Predictors of hematoma enlargement in patients with intracerebral hemorrhage treated with rapid administration of antifibrinolytic agents and strict blood pressure control

OBJECT: Hematoma enlargement is a major cause of poor outcome in patients with intracerebral hemorrhage (ICH). A combination of rapid administration of antifibrinolytics and strict blood pressure (BP) control for prevention of hematoma enlargement has been recently reported. The authors examined the incidence and predictors of hematoma enlargement in patients with ICH who were treated with this therapy. METHODS: Rapid administration of antifibrinolytic agents consisted of intravenous administration of 2 g tranexamic acid over 10 minutes. Systolic BP was strictly maintained below 150 mm Hg using intravenous nicardipine. Immediately after diagnosis of ICH on computed tomography (CT), 188 patients who were admitted within 24 hours of symptom onset were treated with a combination of rapid administration of antifibrinolytic agents and BP control. Hematoma enlargement was determined on the basis of a second CT scan performed the day after admission. Several factors, including those that have been reported to affect hematoma enlargement, were compared between patients with and without hematoma enlargement. Hematoma enlargement (> or =20% volume increase) was observed in eight (4.3%) of 188 patients. Previous use of antiplatelet agents was significantly more frequent in patients with hematoma enlargement (p < 0.05). No significant between-group difference was found for any other factors Conclusions. Previous use of antiplatelet agents was a predictor of hematoma enlargement in patients with ICH treated with rapid administration of antifibrinolytic agents and BP control.     

Involvement of fluctuating high blood pressure in the enlargement of spontaneous intracerebral hematoma.

The correlations between changes in blood pressure after admission and hematoma expansion were investigated in 118 patients with spontaneous intracerebral hematoma admitted within 24 hours of onset who underwent serial computed tomography. Multiple logistic regression was performed to assess correlations between hematoma enlargement and clinical characteristics on admission. Hematoma enlargement was predominantly correlated with time of onset (p = 0.01567), and not well correlated with blood pressure at admission (p = 0.07908). Serial changes in blood pressure were investigated in 57 patients admitted within 6 hours of ictus whose blood pressures were monitored every hour from admission. Wilcoxon signed-rank analysis was used to determine the relationships between hematoma enlargement and blood pressure. Patients with hematoma enlargement was significantly correlated with increased blood pressure (p = 0.0004). Increases in blood pressure after admission may be a factor in hematoma enlargement.     

Effects of nitrendipine on circadian variation of blood pressure in inpatients with renal parenchymal hypertension: assessment by ambulatory blood pressure monitoring

OBJECTIVE: To study the effect of once-daily administration of a nitrendipine tablet 10 mg on 24-hour ambulatory blood pressure in inpatients with renal parenchymal hypertension. METHODS: Sixteen patients participated in the present study, and one patient was withdrawn because the baseline office blood pressure was less than 140/90 mmHg. In the baseline period, ambulatory blood pressure was monitored every 30 minutes for 30 hours. After the baseline measurement, nitrendipine 10 mg was orally administered once daily every morning for 7 days. The 30-hour ambulatory blood pressure monitoring was repeated after Day 6. RESULTS: Fifteen patients (aged 64.9 +/- 15.0 years) completed the study protocol. Baseline office blood pressure was 157.9 +/- 17.5/84.7 +/- 12.5 mmHg (mean +/- SD). Nitrendipine 10 mg tablets significantly reduced both systolic blood pressure (SBP) and diastolic blood pressure (DBP) at least for 11 hours after administration compared with those at baseline. The rate of "Decrease" (reduction in blood pressure > or = 20/10 mmHg and/or achieved blood pressure < 140/90 mmHg at trough point) was 60.0% (9/15). Eleven patients were considered as effective cases at peak point (maximal reduction in blood pressure > or = 20/10 mmHg). The rate of "Decrease" in effective cases at peak point was 72.7% (8/11). CONCLUSION: These results suggest that a once-daily administration of nitrendipine 10 mg tablets is effective for the 24-hour control of blood pressure in patients with renal parenchymal hypertension.     

