added [75]. The results support early initiation of antihypertensive treatment with gradual titration to more aggressive BP treatment targets. The JNC 7 report recommends that BP is maintained at intermediate levels (around 160/100 mmHg) until neurological stability is achieved. Special circumstances such as elevated ICP, progressive cerebral edema, ongoing cerebral ischemia due to occlusive vessel disease or symptomatic cerebral vasospasm, and postoperative cerebral changes require individualized management.

After the first week, or when neurological stability is achieved, a more aggressive treatment can be initiated for secondary prevention of recurrent stroke [7]. The ASA recommends that antihypertensive therapy be considered for all patients with ischemic stroke or transient ischemic attack, because benefit is seen in persons with and without a history of hypertension. Special consideration may be necessary for patients with bilateral severe carotid stenosis, who may bear a high risk of stroke with aggressive BP lowering until carotid revascularization is performed [102,103]. Figure 68.1 shows the algorithm for treatment of acute hypertensive response among patients with stroke and stroke subtypes.

References

1. Whisnant J. Modeling of risk factors for ischemic stroke. The Willis Lecture. Stroke 1997; 28: 1840-4

2. Dozono K, Ishii N, Nishihara Y, et al. An autopsy study of the incidence of lacunes in relation to age, hypertension, and arteriosclerosis. Stroke 1991; 22: 993-6

3. Adams HP Jr, Bendixen BH, Kappelle LJ, et al. Classification of subtype of acute ischemic stroke. Definitions for use in a multicenter clinical trial. TOAST. Trial of Org 10172 in Acute Stroke Treatment. Stroke 1993; 24: 35-41

4. Wityk RJ, Caplan LR. Hypertensive intracerebral hemorrhage. Epidemiology and clinical pathology. Neurosurg Clin N Am 1992; 3: 521-32

5. Qureshi AI. Acute hypertensive response in patients with stroke: pathophysiology and management. Circulation 2008; 118: 176-87

6. Whitworth JA. 2003 World Health Organization (WHO)/International Society of Hypertension (ISH) statement on management of hypertension. J Hypertens 2003; 21: 1983-92

7. Chobanian AV, Bakris GL, Black HR, et al; National Heart, Lung, and Blood Institute Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure; National High Blood Pressure Education Program Coordinating Committee. The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure: the JNC 7 report. JAMA 2003; 289: 2560-72

8. Bath P, Chalmers J, Powers W, et al; International Society of Hypertension Writing Group. International Society of Hypertension (ISH): statement on the management of blood pressure in acute stroke. J Hypertens 2003; 21: 665-72

9. Qureshi AI, Ezzeddine MA, Nasar A, et al. Prevalence of elevated blood pressure in 563,704 adult patients with stroke presenting to the ED in the United States. Am J Emerg Med 2007; 25: 32-8

10. International cardiovascular disease statistics (2007 update). Available at: www.americanheart.org

11. Willmot M, Leonardi-Bee J, Bath M. High blood pressure in acute stroke and subsequent outcome: a systematic review. Hypertension 2004; 43: 18-24

12. Wallace JD, Levy LL. Blood pressure after stroke. JAMA 1981; 246: 2177-80

13. McHenry LC Jr, Merory J, Bass E, et al. Xenon-133 inhalation method for regional cerebral blood flow measurements: normal values and test-retest results. Stroke 1978; 9: 396-9

14. MacKenzie ET, Farrar JK, Fitch W, et al. Effects of hemorrhagic hypotension on the cerebral circulation. I. Cerebral blood flow and pial arteriolar caliber. Stroke 1979; 10: 711-8

15. Paulson OB, Strandgaard S, Edvinsson L. Cerebral autoregulation. Cerebrovasc Brain Metab Rev 1990; 2: 161-92

16. Aaslid R, Lindegaard KF, Sorteberg W, et al. Cerebral autoregulation dynamics in humans. Stroke 1989; 20: 45-52

17. Symon L, Held K, Dorsch NW. A study of regional autoregulation in the cerebral circulation to increased perfusion pressure in normocapnia and hypercapnia. Stroke 1973; 4: 139-47

18. Strandgaard S. Autoregulation of cerebral blood flow in hypertensive patients. The modifying influence of prolonged antihypertensive treatment on the tolerance to acute, drug-induced hypotension. Circulation 1976; 53: 720-7

19. Olsen TS, Larsen B, Herning M, et al. Blood flow and vascular reactivity in collaterally perfused brain tissue. Evidence of an ischemic penumbra in patients with acute stroke. Stroke 1983; 14: 332-41

