Deterioration in carotid baroreflex during carotid endarterectomy

OBJECTIVE: Blood pressure instability after carotid endarterectomy (CEA) has been associated with a disturbance of the baroreflex control mechanism caused by the surgery in the carotid sinus region. The purpose of this study was to determine if a deterioration in carotid baroreceptors occurs during the surgery. METHOD: Heart rate (HR) and blood pressure (BP) were recorded continuously in 60 patients undergoing CEA as well as preoperatively and postoperatively at 2 days and 6 weeks. The baroreflex sensitivity was determined by cross-spectral analysis of HR and systolic blood pressure (SBP). During the surgery, three tests were used to assess the baroreflex response. The first test simulated a sudden fall in systemic blood pressure by clamping the common carotid artery. The second test simulated a rise in systemic blood pressure by applying pressure by using a rubbing action on the luminal surface of the carotid sinus region. The rub test was performed twice, once with the atheromatous plaque in situ and once when the plaque had been removed. The third test is clamp removal and restoration of blood flow through the carotid sinus. RESULTS: Carotid cross-clamping increased mean +/- standard error of the mean SBP from 117 +/- 3 mm Hg before clamping to 125 +/- 3 mm Hg (P <.05) at 30 beats after clamping. The first rub test with the plaque in situ decreased SBP from 121 +/- 3 mm Hg to 117 +/- 3 mm Hg (P <.01) at 10 beats after the rub test, indicating a functioning baroreceptor reflex. The second rub test increased SBP from 126 +/- 3 mm Hg to 128 +/- 3 mm Hg (P <.05). SBP dropped (P <.01) when unclamping suggesting a selective alteration of the baroreflex sensitivity. The baroreflex sensitivity was significantly reduced 2 days postoperatively when compared to preoperative values (P <.05). CONCLUSIONS: These findings suggest that the act of plaque removal could be associated with a partial disruption of baroreceptor mechanism in the carotid artery. This could affect type I baroreceptors.     

Carotid angioplasty and stent-induced bradycardia and hypotension: Impact of prophylactic atropine administration and prior carotid endarterectomy

OBJECTIVE: We compared the physiologic effect of selective atropine administration for bradycardia with routine prophylactic administration, before balloon inflation, during carotid angioplasty and stenting (CAS). We also compared the incidence of procedural bradycardia and hypotension for CAS in patients with primary stenosis vs those with prior ipsilateral carotid endarterectomy (CEA). METHODS: A total of 86 patients were treated with CAS at 3 institutions. Complete periprocedural information was available for 75 of these patients. The median degree of stenosis was 90% (range, 60%-99%). Indications for CAS were severe comorbidities (n = 49), prior CEA (n = 21), and prior neck radiation (n = 5). Twenty patients with primary lesions were treated selectively with atropine only if symptomatic bradycardia occurred (nonprophylactic group). Thirty-four patients with primary lesions received routine prophylactic atropine administration before balloon inflation or stent deployment (prophylactic group). The 21 patients with prior CEA received selective atropine treatment only if symptomatic bradycardia occurred (prior CEA group) and were analyzed separately. Mean age and cardiac comorbidities did not vary significantly either between the prophylactic and nonprophylactic atropine groups or between the primary and prior CEA patient groups. Outcome measures included bradycardia (decrease in heart rate >50% or absolute heart rate <40 bpm), hypotension (systolic blood pressure <90 mm Hg or mean blood pressure <50 mm Hg), requirement for vasopressors, and cardiac morbidity (myocardial infarction or congestive heart failure). RESULTS: The overall incidence of hypotension and bradycardia in patients treated with CAS was 25 (33%) of 75. A decreased incidence of intraoperative bradycardia (9% vs 50%; P < .001) and perioperative cardiac morbidity (0% vs 15%; P < .05) was observed in patients with primary stenosis who received prophylactic atropine as compared with patients who did not receive prophylactic atropine. CAS after prior CEA was associated with a significantly lower incidence of perioperative bradycardia (10% vs 33%; P < .05), hypotension (5% vs 32%; P < .05), and vasopressor requirement (5% vs 30%; P < .05), with a trend toward a lower incidence of cardiac morbidity (0% vs 6%; not significant) as compared with patients treated with CAS for primary carotid lesions. There were no significant predictive demographic factors for bradycardia and hypotension after CAS. CONCLUSIONS: The administration of prophylactic atropine before balloon inflation during CAS decreases the incidence of intraoperative bradycardia and cardiac morbidity in primary CAS patients. Periprocedural bradycardia, hypotension, and the need for vasopressors occur more frequently with primary CAS than with redo CAS procedures. On the basis of our data, we recommend that prophylactic atropine administration be considered in patients with primary carotid lesions undergoing CAS.     

