Abstract
The optimal range of blood pressure levels in the early phase of ischemic stroke with hypertension is still controversial. Based on our stroke registry database, we explored the relationship between blood pressure levels and cerebral perfusion in the early phase of ischemic stroke with hypertension and neurofunctional recovery at 3 months after stroke. Total 732 stroke patients with hypertension were finally analyzed. Patients were divided into quintiles according to systolic blood pressure (SBP) and diastolic blood pressure (DBP) to perform multivariable logistic regression to analyze their relation with neurofunctional recovery, respectively. The cerebral perfusion levels displayed a reverse “U” shape curve with the change of blood pressure levels. Sufficient estimated cerebral blood flow (ECBF) in the early phase of ischemic stroke was associated with good neurofunctional recovery at 3 months after stroke. The best neurofunctional recovery was observed in the middle quintiles with SBP at 161 to 177 mm Hg and DBP at 103 to 114 mm Hg, respectively. So maintaining appropriate blood pressure levels in the early phase of ischemic stroke might be beneficial to cerebral perfusion and neurofunctional recovery.
Keywords: acute phase, hypertension, ischemic stroke, neurofunctional recovery, prognosis
1. INTRODUCTION
Around 65% to 70% of patients with acute stroke present suddenly elevated blood pressure after stroke onset, whether with a history of hypertension or not.1 Blood pressure levels were closely related to the outcome of stroke.2 Antihypertensive treatment had become the main strategy of preventing primary and secondary stroke in hypertensive patients. However, it is still controversial whether or not antihypertensive therapy should be performed in the early phase of ischemic stroke.3, 4
IST trial showed both high blood pressure and low blood pressure were associated with poor outcome after acute ischemic stroke.2 CATIS trial showed mean systolic blood pressure was reduced from 166.7 mm Hg to 144.7 mm Hg (−12.7%) within 24 hours in the antihypertensive treatment group and from 165.6 mm Hg to 152.9 mm Hg (−7.2%) in the control group and antihypertensive therapy did not increase the risk of death and major disability in acute ischemic stroke.5 However, ENOS trial showed the antihypertensive drug lowered blood pressure and had acceptable safety, but did not improve functional outcome in hypertensives with acute stroke.6 Another clinical trial revealed that careful lowering blood pressure treatment with angiotensin‐receptor blocker candesartan was not beneficial to acute stroke patients with elevated blood pressure, leading to a harmful effect.4 Therefore, some investigators suggested that antihypertensive therapy should be cautiously used in the acute phase of stroke, especially within 24 hours of ischemic stroke onset, in case it leads to brain hypoperfusion. Guideline of Diagnosis and Treatment of Acute Ischemic Stroke in China (Chinese Stoke Society, 2010 and 2014) also recommended that antihypertensive treatment should be used carefully within 24 hours after ischemic stroke.
Physiologically, cerebral blood flow (CBF) is matched to the metabolic demands of the brain via autoregulation that maintains relatively stable blood flow with the changes of the systemic blood pressure. Under normal circumstances, organ perfusion depends on interactions of blood pressure, vascular cross‐sectional area, and circulatory volume.7 Effective flow perfusion pressure is vital to sustain cerebral perfusion.8 The disorder of cerebral autoregulatory system concomitant with altered systemic blood pressure after stroke would inevitably influence cerebral perfusion,9 and active strategies should be adopted to control exorbitant blood pressure in the early phase of stroke.10, 11, 12
Hence, it is necessary to clarify the proper blood pressure management of hypertensive patients in the early phase of acute stroke. In this study, we investigated the association of blood pressure levels with cerebral perfusion in the early phase of ischemic stroke and neurofunctional recovery at 3 months after stroke in a large single‐center population.