20. Dawson SL, Panerai RB. Potter JF. Serial changes in static and dynamic cerebral autoregulation after acute ischaemic stroke. Cerebrovasc Dis 2003; 16: 69-75

21. Yamamoto S, Nishizawa S, Tsukada H, et al. Cerebral blood flow autoregulation following subarachnoid hemorrhage in rats: chronic vasospasm shifts the upper and lower limits of the autoregulatory range toward higher blood pressures. Brain Res 1998; 782: 194-201

22. Zaharchuk G, Mandeville JB, Bogdanov AA Jr, et al. Cerebrovascular dynamics of autoregulation and hypoperfusion. An MRI study of CBF and changes in total and microvascular cerebral blood volume during hemorrhagic hypotension. Stroke 1999; 30: 2197-204; discussion 2204-5

23. The Brain Trauma Foundation. The American Association of Neurological Surgeons. The Joint Section on Neurotrauma and Critical Care. Guidelines for cerebral perfusion pressure. J Neurotrauma 2000; 17: 507-11

24. Arboix A, Roig H, Rossich R, et al. Differences between hypertensive and non-hypertensive ischemic stroke. Eur J Neurol 2004; 11: 687-92

25. Aslanyan S, Fazekas F, Weir CJ, et al. Effect of blood pressure during the acute period of ischemic stroke on stroke outcome: a tertiary analysis of the GAIN International Trial. Stroke 2003; 34: 2420-5

26. Resstel LB, Correa FM. Involvement of the medial prefrontal cortex in central cardiovascular modulation in the rat. Auton Neurosci 2006; 126-127: 130-8

27. Hilz MJ, Devinsky O, Szczepanska H, et al. Right ventromedial prefrontal lesions result in paradoxical cardiovascular activation with emotional stimuli. Brain 2006; 129(Pt 12): 3343-55

28. Meyer S, Strittmatter M, Fischer C, et al. Lateralization in autonomic dysfunction in ischemic stroke involving the insular cortex. Neuroreport 2004; 15: 357-61

29. Barron SA, Rogovski Z, Hemli J. Autonomic consequences of cerebral hemisphere infarction. Stroke, 1994; 25: 113-6

30. Robinson TG, James M, Youde J, et al. Cardiac baroreceptor sensitivity is impaired after acute stroke. Stroke 1997; 28: 1671-6

31. Oppenheimer S. The anatomy and physiology of cortical mechanisms of cardiac control. Stroke 1993; 24(12 Suppl): I3-5

32. Ichiyama RM, Waldrop TG, Iwamoto GA. Neurons in and near insular cortex are responsive to muscular contraction and have sympathetic and/or cardiac-related discharge. Brain Res 2004; 1008: 273-7

33. Resstel LB, Correa FM. Medial prefrontal cortex NMDA receptors and nitric oxide modulate the parasympathetic component of the baroreflex. Eur J Neurosci 2006; 23: 481-8

34. Murros K, Fogelholm R, Kettunen S, et al. Serum cortisol and outcome of ischemic brain infarction. J Neurol Sci 1993; 116: 12-7

35. Chamorro A, Amaro S, Vargas M, et al. Catecholamines, infection, and death in acute ischemic stroke. J Neurol Sci 2007; 252: 29-35

36. Rodríguez-Yáñez M, Castellanos M, Blanco M, et al. New-onset hypertension and inflammatory response/poor outcome in acute ischemic stroke. Neurology 2006; 67: 1973-8

37. Qureshi AI, Luft AR, Sharma M, et al. Frequency and determinants of postprocedural hemodynamic instability after carotid angioplasty and stenting. Stroke 1999; 30: 2086-93

38. McGee S, Abernethy WB 3rd, Simel DL. The rational clinical examination. Is this patient hypovolemic? JAMA 1999; 281: 1022-9

39. Jivraj S, Mazer CD, Baker AJ, et al. Case report: profound hypotension associated with labetalol therapy in a patient with cerebral aneurysms and subarachnoid hemorrhage. Can J Anaesth 2006; 53: 678-83

40. McLaren GD, Danta G. Cerebral infarction due to presumed hemodynamic factors in ambulant hypertensive patients. Clin Exp Neurol 1987; 23: 55-66

41. Qureshi AI, Tuhrim S, Broderick JP, et al. Spontaneous intracerebral hemorrhage. N Engl J Med 2001; 344: 1450-60

42. Labovitz DL, Halim A, Boden-Albala B, et al. The incidence of deep and lobar intracerebral hemorrhage in whites, blacks, and Hispanics. Neurology 2005; 65: 518-22

