Acute Blood Pressure Reduction Research Articles

Acute blood pressure reduction in patients with intracerebral hemorrhage does not result in borderzone region hypoperfusion.

The Intracerebral Hemorrhage Acutely Decreasing Arterial Pressure Trial (ICH ADAPT) demonstrated blood pressure (BP) reduction does not affect mean perihematoma or hemispheric cerebral blood flow. Nonetheless, portions of the perihematoma and borderzones may reach ischemic thresholds after BP reduction. We tested the hypothesis that BP reduction after intracerebral hemorrhage results in increased critically hypoperfused tissue volumes. Patients with Intracerebral hemorrhage were randomized to a target systolic BP (SBP) of <150 or <180 mm Hg and imaged with computed tomographic perfusion 2 hours later. The volumes of tissue below cerebral blood flow thresholds for ischemia (<18 mL/100 g/min) and infarction (<12 mL/100 g/min) were calculated as a percentage of the total volume within the internal and external borderzones and the perihematoma region. Seventy-five patients with intracerebral hemorrhage were randomized a median (interquartile range) of 7.8 (13.3) hours from onset. Acute hematoma volume was 17.8 (27.1) mL and mean SBP was 183±22 mm Hg. At the time of computed tomographic perfusion (2.3 [1.0] hours after randomization), SBP was lower in the <150 mm Hg (n=37; 140±18 mm Hg) than in the <180 mm Hg group (n=36; 162±12 mm Hg; P<0.001). BP treatment did not affect the percentage of total borderzone tissue with cerebral blood flow<18 (14.7±13.6 versus 15.6±13.7%; P=0.78) or <12 mL/100 g/min (5.1±5.1 versus 5.8±6.8%; P=0.62). Similar results were found in the perihematoma region. Low SBP load (fraction of time with SBP<150 mmHg) did not predict borderzone tissue volume with cerebral blood flow<18 mL/100 g/min (β=0.023 [-0.073, 0.119]). BP reduction does not increase the volume of critically hypoperfused borderzone or perihematoma tissue. These data support the safety of early BP reduction in intracerebral hemorrhage. http://www.clinicaltrials.gov. Unique identifier: NCT00963976.

Blood Pressure Lowering and Acute Perihematomal Brain Edema After Intracerebral Hemorrhage

See related article, p 1292. Intracerebral hemorrhage (ICH) is a common and often fatal subtype of stroke that produces severe neurological deficits in survivors.1 There are still no proven therapeutic interventions for ICH, but there has been much interest in the potential use of acutely reducing blood pressure to limit hematoma expansion. A key factor affecting ICH outcome is hematoma size, and hematoma expansion occurs in about one third of patients with ICH.2 This has led to 3 clinical trials: Intensive Blood Pressure Reduction in Acute Cerebral Hemorrhage Trial (INTERACT), Antihypertensive Treatment of Acute Cerebral Hemorrhage (ATACH), and The Intracerebral Hemorrhage Acutely Decreasing Arterial Pressure Trial (ICH ADAPT).3–5 INTERACT 2 reported last year6 and suggested an improvement in outcome although this did not reach statistical significance. Understanding the importance of those results requires determination of whether acute blood pressure reductions may have detrimental and beneficial effects in patients with ICH. In this …

Regional cerebral blood flow responses to rapid reductions in blood pressure after high level spinal cord injury: the effect of alpha1‐agonist (1068.8)

Spinal cord injury (SCI) above the T6 level frequently results in orthostatic intolerance, but how cerebral blood flow (CBF) responds to an orthostatic challenge in SCI is poorly understood. It is also unclear how alpha1 agonists, meant to improve orthostatic tolerance, influence the CBF response. This study examined: 1) the acute regional CBF velocity (CBFv) response to acute blood pressure (BP) reductions secondary to orthostatic stress in SCI, compared to able‐bodied controls (AB), and 2) the effect of Midodrine (alpha1‐agonist) on orthostatic tolerance and CBFv regulation in SCI. Ten individuals with SCI &gt;T6, and 10 age‐and sex‐matched controls had beat‐by‐beat BP, as well as middle and posterior cerebral artery blood velocity (MCAv, PCAv) recorded during a progressive tilt‐test to quantify the acute CBF response and orthostatic tolerance. Dynamic CBFv‐BP relationships were evaluated from the first 60s after tilt. The SCI group was tested again after administration of an alpha1‐agonist (10 mg midodrine) in order to elevate BP. The acute (i.e., 0‐30s after tilt) MCAv and PCAv responses were similar in SCI and AB. In contrast, Midodrine led to improved PCAv responses 30‐60 s (10±3 vs. 4±2 %decline; p&lt;0.05) after tilt, and a 59% improvement in orthostatic tolerance (p&lt;0.01). The vertebrobasilar region may be particularly susceptible to hypoperfusion in SCI, leading to increased orthostatic intolerance.Grant Funding Source: Supported by HSFC, NSERC, MSFHR &amp; CNF

Abstract 33: Cerebral Blood Flow in Leukoaraiosis Regions is Unaffected by Acute Lowering of Blood Pressure in Intracerebral Hemorrhage Patients.

