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Stroke and Blood Pressure

Loss of Circadian Rhythm of Blood Pressure Following Acute Stroke
S Jain1, KKN Namboodri1, S Kumari1 and S Prabhakar2, 1Department of Internal Medicine, Postgraduate Institute of Medical Education and Research, Chandigarh, India 160012, 2Department of Neurology, Postgraduate Institute of Medical Education and Research, Chandigarh, India 160012
BMC Neurology 2004, 4:1     doi:10.1186/1471-2377-4-1
© 2004 Jain et al; licensee BioMed Central Ltd. This is an Open Access article: verbatim copying and redistribution of this article are permitted in all media for any purpose, provided this notice is preserved along with the article's original URL.

Abstract

Background

Epidemiology of acute stroke in developing countries differs from that in the developed world, for example, the age at stroke, risk factors, subtypes of stroke and prognosis. Hypertension remains a dominant risk factor and prognostic indicator in patients with stroke in all communities. The risk of stroke is directly related to elevations of blood pressure. A number of clinical studies have shown that the control of hypertension leads to a reduction in the incidence of stroke in a community. However there is still considerable controversy surrounds the changes in blood pressure in various subtypes of strokes and problem of management of elevated BP after stroke. We studied the circadian rhythm of blood pressure in patients following acute stroke.

Methods

To study the circadian rhythm of blood pressure, fifty consecutive patients with an acute stroke who were admitted to medical emergency within 120 hours of onset were included in the study. After a detailed history and clinical examination, a continuous blood pressure monitor (Spacelab 90207) was attached on the side ipsilateral to intracranial lesion (unaffected arm). The blood pressure was recorded for 24 hours at 15 minutes interval during daytime (6.00 am–6.00 pm) and 20 minutes interval overnight (6 pm to 6 am).

Results

Risk factors for stroke in 50 patients included hypertension in 31(62%), diabetes mellitus in 4 (8%), smoking in 13 (26%) and previous history of transient ischemic attack in 7 (14%) patients. Mean systolic pressure and diastolic pressure at admission were higher in patients with hemorrhagic stroke -29 patients (177 ± 24 mmHg and 105 ± 19 mmHg respectively) compared to patients with ischemic strokes-21 patients (150 ± 36 mm Hg and 89 ± 18 mm Hg respectively, p value <0.01 in both comparisons). The normal diurnal variation in blood pressure (night time dipping of more than 10%) was abolished in 44 (88%) of patients. Out of 44 nondippers, 29 patients showed reverse dipping i.e. rise of BP during night time compared to day time levels. None of the risk factors, clinical or laboratory variables, type of stroke or blood pressure changes differed significantly between these two groups.

Conclusions

Therefore, we showed a pathologically reduced or abolished circadian BP variation after stroke. Absence of normal dipping results in a higher 24 hour blood pressure load and may have more target organ damage than those with normal diurnal variation of blood pressure.

 

Background

Epidemiology of acute stroke is different in developing countries from that in developed world. The age at stroke, risk factors, subtypes of stroke and prognosis are different in developing countries. In India, ischemic strokes constitute 70–75% while hemorrhagic strokes account for 20–25% of total cases [1]. However, hypertension remains a dominant risk factor and prognostic indicator in patients with stroke in all communities. The risk of stroke is directly related to elevations of blood pressure. A number of clinical studies have shown that control of hypertension leads to a reduction in the incidence of stroke in a community[2]. Control of hypertension is important for stroke prevention in all age groups. An increased reported incidence of intracerebral hemorrhage in India may be due to undetected and uncontrolled hypertension and a referral bias in a tertiary care center due to the surgical management of many of these patients.

Many studies have focused on the nature and extent of alterations of circadian blood pressure patterns after acute ischemic stroke while only a few studies have studied circadian rhythm of blood pressure in the patients with acute intracerebral hemorrhage[3,4]. The accurate measurement of blood pressure after an acute stroke is important because antihypertensive therapy may be considered in some patients. However, blood pressure may be falsely elevated or depressed immediately after a stroke depending on the level of consciousness, severity of neurological deficit and physical activity. Conventional recordings in the wards may therefore be unreliable or misleading, leading to inappropriate prescribing or withholding of the antihypertensive therapy.

To overcome this problem ambulatory blood pressure monitoring (ABPM) has been proposed as a method of obtaining an accurate clinical assessment. ABPM devices are increasingly being used in the assessment of hypertension but their value in patients after stroke has not been studied systematically. Various studies have shown different changes of circadian blood pressure patterns after stroke depending on the pathogenesis and location of stroke providing some prognostic and therapeutic implications[3,4]. Still, considerable controversy surrounds the changes in blood pressure in various subtypes of strokes and problem of management of elevated BP after stroke. Therefore, we studied the circadian rhythm of blood pressure in patients following acute stroke.