Preoperative blood pressure and intraoperative hypothermia during lower abdominal surgery

BACKGROUND: Preoperative factors including age and body habitus affect intraoperative hypothermia during general anesthesia. We hypothesized that preoperative blood pressure also plays a contributory role in the induction of intraoperative hypothermia. METHODS: We evaluated the effect of preoperative systolic blood pressure (SBP) on core temperature during lower abdominal surgery under general anesthesia. In 36 female patients under 65 years of age, patients with a preoperative SBP of 140 mmHg or greater upon arrival in the operating theater were assigned to the high SBP group (n=18), while those with SBP below 140 mmHg were assigned to the normal SBP group (n=18). Anesthesia was maintained with isoflurane and nitrous oxide combined with epidural buprenorphine, and routine thermal care was provided intraoperatively. RESULTS: There were no significant differences in age, height or weight between the two groups. Tympanic membrane temperature in the normal SBP group started to decrease significantly from 15 min after induction of anesthesia compared to that in the high SBP group, and continued to decrease further at two hours after induction. Vasoconstriction threshold, determined to be tympanic membrane temperature at the time when a forearm minus finger skin surface gradient exceeded 0 degrees C, was significantly higher in the high SBP group than in the normal SBP group. CONCLUSION: These results suggest that preoperative SBP has some preventive effect on the decrease in intraoperative core temperature during lower abdominal surgery under general anesthesia.     

Three-dimensional computerized tomography angiography in patients with hyperacute intracerebral hemorrhage.

OBJECT: The authors confirm the usefulness of extravasation detected on three-dimensional computerized tomography (3D-CT) angiography in the diagnosis of continued hemorrhage and establishment of its cause in patients with acute intracerebral hemorrhage (ICH). METHODS: Thirty-one patients with acute ICH in whom noncontrast and 3D-CT angiography had been performed within 12 hours of the onset of hemorrhage and in whom conventional cerebral angiographic studies were obtained during the chronic stage were prospectively studied. Noncontrast CT scanning was repeated within 24 hours of the onset of ICH to evaluate hematoma enlargement. Findings indicating extravasation on 3D-CT angiography, including any abnormal area of high density on helical CT scanning, were observed in five patients; three of these demonstrated hematoma enlargement on follow-up CT studies. Thus, specificity was 60% (three correct predictions among five positives) and sensitivity was 100% (19 correct predictions among 19 negatives). Evidence of extravasation on 3D-CT angiography indicates that there is persistent hemorrhage and correlates with enlargement of the hematoma. Regarding the cause of hemorrhage, five cerebral aneurysms were visualized in four patients, and two diagnoses of moyamoya disease and one of unilateral moyamoya phenomenon were made with the aid of 3D-CT angiography. Emergency surgery was performed without conventional angiography in one patient who had an aneurysm, and it was clipped successfully. CONCLUSIONS: Overall, 3D-CT angiography was found to be valuable in the diagnosis of the cause of hemorrhage and in the detection of persistent hemorrhage in patients with acute ICH.     

Elevated blood pressure aggravates intracerebral hemorrhage-induced brain injury

Elevated blood pressure (BP) is commonly seen in patients with intracerebral hemorrhage (ICH), and is independently associated with poor functional outcomes. Little is known about how elevated BP influences ICH-related brain injury. In the present study, we investigated the physiological and brain histological changes, as well as functional recovery following ICH in renovascular hypertensive rats. Renovascular hypertension (RVHT) was achieved by applying a silver clip onto the left renal artery of adult Sprague-Dawley rats. ICH was induced by an intrastriatal injection of bacterial collagenase IV about 5-6 weeks after left renal artery clipping or the sham operation. Following induction of ICH, both the normotensive and RVHT rats demonstrated an ultra-acute elevation in BP. Elevated BP increased hematoma volume, brain swelling, and apoptosis in the perihematomal areas. Brain degeneration, including local atrophy and lateral ventricle enlargement, was greater in the RVHT rats. In addition, many proliferating cells were seen over the ipsilateral striatum in the RVHT rats after ICH. The modified limb placing tests were done weekly for 3 weeks. In line with the histological damage, elevated BP worsened neurological deficits. These results suggest that ICH in the hypertensive rats mimics the clinical scenario of hypertensive ICH and may provide a platform to study the mechanisms of ICH-induced brain injury and potential therapies for ICH.     