Introduction: Leukoariosis(LA) is associated with poor prognosis in intracerebral hemorrhage (ICH) patients. Patients with chronic small vessel ischemic changes may be more vulnerable to decreases in cerebral perfusion, in both LA and perihematoma(PH) regions. We tested the hypotheses that acute blood pressure reduction (BP) in ICH patients is associated with decreased cerebral blood flow (CBF) in areas of LA and the PH region. Methods: In the ICH Acutely Decreasing Arterial Pressure Trial (ICH ADAPT), patients with ICH &lt;24 hours duration were randomized to two systolic BP (SBP) target groups (&lt;150 mmHg vs. &lt;180 mmHg). Computed tomography (CT) perfusion imaging was performed 2 h post-randomization. LA tissue volume was planimetrically measured on the acute non-contrast CT, using Hounsfield Unit thresholds of 15-25. CBF, cerebral blood volume (CBV), and Tmax were measured in the LA regions. Results: Seventy-one patients were included with a mean age of 69.3±11.5 years and median (IQR) baseline NIHSS score of 10(11). LA was present in 74.6% (53/71) and the median volume was 8.5(20.6) ml. LA was associated with older age (70.9± 11.2 vs. 64.8 ±11.6, p=0.05) and larger ICH volumes (19.52(29.78) vs. 9.52(16.02) ml, p=0.007). Mean CBF in LA regions (32.5±13.5) was similar to that in normal appearing white matter (35.6±12.1, p=0.3). Despite a significant drop in SBP between aggressive (36.25(40) mmHg) and conservative (18.5(29) mmHg, p=0.01) treatment groups, relative CBF (rCBF) in LA regions was unaffected (0.88±0.1 vs. 0.89±0.09, p=0.6). Similarly, aggressive BP treatment did not affect relative CBV (0.83±0.16 vs. 0.82± 0.15, p=0.8) or Tmax (7.3±3.2 s vs. 6.5 ±2.4 s, p=0.3). The rCBF in the PH regions in patients’ with/without LA was similar (0.88±0.09 vs. 0.86±0.1, p=0.5). There was a trend to worse functional outcome at 90 days, measured with the modified Rankin Scale in patients with LA (4(4) vs. 2(1), p=0.06). Conclusion: LA is associated with larger baseline ICH volumes, but no differences in perihematoma CBF or the response to BP reduction. CBF in LA tissue is also unaffected by BP reduction. These data do not support a less aggressive approach to BP reduction in elderly patients with imaging evidence of chronic small vessel ischemia.

Renal denervation suppresses ventricular arrhythmias during acute ventricular ischemia in pigs

Increased sympathetic activation during acute ventricular ischemia is involved in the occurrence of life-threatening arrhythmias. To test the effect of sympathetic inhibition by renal denervation (RDN) on ventricular ischemia/reperfusion arrhythmias. Anesthetized pigs, randomized to RDN or SHAM treatment, were subjected to 20 minutes of left anterior descending coronary artery (LAD) occlusion followed by reperfusion. Infarct size, hemodynamics, premature ventricular contractions, and spontaneous ventricular tachyarrhythmias were analyzed. Monophasic action potentials were recorded with an epicardial probe at the ischemic area. Ventricular ischemia resulted in an acute reduction of blood pressure (-29%) and peak left ventricular pressure rise (-40%), which were not significantly affected by RDN. However, elevation of left ventricular end-diastolic pressure (LVEDP) during LAD ligation was attenuated by RDN (ΔLVEDP: +1.8 ± 0.6 mm Hg vs +9.7 ± 1 mm Hg in the SHAM group; P = .046). Infarct size was not affected by RDN compared to SHAM. RDN significantly reduced spontaneous ventricular extrabeats (160 ± 15/10 min in the RDN group vs 422 ± 36/10 min in the SHAM group; P = .021) without affecting coupling intervals. In 5 of 6 SHAM-treated animals, ventricular fibrillation (VF) occurred during LAD occlusion. By contrast, only 1 of 7 RDN-treated animals experienced VF (P = .029). Beta-receptor blockade by atenolol showed comparable effects. Neither VF nor transient shortening of monophasic action potential duration during reperfusion was inhibited by RDN. RDN reduced the occurrence of ventricular arrhythmias/fibrillation and attenuated the rise in LVEDP during left ventricular ischemia without affecting infarct size, changes in ventricular contractility, blood pressure, and reperfusion arrhythmias. Therefore, RDN may protect from ventricular arrhythmias during ischemic events.