2. METHODS
2.1. Study design and participants
We carried a single‐center observational study. The cohort has been described previously.13 Briefly, from January 2013 to June 2014, 986 consecutive patients with acute ischemic stroke were registered in the stroke registry database for optimal achieved blood pressure. The early phase of stroke was defined as 24 hours after acute ischemic stroke onset. Patients were included if their systolic blood pressure (SBP) ≥ 140 mm Hg, diastolic blood pressure (DBP) ≥90 mm Hg, or if they had normal blood pressure with a history of hypertension and currently were being treated with antihypertensive drugs. Patients were excluded if they had one of the following characteristics: head CT findings of hemorrhagic stroke, severe conscious disorder and conscious score of the National Institutes of Health stroke scale (NIHSS) >1, the modified Rankin scale (mRS) score >1 before stroke, severe mental disorders and dementia, serious systemic diseases, and expectancy life span <90 days, ALT or AST > 2.0 × ULN or severe liver disease, estimated glomerular filtration rate (eGFR) <30 mL/min/1.73 m2 or sever renal disease or they were not suitable to participate in the study, or they did not complete transcranial doppler (TCD) examination within 24 hours of onset due to severe illness condition.
This study was approved by the ethics committee of the First People’s Hospital of Lianyungang City, and conducted in accordance with the Declaration of Helsinki. Written informed consent was obtained from all of the patients.
Blood pressure was measured by a mercury sphygmomanometer and was confirmed by auscultatory method (YUTU‐XJ11E) synchronously with TCD examination. All patients were lying on the bed for at least half hour before TCD, and effect factors of blood pressure were avoided, including drugs, mental status, pain, cough, bladder filling, and cold. Three consecutive blood pressure determinations (2‐minute intervals) prior to the TCD examination were used to calculate mean blood pressure levels, which was recorded as the blood pressure. Trained nurses completed the blood pressure measurement, and qualified researchers collected the data.
2.2. Cerebral perfusion assessment
Cerebral perfusion assessment was performed within 24 hours after admission. After an initial 30 minutes of rest with the patients in a supine position, the internal carotid arteries (ICA) was examined by a 9‐MHz transducer of a computed sonography system in real‐time by a KJ‐2V7P mobile Doppler system with dual beam. The hemodynamic parameters including the peak systolic velocities, the end diastolic velocities, the mean flow velocities (MVs), the time‐peak velocities and pulse index (PI) of ICA and VA of both sides were explored with a 9‐MHz linear array transducer of a computed sonography system. Flow volume measurements were generally taken in the C4‐C5 intertransverse segment of the VA, and 1 to 2 cm above the carotid bulb in the ICA. The luminal diameter was determined on the enlarged B‐mode image of the vessel as the distance between the internal layers of the parallel walls. The mean of 3 successful measurements was evaluated. Intravascular flow volumes were calculated as the product of averaged flow velocity and the cross‐sectional area of the circular vessel according to the formula, that was MV × A = MV × ([d/2]2 × π).14, 15 The total CBF volume was determined as the sum of flow volumes in the internal carotid and vertebral arteries of both sides.
2.3. Patients follow‐up
The extent of neurological deficits on admission and at 3 months after stroke was evaluated using the NIHSS, and the neurologic prognosis was evaluated using the mRS. The NIHSS and mRS were recorded by trained neurologists following the double‐blind principle. The outcome of good evaluation criteria was as below16: good neurological recovery (≥ 4‐point decrease on the NIHSS during hospitalization or 0 point at discharge); neurological deterioration (≥ 2‐point increase on the NIHSS during hospitalization); and a poor functional outcome (disability, or death, or ≥ 2 on the mRS scale at 3 months after stroke onset).
2.4. Statistical analysis
Analyses were performed with SPSS (SPSS, version 19.0.1 for Windows). Continuous variables were shown as mean ± SD. Categorical variables were given as frequency (percent). One‐way ANOVA or Wilcoxon rank sum test was used to compare continuous variables, and chi‐square test was used to compare categorical variables. Smooth curves that reflected the association between SBP/DBP and estimated cerebral blood flow (ECBF) were drawn using a cubic equation of curve estimation. In the analysis of the association between SBP/DBP and neurofunctional recovery at 3 months after stroke, patients were divided into quintiles according to SBP/DBP. The third quintiles Q3s were as references when SBP and DBP were analyzed. Logistic regression models were used to estimate odds ratios (ORs) and 95% confidence interval (CI). We used 3 multivariable models. As we know, there are many factors affecting the recovery of neurological function after stroke, including age, gender, smoker, hypertension, diabetes mellitus, hyperlipidemia, significant carotid atherosclerosis, coronary artery disease, congestive heart failure, chronic kidney disease, posterior circulation infarction, thrombolytic, modified Rankin scale, National Institute of Health stroke scale, cerebral infarct volume, heart rate, and eGRF. Gender and age are non‐modifiable risk factors, which were firstly adjusted in Model I. Other risk factors served as modifiable conventional risk factors. We wanted to adjust as many risk factors as possible and count their contribution to the outcome in our logistic regression model, and then we used “Enter” strategy to analyze the association of blood pressure levels with neurofunctional recovery after stroke. Due to many risk factors, we included the categorical variables in Model II and all of the variables in Model III. P < .05 was considered statistically significant.