Aspirin does not affect hematoma growth in severe spontaneous intracranial hematoma

Hematoma growth (HG) affects the prognosis of patients with spontaneous intracranial hematoma (ICH), but there is still a lack of evidence about the effects of aspirin (acetylsalicylic acid, ASA) on HG in patients with severe ICH. This study retrospectively analyzed patients with severe ICH who met the inclusion and exclusion criteria in Beijing Tiantan Hospital, Capital Medical University, between January 1, 2015, and July 31, 2019. Severe ICH patients were divided into ASA group and nASA groups according to ASA usage, and the incidence of HG between the groups was compared. Univariate analysis was performed by the Mann–Whitney U test, chi-square test, or Fisher exact test. Multivariate logistic regression analysis was used to analyze the impact of ASA on HG and to screen for risk factors of HG. In total, 221 patients with severe ICH were consecutively enrolled in this study. There were 72 (32.6%) patients in the ASA group and 149 patients in the nASA group. Although the incidence of HG in the nASA group was higher than that in the ASA group (34.9% VS 22.2%, p?=?0.056), ASA did not significantly affect the occurrence of HG (p?=?0.285) after adjusting for initial hematoma volume, high blood pressure at admission, coronary heart disease, and GCS at admission. In addition, we found that high blood pressure at admission was a risk factor for HG. Prior ASA does not increase the incidence of HG in severe ICH patients, and high blood pressure at admission is a risk factor for HG.

     

Ultra-early clot aspiration after lysis with tissue plasminogen activator in a porcine model of intracerebral hemorrhage: edema reduction and blood-brain barrier protection

OBJECT: Ultra-early hematoma evacuation (< 4 hours) after intracerebral hemorrhage (ICH) may reduce mass effect and edema development and improve outcome. To test this hypothesis, the authors induced lobar hematomas in pigs. METHODS: The authors infused 2.5 ml of blood into the frontal cerebral white matter in pigs weighing 8 to 10 kg. In the treatment group, clots were lysed with tissue plasminogen activator ([tPA], 0.3 mg) and aspirated at 3.5 hours after hematoma induction. Brains were frozen in situ at 24 hours post-ICH and hematomal and perihematomal edema volumes were determined on coronal sections by using computer-assisted morphometry. Hematoma evacuation rapidly reduced elevated cerebral tissue pressure from 12.2+/-1.3 to 2.8+/-0.8 mm Hg. At 24 hours, prior clot removal markedly reduced hematoma volumes (0.40+/-0.10 compared with 1.26+/-0.13 cm3, p < 0.005) and perihematomal edema volumes (0.28+/-0.05 compared with 1.46+/-0.24 cm3, p < 0.005), compared with unevacuated control lesions. Furthermore, no Evans blue dye staining of perihematomal edematous white matter was present in brains in which the hematomas had been evacuated, compared with untreated controls. CONCLUSIONS: Hematomas were quickly and easily aspirated after treatment with tPA, resulting in significant reductions in mass effect. Hematoma aspiration after fibrinolysis with tPA enabled removal of the bulk of the hematoma (> 70%), markedly reduced perihematomal edema, and prevented the development of vasogenic edema. These findings in a large-animal model of ICH provide support for clinical trials that include the use of fibrinolytic agents and ultra-early stereotactically guided clot aspiration for treating ICH.     