Blood Pressure Control for Spontaneous Intracerebral Hemorrhage

Blood Pressure Control for Spontaneous Intracerebral Hemorrhage

Autoregulation of Cerebral Blood Flow is Preserved in Primary Intracerebral Hemorrhage

Treatment of acute hypertension after intracerebral hemorrhage (ICH) is controversial. In the context of disrupted cerebral autoregulation, blood pressure (BP) reduction may cause decreased cerebral blood flow (CBF). We used serial computed tomography perfusion to test the hypothesis that CBF remains stable after BP reduction. Patients recruited within 72 hours of ICH were imaged with computed tomography perfusion before and after BP treatment. Change in perihematoma relative (r) CBF after BP treatment was the primary end point. Twenty patients were imaged with computed tomography perfusion at a median (interquartile range) time from onset of 20.2 (25.7) hours and reimaged 2.1 (0.5) hours later, after BP reduction. Mean systolic BP in treated patients (n=16; 4 untreated as BP<target at baseline) decreased significantly between the first (168 ± 21 mm Hg) and second (141 ± 19 mm Hg; P<0.0001) computed tomography perfusion scans. The primary end point of rCBF was not affected by BP reduction (pretreatment=0.89 ± 0.11; post-treatment=0.87 ± 0.11 mL/100 g per minute; P=0.37). Linear regression showed no relationship between changes in systolic BP and perihematoma rCBF (β=0.001 [-0.002 to 0.003]; P=0.63). CBF remained stable after acute BP reduction, suggesting some preservation of cerebral autoregulation.

The Intracerebral Hemorrhage Acutely Decreasing Arterial Pressure Trial

Acute blood pressure (BP) reduction aimed at attenuation of intracerebral hemorrhage (ICH) expansion might also compromise cerebral blood flow (CBF). We tested the hypothesis that CBF in acute ICH patients is unaffected by BP reduction. Patients with spontaneous ICH <24 hours after onset and systolic BP > 150 mm Hg were randomly assigned to an intravenous antihypertensive treatment protocol targeting a systolic BP of <150 mm Hg (n=39) or <180 mm Hg (n=36). Patients underwent computed tomography perfusion imaging 2 hours postrandomization. The primary end point was perihematoma relative (relative CBF). Treatment groups were balanced with respect to baseline systolic BP: 182±20 mm Hg (<150 mm Hg target group) versus 184±25 mm Hg (<180 mm Hg target group; P=0.60), and for hematoma volume: 25.6±30.8 versus 26.9±25.2 mL (P=0.66). Mean systolic BP 2 hours after randomization was significantly lower in the <150 mm Hg target group (140±19 vs 162±12 mm Hg; P<0.001). Perihematoma CBF (38.7±11.9 mL/100 g per minute) was lower than in contralateral homologous regions (44.1±11.1 mL/100 g per minute; P<0.001) in all patients. The primary end point of perihematoma relative CBF in the <150 mm Hg target group (0.86±0.12) was not significantly lower than that in the <180 mm Hg group (0.89±0.09; P=0.19; absolute difference, 0.03; 95% confidence interval -0.018 to 0.078). There was no relationship between the magnitude of BP change and perihematoma relative CBF in the <150 mm Hg (R=0.00005; 95% confidence interval, -0.001 to 0.001) or <180 mm Hg target groups (R=0.000; 95% confidence interval, -0.001 to 0.001). Rapid BP lowering after a moderate volume of ICH does not reduce perihematoma CBF. These physiological data indicate that acute BP reduction does not precipitate cerebral ischemia in ICH patients. Clinical Trial Registration Information- URL:http://clinicaltrials.gov. Unique Identifier: NCT00963976.

Abstract 113: The Intracerebral Haemorrhage Acutely Decreasing Arterial Pressure Trial (ICH ADAPT): Final Results.