Altered autonomic cardiovascular regulation after combined deep and superficial cervical plexus blockade for carotid endarterectomy

Compromised cardiac autonomic modulation can produce cardiovascular disturbances. We investigated whether combined deep and superficial cervical plexus (CP) blockade for carotid endarterectomy (CEA) produces changes in autonomic cardiovascular regulation. To estimate alterations in cardiovascular autonomic control before and after combined CP blockade in 22 patients undergoing CEA, the heart rate (HR) variability, systolic blood pressure (SBP) variability, and baroreflex sensitivity were analyzed. We found that SBP (157 +/- 28 mm Hg versus 191 +/- 38 mm Hg before and after combined CP blockade, respectively) and HR (68 +/- 10 bpm versus 84 +/- 9 bpm) increased after combined CP blockade. The high frequency power of HR variability (3.7 +/- 0.9 versus 2.2 +/- 1.2 ln/ms2) decreased (decrease in parasympathetic drive), whereas the low frequency power of SBP variability (5.5 +/- 4.7 versus 8.6 +/- 9.4 mm Hg2) increased (increase in vascular sympathetic outflow). Baroreflex sensitivity decreased, and this decrease was negatively correlated with a SBP increase (r = -0.455). The present results suggest that combined CP blockade impairs autonomic cardiovascular homeostasis and suggests an association between combined CP blockade and intraoperative or postoperative adverse cardiovascular events in high-risk cardiac patients undergoing CEA that merits further studies.     

Acute device-based blood pressure reduction: electrical activation of the carotid baroreflex in patients undergoing elective carotid surgery

Carotid sinus baroreceptors are involved in controlling blood pressure (BP) by providing input to the cardiovascular regulatory centers of the medulla. The acute effect of temporarily placing an electrode on the carotid sinus wall to electrically activate the baroreflex was investigated. We studied 11 patients undergoing elective carotid surgery. Baseline BP was 146+30/66+/-17 mm Hg and heart rate (HR) 72+/-7 bpm (mean +/- standard deviation). An electrode was placed upon the carotid sinus and after obtaining a steady state baseline of BP and HR, an electric current was applied and increased in 1-volt increments. A voltage dependent and highly significant reduction in BP was observed which averaged 18+/-26* and 8.0+/-12 mm Hg for systolic BP and diastolic BP, respectively. Maximal reductions occurred at 4.4+/-1.2 V: 23+/-24 mm Hg*, 16+/-10 mm Hg* and 7+/-12 bpm* for systolic BP, diastolic BP and HR, respectively ( = p <.05). Thus, electrical stimulation of the carotid sinus activates the carotid baroreflex resulting in a reduction in BP and HR. This presents a proof of concept for device based baroreflex modulation in acute BP regulation and adds to the available data which provide a rationale for evaluating this system in the context of chronic BP reduction in hypertensive patients.     

Decreased oxygen consumption as a toxic manifestation of protamine sulfate reversal of heparin anticoagulation

Protamine sulfate has been observed to interfere with the control of isolated mitochondrial respiration in vitro. This study was designed to determine if oxygen consumption changes in intact animals occur in vivo during protamine administration. Oxygen consumption was assessed in seven dogs anticoagulated with heparin (150 IU/kg) and reversed 30 minutes later with protamine sulfate (1.5 mg/kg). Oxygen saturations measured included arterial (SaO2 arterial), mixed venous (SvO2 systemic), jugular (SvO2 jugular), portal (SvO2 portal), and coronary (SvO2 coronary). Cardiac output (CO) and carotid artery flow determinations allowed calculation of systemic oxygen consumption (VO2 systemic) and cerebral oxygen consumption VO2 cerebral. Hemodynamic measurements included arterial blood pressure (BP), pulmonary artery systolic and diastolic pressures (PAS, PAD), and heart rate (HR). Protamine sulfate administration resulted in hypotension (delta BP -64 mm Hg), pulmonary hypertension (delta PAS + 13 mm Hg, delta PAD + 11 mm Hg), and bradycardia (delta HR -30). Shortly after protamine administration, CO fell 54% and carotid artery flow fell more than 50%, yet declines in SvO2 systemic and SvO2 jugular were not observed. In fact these parameters increased 3% and 2%, respectively. VO2 systemic fell 55% and VO2 cerebral fell 57%. Similarly, SvO2 portal and SvO2 coronary increased 6% and 9%, respectively. Significant correlations existed between changes in VO2 systemic and BP (r = 0.05, p less than 0.001), HR (r = 0.3, p less than 0.01, PAD (r = -0.3, p less than 0.05, and CO (r = 0.8, p less than 0.001). Impaired oxygen utilization was most evident during the first 5 minutes after protamine administration. This investigation, for the first time, establishes that protamine sulfate decreases in vivo oxygen consumption, a finding that may account for certain of the drug's adverse side effects.     