Management of primary hypertensive hemorrhage of the brain

Opinion statement Intracerebral hemorrhage (ICH) can be prevented by adequate treatment of hypertension. Angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, and calcium channel blockers seem particularly effective. ICH also is associated with apolipoprotein E 4 genotype and with low cholesterol, but not statin therapy for high cholesterol. Microbleeds identified on magnetic resonance imaging scans also confer increased risk of ICH. Experimental drug regimens that target metalloproteinases and inflammation reduce damage in animal models of ICH, but none are proven effective in humans. Cerebral edema after ICH has varied mechanisms and significance, and may be another target for therapy. Cerebral blood flow is not substantially reduced in most patients with ICH. Lowering systolic blood pressure below 160 mm Hg in the first hours after ICH may prevent additional bleeding. Activated factor 7 is a promising new therapy to limit hematoma enlargement and consequently reduce morbidity and mortality after ICH. Dosages of 80 to 160 μg/kg given within the first 3 to 4 hours after symptom onset, or in patients at risk of additional bleeding such as those with coagulopathy, is logical but is unapproved. The role of activated factor 7 hopefully will be clarified by additional study. Open surgical evacuation of most spontaneous supratentorial hematomas has been shown to be ineffective in reducing mortality or disability except in certain circumstances, such as large or enlarging superficially located clots in patients who are awake. Stereotactic and endoscopic clot aspiration, often using instillation of lytic agents to liquefy the hematoma, is the most active area of surgical intervention research. Such minimally invasive approaches have been shown to safely produce more rapid removal of blood compared with standard treatment. This is particularly true for intraventricular hemorrhages. Future research will focus on the use of stem cells to restore the damaged architecture around the hematoma. The impressive scope and progress of ongoing clinical and basic research show that there is no longer a place for nihilism in the approach to ICH.     

Improved Long-Term Outcomes After Renal Transplantation Associated with Blood Pressure Control

Hypertension has a negative impact on long-term outcomes after renal transplantation. We investigated the effect of a recent decline in blood pressure among renal transplant patients in the Collaborative Transplant Study (CTS) database on long-term graft and patient survival. CTS data were used to evaluate transplant outcomes in relation to recipient systolic blood pressure (SBP) for 24,404 first cadaver kidney recipients transplanted between 1987 and 2000. Patients whose SBP was > 140 mmHg at 1 year posttransplantation but controlled to < or = 140 mmHg by 3 years had significantly improved long-term graft outcome compared with patients with sustained high SBP to 3 years (RR 0.79; CI 0.73-0.86; p < 0.001). Additional examination at 5 years showed that SBP lowering after year 3 was associated with improved 10-year graft survival (RR 0.83; CI 0.72-0.96; p = 0.01), whereas even a temporary increase in SBP at 3 years was associated with worse survival (RR 1.37; CI 1.19-1.58; p < 0.001). Changes in SBP were paralleled by changes in the incidence of cardiovascular death among recipients younger than 50 but not in older recipients. Lowering SBP, even after several years of posttransplantation hypertension, is associated with improved graft and patient survival in renal allograft recipients.     