3. RESULTS
3.1. Baseline characteristics
As shown in Figure 1, 986 acute ischemic stroke patients with hypertension were registered, and 732 patients were analyzed finally in this study. Baseline characteristics of these patients were shown in Table 1. There were no significant differences among these quintiles (Q1‐Q5) of SBP and DBP in NIHSS and modified Rankin scale points as well as the history of related diseases, such as diabetes mellitus, dyslipidemia, coronary artery disease, significant carotid atherosclerosis, congestive heart disease, and chronic kidney disease.
Figure 1.
Study flow chart showing the number of patients included in the final analysis
Table 1.
Baseline characteristics of the study population based on SBP/DBP quintile
| Characteristic | SBP, mm Hg | DBP, mm Hg | ||||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|
| Q1 (<143) | Q2 (143‐160) | Q3 (161‐177) | Q4 (178‐191) | Q5 (≥192) | P | Q1 (<90) | Q2 (90‐102) | Q3 (103‐114) | Q4 (114‐123) | Q5 (≥124) | P | |
| N | 146 | 145 | 144 | 149 | 148 | 141 | 149 | 145 | 149 | 148 | ||
| Age, y | 63.51 ± 13.32 | 65.48 ± 12.68 | 64.24 ± 13.20 | 64.1 ± 13.04 | 63.64 ± 12.20 | .711 | 63.01 ± 13.35 | 66.12 ± 12.75 | 64.01 ± 13.00 | 64.1 ± 13.04 | 63.64 ± 12.20 | .304 |
| Male, n (%) | 82 (56.16) | 78 (53.79) | 75 (52.08) | 72 (48.32) | 76 (51.35) | .735 | 84 (59.57) | 76 (51.01) | 75 (51.72) | 72 (48.32) | 76 (51.35) | .392 |
| Current smoker, n (%) | 33 (22.60) | 50 (34.48) | 41 (28.47) | 29 (19.46) | 15 (10.14) | <.001 | 32 (22.70) | 50 (33.56) | 42 (28.97) | 29 (19.46) | 15 (10.14) | <.001 |
| HR (bpm) | 88.17 ± 8.45 | 88.58 ± 9.34 | 89.6 ± 7.81 | 87.3 ± 8.01 | 88.27 ± 9.77 | .258 | 88.48 ± 8.17 | 88.64 ± 9.53 | 89.22 ± 7.894 | 87.3 ± 8.01 | 88.27 ± 9.77 | .434 |
| mRS score | 2.75 ± 0.87 | 2.84 ± 0.83 | 2.84 ± 0.83 | 2.77 ± 0.97 | 2.78 ± 0.86 | .861 | 2.8 ± 0.85 | 2.75 ± 0.82 | 2.88 ± 0.85 | 2.77 ± 0.97 | 2.78 ± 0.86 | .733 |
| NIHSS score | 11.05 ± 5.05 | 10.92 ± 4.88 | 10.75 ± 4.81 | 10.81 ± 5.12 | 11.1 ± 5.23 | .970 | 10.79 ± 5.14 | 10.74 ± 4.68 | 11.18 ± 4.93 | 10.81 ± 5.12 | 11.1 ± 5.23 | .921 |
| CIV (cm3) | 11.11 ± 3.98 | 11.30 ± 3.09 | 12.47 ± 2.45 | 11.32 ± 2.46 | 11.68 ± 3.86 | .003 | 10.24 ± 3.43 | 12.28 ± 3.52 | 12.3 ± 2.36 | 11.32 ± 2.46 | 11.68 ± 3.86 | <.001 |
| PCI, n (%) | 42 (28.77) | 41 (28.28) | 41 (32.43) | 51 (34.23) | 48 (34.23) | .724 | 44 (31.20) | 43 (28.86) | 37 (25.52) | 51 (34.23) | 48 (32.43) | .531 |
| TT, n (%) | 7 (4.79) | 7 (4.83) | 11 (7.64) | 10 (6.71) | 9 (6.08) | .818 | 9 (6.38) | 8 (5.37) | 8 (5.51) | 10 (6.71) | 9 (6.08) | .987 |