Background: Acute blood pressure (BP) reduction aimed at attenuation of intracerebral hemorrhage (ICH) expansion might also result in a harmful compromise of cerebral blood flow (CBF) in the region surrounding the hematoma. We tested the hypothesis that CBF in acute ICH patients is affected by BP reduction. Methods: Seventy-five patients with spontaneous ICH with baseline systolic BP&gt;150 mmHg were randomly assigned to an intravenous antihypertensive treatment protocol (labetalol, hydralazine and enalapril) targeting a systolic BP of either &lt;150 mmHg or &lt;180 mmHg within 24 hours of symptom onset. Patients underwent CT perfusion (CTP) imaging 2 hours post-randomization. The primary endpoint was relative CBF (rCBF) within the 1 cm perihematoma region. Results: Treatment groups were balanced with respect to baseline systolic BP: 182±20 mmHg (&lt;150 mmHg target group, n=39) vs. 184±25 mmHg (&lt;180 mmHg target group, n=36, p=0.60), hematoma volume: 25.6±30.8 vs. 26.9±25.2 ml (p=0.66) and median (IQR) time to randomization: 7.8 (13.5) and 8.5 (11.9) h (p=0.94). Mean systolic BP two hours after randomization was significantly lower in the &lt;150 mmHg target group (140±19 vs 162±12 mmHg in the &lt;180 target group, p&lt;0.001). Perihematoma CBF (38.7±11.9 ml/100g/min) was lower than in contralateral homologous regions (44.1±11.1 ml/100g/min, p&lt;0.001) in all patients. The primary endpoint of perihematoma rCBF in the &lt;150 mmHg target group (0.86±0.12) was not significantly lower than that in the &lt;180 mmHg group (0.89±0.09, p=0.19; absolute difference 0.03 95% CI -0.018, 0.078). There was no relationship between the magnitude of the BP change and perihematoma rCBF in the &lt;150 mmHg (R=0.00005, 95% CI -0.001, 0.001) or &lt;180 mmHg target groups (R=0.000, 95% CI -0.001, 0.001). There were no effects on rCBF in patients treated within 6 hours (0.78±0.22 in the &lt;150 mmHg group and 0.88±0.10 in the &lt;180 mmHg group, p=0.08) or in those treated 6-24 hours after onset (0.85±0.21 in the &lt;150 mmHg group and 0.89±0.10 in the &lt;180 mmHg group, p=0.46). Conclusions: Rapid BP lowering following ICH does not reduce perihematoma CBF. These physiological data support the safety of acute and aggressive BP reduction following ICH.

Abstract WP295: Acute Blood Pressure Reduction in Intracerebral Hemorrhage Patients Does Not Increase Hypoperfused Tissue Volume: a CT Perfusion Threshold Study

Background: The Intracerebral Hemorrhage Acutely Decreasing Arterial Pressure Trial (ICH ADAPT) demonstrated that aggressive blood pressure (BP) reduction does not affect mean perihematoma cerebral blood flow (CBF). It remains unknown if portions of the perihematoma region or watershed vascular territories (borderzones, BZs) reach ischemic thresholds after BP reduction. We tested the hypothesis that aggressive BP reduction was associated with an increased volume of critically hypoperfused tissue in ICH ADAPT patients. Methods: ICH patients were randomized to a target systolic BP (SBP) of &lt;150 or &lt;180 mmHg and imaged with CT perfusion (CTP) 2h later. A 1cm perihematoma region, and ipsilateral and contralateral internal and external BZs were outlined. The volume of tissue below CBF thresholds for ischemia (&lt;18ml/100g/min) and infarction (&lt;12ml/100g/min) was calculated as a percentage of the total volume of each region of interest. Results: ICH patients (n=73) were randomized a median (IQR) of 7.8 (13.3) h from onset and imaged with CTP 2.3 (1.0) h later. Acute hematoma volume was 17.8 (27.1) ml and mean SBP was 183±22 mmHg. At the time of CTP, SBP was lower in the &lt;150 mmHg group (n=37, 140±18 mmHg) than the &lt;180 mmHg group (n=36, 162±12 mmHg, P&lt;0.001). Mean CBF in the perihematoma region did not differ between groups (&lt;150 mmHg: 38.9±13.0 vs. &lt;180 mmHg: 38.5±10.9 ml/100g/min, P=0.86). BP treatment did not affect the percentage of perihematoma tissue with CBF &lt;18 (17.5±15.4 (&lt;150 group) vs. 16.5±14.3% (&lt;180 group), P=0.82) or &lt;12 ml/100g/min (7.0±7.2 vs. 6.6±7.6%, P=0.93). Similar results were found in all BZs. Linear regression revealed no relationship between low SBP load (the fraction of time between randomization and CTP with SBP &lt;150mmHg) and the percentage of perihematoma tissue with CBF &lt;18 (β=3.62, [-6.86, 14.10]) or &lt;12 ml/100g/min (β=1.89, [-3.30, 7.08]). There was no relationship between low SBP load and percentage of hypoperfused tissue in any BZ. Perfusion threshold analysis of time domain parameters and cerebral blood volume yielded similar results. Conclusion: BP reduction does not increase the volume of hypoperfused tissue, at any threshold examined, in the perihematoma region or any BZ. These data support the safety of early BP reduction in ICH.