Pathophysiology of brain edema formation

A number of mechanisms seem to be involved in edema formation after an ICH. At least three phases of edema are involved in ICH. These include a very early phase (first several hours) involving hydrostatic pressure and clot retraction, a second phase (first 2 days) involving the activation of the coagulation cascade and thrombin production, and a third phase (after 3 days) involving RBC lysis and hemoglobin-induced neuronal toxicity. Activation of the complement system in brain parenchyma also plays an important role in the second and third phases. There are potential therapeutic strategies to address each of these mechanisms. Because the adverse effect of an ICH seems to result from a toxic effect of blood components on brain tissue, early clot removal may be the best strategy, because it results in the removal of all the toxic components [93]. Hematoma aspiration after tissue plasminogen activator (tPA) infusion has also been shown to be relatively safe and effective in animal models. Kaufman et al [94] reported that tPA lysed the hematoma in minutes and did not cause inflammation or bleeding in rabbits. Because clots lysed with tPA can be aspirated through a needle or catheter, mechanical brain injury by this method is minimized. In a rat model, aspiration of clot with tPA reduced clot volume and brain injury [95,96]. Recently, Wagner et al [97] infused tPA into hematomas in a porcine model at 3 hours after induction and aspirated the liquified clots 1 hour later. Clot removal after tPA treatment resulted in a 72% reduction in hematoma volume compared with untreated controls. Clot removal also reduced brain edema volume and BBB disruption and improved cerebral tissue pressure [93]. Six randomized trials have been accomplished, but surgical evacuation of the clot remains controversial [98-103]. Recently, thrombolysis and aspiration under CT guidance reduced the hematoma volume effectively [104]. Infusion of tPA directly into the hematoma before clot aspiration has also been used in human beings. Up to 90% of the original hematoma volume can be removed [105, 106]. Schaller et al [107] injected tPA directly into a hematoma 72 hours after the ictus in patients. The hematomas were lysed, and the liquified clots were drained in 14 patients. Two patients died, but none had recurrent hemorrhage. In conclusion, much has been learned about the basic mechanisms involved in edema formation after ICH. Animal models indicate that a number of components of blood are capable of inducing brain injury and brain edema. Now, it is time to translate that basic information into clinical trials.     

Traumatic intracerebral hematomas: timing of appearance and indications for operative removal

Immediate and delayed traumatic intracerebral hematomas (ICH) can produce devastating secondary brain damage after severe head injury. The relationship between the initial injury and eventual occurrence, size, and time of appearance of such hematomas is not well understood, but has great importance since delayed appearance may necessitate delayed surgical decompression of developing lesions not present on early CT scans. We reviewed the records of 35 consecutive patients with operated post-traumatic ICH to document when these lesions appeared on CT, what were the indications for surgery, and what was eventual outcome. Time between injury and ICH appearance was categorized as immediate (0-3 hours), intermediate (3-6), delayed (6-24) or very delayed (later than 24 hours). ICH appearance was immediate in 20%, intermediate in 6%, delayed in 29%, and very delayed in 46%. Half of the patients were not comatose at the time of admission (GCS greater than or equal to 8). Hematoma removal was prompted by clinical deterioration or failure to improve in half the patients and by uncontrolled intracranial hypertension in the other half. Half the patients died, generally those in traumatic coma immediately after injury although advanced age also was associated with poor outcome. Only about one quarter of patients who require surgical removal of ICH can be shown to have their lesions soon after injury. Most operable intraparenchymal clots develop after initial CT scanning and trauma surgeons must be prepared to recognize and treat this delayed complication of brain injury. Even with aggressive management, ICH contribute significantly to poor outcome and improved treatment must be sought.     

Factors affecting outcome of intracerebral hemorrhage in patients undergoing chronic hemodialysis

To date, despite a markedly high incidence of intracerebral hemorrhage (ICH) in patients with end-stage renal disease, only few studies have focused on factors that affect patient's prognosis. To elucidate these factors, we retrospectively investigated 22 consecutive patients who had chronic renal failure, were maintained by hemodialysis (HD), had suffered from ICH, and were hospitalized and treated in our institute from 2006 to 2008. Hematoma volume, blood pressure on admission, blood pressure 3 days after ICH onset, and neurological deterioration significantly affected patient mortality. Progression of neurological symptoms during HD was observed often in patients with hematoma of more than 60 mL or in patients with pontine hemorrhages. Age, gender, duration of HD, anti-platelet or anticoagulant therapies, or maximal dose of nicardipine did not affect patient's prognosis. Based on this study we conclude that controlling blood pressure on admission and within 3 days after onset of ICH may be the most important factor that would improve patient's prognosis. Further, special care might be required for patients with large hematomas (more than 60 mL) or those with brainstem hemorrhages, because progression of neurological symptoms occurs often in such patients.     

