Hg Mean Research Articles

Intensive atmospheric mercury measurements at Terra Nova Bay in Antarctica during November and December 2000

It is well known that due to its long atmospheric residence time, mercury is distributed on a global scale and aeolian transport is believed to be the major contributor to mercury in polar environments. No measurements of reactive gaseous mercury (RGM) at all have ever been performed in the Antarctic before. Hg0(g) concentrations were in the range 0.29 to 2.3 ng m−3, with an average value of 0.9 ± 0.3 ng m−3. RGM was measured using KCl‐coated annular denuders and a speciation unit coupled to a TGM analyzer; concentrations ranged from 10.5 to 334 pg m−3, with an average of 116.2 ± 77.8 pg m−3. The Hg0(g) measurements are in good agreement with the few data available for such southerly latitudes. The RGM concentrations are as high as those found in some industrial environments; the high concentrations in the absence of local sources (anthropogenic or natural) show that in situ gas phase oxidation of Hg0 is the most important factor influencing RGM production and therefore also Hg deposition. The toxicity of Hg means that the consequences of high concentrations of oxidized and soluble Hg species depositing in the fragile Antarctic environment could be serious indeed.

Noninvasive estimation of both systolic and diastolic pulmonary artery pressure from Doppler analysis of tricuspid regurgitant velocity spectrum in patients with chronic heart failure

Background Noninvasive estimation of pulmonary artery systolic and diastolic pressures usually requires the investigation of both tricuspid and pulmonary regurgitant jets and an estimate of right atrial pressure. A new, noninvasive method to obtain pulmonary diastolic pressure (based on the hemodynamic demonstration that right ventricular systolic pressure and pulmonary artery diastolic pressure are equal at the time of pulmonary valve opening) from the analysis of tricuspid regurgitation alone has been described in a small cohort of patients. We sought to verify the accuracy of this method in a large population of patients with heart failure. Methods An estimate of pulmonary artery diastolic pressure was obtained by transposing the pulmonary opening time (from the onset of the R wave on the electrocardiographic tracing to the beginning of pulmonic forward flow on Doppler examination) onto the tricuspid regurgitant velocity curve and calculating the pulmonary artery diastolic pressure value as the pressure gradient between the right ventricle and right atrium at this time. The study group included 86 consecutive patients (64 men, aged 52 ± 11 years) with heart failure (New York Heart Association class ≥II, 94%) who were in stable clinical condition with a chiefly idiopathic (57%), ischemic (24%), or other form (13%) of dilated cardiomyopathy. Noninvasive, right-sided pressures were compared with invasive measurements obtained during right heart catheterization performed within 24 hours. The Bland and Altman graphic method was used together with the calculation of the Lin concordance correlation coefficient and its 95% CI to assess the agreement between hemodynamic and echocardiographic measurements. Results Catheter-derived pulmonary artery systolic pressure ranged from 8 to 119 mm Hg (mean 42 ± 21 mm Hg), pulmonary artery diastolic pressure from 1 to 59 mm Hg (mean 20 ± 11 mm Hg), and right atrial pressure from −5 to 20 mm Hg (mean 6 ± 5 mm Hg). Tricuspid regurgitation was detected in 75 of 86 patients (87%). Pulmonary artery systolic pressure ranged from 13 to 110 mm Hg (mean 44 ± 21 mm Hg); the pressure gradient between the right ventricle and right atrium at time t of the pulmonary valve opening on the tricuspid regurgitation velocity curve was measurable in 70 of 75 (93%) cases and ranged from 3.5 to 64 mm Hg (mean 22 ± 11 mm Hg). Good agreement was observed not only for pulmonary artery systolic pressure but also for pulmonary artery diastolic pressure, based on the analysis of the tricuspid regurgitation velocity jet, with a slight difference between measurements (−1.8 and 0.1, respectively), no evident pattern of point scattering, and a high concordance correlation coefficient that was elicited by the virtually total overlapping of lines on the graph. Overall results were not significantly different whether patients with depressed right ventricular function (right ventricular ejection fraction ≤35%), with a tricuspid regurgitation grade ≥2 and atrial fibrillation were included in the analysis. Conclusions The narrow paired difference for the estimate of pulmonary artery systolic pressure and the even better difference for pulmonary artery diastolic pressure using the tricuspid regurgitation velocity curve analysis indicates that this new method reliably estimates invasive right-sided pressures over a wide range of pressure values in patients with heart failure. The overall good correlation with invasive values indicates that Doppler examination of tricuspid regurgitation alone may provide a simple and comprehensive new method for the noninvasive evaluation of right ventricular and pulmonary hemodynamics in patients with heart failure. (Am Heart J 2002;144:1087-94.)