Abstract WP435: Acute Blood Pressure Reduction and Cerebral Infarction After Aneurysmal Subarachnoid Hemorrhage

Background: Radiographic cerebral infarction (RCI) is a prominent cause of disability after aneurysmal subarachnoid hemorrhage (SAH). Current guidelines for acute blood pressure (BP) management of SAH patients are intended to prevent rebleeding, but their potential impact on RCI is unknown. HYPOTHESIS: RCI after SAH is associated with more acute BP reduction and lower BP. METHODS: We evaluated 49 patients with SAH. Clinical and radiographic data were prospectively collected. BP data were electronically retrieved from the medical record. BP was compared with multivariate generalized linear models. RESULTS: RCI was detected in 19 of 49 patients (38.8%). No rebleeding occurred in any of the patients during their hospital stay. Vasospasm occurred in 8 (16.3%) of patients and was associated with higher systolic and diastolic BP (P&lt;0.001 for both) between days 4 and 14. Historical hypertension was associated with RCI (52.6% vs. 23.3%, P=0.036), although initial systolic (168±37 vs. 151±26 mm Hg, P=0.1) and diastolic BP (90±20 vs. 83±19, P=0.2) were not. In a generalized linear model accounting for time from symptom onset, vasospasm, historical hypertension and a vasospasm by time interaction (since BP augmentation depended on the time from symptom onset), lower systolic (-7, 95%CI -8 to -6 mm Hg, (P&lt;0.001) and diastolic BP (-5, 95%CI -6 to -4 mm Hg, P&lt;0.001) were associated with RCI. There were similar data for change in BP from initial BP. CONCLUSIONS: RCI after SAH is associated with greater BP reductions and historical hypertension may contribute to this risk. More aggressive BP reduction than recommended by current guidelines, while potentially decreasing the risk of aneurysm rebleeding, may be associated with RCI. Routine perfusion scanning to determine the risk of RCI from reduced perfusion may be warranted.

Anaphylactic Shock Decreases Cerebral Blood Flow More Than What Would Be Expected From Severe Arterial Hypotension

The effects of acute reduction in arterial blood pressure in severe anaphylactic shock (AS) on cerebral blood flow are of paramount importance to be investigated. We studied cerebral circulation and oxygenation in a model of severe AS and compared it with a pharmacologically induced arterial hypotension of similar magnitude. Anaphylactic shock was induced by 1 mg intravenous ovalbumin (OVA) in sensitized rats. Rats were randomized to three groups: (i) no resuscitation (OVA; n = 10) (ii) intravenous volume expansion (10 mL in 10 min after OVA injection) (OVA + VE; n = 10); (iii) control hypotension (100 μg of nicardipine followed by continuous infusion of 1 mg · 100 g · h intravenously; NICAR; n = 10). Mean arterial pressure (MAP), carotid blood flow (CBF), cardiac output, cerebral cortical blood flow (CCBF; estimated by laser Doppler technique), and cerebral tissue oxygen pressure (PtiO2) were recorded over the 15 min following AS induction in all three groups. Results are expressed as mean (SD). One minute after OVA or nicardipine injection, there was a rapid and significant 50% decrease in MAP from basal values. In the OVA group, AS severely altered systemic and cerebral hemodynamics in 5 min: 93% (SD, 4%) decrease in CBF, 66% (SD, 8%) in CCBF, and 44% (SD, 8%) in PtiO2; the decrease in CBF was significantly (P < 0.05) attenuated in the OVA + VE group; however, CCBF and PtiO2 were not statistically different in the OVA versus OVA + VE groups. On the contrary, nicardipine-induced hypotension had only a limited impact on CBF, cardiac output, CCBF, and PtiO2 for a similar MAP decrease. There was a linear relation between CCBF and blood pressure in the OVA (regression slope: 0.87 [SD, 0.06]; median r = 0.81) but not in the NICAR group (regression slope: 0.23 [SD, 0.32]; median r = 0.33). Anaphylactic shock resulted in severe impairment of cerebral blood flow and oxygenation, beyond what could be expected from the level of arterial hypotension.