43. Takebayashi S, Kaneko M. Electron microscopic studies of ruptured arteries in hypertensive intracerebral hemorrhage. Stroke 1983; 14: 28-36

44. Qureshi AI, Suri MF, Ostrow PT, et al. Apoptosis as a form of cell death in intracerebral hemorrhage. Neurosurgery 2003; 52: 1041-7; discussion 1047-8

45. Qureshi AI, Ali Z, Suri MF, et al. Extracellular glutamate and other amino acids in experimental intracerebral hemorrhage: an in vivo microdialysis study. Crit Care Med 2003; 31: 1482-9

46. Lusardi TA, Wolf JA, Putt ME, et al. Effect of acute calcium influx after mechanical stretch injury in vitro on the viability of hippocampal neurons. J Neurotrauma 2004; 21: 61-72

47. Shah QA, Ezzeddine MA, Qureshi AI. Acute hypertension in intracerebral hemorrhage: pathophysiology and treatment. J Neurol Sci 2007; 261: 74-9

48. Qureshi AI, Hanel RA, Kirmani JF, et al. Cerebral blood flow changes associated with intracerebral hemorrhage. Neurosurg Clin N Am 2002; 13: 355-70

49. Zazulia AR, Diringer MN, Videen TO, et al. Hypoperfusion without ischemia surrounding acute intracerebral hemorrhage. J Cereb Blood Flow Metab 2001; 21: 804-10

50. Nakamura T, Xi G, Park JW, et al. Holo-transferrin and thrombin can interact to cause brain damage. Stroke 2005; 36: 348-52

51. Xi G, Keep RF, Hoff JT. Mechanisms of brain injury after intracerebral hemorrhage. Lancet Neurol 2006; 5: 53-63

52. Nakamura T, Keep RF, Hua Y, et al. Iron-induced oxidative brain injury after experimental intracerebral hemorrhage. Acta Neurochir Suppl 2006; 96: 194-8

53. Wagner KR, Packard BA, Hall CL, et al. Protein oxidation and heme oxygenase-1 induction in porcine white matter following intracerebral infusions of whole blood or plasma. Dev Neurosci 2002; 24: 154-60

54. Davis SM, Broderick J, Hennerici M, et al. Hematoma growth is a determinant of mortality and poor outcome after intracerebral hemorrhage. Neurology 2006; 66: 1175-81

55. Kazui S, Minematsu K, Yamamoto H, et al. Predisposing factors to enlargement of spontaneous intracerebral hematoma. Stroke 1997; 28: 2370-5

56. Dandapani BK, Suzuki S, Kelley RE, et al. Relation between blood pressure and outcome in intracerebral hemorrhage. Stroke 1995; 26: 21-4

57. Vemmos KN, Tsivgoulis G, Spengos K, et al. Association between 24-h blood pressure monitoring variables and brain oedema in patients with hyperacute stroke. J Hypertens 2003; 21: 2167-73

58. Kim-Han JS, Kopp SJ, Dugan LL, et al. Perihematomal mitochondrial dysfunction after intracerebral hemorrhage. Stroke 2006; 37: 2457-62

59. Powers WJ, Zazulia AR, Videen TO, et al. Autoregulation of cerebral blood flow surrounding acute (6 to 22 hours) intracerebral hemorrhage. Neurology 2001; 57: 18-24

60. Qureshi AI, Mohammad YM, Yahia AM, et al. A prospective multicenter study to evaluate the feasibility and safety of aggressive antihypertensive treatment in patients with acute intracerebral hemorrhage. J Intensive Care Med 2005; 20: 34-42

61. Qureshi AI, Harris-Lane P, Kirmani JF, et al. Treatment of acute hypertension in patients with intracerebral hemorrhage using American Heart Association guidelines. Crit Care Med 2006; 34: 1975-80

62. Broderick J, Connolly S, Feldmann E, et al; American Heart Association; American Stroke Association Stroke Council; High Blood Pressure Research Council; Quality of Care and Outcomes in Research Interdisciplinary Working Group. Guidelines for the management of spontaneous intracerebral hemorrhage in adults: 2007 update: a guideline from the American Heart Association/American Stroke Association Stroke Council, High Blood Pressure Research Council, and the Quality of Care and Outcomes in Research Interdisciplinary Working Group. Stroke 2007; 38: 2001-23