Effectiveness of percutaneous device occlusion for atrial septal defect in adult patients with pulmonary hypertension.

Adult patients with atrial septal defect (ASD) and pulmonary hypertension have a more advanced degree of disease, frequently having functional class deterioration and atrial arrhythmias when they are aged >40 years. Surgery at this age prolongs life expectancy and limits functional deterioration. Although percutaneous ASD device occlusion is an accepted alternative to surgery, there is limited information on the immediate and long-term effects of device occlusion in middle-aged and elderly patients with ASD and pulmonary hypertension. From a total of 101 patients with secundum ASD who were receiving treatment with percutaneous device occlusion, we selected for analysis 29 adult patients (mean age 56 +/- 14 years) with a baseline peak pulmonary pressure of >40 mm Hg (mean 65 +/- 23 mm Hg). Three of the patients had suprasystemic pulmonary pressure and a bidirectional shunt. Six patients were asymptomatic at treatment. The remaining 23 had different degrees of dyspnea; 14 of them had an advanced New York Heart Association functional class (III-IV). Twelve patients had chronic atrial fibrillation. At cardiac catheterization, the mean ratio of pulmonary to systemic flow was 1.8 +/- 0.5, and the pulmonary-to-systemic pressure ratio was 0.66 +/- 0.22. The mean diameter of the defect, as evaluated by the stretching balloon method, was 26 +/- 7 mm. All patients received an Amplatzer septal occluder (Golden Valley, Minn). Seven patients had combined therapeutic procedures for associated anomalies before the implant: mitral balloon valvuloplasty (n = 1), stent coronary revascularization (n = 1), stent in pulmonary vein stenosis (n = 1), and internal catheter defibrillation (n = 4). After treatment, patients were followed up by clinical and echocardiographic Doppler studies every 6 months. Immediately after the implantation, the peak systolic pulmonary pressure significantly decreased to 54 +/- 21 mm Hg (P <.001). A clear improvement in functional status was observed after the treatment in all symptomatic patients, especially in those with refractory heart failure. There were no major complications. Six patients who had atrial fibrillation at baseline study recovered to a stable sinus rhythm after treatment, and it was maintained at discharge. Complete ASD occlusion by echocardiographic Doppler at discharge was observed in 28 patients (97%). After a mean follow up of 21 +/- 14 months, clinical improvement persisted in all previously symptomatic patients, and the peak systolic pulmonary pressure, obtained by echocardiographic Doppler, further decreased to 31 +/- 11 mm Hg (P <.001) compared with baseline and immediately after hemodynamic measurements. Our findings suggest that percutaneous device occlusion of ASD in adult patients with pulmonary hypertension is safe and effective and provides significant and prolonged relief.

Effectiveness of percutaneous device occlusion for atrial septal defect in adult patients with pulmonary hypertension