Acute, NO‐mediated, effects of erythropoietin are not associated with its cardioprotective properties

Our serendipitous observation of acute reduction of blood pressure associated with a systemic injection of recombinant human erythropoietin (rhEPO) in the rat prompted a systematic evaluation of the acute effects of rhEPO on cardiovascular function and cardioprotection. Four groups of rats (Wistar, male, 3‐mo old) received bolus i.v. injection of one of the following: physiological saline, rhEPO (3000 U/kg), saline+L‐NAME (15 mg/kg), or rhEPO+L‐NAME. Two hours after injections rats were anesthetized with Isoflurane and subjected to detailed analyses of cardiovascular performance via open chest pressure‐volume loops analyses. In the second experiment four groups of rats were subjected to a permanent ligation of descending coronary artery immediately followed by the same i.v. injections as in the first experiment. Twenty four hours following coronary ligation hearts were harvested and myocardial infarct size (MI) was measured histologically. A significant reduction of arterial blood pressure two hours after a rhEPO injection was accompanied with a reduction of left ventricular systolic function (Table). L‐NAME completely suppressed this acute cardiovascular response to rhEPO. In contrast, the 50% reduction of MI size observed 24 hrs after coronary ligation in rhEPO‐treated vs untreated rats was not affected by L‐NAME treatment. Thus, these novel NO‐mediated acute hemodynamic effects of rhEPO are not associated with EPO‐associated cardioprotection. Parameters Saline rhEPO ESP 85±5 66±5* dP/dt+ 7136±530 5420±382* PRSW 51.8±3.9 34.6±2.5* BPs 90±6 70±3* BPd 55±5 38±3 BPm 66±6 49±3* ‐p&lt;0.05

Hemodynamic Stability After Intraarterial Injection of Verapamil for Cerebral Vasospasm

Vasospasm after subarachnoid hemorrhage is a common and potentially life-threatening complication. Treatment of vasospasm may include intraarterial (IA) injections of verapamil into the cerebral vasculature. Clinical experience suggests that the average patient experiences an acute reduction in systemic blood pressure after IA verapamil. Our study objective was to (1) identify the effects of IA injection of verapamil on mean arterial blood pressure (MAP) and heart rate (HR) in patients with cerebral vasospasm and (2) determine the effect of verapamil dose on change in MAP and HR. We hypothesized that (1) selective IA injection of verapamil for treatment of cerebral vasospasm is associated with a reduction in MAP and an increase in HR and (2) the change in MAP and HR are linearly related to the dose of verapamil administered. We prospectively studied subjects with vasospasm scheduled for cerebral angiography with possible IA injection of verapamil. All subjects were given a general anesthetic. Invasive arterial blood pressure and HR were monitored continuously and recorded at 10-second intervals throughout the procedure. We identified the lowest MAP and highest HR before and after verapamil injection. The association between IA verapamil and change in MAP and HR was determined using repeated-measures multivariate regression analysis, adjusting for potential confounding factors (weight, preoperative vasopressor use, and preinjection MAP). Data are reported as adjusted coefficients and 95% confidence intervals (CI). We included 20 subjects who underwent a total of 46 injections of IA verapamil. On the basis of our multivariate model, on average, each 5 mg of IA verapamil was associated with a 3.5 mm Hg reduction in MAP (95% CI -5.0 to -2.0, P < 0.001). HR was not significantly altered by IA verapamil on both unadjusted and adjusted analyses (nonsignificant increase of 0.4 beats per minute for each 5 mg of IA verapamil, 95% CI -1.6 to 2.4, P = 0.70). Under general anesthesia, injection of IA verapamil into cerebral arteries reduces MAP but does not change HR in the average patient. Further research is required to determine the clinical significance of these results.

Abstract 2619: Autoregulation of Cerebral Blood Flow is Preserved in Primary Intracerebral Hemorrhage