63. Steiner T, Kaste M, Forsting M, et al. Recommendations for the management of intracranial hemorrhage – part I: spontaneous intracerebral hemorrhage. The European Stroke Initiative Writing Committee and the Writing Committee for the EUSI Executive Committee. Cerebrovasc Dis 2006; 22: 294-316

64. Ohwaki K, Yano E, Nagashima H, et al. Blood pressure management in acute intracerebral hemorrhage: relationship between elevated blood pressure and hematoma enlargement. Stroke 2004; 35: 1364-7

65. Qureshi AI. Antihypertensive Treatment of Acute Cerebral Hemorrhage (ATACH): rationale and design. Neurocrit Care 2007; 6: 56-66

66. Anderson CS, Huang Y, Wang JG, et al. Intensive blood pressure reduction in acute cerebral hemorrhage trial (INTERACT): a randomised pilot trial. Lancet Neurol 2008; 7: 391-9

67. Janardhan V, Qureshi AI. Mechanisms of ischemic brain injury. Curr Cardiol Rep 2004; 6: 117-23

68. Astrup J, Symon L, Branston NM, et al. Cortical evoked potential and extracellular K+ and H+ at critical levels of brain ischemia. Stroke 1977; 8: 51-7

69. Elewa HF, Kozak A, Johnson MH, et al. Blood pressure lowering after experimental cerebral ischemia provides neurovascular protection. J Hypertens 2007; 25: 855-9

70. Leonardi-Bee J, Bath PM, Phillips SJ, et al. Blood pressure and clinical outcomes in the International Stroke Trial. Stroke 2002; 33: 1315-20

71. Stead LG, Gilmore RM, Vedula KC, et al. Impact of acute blood pressure variability on ischemic stroke outcome. Neurology 2006; 66: 1878-81

72. Barer DH, Cruickshank JM, Ebrahim SB, et al. Low dose beta blockade in acute stroke (“BEST” trial): an evaluation. Br Med J (Clin Res Ed) 1988; 296: 737-41

73. Ahmed N, Nasman, Wahlgren NG. Effect of intravenous nimodipine on blood pressure and outcome after acute stroke. Stroke 2000; 31: 1250-5

74. Horn J, Limburg M. Calcium antagonists for acute ischemic stroke. Cochrane Database Syst Rev 2000; (2): CD001928

75. Schrader J, Lüders S, Kulschewski A, et al. The ACCESS Study: evaluation of Acute Candesartan Cilexetil Therapy in Stroke Survivors. Stroke 2003; 34: 1699-703

76. Brott T, Lu M, Kothari R, et al. Hypertension and its treatment in the NINDS rt-PA Stroke Trial. Stroke 1998; 29: 1504-9

77. Adams HP Jr, del Zoppo G, Alberts MJ, et al. Guidelines for the early management of adults with ischemic stroke: a guideline from the American Heart Association/American Stroke Association Stroke Council, Clinical Cardiology Council, Cardiovascular Radiology and Intervention Council, and the Atherosclerotic Peripheral Vascular Disease and Quality of Care Outcomes in Research Interdisciplinary Working Groups: The American Academy of Neurology affirms the value of this guideline as an educational tool for neurologists. Circulation 2007; 115: e478-534

78. Oliveira-Filho J, Silva SC, Trabuco CC, et al. Detrimental effect of blood pressure reduction in the first 24 hours of acute stroke onset. Neurology 2003; 61: 1047-51

79. Castillo J, Leira R, García mm, et al. Blood pressure decrease during the acute phase of ischemic stroke is associated with brain injury and poor stroke outcome. Stroke 2004; 35: 520-6

80. Klijn CJ, Hankey GJ. Management of acute ischaemic stroke: new guidelines from the American Stroke Association and European Stroke Initiative. Lancet Neurol 2003; 2: 698-701

81. Broderick J, Brott T, Barsan W, et al. Blood pressure during the first minutes of focal cerebral ischemia. Ann Emerg Med 1993; 22: 1438-43

82. Mattle HP, Kappeler L, Arnold M, et al. Blood pressure and vessel recanalization in the first hours after ischemic stroke. Stroke 2005; 36: 264-8

83. Tanne D, Kasner SE, Demchuk AM, et al. Markers of increased risk of intracerebral hemorrhage after intravenous recombinant tissue plasminogen activator therapy for acute ischemic stroke in clinical practice: the Multicenter rt-PA Stroke Survey. Circulation 2002; 105: 1679-85

84. Katzan IL, Furlan AJ, Lloyd LE, et al. Use of tissue-type plasminogen activator for acute ischemic stroke: the Cleveland area experience. JAMA 2000; 283: 1151-8