Background Adult patients with atrial septal defect (ASD) and pulmonary hypertension have a more advanced degree of disease, frequently having functional class deterioration and atrial arrhythmias when they are aged >40 years. Surgery at this age prolongs life expectancy and limits functional deterioration. Although percutaneous ASD device occlusion is an accepted alternative to surgery, there is limited information on the immediate and long-term effects of device occlusion in middle-aged and elderly patients with ASD and pulmonary hypertension. Methods From a total of 101 patients with secundum ASD who were receiving treatment with percutaneous device occlusion, we selected for analysis 29 adult patients (mean age 56 ± 14 years) with a baseline peak pulmonary pressure of >40 mm Hg (mean 65 ± 23 mm Hg). Three of the patients had suprasystemic pulmonary pressure and a bidirectional shunt. Six patients were asymptomatic at treatment. The remaining 23 had different degrees of dyspnea; 14 of them had an advanced New York Heart Association functional class (III-IV). Twelve patients had chronic atrial fibrillation. At cardiac catheterization, the mean ratio of pulmonary to systemic flow was 1.8 ± 0.5, and the pulmonary-to-systemic pressure ratio was 0.66 ± 0.22. The mean diameter of the defect, as evaluated by the stretching balloon method, was 26 ± 7 mm. All patients received an Amplatzer septal occluder (Golden Valley, Minn). Seven patients had combined therapeutic procedures for associated anomalies before the implant: mitral balloon valvuloplasty (n = 1), stent coronary revascularization (n = 1), stent in pulmonary vein stenosis (n = 1), and internal catheter defibrillation (n = 4). After treatment, patients were followed up by clinical and echocardiographic Doppler studies every 6 months. Results Immediately after the implantation, the peak systolic pulmonary pressure significantly decreased to 54 ± 21 mm Hg ( P <.001). A clear improvement in functional status was observed after the treatment in all symptomatic patients, especially in those with refractory heart failure. There were no major complications. Six patients who had atrial fibrillation at baseline study recovered to a stable sinus rhythm after treatment, and it was maintained at discharge. Complete ASD occlusion by echocardiographic Doppler at discharge was observed in 28 patients (97%). After a mean follow up of 21 ± 14 months, clinical improvement persisted in all previously symptomatic patients, and the peak systolic pulmonary pressure, obtained by echocardiographic Doppler, further decreased to 31 ± 11 mm Hg ( P <.001) compared with baseline and immediately after hemodynamic measurements. Conclusions Our findings suggest that percutaneous device occlusion of ASD in adult patients with pulmonary hypertension is safe and effective and provides significant and prolonged relief. (Am Heart J 2002;144:877-80.)

Blood pressure control--effects on diabetic nephropathy progression: how low does blood pressure have to be?

Hypertension and diabetes are independent risk factors for both cardiovascular disease and renal complications. Coexistence of these comorbid conditions predisposes the patient to a much greater risk of progression to end-stage renal disease. Combined with the increased cardiovascular mortality, this has led to recent Joint National Committee-VI recommendations for the initiation of antihypertensive therapy for people with diabetes at a blood pressure of 130/85 mm Hg, a level lower than that recommended for the nondiabetic population. Results of a review of recently published investigations on the effects of blood pressure on diabetic nephropathy progression are presented in this article. This review finds evidence to support reducing the mean arterial blood pressure to levels below 95 mm Hg, a level that is even lower than the blood pressure of 130/80 mm Hg (mean arterial pressure of 97 mm Hg) recommended by the American Diabetes Association and National Kidney Foundation. The effect of blood pressure on renal disease progression is linear and appears to have no lower threshold for the benefits of blood pressure reduction on limiting nephropathy progression. The answer to the question of how low does blood pressure have to be to minimize the effects of blood pressure on diabetic nephropathy progression might be "the lower, the better."

Percutaneous inferior vena cava-to-portal vein shunt (PIPS) using a stent-graft: preliminary results.

To present preliminary results of an inferior vena cava (IVC)-to-portal vein shunt (PIPS) that is created through the caudate lobe of the liver. Sixteen patients (13 men; mean age 50 years, range 32-63) were referred for PIPS procedures because of bleeding varices (n = 11), intractable ascites (n = 4), and hepatorenal syndrome (n = 1). The severity of liver disease was Child's B in 2 and Child's C in 14. The PIPS was created by a transhepatic puncture through the IVC and the portal vein; an endograft made of polytetrafluoroethylene sutured to a Palmaz stent was placed through a jugular approach. In 13 (81%) patients, the portal vein-to-IVC tracts were successfully created. The postprocedural portal vein-IVC gradients varied from 1 to 9 mm Hg (mean 5). There were 2 deaths in the 30-day periprocedural period from adult respiratory distress syndrome and hepatorenal syndrome. A third patient died at 31 days from liver failure owing to continuing alcohol abuse. In addition, there was 1 case of peritoneal bleeding treated with blood product replacement. The follow-up period ranged from 14 to 671 days (mean 343). None of the patients treated for variceal bleeding had another bleeding episode, but 2 patients who had a PIPS procedure for refractory ascites did not benefit from the procedure. Postprocedure, 46% (6/13) of the patients had hepatic encephalopathy, which was unchanged from baseline. The primary and secondary patency rates at 365 days were 60% and 65%, respectively. The preliminary results using a stent-graft to create an IVC-portal vein shunt are encouraging and support further work to better determine the role of this procedure.

Abnormal pulmonary vascular tone in canine oleic acid lung injury.