Correlation of carotid artery stump pressure and neurologic changes during 474 carotid endarterectomies performed in awake patients

PURPOSE: A carotid artery stump pressure (SP) of < 50 mm Hg and abnormal electroencephalography (EEG) changes have been suggested as indications for selective shunting in patients undergoing carotid endarterectomy (CEA) under general anesthesia. We attempted to determine the optimal SP threshold that correlated with neurologic changes in awake patients undergoing CEA using cervical block anesthesia (CBA) and performed a cost comparison with EEG monitoring. METHODS: Between July 1, 1995, and December 31, 2004, SP was measured during 474 CEAs performed under CBA by inserting a 19-gauge butterfly needle into the common carotid artery. A saline-filled intravenous bag in the patient's contralateral hand was connected to pressure tubing to generate waveforms with hand squeezing that could be visualized on a monitor. Systemic pressure was maintained approximately 10 mm Hg higher than baseline. Accurate SPs were confirmed by the finding of flatline waveforms after internal carotid artery clamping. Selective shunting was performed when neurologic changes occurred (aphasia, inability to squeeze the contralateral hand, decreased consciousness), regardless of SP. During this same period, 142 patients underwent CEA using GA, and SP was also measured. RESULTS: Shunting was necessary because of neurologic changes in 7.2% (34/474) of all CEAs performed using CBA: 0.9% (3/335) with SPs > or = 50 mm Hg systolic vs 1.0% (4/402) with SPs > or = 40 mm Hg systolic, and 22% (31/139) with SPs < 50 mm Hg systolic vs 42% (30/72) with SPs < 40 mm Hg systolic. If these 474 CEAs had been performed using GA, shunts would have been used in 29% (139/474) of patients for a SP < 50 mm Hg systolic vs 15% (72/474) for a SP < 40 mm Hg systolic. In patients not shunted, the perioperative stroke/death rate was 1.2% in patients (4/332) with SPs > or = 50 mm Hg vs 1.0% (4/398) with SPs > or = 40 mm Hg. Three of the four strokes occurred > 24 hours postoperatively and were unrelated to lack of shunting and ischemia. There was no significant difference in the percentage of patients with SPs > or = 50 mm Hg who underwent CEA using CBA (70%, 335/474) vs GA (67%, 96/142) during this time period. At our hospital, charges for SPe measurement, including anesthesia charges and tubing, were 229 dollars per case vs 3439 dollars per case for EEG monitoring. Use of SP measurements in these 474 patients would have resulted in reduced charges of 1,521,540 dollars compared with EEG monitoring if CEA had been performed under GA. CONCLUSION: Using 40 mm Hg systolic as a threshold, the need for shunting (15%) and the false-negative rate (1.0%) for SP in our series were equivalent to the results of EEG monitoring during CEA reported in the literature. However, charges for SP measurements are dramatically lower compared with EEG monitoring. Our results suggest that a carotid artery SP > or = 40 mm Hg systolic may be considered as an equally reliable but more cost-effective method to predict the need for carotid shunting during CEA under GA compared with EEG monitoring, but further investigation is warranted.     

Factors associated with hypotension and bradycardia after carotid angioplasty and stenting

BACKGROUND: Acute procedurally induced hemodynamic depression can occur after carotid angioplasty and stenting (CAS). This study was performed to determine the frequency and risk factors for hypotension and bradycardia after the CAS procedure. METHODS: The study reviewed clinical variables and angiographic data of all patients undergoing elective CAS with neuroprotection during a recent 5-year period. Intravenous atropine was given selectively in cases of bradycardia (heart rate <60 beats/min or a decrease of >20 beats/min). We further defined hemodynamic depression as bradycardia or severe hypotension (systolic blood pressure fall >30 mm Hg). Frequency and potential risk factors for hemodynamic depression were analyzed by logistic regression. RESULTS: During the study period, 416 patients (99% male; mean age, 74 +/- 11 years) underwent the CAS procedure. The median degree of stenosis was 93% (range, 60% to 99%). The frequencies of post-CAS hemodynamic depression include hypotension in 58 (14%), bradycardia in 112 (27%), or both in 21 (5%). All patients with bradycardia received intraprocedural atropine, and all heart rates returned to the baseline level. Persistent hypotension occurred in 45 patients (11%). Increased age was associated with CAS-induced bradycardia or hypotension. Adjusted risk factors associated with hemodynamic depression include age >78 years (odds ratio [OR], 5.25; 95% confidence interval [CI], 2.32 to 15.25; P = .01) and ejection fraction of <25% (OR, 3.25; 95% CI, 0.58 to 6.58; P = .02). CEA-related restenosis was associated with a reduced risk of hemodynamic depression (OR, 0.21; 95% CI, 0.12 to 0.69, P = .001). Persistent hypotension after CAS was associated with an increased risk of an adverse clinical event (44%, P = .001). CONCLUSIONS: Hemodynamic depression, including hypotension and bradycardia, is frequent after CAS. However, CAS-induced hemodynamic depression is rare in patients with postendarterectomy stenosis. Patients with compromised ejection fraction and increased age are at a higher risk of presenting with CAS-induced hemodynamic instability, and persistent hypotension after CAS is associated with an increased postprocedural complication rate.     