85. Katzan IL, Hammer MD, Furlan AJ, et al; Cleveland Clinic Health System Stroke Quality Improvement Team. Quality improvement and tissue-type plasminogen activator for acute ischemic stroke: a Cleveland update. Stroke 2003; 34: 799-800

86. Hart RG, Tonarelli SB, Pearce LA. Avoiding central nervous system bleeding during antithrombotic therapy: recent data and ideas. Stroke 2005; 36: 1588-93

87. Aguilar MI, Hart RG, Kase CS, et al. Treatment of warfarin-associated intracerebral hemorrhage: literature review and expert opinion. Mayo Clin Proc 2007; 82: 82-92

88. Arima H, Hart RG, Colman S, et al; PROGRESS Collaborative Group Perindopril-based blood pressure-lowering reduces major vascular events in patients with atrial fibrillation and prior stroke or transient ischemic attack. Stroke 2005; 36: 2164-9

89. Rothwell PM, Coull AJ, Giles MF, et al; Oxford Vascular Study. Change in stroke incidence, mortality, case-fatality, severity, and risk factors in Oxfordshire, UK from 1981 to 2004 (Oxford Vascular Study). Lancet 2004; 363: 1925-33

90. Chapman N, Huxley R, Anderson C, et al; Writing Committee for the PROGRESS Collaborative Group. Effects of a perindopril-based blood pressure-lowering regimen on the risk of recurrent stroke according to stroke subtype and medical history: the PROGRESS Trial. Stroke 2004; 35: 116-21

91. Perry HM Jr, Davis BR, Price TR, et al. Effect of treating isolated systolic hypertension on the risk of developing various types and subtypes of stroke: the Systolic Hypertension in the Elderly Program (SHEP). JAMA 2000; 284: 465-71

92. Harper SL, Bohlen HG. Microvascular adaptation in the cerebral cortex of adult spontaneously hypertensive rats. Hypertension 1984; 6: 408-19

93. Baumbach GL, Heistad DD. Remodeling of cerebral arterioles in chronic hypertension. Hypertension 1989; 13: 968-72

94. Williams JL, Furlan AJ. Cerebral vascular physiology in hypertensive disease. Neurosurg Clin N Am 1992; 3: 509-20

95. Chamorro A, Sacco RL, Mohr JP, et al. Clinical-computed tomographic correlations of lacunar infarction in the Stroke Data Bank. Stroke 1991; 22: 175-81

96. Matsushita K, Kuriyama Y, Nagatsuka K, et al. Periventricular white matter lucency and cerebral blood flow autoregulation in hypertensive patients. Hypertension 1994; 23: 565-8

97. Hachinski VC, Potter, Merskey H. Leuko-araiosis. Arch Neurol 1987; 44: 21-3

98. Ovbiagele B, Hills NK, Saver JL, et al. Antihypertensive medications prescribed at discharge after an acute ischemic cerebrovascular event. Stroke 2005; 36: 1944-7

99. Gueyffier F, Boissel JP, Boutitie F, et al. Effect of antihypertensive treatment in patients having already suffered from stroke. Gathering the evidence. The INDANA (INdividual Data ANalysis of Antihypertensive intervention trials) Project Collaborators. Stroke 1997; 28: 2557-62

100. Rezaiefar, Pottie K. Blood pressure and secondary prevention of strokes. How low should we go? Randomised trial of a perindopril-based blood-pressure-lowering regimen among 6,105 individuals with previous stroke or transient ischaemic attack. Can Fam Physician 2002; 48: 1625-9

101. Arima H, Chalmers J, Woodward M, et al; PROGRESS Collaborative Group. Lower target blood pressures are safe and effective for the prevention of recurrent stroke: the PROGRESS trial. J Hypertens 2006; 24: 1201-8

102. Sacco RL, Adams R, Albers G, et al; American Heart Association/American Stroke Association Council on Stroke; Council on Cardiovascular Radiology and Intervention; American Academy of Neurology Guidelines for prevention of stroke in patients with ischemic stroke or transient ischemic attack: a statement for healthcare professionals from the American Heart Association/American Stroke Association Council on Stroke: co-sponsored by the Council on Cardiovascular Radiology and Intervention: the American Academy of Neurology affirms the value of this guideline. Circulation 2006; 113: e409-49

103. Rothwell M, Howard SC, Spence JD. Relationship between blood pressure and stroke risk in patients with symptomatic carotid occlusive disease. Stroke 2003; 34: 2583-90

Only gold members can continue reading. Log In or Register to continue