To characterize the endothelium-dependent and endothelium-independent components of abnormal pulmonary vascular tone in canine oleic acid lung injury. Prospective, interventional study. University laboratory. Twenty anesthetized mongrel dogs. Right heart catheterization was performed to measure pulmonary vascular resistance before and after induction of oleic acid lung injury in ten anesthetized and ventilated dogs. Pulmonary and internal mammary artery rings were sampled in these ten dogs with oleic acid injury and in ten anesthetized healthy control dogs. We also studied the responses to acetylcholine, to phenylephrine, and to hypoxia of the intact or endothelium-denuded rings mounted in organ baths. Oleic acid lung injury was associated with an increase in pulmonary vascular resistance from 118 +/- 11 to 245 +/- 47 dyne.sec.cm-5.m-2 and a decrease in the Pao2/Fio2 ratio from 451 +/- 42 to 139 +/- 26 mm Hg (mean +/- se, p <.05 and p <.01, respectively). Acetylcholine-induced relaxation was decreased in the oleic acid pulmonary artery rings compared with the controls (85 +/- 3% vs. 99 +/- 6% of precontraction level, p <.05). Phenylephrine-induced contraction was decreased in denuded oleic acid pulmonary artery rings compared with the controls (81 +/- 8% vs. 102 +/- 10% of contraction to KCl 120 mM, p <.05). In vitro hypoxia induced a small endothelium-dependent contraction followed by an endothelium-independent relaxation. These responses were not different in oleic acid lung artery rings and in controls, except for a decrease in hypoxic contraction in the oleic acid pulmonary artery rings. In vitro hypoxic pulmonary vasoconstriction and relaxation were, respectively, directly (r =.48) and inversely (r = -.67) correlated with oleic acid-induced increase in pulmonary vascular resistance. There was no correlation between in vitro internal mammary artery reactivity and oleic acid-induced increase in pulmonary vascular resistance. Oleic acid-induced lung injury slightly impairs pulmonary arterial endothelium-dependent relaxation and endothelium-independent contraction. In vitro hypoxic pulmonary vasoreactivity is related to in vivo oleic acid-induced increase in pulmonary vascular resistance.

Dalteparin sodium treatment during resuscitation inhibits hemorrhagic shock-induced leukocyte rolling and adhesion in the mesenteric microcirculation.

Ischemia/reperfusion-induced polymorphonuclear neutrophil leukocyte (PMN) adhesion and extravasation are pivotal for the development of postinjury multiple organ failure. We hypothesized that the deleterious microcirculatory consequences of hemorrhagic shock (HS) could be altered by low-molecular-weight heparin (LMWH) therapy. Our aim was to investigate the effects of dalteparin sodium on leukocyte-endothelial cell interactions when LMWH treatment was initiated before HS or during resuscitation. Anesthetized dogs underwent HS (40 mm Hg mean arterial pressure for 60 minutes) and resuscitation either with shed blood or with lactated Ringer's (LR) solution. LMWH or conventional heparin sodium pretreatment was administered subcutaneously before hemorrhage; or LMWH was given intravenously during resuscitation. Mesenteric postcapillary venules were observed by intravital video microscopy before and after HS, and 60 minutes, 120 minutes, and 180 minutes after resuscitation, and leukocyte rolling and firm adherence were determined. HS significantly increased PMN rolling and adhesion in the mesenteric microcirculation. LMWH, but not heparin sodium pretreatment, significantly inhibited both primary and secondary interactions. LMWH treatment was also effective when initiated during resuscitation. LMWH exerted the same inhibitory effect regardless of the type of resuscitation. LMWH treatment during resuscitation effectively inhibits PMN rolling and adhesion.

Toward a durable impeller pump with mechanical bearings.

Our former work demonstrated that our impeller pump could support the circulation of experimental animals for several months without harm to blood elements or organ function. The termination of the experiments was mostly related to wear of the mechanical bearing and thrombosis along the bearing. To solve the bearing problem, we investigated a magnetic bearing in our lab, which resulted in some new problems, such as complicated design and control, considerable energy consumption, and lesser reliability. Progress in developing an impeller pump for long-term application has recently been achieved. Instead of using a sliding bearing system, we devised a rolling bearing system. Its service life is more than 10 years because of a wearproof roller made of ultra high molecular weight polythene. To avoid thrombus formation, we introduced a special purge system to the bearing, allowing the saline with heparin to be infused through the bearing into the pump. The bearing, therefore, keeps working in the saline, and no thrombus will be formed. Animal experiments demonstrated that a 30 ml fluid infusion per hour is enough to prevent thrombus formation. With these improvements, the impeller pump has continuously run for 8 months, and no bearing wear can be measured. The device, weighing 150 g, is fully implantable, consumes approximately 9.6 watts, and delivers a 9L/min blood flow against a 120 mm Hg mean pressure and reaches a highest total efficiency of 24.7% for the motor (including the controller) and pump. The system can produce both pulsatile and nonpulsatile flow according to requirements.