Regional cerebral blood flow and response to carbon dioxide during controlled hypotension with isoflurane anesthesia in the rat

Regional (frontal, parietal, occipital, cortical, and basal ganglia) cerebral blood flow (rCBF) was examined at 1.5 and 3.5 MAC inspired isoflurane/O2 anesthesia in the rat using the radioactive microsphere technique to determine the effects of controlled hypotension with deep isoflurane anesthesia on rCBF and the response of rCBF to changes in PaCO2 when mean blood pressure (BP) was decreased to levels below the lower limit of the autoregulatory threshold. Four groups of six rats were studied with rCBF 1 determined at 1.5 MAC (mean BP 80-90 mm Hg) followed by two rCBF determinations at 3.5 MAC (mean BP 46-48 mm Hg). For CBF 1 the regional CO2 response was a 3.1-3.9% increase in rCBF/mm Hg increase in CO2. Regional cerebral blood flow (ml/g/min) ranged from 0.64 +/- 0.05-0.83 +/- 0.15 at PaCO2 of 19 mm Hg to 1.34 +/- 0.11-1.80 +/- 0.33 at PaCO2 of 41 mm Hg to 2.61 +/- 0.26-3.72 +/- 0.37 at PaCO2 of 59 mm Hg (mean +/- SEM). With controlled hypotension (CBF 2) rCBF was unchanged during normocarbia, increased 100% during hypocarbia, P less than 0.01 vs CBF 1 and decreased 30% during hypercarbia, P less than 0.01 vs CBF 1. For rCBF 3 measurements, the BP and inspired concentration of isoflurane were kept constant, while PaCO2 was increased in two and decreased in two of the four groups. Within-group comparisons between rCBF 2 and rCBF 3 results demonstrated loss of CO2 responsiveness of the rat cerebrovasculature in every region during controlled hypotension to below the autoregulatory threshold at 3.5 MAC isoflurane/O2 anesthesia.(ABSTRACT TRUNCATED AT 250 WORDS)     

Airtraq(R)喉镜和Macintosh直接喉镜在经口气管插管时血流动力学的比较

目的比较Airtraq(R)视频喉镜和Macintosh直接喉镜经口气管插管时心血管反应。方法40例拟择期经口气管插管全麻下手术的患者,按照随机数字表随机分为两组,Airtraq(R)组（A组）和Macintosh喉镜组（M组）,每组20例。观察麻醉诱导前、诱导后、插管即刻、插管后1、3 min时的心率(HR)、血压和...     

Hemodialysis with low-temperature dialysate: a long-term experience

The effect of cool dialysate in hemodialysis (HD)-induced symptoms was studied in a group of 8 patients, neither diabetic nor anephric, with a high incidence of HD-induced hypotension (20-90%). Patients were studied during two consecutive periods of 6 months, the first one with dialysate at 37 degrees C (598 sessions) and the second one at 35 degrees C (599 sessions). Dialysis at low temperature was associated with a decrease in symptomatic hypotension (SH) (47.4 vs. 33.9%, p less than 0.001), a greater loss of weight during HD (1.52 +/- 0.03 vs. 1.71 +/- 0.03 kg, p less than 0.001) and stabilization of predialysis systolic blood pressure (SBP) at a lower level (144 +/- 0.69 vs. 139 +/- 0.98 mm Hg, p less than 0.001). At 37 degrees C, SH was associated with a higher ultrafiltration (1.71 +/- 0.05 vs. 1.32 +/- 0.05 kg, p less than 0.001). There was an improvement of symptoms both taken as a whole (55.6 vs. 45.8%, p less than 0.01) or one by one, cramps were the only exception as they increased at 35 degrees C (2.7 vs. 10.9%, p less than 0.001) being related with a greater weight loss at both temperatures (1.47 +/- 0.04 vs. 2.04 +/- 0.25 kg at 37 degrees C, p less than 0.001; 1.76 +/- 0.03 kg vs. 2.23 = 0.10 kg at 35 degrees C, p less than 0.001). In spite of the increase in the frequency of cramps, 7 out of 8 patients experienced some amelioration of dialysis symptoms (range between 7 and 21.4%).(ABSTRACT TRUNCATED AT 250 WORDS)     

Treatment of post-dialytic orthostatic hypotension with an inflatable abdominal band in hemodialysis patients