| eGFR (mL/min/1.73 m2) | 130.7 ± 11.34 | 129.17 ± 9.87 | 131.33 ± 11.16 | 128.77 ± 9.41 | 132.19 ± 10.22 | .024 | 128.92 ± 9.93 | 131.9 ± 10.48 | 130.3 ± 11.82 | 128.77 ± 9.41 | 132.19 ± 10.22 | .008 |
| Medical history | ||||||||||||
| Hypertension, n (%) | 136 (93.15) | 118 (81.38) | 133 (92.36) | 133 (89.26) | 124 (83.78) | .005 | 132 (93.62) | 122 (81.88) | 133 (91.72) | 133 (89.26) | 124 (83.78) | .007 |
| Diabetes mellitus, n (%) | 28 (19.18) | 35 (24.14) | 35 (24.31) | 39 (26.17) | 25 (16.89) | .263 | 27 (19.15) | 37 (24.83) | 34 (23.45) | 39 (26.17) | 25 (16.89) | .260 |
| Hyperlipidemia, n (%) | 80 (54.79) | 80 (55.17) | 82 (56.94) | 93 (62.42) | 77 (52.03) | .463 | 80 (56.73) | 82 (55.03) | 80 (55.17) | 93 (62.42) | 77 (52.03) | .471 |
| SCS, n (%) | 20 (13.70) | 27 (18.62) | 26 (18.06) | 24 (16.11) | 18 (12.16) | .494 | 20 (14.18) | 28 (18.79) | 25 (17.24) | 24 (16.11) | 18 (12.16) | .558 |
| Coronary artery disease, n (%) | 15 (10.27) | 26(17.93) | 21(14.58) | 16(10.74) | 20(13.51) | .299 | 15 (10.64) | 25 (16.78) | 22 (15.17) | 16 (10.74) | 20 (13.51) | .448 |
| Congestive heart failure, n (%) | 1 (0.68) | 10 (6.90) | 8 (5.56) | 6 (4.03) | 6 (4.05) | .103 | 2 (1.42) | 8 (5.37) | 9 (6.21) | 6 (4.03) | 6 (4.05) | .325 |
| Chronic kidney disease, n (%) | 9 (6.16) | 8 (5.52) | 9 (6.25) | 7 (4.70) | 5 (3.38) | .790 | 8 (5.67) | 8 (5.37) | 10 (6.90) | 7 (4.70) | 5 (3.38) | .737 |
CAD, coronary artery disease; CHF, congestive heart failure; CIV, cerebral infarct volume; CKD, chronic kidney disease; HR, heart rates; mRS, modified Rankin scale; NIHSS, National Institute of Health stroke scale; PCI, posterior circulation infarcts; SCS, significant carotid stenosis; TT, thrombolytic therapy.
3.2. The association of blood pressure with ECBF
The association between SBP/DBP and ECBF was shown in Figure 2. High ECBF located mostly in the area with moderate SBP or DBP, so a cubic curve fitting displayed a reverse U‐shape curve between ECBF and SBP/DBP. ECBF showed a rapid increase when SBP increased from 100 to 150 mm Hg, then a gradual increase when SBP increased from 150 to 170 mm Hg, and reached maximum value at approximate 170 mm Hg. After that, ECBF showed a gradual decrease with further increasing of SBP from 170 to 200 mm Hg, and finally a rapid decrease with SBP increasing from 200 mm Hg to higher. ECBF showed a similar change with increasing of DBP: a rapid increase from 75 to 100 mm Hg, then a gradual increase from 100 to 110 mm Hg, furthermore, a gradual decrease from 110 to 125 mm Hg, and finally a rapid decrease from 125 mm Hg to higher.
Figure 2.