A Study of Glaucoma After Penetrating Keratoplasty

To identify the incidence and risk factors associated with the development of glaucoma after penetrating keratoplasty. A retrospective study was carried out in 228 patients who underwent penetrating keratoplasty from January 1995 to January 2000 at the Cornea Section of the Ophthalmology Service at the School of Medicine, Federal University of Uberlândia MG, Brazil. Follow-up time ranged from 4 to 60 months (mean, 17.14 +/- 13.65). Two hundred twenty-eight patients undergoing penetrating keratoplasty were evaluated and 49 (21.5%) developed glaucoma. Risk factors for developing glaucoma were bullous keratopathy [relative risk (RR) = 2.1774), herpesvirus (RR = 1.8979), and trauma (RR = 1.0575). Mean intraocular pressure before transplantation was 15.26 +/- 5.37 mm Hg. Intraocular pressure after transplantation ranged from 22 to 58 mm Hg, with a mean value of 30.04 +/- 7.06 mm Hg. Thirty-six (73.5%) patients had medical treatment, 10 (20.4%) had medical and surgical treatment, and three (6.1%) had surgical treatment. Final intraocular pressure ranged from 4 to 34 mm Hg (mean, 16.79 +/- 5.36). The incidence of glaucoma after penetrating keratoplasty is high, and the risk factors include aphakic/pseudophakic bullous keratopathy, herpes simplex virus, and trauma.

Rounded Mass in the Middle Lobe After Swan-Ganz Catheterization

A 76 -year-old woman was admitted to the hospital because of episodes of ventricular tachycardia. She had a history of myocardial infarction in 1973 and underwent coronary artery bypass surgery in 1993. Transesophageal echocardiography revealed grade 3 mitral valve regurgitation. A left and right cardiac catheterization was performed with insertion of a Swan-Ganz catheter via the right femoral vein. Shortly after inflating the balloon in the wedge position, the patient experienced an episode of hemoptysis of approximately 50 mL. The pulmonary artery pressure was 40/20 mm Hg (mean, 21 mm Hg). Because of oxygen desaturation, she was transferred to the ICU. The chest radiograph then obtained showed a well-circumscribed rounded mass in the right middle lung zone (Fig 1), which was not seen on prior chest radiographs.

One MAC of sevoflurane provides protection against reperfusion injury in the rat heart in vivo

Volatile anaesthetics protect the heart against reperfusion injury. We investigated whether the cardioprotection induced by sevoflurane against myocardial reperfusion injury was concentration-dependent. Fifty-eight alpha-chloralose anaesthetized rats were subjected to 25 min of coronary artery occlusion followed by 90 min of reperfusion. Sevoflurane was administered for the first 15 min of reperfusion at concentrations corresponding to 0.75 (n=11), 1.0 (n=11), 1.5 (n=13), or 2.0 MAC (n=12). Eleven rats served as untreated controls. Left ventricular peak systolic pressure (LVPSP, tipmanometer) and cardiac output (CO, flowprobe) was measured. Infarct size (IS, triphenyltetrazolium staining) was determined as percentage of the area at risk. Baseline LVPSP was 131 (126-135) mm Hg (mean (95% confidence interval)) and CO 33 (31-36) ml min(-1), similar in all groups. During early reperfusion, sevoflurane reduced LVPSP in a concentration-dependent manner to 78 (67-89)% of baseline at 0.75 MAC (not significant vs controls 99 (86-112)%), 71 (62-80)% at 1 MAC (P<0.05), 66 (49-83)% at 1.5 MAC (P<0.05) and 56 (47-65)% at 2 MAC (P<0.05). CO remained constant. While 0.75 MAC of sevoflurane had no effect on IS (34 (27-41)% of the area at risk) compared with controls (38 (31-45)%, P=0.83), 1.0 MAC reduced IS markedly to 23 (17-30)% (P<0.05). Increasing the concentration to 1.5 MAC (23 (17-30)%) and 2 MAC (23 (13-32)%, both P<0.05 vs controls) had no additional protective effect. One MAC sevoflurane protected against myocardial reperfusion injury. Increasing the sevoflurane concentration above 1 MAC resulted in no further protection.