Background: Treatment of hypertension during acute intracerebral hemorrhage (ICH) is controversial. There are concerns that in the context of disrupted cerebral autoregulation, blood pressure (BP) reduction may cause decreased cerebral blood flow (CBF), particularly in the perihematoma region. CBF was assessed using serial CT perfusion (CTP) studies. We hypothesized that CBF would remain stable following BP reduction. Methods: Acute primary ICH patients were imaged pre and post BP treatment. Perfusion maps were calculated from CTP source images. Mean CBF was measured in a 1cm perihematoma region, contralateral homologous regions and in both hemispheres. Mean cerebral blood volume (CBV), mean transit time (MTT), and time to drain (TTD) were calculated in the same manner. Relative measures (i.e. rCBF) were calculated as ratios/differences between ipsilateral and contralateral regions. Results: Sixteen patients (median age 75 (54-91)) were imaged with CTP (median time from onset 19.4 (2.0-72.2) h) and re-imaged 2.0 (1.1-3.3) h later. Median NIHSS at baseline was 9 (2-24); this remained stable at the time of the second CTP (10 (2-24), P=0.14). Baseline hematoma volume was 24.8±19.9 ml and there was no change at the time of the second CTP (26.3±22.1 ml, P=0.16). Patients were recruited from an ongoing trial, in which they were randomly treated to a target systolic BP of &lt;150mmHg (n=9) or &lt;180mmHg (n=7). Four patients received no antihypertensives as BP was below target at the time of randomization. Mean systolic BP in treated patients (n=12) decreased significantly between the first (165±23 mmHg) and second (143±18 mmHg, P&lt;0.0001) CTP scans. Mean perihematoma CBF in treated patients was stable with BP reduction (pre=35.1±7.1 vs. post=35.4±6.2 ml/100g/min, P=0.87). Ipsilateral hemispheric CBF was also stable (pre=47.3±7.2 vs. post=46.4±7.1 ml/100g/min, P=0.66). Although perihematoma CBF was lower than in contralateral homologous regions (rCBF=0.72±0.11), BP reduction did not decrease this further (0.74±0.14 post-treatment, P=0.58). Ipsilateral hemispheric rCBF (0.96±0.06) was also unaffected by BP treatment (0.95±0.08, P=0.64). Perihematoma rCBF decreased in 5 treated patients, but never by &gt;12%. Linear regression showed no relationship between changes in systolic BP and perihematoma rCBF (R=-0.002, [-0.005, 0.001], P=0.18). Perihematoma rCBV (pre=0.77±0.11 vs. post=0.79±0.10, P=0.20), rMTT (pre=0.51±0.54s vs. post=0.70±0.65s, P=0.26) and rTTD (pre=0.71±1.01s vs. post=0.89±0.84s, P=0.42) also remained stable following BP treatment. Conclusions: Acute BP reduction does not appear to exacerbate perihematoma oligaemia. Stability of CBF following acute BP treatment suggests preservation of cerebral autoregulation in ICH, within the range of arterial pressures studied. These findings support the safety of early BP treatment in ICH.

Korean red ginseng improves blood pressure stability in patients with intradialytic hypotension.

Introduction. Intradialytic hypotension (IDH) is a common complication during hemodialysis which may increase mortality risks. Low dose of Korean red ginseng (KRG) has been reported to increase blood pressure. Whether KRG can improve hemodynamic stability during hemodialysis has not been examined. Methods. The 8-week study consisted of two phases: observation phase and active treatment phase. According to prehemodialysis blood pressure (BP), 38 patients with IDH were divided into group A (BP ≥ 140/90 mmHg, n = 18) and group B (BP < 140/90 mmHg, n = 20). Patients were instructed to chew 3.5 gm KRG slices at each hemodialysis session during the 4-week treatment phase. Blood pressure changes, number of sessions disturbed by symptomatic IDH, plasma levels of vasoconstrictors, blood biochemistry, and adverse effects were recorded. Results. KRG significantly reduced the degree of blood pressure drop during hemodialysis (P < 0.05) and the frequency of symptomatic IDH (P < 0.05). More activation of vasoconstrictors (endothelin-1 and angiotensin II) during hemodialysis was found. The postdialytic levels of endothelin-1 and angiotensin II increased significantly (P < 0.01). Conclusion. Chewing KRG renders IDH patients better resistance to acute BP reduction during hemodialysis via activation of vasoconstrictors. Our results suggest that KRG could be an adjuvant treatment for IDH.

Response to Letter by Nishikawa Regarding Article, “Blood Pressure Reduction, Decreased Diffusion on MRI, and Outcomes After Intracerebral Hemorrhage”