Relationship between SBP/DBP and ECBF. A, Relationship between SBP and ECBF, R2 = 0.199, F = 90.745, P < .001; B, Relationship between DBP and ECBF, R2 = 0.245, F = 118.154, P < .001 Data were analyzed using a cubic equation of curve estimation. SBP, systolic blood pressure; DBP, diastolic blood pressure
3.3. The association of ECBF with neurofunctional recovery
As shown in Table 2, sufficient ECBF in the acute phase of ischemic stroke was associated with good neurofunctional recovery at 3 months of stroke. After adjustment with confounding factors, the trend still remained in Model I, II and Model III. E/T means number at events/total cases, ie, the number of patients with good recovery/the number of total patients in this study in Table 2.
Table 2.
The relationships between ECBF and good recovery at 3‐month of stroke onset
| No. at E/Ta, % | Unadjusted | Model I | Model II | Model III | |||||
|---|---|---|---|---|---|---|---|---|---|
| OR (95% CI) | P | OR (95% CI) | P | OR (95% CI) | P | OR (95% CI) | P | ||
| Good recovery | 236/732 (32.24) | 1.15 (1.03‐1.28) | .016 | 1.14 (1.02‐1.28) | .02 | 1.14 (1.01‐1.27) | .027 | 1.16 (1.03‐1.30) | .016 |
CI, confidence interval; OR, Odds Ratio.
Logistic regression models were used in the analyses. Model I was adjusted for mean age, gender. Model II was adjusted for the multivariate (based on Model I, plus current smoker, hypertension, diabetes mellitus, hyperlipidemia, significant carotid atherosclerosis, coronary artery disease, congestive heart failure, chronic kidney disease, posterior circulation infarction, thrombolytic). Model III was adjusted for the multivariate (based on Model II plus modified Rankin scale, National Institute of Health stroke scale, cerebral infarct volume and heart rate and eGRF).
No. at E/T, number at events/total cases, means the number of patients with good recovery/the number of total patients in this study.
3.4. The association of blood pressure with neurofunctional recovery
At 3 months of stroke, the most patients in Q3s (SBP of 161 to 177 mm Hg and DBP of 103 to 114 mm Hg, respectively) demonstrated a good neurofunctional recovery. As shown in Tables 3 and 4, a higher or lower blood pressure levels was negatively associated with good prognosis, when Q3 was as reference. The significant associations still remained after adjusting for conventional risk factors in Model I, II and Model III.
Table 3.
The multi‐parameter logistic regression analysis of SBP and good neurological functional recovery at 3‐month of onset
| Quintile | No. at E/Ta(%) | Unadjusted | Model I | Model II | Model III | ||||
|---|---|---|---|---|---|---|---|---|---|
| OR (95% CI) | P | OR (95% CI) | P | OR (95% CI) | P | OR (95% CI) | P | ||
| Q1 (<143) | 41/146 (28.08) | 0.44 (0.27‐0.71) | .001 | 0.44 (0.27‐0.72) | .001 | 0.42 (0.25‐0.71) | .001 | 0.41 (0.21‐0.80) | .008 |
| Q2 (144‐160) | 54/145 (37.24) | 0.66 (0.41‐1.06) | .086 | 0.66 (0.41‐1.06) | .084 | 0.61 (0.38‐1.00) | .052 | 0.67 (0.40‐1.11) | .119 |
| Q3 (161‐177) | 68/144 (47.22) | 1 | 1 | 1 | 1 | ||||
| Q4 (178‐191) | 41/149 (27.51) | 0.42 (0.26‐0.69) | .001 | 0.42 (0.26‐0.69) | .001 | 0.43 (0.25‐0.73) | .002 | 0.51 (0.29‐0.89) | .017 |
| Q5 (≥192) | 32/148 (21.62) | 0.31 (0.19‐0.51) | <.001 | 0.31 (0.18‐0.51) | <.001 | 0.35 (0.20‐0.60) | <.001 | 0.36 (0.20‐0.64) | <.001 |
CI, confidence interval; OR, Odds Ratio.
Q was quintile according to the levels of SBP. Logistic regression models were used in the analyses. Model I was adjusted for mean age, gender. Model II was adjusted for the multivariate (based on Model I, plus current smoker, hypertension, diabetes mellitus, hyperlipidemia, significant carotid atherosclerosis, coronary artery disease, congestive heart failure, chronic kidney disease, posterior circulation infarction, thrombolytic). Model III was adjusted for the multivariate (based on Model II plus modified Rankin scale, National Institute of Health stroke scale, cerebral infarct volume and heart rate and eGRF).