Repair of double-chambered right ventricle: surgical results and long-term follow-up

Background. We reviewed the outcomes of double-chambered right ventricle repair. Methods. Between 1969 and 1998, 40 patients underwent surgical repair of a double-chamber right ventricle. The patients ranged in age from 3 months to 52 years (mean, 12.8 ± 11.6 years). Right ventricular outflow tract pressure gradients were from 20 to 170 mm Hg (mean, 65.0 ± 38.5 mm Hg) An associated ventricular septal defect was present in 27 patients (67.5%). Four patients were older than 30 years of age. Results. There were no hospital or late deaths. Mean postsurgical follow-up was 16.5 ± 8.9 years (range, 2.5 to 31 years). No patient required further surgery to relieve obstruction of right ventricular outflow tract. Conclusions. Surgical repair of a double-chambered right ventricle yields excellent hemodynamic and functional results over both the short and long term.

Factors associated with the occurrence and magnitude of earthquake-induced increases in blood pressure

Background Blood pressure increases transiently after a major earthquake, but the characteristics and the mechanism of this increase are unknown. Methods The study involved 124 elderly hypertensive outpatients from two clinics near the epicenter of the Hanshin-Awaji earthquake (7.2 on the Richter scale) for whom ambulatory blood pressure monitoring and assessment of end-organ damage had been performed before the earthquake. Results During the 1 to 2 weeks after the earthquake, while major aftershocks persisted, mean (± SD) systolic blood pressure was 14 ± 16 mm Hg greater and mean diastolic blood pressure was 6 ± 10 mm Hg greater, but these values returned to baseline by 3 to 5 weeks after the earthquake. The earthquake-induced increase in blood pressure correlated significantly with the “white coat” effect ([clinic systolic blood pressure minus 24-hour systolic blood pressure] r = 0.34, P <0.001), body mass index ( r = 0.28, P <0.001), and age ( r = 0.24, P <0.01). The earthquake-induced blood pressure increase was prolonged in patients with microalbuminuria for at least 2 months after the earthquake, whereas it was less pronounced in patients who had been treated with an alpha-blocker and in patients with diabetes mellitus. Conclusions These elderly patients with hypertension had a substantial increase in blood pressure after a major earthquake; the increase was usually transient, except in patients who had microalbuminuria. The correlation with white-coat hypertension suggests that both phenomena are related to sympathetic activation.

Incidence, location, pathology, and significance of pulmonary homograft stenosis after the Ross operation.

The Ross operation has several theoretical advantages. However, concern exists regarding evolving pathology in the pulmonary homograft. Consecutive patients (n=144; mean age 31 years, range 2 months to 64 years) undergoing the Ross operation were studied between 1993 and 2000. Echocardiographic examination of the pulmonary homograft was performed immediately after surgery, then at yearly intervals for a mean interval of 48 months. Fifteen patients (mean age 37 years) in whom echocardiography revealed peak pulmonary gradients >/=30 mm Hg (mean 46+/-18 mm Hg) underwent MRI with velocity mapping in a Picker 1.5-T magnet. No patient had more than mild pulmonary regurgitation. Four patients required reoperation for rapidly progressive pulmonary homograft stenosis; in all 4, there was macroscopic and microscopic evidence of a pronounced chronic adventitial reaction, with perivascular infiltration producing extrinsic compression. Freedom from any pulmonary homograft stenosis at 7-year follow-up was 79.7%, with instantaneous hazard falling to zero after 4 years. Freedom from reoperation at 7 years was 96.7%. In those studied with MRI, there was evidence of narrowing of the whole homograft or distal suture line in 14 of 15 patients, with obvious excess surrounding tissue in 11. Mean minimum diameter and peak velocity by MRI were 11+/-2 mm and 3.2+/-0.7 m/s, respectively. Multivariate analysis of patient-, surgery-, and homograft-related variables did not reveal any significant risk factors for development of neopulmonary stenosis. Pulmonary homograft stenosis after the Ross operation is clinically important and appears to represent an early postoperative inflammatory reaction to the pulmonary homograft that leads to extrinsic compression and/or shrinkage.