 

Methods

50 consecutive patients (age 75 years or younger) who were admitted after an acute stroke within 120 hours of its onset were included in the study. Definition of stroke was based on World Health Organisation criteria; rapidly developing clinical signs of focal and at times global loss of cerebral function with symptoms lasting more than 24 hours or leading to death with no apparent cause other than that of vascular origin. Patients with transient ischemic attacks, subarachnoid hemorrhage, cortical vein thrombosis or atrial fibrillation were excluded from the study. All patients had a detailed clinical examination, laboratory studies and a CT scan study of the brain on admission. As per our study protocol, patients who were receiving antihypertensive therapy at the time of admission to the hospital were maintained on the same medication for the duration of the study. No new antihypertensive medication was given during the study period. The Spacelab 90207 ambulatory oscillometric blood pressure monitor (ABPM) was attached at the time of admission. ABPM device was attached on the side ipsilateral to intracranial lesion after relevant difference between the two limbs was ruled out by conventional checks of blood pressure. The first reading obtained with the ABPM device was compared with immediately preceding and following manual measurements. The blood pressure was automatically recorded for 24 hours after application of the blood pressure monitor at 15 minutes interval during day time (6.00 a.m. – 6.00 p.m.) and 20 minutes interval overnight (6.00 p.m. – 6.00 a.m.). The mean daytime and nighttime BP were calculated and the values were analyzed to determine diurnal variation and any evidence of nocturnal fall of blood pressure. Patients were considered to have dipping if the mean arterial pressure (MAP) at night was less than 90% of MAP during daytime. The blood pressure changes were calculated and a relationship with risk factors and nature of stroke was studied. Patients were bedridden at the time of admission and were subjected to ambulatory blood pressure monitoring in that state only

Statistical comparisons between BP and heart rate measurements were made with unpaired 't' test and chi square test. A value of p < 0.05 was considered statistically significant.

 

Results

50 patients (26 males, 24 females; age 57.5 ± + 11.5 years with range 22–74 years) admitted with acute stroke (within 120 hours of onset) to the emergency department of PGIMER, Chandigarh were studied (Table 1). The stroke patients were subclassified into hemorrhagic stroke (29 patients, 58%) and ischemic stroke (21 patients, 42%) based on CT scan findings. Hypertension was the commonest risk factor (31 patients, 62%). Other risk factors included diabetes mellitus in 4 (8%), smoking in 13 (26%) and previous history of transient ischemic attack in 7 (14%) patients. The incidence of risk factors namely hypertension, diabetes mellitus, smoking, history of transient ischemic attacks and coronary artery disease did not differ significantly between patients with hemorrhagic and ischemic strokes. 81% (25 patients) of the patients with a history of hypertension were on antihypertensive medication prior to the development of stroke. In all the patients, who were treated too, also had an uncontrolled blood pressure as could be assessed from the previous medical records. This was attributed to a poor compliance.

Mean systolic blood pressure at admission in this study was 166 ± 32 mm Hg and it was higher in patients with hemorrhagic stroke (177 ± 24 mm Hg) compared to that with ischemic stroke (150 ± 36 mm Hg, p < 0.01) (Table 2). Similarly, mean diastolic blood pressure at admission was also higher in hemorrhagic group compared to ischemic subgroup (105 ± 19 mmHg vs 89 ± 18 mm Hg, p < 0.01). All parameters of blood pressure changes monitored under this study (mean, SBP, mean DBP, mean MAP) were significantly higher in patients with hemorrhagic stroke compared to those in ischemic stroke during day time, night time and total 24 hours. Admission SBP and DBP were higher in patients with history of prior hypertension (174 ± 32 mm Hg and 103 ± 21 mmHg respectively) than in patients without history of previous hypertension (152 ± 30 mm Hg and 91 ± 18 mm Hg respectively, p value < 0.05 in both comparisons). Admission SBP was positively correlated with age of the patient (p < 0.005) and negatively correlated with time after onset of stroke. The admission SBP or DBP was not influenced by previous history of coronary artery disease, smoking, diabetes mellitus, and transient ischemic attack at the time of admission.

The normal diurnal variation in blood pressure i.e. night time dipping was abolished in 44 (88%) of patients. This nondipping was seen equally in both hemorrhagic and ischemic subgroups without any statistically significant difference.

Out of 44 nondippers, 23 patients showed reverse dipping i.e. rise of BP during nighttime compared to daytime levels. None of the risk factors, clinical or laboratory variables or blood pressure changes differed significantly between these two subgroups (Table 1,3). None of the patients had a recurrence of stroke during the study period.