Multivariate analysis of risk factors of hematoma expansion in spontaneous intracerebral hemorrhage

BACK GROUND: We focused on the cause of hematoma expansion after admission because the volume of hematoma after S-ICH plays a crucial role in the cause of mortality and morbidity. METHODS: In a retrospective review, 51 patients with hematoma expansion of S-ICH were identified among 880 cases of S-ICH treated between 2001 and May 2006. We divided cases into 2 groups according to the time of hematoma expansion. An enlargement of hematoma within 2 weeks after hospitalization was categorized as the acute stage group and after 2 weeks was categorized as the chronic stage group. Spontaneous intracerebral hemorrhage without hematoma expansion group (100 cases) had been consecutively selected as a control group. We analyzed the risk factors of hematoma expansion in patients with S-ICH especially in the acute stage group. RESULTS: Fifty-one of 880 patients had the enlargement of hematoma (5.8%). Forty-three (84%) of 51 cases were acutely developed and 8 cases (16%) were developed chronically. On univariate analysis there were significant differences in BP within the initial 48 hours (P < .0001), GOS (P < .0001), and previously taking anticoagulant agents (P = .0053). Especially the difference in SBP and DBP within 48 hours between groups was 19 (11%) and 13 mm Hg (14%), respectively. The DBP within the initial 24 hours had a meaningful odds ratio (1.06) on logistic regression analysis. CONCLUSION: A reduction of BP by 15% (SBP < or =140 mm Hg, DBP < or =80 mm Hg) is necessary at acute stage in S-ICH.     

Acute brain edema in fatal head injury: analysis by dynamic CT scanning

Dynamic computerized tomography (CT) was performed on 42 patients with acute head injury to evaluate the hemodynamics and to elucidate the nature of fatal diffuse brain bulk enlargement. Patients were divided into two groups according to the outcome: Group A included 17 nonfatally injured patients, eight with acute epidural hematomas and nine with acute subdural hematomas; Group B included 25 fatally injured patients, 16 with acute subdural hematomas and nine with bilateral brain bulk enlargement. Remarkable brain bulk enlargement could be seen in all fatally injured patients with acute subdural hematoma. In 29 (69%) of 42 patients, dynamic CT was performed within 2 hours after the impact. In the nonfatally injured patients with brain bulk enlargement, dynamic CT scans suggested a hyperemic state. On the other hand, in 17 (68%) of the 25 fatally injured patients, dynamic CT scans revealed a severely ischemic state. In the fatally injured patients with acute subdural hematoma, CT Hounsfield numbers in the enlarged hemisphere (hematoma side) were significantly lower than those of the opposite side (p less than 0.001). Severe diffuse brain damage confirmed by follow-up CT scans and uncontrollable high intracranial pressure were noted in the fatally injured patients. Brain bulk enlargement following head injury originates from acute brain edema and an increase of cerebral blood volume. In cases of fatal head injury, acute brain edema is the more common cause of brain bulk enlargement and occurs more rapidly than is usually thought.     

Telmisartan in patients with mild/moderate hypertension and chronic kidney disease