The purpose of this study was to ascertain whether abdominal compression with an inflatable abdominal band, a device we developed, improved post-dialytic orthostatic hypotension (OH) in hemodialysis (HD) patients. Twenty-five chronic HD patients with intractable post-dialytic OH were recruited. Post-HD changes in systolic blood pressure (DeltaSBP) in the supine and standing positions were compared in the patients, measured with or without the use of the band. The study showed DeltaSBP after HD without the band was significantly greater than that measured before HD (-36.1+/-18.2 vs -13.1+/-16.8 mm Hg; P<0.0001). DeltaSBP after HD with the band was reduced significantly in comparison to DeltaSBP after HD without the band (-19.4+/-21.2 vs -36.1+/-18.2 mm Hg; P<0.002). Use of the band did not cause an elevation in SBP in the supine position (149.0+/-29.6 vs 155.4+/-25.7 mm Hg); however, it did increase SBP upon standing (129.6+/-27.3 vs 117.2+/-22.6 mm Hg; P<0.05). Eight patients in whom an increase in SBP of 25 mm Hg or more was achieved with the band were classified as responders. Ejection fraction was significantly higher (76.4+/-11.1 vs 61.9+/-13.6%; P<0.02) and atrial natriuretic peptide concentration significantly lower (27.9+/-22.0 vs 68.9+/-47.5 pg/ml; P<0.02) in responders than in non-responders. We conclude that the abdominal band was effective for overcoming post-dialytic OH, without elevating supine SBP in some patients.     

Comparison of blood pressure profiles with flunitrazepam/fentanyl/nitrous oxide vs cervical epidural anesthesia in surgery of the carotid artery

A study was carried out to compare the evolution of arterial blood pressure during carotid endarterectomy performed under either general anaesthesia (GA) or cervical epidural anaesthesia (CEA). 20 patients were randomly assigned to two equal groups. In the CEA group, 15 ml of 0.375% bupivacaine and 150 micrograms fentanyl were injected into the epidural space at C7-D1 level. In the GA group, patients were anaesthetized with 0.2 mg.kg-1 flunitrazepam and 5 micrograms.kg-1 fentanyl; intubation was carried out using 0.08 mg.kg-1 vecuronium, and the patients were ventilated with a mixture of nitrous oxide and oxygen (50% of each). Further injections, every 30 min, of 2 micrograms.kg-1 fentanyl were given to the patients in group GA. Blood pressure was monitored continuously, up to 4 h postoperatively, with a radial arterial catheter. Per- or postoperative hypertension was defined as a rise in systolic arterial blood pressure (Pasys) over 180 mmHg for greater than 3 min; this was treated with 20 mg nifedipine intranasally (group CEA) or 100 micrograms fentanyl with 0.5 mg flunitrazepam with or without nifedipine (group GA). Per- or postoperative hypotension was defined as a fall in Pasys below 100 mmHg and or a 30% fall in mean arterial blood pressure for greater than 3 min; this was treated, in both groups, with an intravenous bolus of 3 mg ephedrine. Patients in group CEA experienced more frequent episodes of peroperative hypertension (8/2; p less than 0.02) and postoperative hypotension (5/1) than group GA.(ABSTRACT TRUNCATED AT 250 WORDS)     

Airtraq喉镜和Macintosh直接喉镜在经口气管插管时血流动力学的比较

目的比较Airtraq视频喉镜和Macintosh直接喉镜经口气管插管时心血管反应。方法40例拟择期经口气管插管全麻下手术的患者,按照随机数字表随机分为两组,Airtraq组（A组）和Macintosh喉镜组（M组）,每组20例。观察麻醉诱导前、诱导后、插管即刻、插管后1、3min时的心率（HR）、血压和心率收缩压乘积（ratepressureproduct,RPP）。结果两组声门暴露时间差异无统计学意义（P〉0．05）,导管置入时间A组（6±4）S短于M组（10±4）S（P〈0．01）。两组诱导后的HR、血压和RPP值都较诱导前的基础值明显下降（P〈0．05）,插管即刻、插管后1min的心血管指标较诱导后明显增高（P〈0．05）。A组插管后3min心血管指标与诱导后比较差异无统计学意义（P〉0．05）,而M组3min时心血管指标[收缩压（SBP）（106±17）mmHg（1mmHg=0．133kPa）,舒张压（DBP）（65±10）mmHg,平均动脉压（MAP）（78±19）mmHg,HR（92±12）次／分,RPP（9748±2072）]与诱导后[SBP（93±15）mmHg,DBP（54±9）mmHg,MAP（67±10）mmHg,HR（85±12）次／分,RPP（8117±1886）]比较差异仍有统计学意义（R0．05）。A组、M组插管后5min心血管指标与诱导后比较差异均无统计学意义。结论与Macintosh直接喉镜相比,应用Airtraq视频喉镜行经口气管插管可减少插管置入时间,且血流动力学反应较轻。     

Telemetric blood pressure monitoring in conscious rats before and after compression injury of spinal cord