No. at E/T, number at events/total cases, means the number of patients with good recovery/the number of total patients in each quintile.
Table 4.
The multi‐parameter logistic regression analysis of DBP and good neurological functional recovery at 3‐month of onset
| Quintile | No.at E/Ta(%) | Unadjusted | Model I | Model II | Model III | ||||
|---|---|---|---|---|---|---|---|---|---|
| OR (95% CI) | P | OR (95% CI) | P | OR (95% CI) | P | OR (95% CI) | P | ||
| Q1 (<90) | 19/144 (13.19) | 0.13 (0.07‐0.24) | <.001 | 0.14 (0.08‐0.24) | <.001 | 0.12 (0.07‐0.23) | <.001 | 0.13 (0.07‐0.27) | <.001 |
| Q2 (91‐102) | 66/149 (44.30) | 0.68 (0.43‐1.08) | .683 | 0.68 (0.43‐1.08) | .102 | 0.65 (0.40‐1.05) | .077 | 0.61 (0.37‐1.01) | .054 |
| Q3 (103‐114) | 78/145 (53.79) | 1 | 1 | 1 | 1 | ||||
| Q4 (115‐123) | 41/149 (27.52) | 0.33 (0.20‐0.53) | <.001 | 0.32 (0.20‐0.53) | <.001 | 0.32 (0.19‐0.54) | <.001 | 0.34 (0.19‐0.58) | <.001 |
| Q5 (≥124) | 32/148 (21.62) | 0.24 (0.14‐0.39) | <.001 | 0.24 (0.14‐0.39) | <.001 | 0.25 (0.15‐0.43) | <.001 | 0.26 (0.15‐0.46) | <.001 |
CI, Confidence Interval; OR, Odds Ratio.
Q was quintile according to the levels of DBP. Logistic regression models were used in the analyses. Model I was adjusted for mean age, gender. Model II was adjusted for the multivariate (based on Model I, plus current smoker, hypertension, diabetes mellitus, hyperlipidemia, significant carotid atherosclerosis, coronary artery disease, congestive heart failure, chronic kidney disease, posterior circulation infarction, thrombolytic). Model III was adjusted for the multivariate (based on Model II plus modified Rankin scale, National Institute of Health stroke scale, cerebral infarct volume and heart rate, and eGRF).
No. at E/T, number at events/total cases, means the number of patients with good recovery/the number of total patients in each quintile.
4. DISCUSSION
In this study, we investigated the association between the blood pressure levels in stroke patients with hypertension and their cerebral blood flow in the early phase of ischemic stroke and their neurofunctional recovery at 3 months after stroke in a large single‐center population. We found that a reverse “U” shape curve relationship between blood pressure levels and cerebral perfusion in the early phase of ischemic stroke with hypertension, and the similar relation with neurofunctional recovery at 3 months after stroke. The most patients in the middle quintile (SBP of 161 to 177 mm Hg and DBP of 103 to 114 mm Hg, respectively) demonstrated a good neurofunctional recovery, while higher or lower blood pressure levels were negatively associated with good prognosis.
Normally, the brain can maintain relatively stable cerebral flow via its auto‐regulation function while blood pressure levels fluctuate in a certain range. The autoregulation capability of cerebral arteries will be weakened if blood pressure levels exceed the BP threshold and the autoregulatory capability of cerebral arteries is compromised, and the CBF becomes a more passive process and will decrease dramatically.9 To keep sufficient cerebral blood flow at relatively stabilized levels, it is necessary to control blood pressure levels within a certain range. Accordingly, cerebral blood flow can meet the needs of brain metabolic with the increase of blood pressure after stroke as long as blood pressure keeps in a reasonable range. However, exorbitant blood pressure may reflexly cause intensive cerebral vasospasm through the endogenous vasomotor mechanism, which in turn decreases cerebral flow and may lead to poor clinical outcomes.16 Hence, antihypertensive treatment should be started at the levels of SBP ≥190 mm Hg/DBP ≥120 mm Hg (the initiation levels of blood pressure lowering) within 24 hours after stroke, which is consistent with the recommendations of the Chinese diagnosis and therapy guideline of acute ischemic stroke (2014). On the other hand, aggressive blood pressure lowering might decrease cerebral perfusion15, 17, 18 and induce the expansion of the original cerebral ischemic region or creation of a new ischemic area, particularly in areas where there is a narrow artery. Our study also showed that higher and lower blood pressure levels were associated with hypoperfusion and poor prognosis.