AIMS: This study assessed the clinical efficacy and safety of telmisartan, an angiotensin II receptor blocker with a long terminal elimination half-life and almost exclusively excreted in bile, in patients with varying severity of chronic kidney disease (CKD). PATIENTS AND METHODS: Adults with diastolic blood pressure (DBP) 90 - 109 mmHg and stable CKD were enrolled: mild/moderate (creatinine clearance (CrCl) 30 - 74 ml/ min/1.73 m2), severe (CrCl < 30 ml/min/1.73 m2) or requiring maintenance hemodialysis. A two- to four-week single-blind, placebo run-in period preceded once-daily telmisartan 40 mg administration for four weeks. Telmisartan 80 mg was given after four- or eight-week treatment ifDBP > or = 85 mmHg. After 12-week treatment, trough DBP/systolic blood pressure (SBP), DBP and SBP control rates, renal function and tolerability were recorded. RESULTS: Mean changes in DBP/SBP were 10.5/-10.7 mmHg for mild/moderate CKD (n = 27), -11.2/-14.9 mmHg for severe CKD (n = 27) and -15.0/-21.1 mmHg for hemodialysis patients (n = 28). DBP control rates (< 90 mmHg)/SBP responses (< 140 mmHg or > 10 mmHg reduction) occurred in 59.3%/66.7%, 63.0%/70.4% and 71.4%/92.9% of mild/moderate CKD, severe CKD and hemodialysis patients, respectively. Incidences of drug-related adverse events were low, and all were known adverse events of telmisartan and common to other angiotensin II receptor blockers. At the end of treatment, a decrease in 24-h urine creatinine occurred in 5/53 (9.4%) patients. Two patients discontinued treatment prematurely due to the worsening of CKD and one due to aggravated proteinuria. CONCLUSION: Once-daily telmisartan provided effective and well-tolerated treatment of mild/moderate hypertension in CKD patients, with no worsening of renal function.     

Preoperative blood pressure and catecholamines related to hypothermia during general anesthesia

BACKGROUND: We previously demonstrated that preoperative blood pressure values affect intraoperative hypothermia during general anesthesia. We hypothesized that increased catecholamine secretion could be responsible for the relationship between preoperative blood pressure and hypothermia. METHODS: To evaluate the effect of preoperative systolic blood pressure (SBP) and plasma catecholamine levels on core temperature during general anesthesia, 40 male patients who were scheduled for open abdominal surgery were allocated to two groups: those whose preoperative SBP was 140 mmHg or greater (high SBP group, n = 20), and those whose SBP was less than 140 mmHg (normal SBP group, n = 20). Anesthesia was maintained with 0.4% isoflurane and opioids. RESULTS: The average age, height, and weight of the patients in the two groups did not differ. Preoperative SBP, mean blood pressure, diastolic blood pressure and heart rate in the high SBP group were significantly higher than those in the normal SBP group. Plasma norepinephrine concentrations in the high SBP group were significantly greater than those in the normal SBP group before and 1 h after the induction of anesthesia. Tympanic membrane temperatures in the normal SBP group started to decline further just after the induction of anesthesia, more so than that in the high SBP group. The vasoconstriction threshold in the normal SBP group was significantly lower than that in the high SBP group. CONCLUSION: These results suggest that the higher levels of preoperative catecholamine secretion contributed to the lesser degree of intraoperative hypothermia observed in the high SBP group.     

The study of aortic stiffness in different hypertension subtypes in patients with chronic kidney disease

Objective To investigate whether there is any difference in aortic stiffness among different hypertension subtypes in patients with chronic kidney disease. Methods Six hundred and twenty-six patients with chronic kidney disease were included in the present analysis. They were classified into four groups: normotension (n＝391) with systolic blood pressure (SBP) ＜140 mmHg and diastolic blood pressure (DBP) ＜90 mmHg; isolated systolic hypertension (ISH, n＝141) with SBP≥140 mmHg and DBP＜90 mmHg; isolated diastolic hypertension (IDH, n＝25) with SBP＜140 mmHg and DBP≥90 mmHg; systolic-diastolic hypertension (SDH, n＝69) with SBP≥140 mmHg and DBP≥90 mmHg. Aortic stiffness was assessed by pulse pressure and pulse wave velocity. Results The IDH group had lower mean age than the other groups(P＜0.01). The percentage of diabetes in the ISH group was higher than that in the other groups. The comparison of aortic stiffness showed that the ISH and SDH groups had higher aortic stiffness than the normotension and IDH groups (P＜0.01), but no significant difference in aortic stiffness was observed neither between the normotension and IDH groups nor between ISH and SDH groups.Conclusion Aortic stiffness is significantly different among different hypertension subtypes, which may be an underlying cause for the different cardiovascular mortality among the hypertension subtypes.