 

Discussion about the Result of Loss of Circadian Rhythm of Blood Pressure Following Acute Stroke

Conclusion on the Result of Loss of Circadian Rhythm of Blood Pressure Following Acute Stroke

Symptoms of Stroke

Resources
1.   Arjundas G: Personal experience in tubercular meningitis and strokes.
Neurol India 1995, 43:127-37. OpenURL
    Return to citation in text: [1]
 
2.   Collins R, MacMahon S: Blood pressure, antihyhpertensive drug treatment and the risks of stroke and of coronary heart disease.
Br Med Bull 1994, 50:272-298.
    Return to citation in text: [1]
 
3.   Sander D, Klingelhoter J: Changes of circardian blood pressure patterns after hemodynamic and thromboembolic brain infarction.
Stroke 1994, 25:1730-37.
    Return to citation in text: [1] [2]
 
4.   Morfis L, Schwartz RS, Poulos R, Howes LG: Blood Pressure changes in acute cerebral infarction and hemorrhage.
Stroke 1997, 28:1401-05.
    Return to citation in text: [1] [2]

Tables

Table 1 [1] [2]
Demographic and laboratory variables of patients with stroke
Variables Total Dippers Nondippers P value

No of patients 50 6(12%) 44(88%) <0.001
Age (in years) 57.5 ± 11.5 67.2 ± 6.6 56.2 ± 11.5 <0.05
Sex (M:F) 26:24 2:4 24:20 NS
Previous hypertension 31(62%) 3(50%) 28(63.6%) NS
Diabetes mellitus 4(8%) 1(16.7%) 3(6.8%) NS
CAD* 6(12%) 0 6(13.6%) NS
Smoking 13(26%) 0 13(29.6%) NS
Previous TIA** 7(14%) 1(16.7%) 6(13.9%) NS
Time between onset to ABPM (hours) 34.7 ± 17.7 32.3 ± 14.2 34.9 ± 18.3 NS
Altered sensorium at admission(numbers) 34(68%) 2(33.3%) 32(66.6%) NS
Blood Sugar (mg%) 138 ± 48 139 ± 34 138 ± 49 NS
Serum Creatinine(mg%) 0.91 ± 0.2 0.84 ± 0.2 0.92 ± 0.22 NS
Site of lesion        
Cortical 23 3 20 NS
Thalamus 14 3 11 NS
Basal ganglia 25 2 23 NS
Pons 2 0 2 NS

* Coronary artery disease **Transient ischemic attack

Table 2 [1]
Blood pressure changes in patients with stroke-hemorrhage versus infarct
Variable Total (n = 50) Hemorrhage (n = 29) Infarct (n = 21) P value

Admission BP        
Mean SBP* 165.5 ± 32 176.9 ± 24 149.8 ± 36 <0.01
Mean DBP** 98.1 ± 20 105.0 ± 19 88.6 ± 17.8 <0.01
24 hour BP        
Mean SBP 159.2 ± 25.8 169.6 ± 21.7 144.8 ± 24.4 <0.001
Mean DBP 95.7 ± 16.4 102.3 ± 16.1 86.4 ± 12.1 <0.001
Mean MAP*** 115 ± 23.7 125.9 ± 16.5 101.2 ± 25.0 <0.001
Daytime BP        
Mean SBP 160.4 ± 26.2 171.1 ± 21.8 145.6 ± 24.9 <0.001
Mean DBP 95.7 ± 17.6 103.3 ± 15.7 85.3 ± 14.7 <0.001
Mean MAP 116.6 ± 18.8 125.4 ± 15.2 104.5 ± 16.6 <0.001
Nighttime BP        
Mean SBP 158.5 ± 28.3 168.7 ± 26.1 144.4 ± 13.2 <0.01
Mean DBP 95.4 ± 18.5 101.7 ± 19.1 86.1 ± 25.3 <0.01
Mean MAP 121.5 ± 30.8 128.6 ± 29.6 111.6 ± 13.3 NS

*Systolic blood pressure,** Diastolic blood pressure,***Mean blood pressure

Table 3 [1]
Blood pressure changes in patients with stroke-dippers versus nondippers
Variable Total (n = 50) Dippers (n = 6) Nondippers (n = 44) P value

24 hour Mean BP        
Mean SBP 159.2 ± 25.8 163.3 ± 11.2 158.6 ± 27.2 NS
Mean DBP 95.7 ± 16.4 93.5 ± 9.3 95.9 ± 1.2 NS
Mean MAP 115 ± 23.7 117.67 ± 8.6 115.3 ± 25.1 NS
Daytime BP        
Mean SBP 160.4 ± 26.2 177.7 ± 14.6 158.1 ± 26.7 NS
Mean DBP 95.7 ± 17.6 102 ± 11.0 95.0 ± 18.2 NS
Mean MAP 116.6 ± 18.8 128.5 ± 9.2 115 ± 19.4 NS
Nighttime BP        
Mean SBP 158.5 ± 28.3 148.5 ± 14.2 159.9 ± 29.5 NS
Mean DBP 95.4 ± 18.5 85 ± 11.5 96.5 ± 18.9 NS
Mean MAP 121.5 ± 30.8 106.2 ± 12.6 123.6 ± 32.0 NS
Admission BP        
Mean SBP 165.5 ± 32 177.5 ± 23 163.9 ± 33.4 NS
Mean DBP 98.1 ± 20 97 ± 18 98.3 ± 20.8 NS

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