A relatively high blood pressure level is beneficial to global cerebral blood flow in the case of local cerebral hypoperfusion. Some studies have noted a decreased risk of neurologic deterioration from stroke with higher blood pressure.19 Semplicini and colleagues found that induced hypertension resulted in partial but objective neurologic improvement when started 7 days after onset of stroke.20 Our study also showed that maintaining a relatively higher blood pressure levels was beneficial to cerebral perfusion in the early phase of ischemic stroke.
Currently, there are a few reports on the blood pressure levels at which antihypertension therapy should initiate or cease in the acute phase of ischemic stroke. A “U” shape curve relationship between initial blood pressure and prognosis in IST trial indicated that SBP between 140 mm Hg and 180 mm Hg was associated with the best outcome.21 Low blood pressure (SBP <140 mm Hg) was also associated with a poor outcome in the acute stroke period.22 However, lower blood pressure levels in those who continued antihypertensive treatment after acute stroke were not associated with an increase in adverse events.23 As a result, there is no definite conclusion on the ideal blood pressure levels and the levels for initiating or ceasing antihypertension therapy. The possible reasons included different time of admitting to the hospital after stroke onset, different time of initiating antihypertension treatment, and different therapies of antihypertension. In our study, the optimal blood pressure in the 24 hours after stroke onset was at SBP 161 to 177 mm Hg/DBP 103 to 114 mm Hg.
There were some limitations in this study. First, compared with other methods such as MR perfusion scanning, TCD is less precise in assessing cerebral perfusion. However, TCD is a convenient, simple, noninvasive procedure that does not cause adverse events and it has already been widely used in detecting ICA hemodynamics at the bedside. Second, thrombolysis is a therapeutic approach to maintain perfusion in injured arteries, and slightly lowered blood pressure is required in the patients treated with thrombolysis. Thus undergoing thrombolysis has an important effect on the association between blood pressure and neurofunctional recovery. However, only 48 patients underwent thrombolysis in our study, so we did not subgroup patients according to thrombolysis or not. Third, our cohort was drawn from a single center with a relatively small sample size. Further studies with larger samples in different centers are needed to verify the effects of blood pressure levels on cerebral perfusion at an early stage of ischemic stroke.
5. CONCLUSIONS
In summary, there was a reverse “U” shape curve relationship between blood pressure levels and cerebral perfusion in the early phase of ischemic stroke. ECBF would decrease dramatically if SBP ≥ 200 mm Hg/DBP ≥ 125 mm Hg or SBP < 100 mm Hg/DBP < 75 mm Hg, leading to neurological deteriorate. Maintaining blood pressure levels at SBP 161 to 177 mm Hg/DBP 103 to 114 mm Hg within 24 hours after stroke onset might be beneficial to cerebral perfusion and neurofunctional recovery at 3 months after stroke.
CONFLICT OF INTEREST
The authors have declared no conflicts of interest.
DISCLOSURES
This study was funded by National Key R&D Program of China with grant 2017YFC0909403, Chinese Academy of Medical Sciences with grant 2017‐I2M‐1‐008, National Natural Science Foundation of China with grant 81770424, and the State Key Laboratory of Cardiovascular Disease with grants 2017KF‐01/2017ZR0‐05/2017‐14 to Yibo Wang, the Bureau of Science and Technology of Jiangsu Province with Medical Scientific Specific Fund BL2014062 and the Health Bureau of Jiangsu Province with Science Research Fund H2014061 to Mingli He, Preventive Medicine Scientific Research Foundation of Jiangsu Province with grant Y2013032 to Guanghui Zhang.
ACKNOWLEDGMENTS
We want to thank the Health Bureau of Lianyungang City and the Health Bureau of Ganyu County for their help on research implementation, researcher training, and coordination.
He M, Cui B, Wu C, et al. Blood pressures immediately following ischemic strokes are associated with cerebral perfusion and neurologic function. J Clin Hypertens. 2018;20:1008–1015. 10.1111/jch.13310
Mingli He and Bing Cui equally contributed to this study.
Clinical Trial Registration URL: http://www.chictr.org. Unique identifier: ChiCTRTRC‐14004804.
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