Abnormal cardiovascular control after spinal cord injury (SCI) results in hypotension soon after injury. Later, paroxysmal hypertension and bradycardia in response to sensory stimulation below the level of injury develop in most people with SCI. In this study, we used a radiotelemetry system, in rats (n = 7), to investigate the effect of a clinically relevant compression model of SCI at T5 spinal segment on mean arterial pressure (MAP) and heart rate (HR) at rest and in response to colorectal distension. The transducers were implanted 1 month before clip compression (50-g) injury and continuous recording of MAP and HR was established for a period of 2.5 months. SCI was associated with hypotension (86+/-3 mm Hg) at 1 day after injury. In the following 2 days, MAP gradually returned to preinjury levels. By contrast, HR increased at 1 day after SCI and remained unchanged thereafter. Three days after SCI, colorectal distension caused an increase in MAP of 8+/-2 mm Hg accompanied by bradycardia (-18 bpm). One week after SCI, colorectal distension induced an increase in MAP of 9+/-2 mm Hg and bradycardia (-41 bpm). In the following days, the magnitude of reflex hypertension gradually increased, reaching 21+/-4 mm Hg at 1.5 months after SCI. In summary, our data show that resting MAP rapidly returns to control values after SCI. Episodic hypertension associated with autonomic dysreflexia can develop in rats within 1 month after incomplete SCI.     

Effect of sertraline hydrochloride on dialysis hypotension

Hemodialysis hypotension (HH) is a very common disorder and has a multifactorial etiology. Autonomic dysfunction occurs in up to 50% of patients with end-stage renal disease (ESRD) and plays a key role in HH in some patients. Sertraline hydrochloride, a central nervous system serotonin reuptake inhibitor, has been shown to be an effective treatment of hypotension caused by autonomic dysfunction in disorders such as neurocardiogenic syncope and idiopathic orthostatic hypotension. This study sought to determine whether sertraline was effective in ameliorating HH. A retrospective chart analysis was performed that included nine consecutive patients (aged > or = 54 years, time on hemodialysis > or = 2.2 years) placed on sertraline (50 to 100 mg/d) for depression who also had HH (defined as prehemodialysis systolic blood pressure [SBP] < or = 100 mm Hg, > or = 40 mm Hg decrease in SBP during hemodialysis, SBP <90 mm Hg, any diastolic blood pressure <40 mm Hg, or a decrease in blood pressure-causing symptoms) before treatment with sertraline. The data from a 6-week pre-sertraline period were compared with the data from a 6-week sertraline period (defined as 6 weeks after drug begun). Blood pressure medications were unchanged during the trial period of sertraline. However, nadir mean arterial pressure recorded during a given dialysis session in the pre-sertraline period (55+/-4 mm Hg) was significantly lower than that recorded in the sertraline period (68+/-5 mm Hg; P < 0.05). In addition, the number of hypotensive episodes (same definition as HH) per dialysis session during the sertraline period was significantly lower than that during the pre-sertraline period (mean, 0.6+/-0.2 episodes per session v 1.4+/-0.3 episodes per session; P < 0.005). The number of therapeutic interventions required for hypotension during the sertraline period was also significantly less than that during the pre-sertraline period (mean, 1.7+/-0.8 interventions v 11.0+/-3.0 interventions; P < 0.005). The urea reduction ratio (62.7%+/-4.7% v 63.1%+/-9.3%; P = NS) and hematocrit (28.9%+/-0.8% v 29.5%+/-1.0%; P = NS) did not change significantly. It is concluded that the short-term (6 weeks) use of sertraline hydrochloride reduces HH in some patients with ESRD. A possible mechanism for this effect is sertraline-induced attenuation of the paradoxical sympathetic withdrawal that may underlie HH in some patients with ESRD.     

Renal stenting for incidentally discovered renal artery stenosis: is there any outcome benefit?

We evaluated whether there was a clinical outcome benefit in patients incidentally discovered to have high-grade renal artery stenosis (RAS) and treated with percutaneous transluminal renal angioplasty and stenting (PTRAS) at the time of angiogram for another indicated procedure. A retrospective chart review was performed on all patients undergoing renal arteriography over 4 years at our academic tertiary-care referral center. Review of catheterization reports was used to identify patients diagnosed with high-grade RAS (reduction of > or =70% luminal diameter by arteriogram). Patients treated with PTRAS were identified. Baseline and postprocedure blood pressure (BP, an average of at least three independent measurements), glomerular filtration rate, serum creatinine, and antihypertensive medication regimen were compared for 12 months of follow-up. Over 4 years, 124 patients underwent renal arteriography and 78 (63%) were diagnosed with high-grade RAS. Fifty-eight patients (74% of those with high-grade RAS) received PTRAS. Patients treated with PTRAS had similar baseline characteristics to those with high-grade RAS with no intervention, with the exception of lower diastolic BP (DBP; 74 +/- 11.2 vs. 80 +/- 14.2 mm Hg, p = 0.04) and a higher proportion of hyperlipidemia (78 vs. 55%, p = 0.05). Thirty-eight out of 58 PTRAS patients (66%) received sufficient follow-up to assess outcomes. When baseline and postprocedure variables were compared in PTRAS patients with 12-month follow-up, there was a reduction in systolic BP (SBP, 153 +/- 20.8 vs. 136 +/- 27.2 mm Hg, p = 0.01) and mean arterial pressure (MAP, 103 +/- 11.2 vs. 95 +/- 14 mm Hg, p = 0.04). When these patients were stratified by those with an increase, decrease, or no change in postprocedure antihypertensive medications, significant reductions in SBP, MAP, and DBP were noted only in the patient population that also had an increase in the number of antihypertensive medications. No differences in renal insufficiency were detected. Patients with high-grade RAS incidentally discovered during arteriography performed for extrarenal disease and treated with PTRAS have a modest reduction in BP, which is significant only in those patients with an increased number of antihypertensive medications postprocedure. Caution must be taken in stenting patients with incidental RAS as outcome benefit may be minimal when compared to medical management only.     