Incidence, Location, Pathology, and Significance of Pulmonary Homograft Stenosis After the Ross Operation

Background The Ross operation has several theoretical advantages. However, concern exists regarding evolving pathology in the pulmonary homograft. Methods and Results Consecutive patients (n=144; mean age 31 years, range 2 months to 64 years) undergoing the Ross operation were studied between 1993 and 2000. Echocardiographic examination of the pulmonary homograft was performed immediately after surgery, then at yearly intervals for a mean interval of 48 months. Fifteen patients (mean age 37 years) in whom echocardiography revealed peak pulmonary gradients ≥30 mm Hg (mean 46±18 mm Hg) underwent MRI with velocity mapping in a Picker 1.5-T magnet. No patient had more than mild pulmonary regurgitation. Four patients required reoperation for rapidly progressive pulmonary homograft stenosis; in all 4, there was macroscopic and microscopic evidence of a pronounced chronic adventitial reaction, with perivascular infiltration producing extrinsic compression. Freedom from any pulmonary homograft stenosis at 7-year follow-up was 79.7%, with instantaneous hazard falling to zero after 4 years. Freedom from reoperation at 7 years was 96.7%. In those studied with MRI, there was evidence of narrowing of the whole homograft or distal suture line in 14 of 15 patients, with obvious excess surrounding tissue in 11. Mean minimum diameter and peak velocity by MRI were 11±2 mm and 3.2±0.7 m/s, respectively. Multivariate analysis of patient-, surgery-, and homograft-related variables did not reveal any significant risk factors for development of neopulmonary stenosis. Conclusions Pulmonary homograft stenosis after the Ross operation is clinically important and appears to represent an early postoperative inflammatory reaction to the pulmonary homograft that leads to extrinsic compression and/or shrinkage.

Omapatrilat in subtotal nephrectomy-salt hypertension: role of calcitonin gene-related peptide.

Calcitonin gene-related peptide (CGRP), a potent vasodilator neuropeptide, plays a counterregulatory role in subtotal nephrectomy-salt (SN-salt)-induced hypertension, reflecting a stimulation of the efferent vasodilator function of perivascular sensory nerves. To determine the effect of omapatrilat, a dual ACE and neutral endopeptidase inhibitor, on blood pressure and the potential antihypertensive role for CGRP, 24 male Sprague-Dawley rats were separated into 4 groups: (1) SN-salt, (2) SN-salt plus omapatrilat (80 mg. kg(-1). d(-1) in the drinking water), (3) sham-operated plus salt, (4) sham-operated plus salt and omapatrilat. After 11 days the mean arterial pressure was higher in the SN-salt group (174+/-10 mm Hg) versus the sham-operated-salt (109+/-4 mm Hg) and sham-operated-salt plus omapatrilat (105+/-3 mm Hg) groups. Omapatrilat treatment of the SN-salt rats significantly decreased the mean arterial pressure to 123+/-7 mm Hg and significantly reduced the heart-to-body weight ratio. Intravenous administration of a specific CGRP receptor antagonist produced a significant 10+/-2 mm Hg mean arterial pressure increase in the untreated SN-salt hypertensive rats but was without effect in the other groups. This indicates that CGRP does not contribute to the antihypertensive actions of omapatrilat. In addition, CGRP mRNA and protein content in dorsal root ganglia were decreased approximately 25% in the SN-salt plus omapatrilat rats. Thus, omapatrilat not only markedly reduces the blood pressure in this model of renal failure-induced hypertension but may also prevent the abnormal compensatory stimulation of the vasodilator activity of the peripheral sensory nervous system.

Is endotracheal adrenaline deleterious because of the beta adrenergic effect?

IV adrenaline increases coronary and cerebral perfusion pressures during cardiopulmonary resuscitation. We recently showed that endotracheal adrenaline can decrease blood pressure (BP), a detrimental effect presumably mediated by the beta 2-adrenergic receptor unopposed by alpha-adrenergic vasoconstriction. This prospective, randomized, laboratory comparison of endotracheal adrenaline (0.05 mg/kg diluted with normal saline to 10 mL total volume) with or without nonselective beta-blocker (propranolol) pretreatment was conducted in an attempt to clarify the mechanism of this BP decrease. Five mongrel dogs were given 0.05 mg/kg endotracheal adrenaline (diluted) or 0.05 mg/kg endotracheal adrenaline followed by an IV propranolol (0.1 mg/kg) pretreatment. Each dog served as its own control (10 mL of normal saline administered endotracheally) and received each regimen at least one week apart. Endotracheal adrenaline given after the propranolol pretreatment produced an increase in systolic, diastolic, and mean arterial BPs, from 165/110 mm Hg (mean 128 mm Hg) to 177.5/125 mm Hg (mean 142.5 mm Hg), respectively, as opposed to the hypotensive effect of isolated endotracheal adrenaline (P < 0.03). Thus, endotracheal adrenaline was associated with predominantly beta-adrenergic-mediated effects, causing hypotension via peripheral vasodilatation unopposed by alpha-adrenergic vasoconstriction. The search for the optimal dose of endotracheal adrenaline should be aimed at achieving the higher alpha-adrenergic vasoconstrictive threshold.