HomeStrokeVol. 43, No. 1Response to Letter by Nishikawa Regarding Article, “Blood Pressure Reduction, Decreased Diffusion on MRI, and Outcomes After Intracerebral Hemorrhage” Free AccessReplyPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessReplyPDF/EPUBResponse to Letter by Nishikawa Regarding Article, “Blood Pressure Reduction, Decreased Diffusion on MRI, and Outcomes After Intracerebral Hemorrhage” Andrew M. Naidech, MD, MSPH, Matthew B. Maas, MD, Alexander J. Nemeth, MD and Eric J. Russell, MD Andrew M. NaidechAndrew M. Naidech Northwestern University Feinberg School of Medicine Chicago, IL (Naidech, Maas, Nemeth, Russell) Search for more papers by this author , Matthew B. MaasMatthew B. Maas Northwestern University Feinberg School of Medicine Chicago, IL (Naidech, Maas, Nemeth, Russell) Search for more papers by this author , Alexander J. NemethAlexander J. Nemeth Northwestern University Feinberg School of Medicine Chicago, IL (Naidech, Maas, Nemeth, Russell) Search for more papers by this author and Eric J. RussellEric J. Russell Northwestern University Feinberg School of Medicine Chicago, IL (Naidech, Maas, Nemeth, Russell) Search for more papers by this author Originally published15 Dec 2011https://doi.org/10.1161/STROKEAHA.111.643007Stroke. 2012;43:e15Other version(s) of this articleYou are viewing the most recent version of this article. Previous versions: January 1, 2011: Previous Version 1 Response:Nishikawa1 notes that we found a high incidence of decreased diffusion (DD) in patients with intracerebral hemorrhage compared with other studies. We are glad that he agrees, and his unpublished data confirm, that whether DD is common is not the issue, but rather, how common it is. A few methodological differences may account for the differences between cohorts. Patients in the sample reported by the Massachusetts General Hospital2 group were not acutely symptomatic from cerebral amyloid angiography (1 was excluded for that reason), a different population than our sample (acute intracerebral hemorrhage generally from amyloid angiopathy or hypertension). In the cohort from our colleagues across town at Rush,3 MRI scans were interpreted by stroke neurologists; perhaps neuroradiologists are more sensitive, although the interrater reliability for assessing DD is high, as we noted. A multicenter European study that was not yet published at the time that we submitted our work also documented DD after intracerebral hemorrhage,4 although not all of the patients were scanned acutely (some >2 months from symptom onset), as opposed to our cohort. We stand by our methods of scanning soon after symptom onset and meticulous MRI interpretation by experts. The confirmation of acute blood pressure reduction as a clinical risk factor for DD and its impact on 3-month functional outcomes in multivariate models underscore its importance as a subject for future research.Andrew M. Naidech, MD, MSPHMatthew B. Maas, MDAlexander J. Nemeth, MDEric J. Russell, MD Northwestern University Feinberg School of Medicine Chicago, ILDisclosuresNone.FootnotesStroke welcomes Letters to the Editor and will publish them, if suitable, as space permits. Letters must reference a Stroke published-ahead-of-print article or an article printed within the past 3 weeks. The maximum length is 750 words including no more than 5 references and 3 authors. Please submit letters typed double-spaced. Letters may be shortened or edited. Include a completed copyright transfer agreement form (available online at http://stroke.ahajournals.org and http://submit-stroke.ahajournals.org).

Letter by Nishikawa Regarding Article, “Blood Pressure Reduction, Decreased Diffusion on MRI, and Outcomes After Intracerebral Hemorrhage”

To the Editor: We read with great interest the article by Garg et al.1 The authors showed that decreased diffusion on MRI in patients with intracerebral hemorrhage was associated with greater acute blood pressure reductions and associated with disability and death at 3 months in multivariate analysis. The authors insisted that data confirmed the results of a previous report.2 However, the prevalence of decreased …

Blood Pressure Reduction, Decreased Diffusion on MRI, and Outcomes After Intracerebral Hemorrhage

Decreased diffusion (DD) consistent with acute ischemia may be detected on MRI after acute intracerebral hemorrhage (ICH), but its risk factors and impact on functional outcomes are not well-defined. We tested the hypotheses that DD after ICH is related to acute blood pressure (BP) reduction and lower hemoglobin and presages worse functional outcomes. Patients who underwent MRI were prospectively evaluated for DD by certified neuroradiologists blinded to outcomes. Hemoglobin and BP data were obtained via electronic queries. Outcomes were obtained at 14 days and 3 months with the modified Rankin Scale, a functional scale scored from 0 (no symptoms) to 6 (dead). We used logistic regression for dependence or death (modified Rankin Scale score 4-6). DD distinct from the hematoma was found on MRI in 39 of 95 patients (41%). DD was associated with greater BP reductions from baseline and a higher risk of dependence or death at 3 months (odds ratio, 4.8; 95% confidence interval, 1.7-13.9; P=0.004) after correction for ICH score (1.8 per point; 95% confidence interval, 1.2-3.1; P=0.01). Lower hemoglobin was associated with worse ICH score, larger hematoma volume, and worse outcomes, but not DD. DD is common after ICH, associated with greater acute BP reductions, and associated with disability and death at 3 months in multivariate analysis. The potential benefits of acute BP reduction to reduce hematoma growth may be limited by DD. The prevention and treatment of cerebral ischemia manifested as DD are potential methods to improve outcomes.

183 Acute Blood Pressure Reduction and Outcomes in Asymptomatic Hypertension: A Retrospective Cohort Study

183 Acute Blood Pressure Reduction and Outcomes in Asymptomatic Hypertension: A Retrospective Cohort Study