Hemodialysis-associated hypotension as an independent risk factor for two-year mortality in hemodialysis patients

BACKGROUND: The relationship between blood pressure (BP) and mortality in hemodialysis patients has remained controversial. Some studies suggested that a lower pre- or postdialysis BP was associated with excess mortality, while others showed poorer outcome in patients with uncontrolled hypertension. We conducted a multicenter prospective cohort study to evaluate the impact of hemodialysis-associated hypotension on mortality. METHODS: We recruited 1244 patients (685 males; mean age, 60 +/- 13 years) who underwent hemodialysis in 28 units during the two-year study period beginning in December 1999. Pre-, intra-, and postdialysis BP, and BP upon standing soon after hemodialysis, were measured in all patients at entry. Logistic regression analysis was used to assess the effect on mortality of pre-, intra-, and postdialysis BP, a fall in BP during hemodialysis, and a fall in BP upon standing soon after hemodialysis. RESULTS: During the study period, 149 patients died. Logistic models identified the lowest intradialysis systolic blood pressure (SBP) and degree of fall in SBP upon standing soon after hemodialysis as significant factors affecting mortality, but not pre- or postdialysis SBP and diastolic BP. The adjusted odds ratio for death was 0.79 (95% CI 0.64-0.98) when the lowest intradialysis SBP was analyzed in increments of 20 mm Hg, and was 0.82 (95% CI 0.67-0.98) when the fall in SBP upon standing soon after hemodialysis was analyzed in increments of 10 mm Hg. CONCLUSION: These results suggest that intradialysis hypotension and orthostatic hypotension after hemodialysis are significant and independent factors affecting mortality in hemodialysis patients.     

Prospective evaluation of electroencephalography, carotid artery stump pressure, and neurologic changes during 314 consecutive carotid endarterectomies performed in awake patients

OBJECTIVE: This study attempted to correlate neurologic changes in awake patients undergoing carotid endarterectomy (CEA) under cervical block anesthesia (CBA) with electroencephalography (EEG) and measurement of carotid artery stump pressure (SP). METHODS: Continuous EEG and SP monitoring was measured prospectively in 314 consecutive patients undergoing CEA between April 1, 2003, and July 30, 2006, under CBA. Indications for CEA were asymptomatic 70% to 99% internal carotid artery stenosis in 242 (77.1%), transient ischemic attacks (including transient monocular blindness) in 45 (14.3%), and prior stroke in 27 (8.6%). Mean common carotid artery pressure before clamping, mean SP after carotid clamping, and intraarterial pressure were continuously monitored in all patients. An indwelling shunt was placed when neurologic events (contralateral motor weakness, aphasia, loss of consciousness, or seizures) occurred, regardless of SP or EEG changes. RESULTS: Shunt placement was necessary because of neurologic changes in 10% (32/314) of all CEAs performed under CBA. Only 3 patients (1.4%) of 216 required shunt placement if SP was 50 mm Hg or more, vs 29 (29.6%) of 98 if SP was less than 50 mm Hg (P < .00001; sensitivity, 29.8%; specificity, 98.6%). In patients with SP of 40 mm Hg or more, 7 (2.6%) of 270 required shunt placement, vs 25 (56.8%) of 44 if SP was less than 40 mm Hg (P < .00001; sensitivity, 56.8%; specificity, 97.4%). Ischemic EEG changes were observed in 19 (59.4%) of 32 patients (false-negative rate, 40.6%) requiring shunt placement under CBA. Three patients had false-positive EEG results and did not require shunt placement (false-positive rate, 1.0%). The perioperative stroke/death rate was 4 (1.2%) in 314. All strokes occurred after surgery and were unrelated to cerebral ischemia or lack of shunt placement. CONCLUSIONS: Ten percent of patients required a shunt placement during CEA under CBA. Shunt placement was necessary in 56.8% of patients with SP less than 40 mm Hg. EEG identified cerebral ischemia in only 59.4% of patients needing shunt placement, with a false-positive rate of 1.0% and a false-negative rate of 40.6%. Both SP and EEG as a guide to shunt placement have poor sensitivity. Intraoperative monitoring of the awake patients under regional anesthesia (CBA) is the most sensitive and specific method to identify patients requiring shunt placement.     