Short-term hemodynamic performance of the mitral Carpentier-Edwards PERIMOUNT pericardial valve

Background. Although long-term durability data exist, little data are available concerning the hemodynamic performance of the Carpentier-Edwards PERIMOUNT pericardial valve in the mitral position.Methods. Sixty-nine patients who were implanted with mitral PERIMOUNT valves at seven international centers between January 1996 and February 1997 consented to participate in a short-term echocardiography follow-up. Echocardiographs were collected at a mean of 600 ± 133 days after implantation (range, 110 to 889 days); all underwent blinded core lab analysis.Results. At follow-up, peak gradients were 9.09 ± 3.43 mm Hg (mean, 4.36 ± 1.79 mm Hg) and varied inversely with valve size (p < 0.05). The effective orifice areas were 2.5 ± 0.6 cm2 and tended to increase with valve size (p = 0.08). Trace mitral regurgitation (MR) was common (n = 48), 9 patients had mild MR, 1 had moderate MR, none had severe MR. All MR was central (n = 55) or indeterminate (n = 3). No paravalvular leaks were observed. Mitral regurgitation flow areas were 3.4 ± 2.8 cm2 and were without significant volumes.Conclusions. In this multicenter study, these mitral valves are associated with trace, although physiologically insignificant, central MR. Despite known echocardiographic limitations, the PERIMOUNT mitral valves exhibit similar hemodynamics to other prosthetic valves.

Intravascular US-guided Direct Intrahepatic Portacaval Shunt with a PTFE-covered Stent-Graft: Feasibility Study in Swine and Initial Clinical Results

To determine the feasibility of the creation of a direct intrahepatic inferior vena cava (IVC)-to-portal-vein shunt with puncture guided by a transfemorally placed intravascular ultrasound (IVUS) probe and use of a polytetrafluoroethylene (PTFE)-covered stent-graft. In five swine, transjugular access was used to perform a direct puncture from the IVC to the portal vein with use of a modified Rosch-Uchida Portal Access set directed with real-time IVUS (9 MHz) introduced from a transfemoral venous approach. The direct intrahepatic portocaval shunt (DIPS) was then created with single or overlapping PTFE-covered Palmaz stents placed through a 10-F sheath and dilated to a diameter of 8 mm. Follow-up was performed with transhepatic portography at 2, 4, and 8 weeks. Animals were killed when shunts occluded or at the termination of the study at 8 weeks. Gross and microscopic histologic study was performed on sacrificed animals. A similar technique was used to create DIPS in five patients with intractable ascites, with follow-up by US and venography. All experimental DIPS created in swine were created without complications. Portal vein punctures were achieved in four of five swine on the first or second pass of the needle. Follow-up transhepatic portography at 2 weeks demonstrated occlusion of two shunts, both explained by technical reasons at sacrifice. At 4 and 8 weeks, the remaining three shunts were patent on portography. Histology showed a thin neointimal lining with no significant tissue ingrowth or hyperplasia. Clinically, in five patients, successful puncture of the portal vein from the IVC was achieved in one to three passes. Creation of DIPS led to a reduction of mean portosystemic gradient from 18-29 mm Hg (mean, 24 mm Hg) to 9-10 mm Hg (mean, 9 mm Hg). One patient died of liver failure 2 days after creation of DIPS. The other four patients were doing well 2-15 months (mean, 8 months) after the procedure, with patency confirmed by US and venography. Creation of DIPS is technically feasible, and the direct IVC-to-portal-vein puncture can be done accurately with real-time IVUS guidance. Further studies and longer follow-up are necessary to determine if the short length of the PTFE-covered stent-graft and avoidance of the hepatic vein will increase the long-term patency compared to standard transjugular intrahepatic portosystemic shunt creation.