The use of inhaled prostacyclin in nitroprusside-resistant pulmonary artery hypertension

Because nitroprusside NTP infusion used to differentiate between fixed and reversible pulmonary artery hypertension in heart transplant candidates can result in systemic hypotension before reducing pulmonary artery pressures, we observed the effect or inhaled prostacyclin (PGI(2)) on pulmonary artery pressures and transpulmonic gradient (TPG) in patients with NTP-resistant pulmonary artery hypertension. Six patients undergoing evaluation for orthotropic heart transplant (OHTX) with NTP-resistant pulmonary artery hypertension received inhaled PGI(2), with hemodynamic measurements made at baseline, on NTP- and PGI(2) inhaled after returning to baseline. Compared with hemodynamic results with NTP, inhaled PGI(2) caused significant decrease in pulmonary artery systotic pressure, 43.8 +/- 4.8 mm Hg vs 63.2 +/- 2.04 mm Hg (p < 0.001); Mean pulmonary artery pressure, 22.7 +/- 4.18 vs 32.3 +/- 3.39 mm Hg (p < 0.05); and TPG, 11.5 +/- 3.73 vs 17.0 +/- 4.69 mm Hg (p < 0.05), with a 40% decrease in pulmonary vascular resistance/systemic vascular resistance ratio. We conclude that inhaled PGI(2) has benefit in reversing pulmonary artery hypertension resistant to NTP, in patients undergoing OHTX evaluation which is due to its more selective pulmonary vasodilation.     

Cardiovascular parameter changes in patients with erectile dysfunction using pde-5 inhibitors: a study with sildenafil and vardenafil

Sildenafil is the most prescribed oral agent for patients with erectile dysfunction (ED). Vardenafil is a new phosphodiesterase type 5 (Pde-5) inhibitor that was approved by the US Food and Drug Administration last year to treat patients with ED of various causes. Both of these Pde-5 inhibitors have vasodilating properties and effects on blood pressure (BP), and like nitrates, they work through the nitric oxide cyclic guanosine monophosphate pathway. The aim of this study was to investigate the influence of these Pde-5 inhibitors on BP and heart rate (HR) in normotensive men with ED by a crossover comparison. Thirty-five patients with ED were enrolled to evaluate and compare the effect of sildenafil (50 mg) and vardenafil (10 mg) on BP and HR. At the screening (baseline [B]) visit, sitting systolic blood pressure (B-SBP), diastolic blood pressure (B-DBP), and HR were measured. We performed a multiple administration for both drugs and, therefore, multiple measurements of BP and HR changes, 3 doses a week, on alternate days, late in the afternoon, and on an empty stomach. B-SBP, B-DBP, and HR were recorded before each 50-mg sildenafil dosing and after 30, 60, 120, and 240 minutes. Data were averaged over the 4 time points and compared with the baseline values obtained before each dosing. After a 3-week wash-out period, patients were crossed over to vardenafil (10 mg) with the same study design. After administration of both drugs, we observed a statistically significant decrease of BP and an increase of HR. On average, sildenafil caused a decrease of SBP ranging from 5.1 +/- 3.9 mm Hg during the first dosing to 4.7 +/- 4.2 mm Hg during the third dosing, DBP ranged from 4.4 +/- 4.9 to 4 +/- 4.1 mm Hg, and HR increased 1.8 +/- 2.0 bpm (first dose) and 1.2 +/- 0.9 bpm (third dose). With vardenafil, we recorded a greater variation for SBP and DBP. SBP decreased from 8.02 +/- 8.0 mm Hg during the first dosing to 5.4 +/- 5.5 mm Hg during the third dosing, whereas DBP decreased from 6.6 +/- 7.2 to 5.0 +/- 5.3 mm Hg, respectively. Recorded HR showed an increase of 3.1 +/- 3.2 bpm (first dose) and 2.4 +/- 2.3 bpm (third dose). After the first vardenafil administration, we recorded fainting episodes in 3 patients because of a decrease in BP greater than 20 mm Hg. Two of the patients were in therapy with doxazosin for benign prostatic hyperplasia (BPH). Cardiovascular response was not significantly different after the first dose between the 2 treatments. Vardenafil demonstrated clinically significant differences (fainting) with respect to sildenafil only during the first doses. We suggest that before starting therapies with Pde-5 inhibitors, particularly with the newer ones, that baseline cardiovascular parameters are measured and monitored, especially during the first dose, because of the presence of a "first dose effect." Moreover, it is necessary to pay particular attention to those patients in treatment with other drugs that could have a synergistic hypotensive effect as a result of vasodilation potentiation.