Fall In Pulmonary Artery Pressure Research Articles

Abstract 10881: Assess Response of Phosphodiesterase-5 Inhibitor in Pulmonary Artery Hypertension by Flow Mediated Dilation of Brachial Artery

Introduction: Endothelial dysfunction is a significant component in the development of pulmonary artery hypertension (PAH). Current treatment guidelines recommend phosphodiesterase-5 inhibitors (PDE-5i) in PAH. The responder status to PDE-5i is not assessed unlike invasive vasoreactivity testing done for calcium channel blockers. This study aims to determine the effectiveness of PDE-5 inhibitors by non-invasively testing flow mediated dilation (FMD) of brachial artery. Hypothesis: We hypothesise that FMD of brachial artery predicts the responsiveness of the PDE-5i earlier than fall in pulmonary artery pressures on echocardiography. Methods: It is a single centre prospective study over a period of 18 months where we randomly assigned PAH patients with PDE-5i. FMD in brachial artery, pulmonary arterial pressure by right ventricular systolic pressure (RVSP) by TR jet velocity and tricuspid annular planar systolic excursion (TAPSE) is measured before and after starting PDE-5i at 1 st week and at 6 th month. Primary end point is to predict the response of PDE-5i by FMD of brachial artery earlier than fall in pulmonary artery pressures through echocardiography. Secondary end point is to determine the 6 th month outcome of patients with PAH by FMD and echocardiography by RVSP and TAPSE. Results: In this study we enrolled 21 randomized cases with mean age of 40.00 ± 10.79 years, majority being females (n=17; 81%). Over a period of 18 months, primary end point is reached in 29% patients (p=0.05). Secondary end points of RVSP is achieved by 57% patients (p= 0.0014), TAPSE by 76% patients (p<0.002). FMD was seen in 14 cases after 1 week and 16 cases after 6 months. Of these 14 cases all of them had a fall in RVSP and improvement in TAPSE after 6 months. Mean RVSP after 1 week is 49.24±9.56 mmHg and after 6 months is 46.00 ± 9.18 mmHg (p<0.006). Mean TAPSE at 1 week is 17.10 ± 2.86 mm and at 6 months is 17.90±2.49 mm (p<0.002). Conclusions: In conclusion patients having PAH initiated on PDE-5i, FMD of brachial artery predicts the responsiveness of this drug earlier than fall in pulmonary artery pressures on echocardiography by as early as 1 st week. It is a non-invasive method that helps in assessing the response of this commonly used drug in PAH in clinics.

FACTORS RESPONSIBLE FOR INSIGNIFICANT DECREASE IN PULMONARY ARTERY PRESSURE IMMEDIATELY AFTER PER CUTANEOUS TRANS-MITRAL COMMISSUROTOMY IN PATIENTS OF RHEUMATIC MITRAL STENOSIS

OBJECTIVES: To determine the factors responsible for insignificant decrease in pulmonary artery pressure immediately after percutaneous trans-mitral commissurotomy (PTMC) in patients of rheumatic mitral stenosis. METHODS: This cross-sectional study was conducted on patients undergoing PTMC at Cardiology Unit, Lady Reading Hospital, Peshawar, Pakistan from 11th February, 2016 to 28th February, 2018. Pulmonary artery pressure (PAP) was noted before and after PTMC through echocardiography. Data was analyzed with SPSS Version 20.0, categorical and continuous variables were described as frequencies/percentages and mean±SD respectively. Odds Ratio was determined for factors negatively affecting the fall in PAP. RESULTS: Out of 159 patients, 108 (67.9%) were females. Mean age was 25.38±10.67 years. PAP was insignificantly decreased in patients >30 years (p>0.05), symptoms for >5 years (p>0.05), left atrium diameter >4.5cm (p>0.05), atrial fibrillation (p>0.05), right ventricle diameter >2.5cm (p>0.05) and NYHA IV dyspnea (p>0.05). Odds Ratio for failure of significant decrease in PAP immediately post-PTMC was 1.68 for age more than 30 years, 1.10 for symptoms more than 5 years, 3.73 for LA diameter more than 4.5 cm, 2.31 for RV diameter more than 2.5 cm , 2.32 for history of atrial fibrillation and 6.71 for NYHA IV dyspnea. CONCLUSION: Factors which negatively affect the immediate fall in PAP post-PTMC are age >30years, duration of symptoms >5years, LA diameter >4.5cm, history of atrial fibrillation, RV diameter >2.5cm and NYHA IV dyspnea and hence are the poor predictors of successful PTMC while NYHA IV dyspnea has highest Odds for insignificant decrease.

Catheter-based management of pulmonary embolism

Background: Pulmonary embolism (PE) is a major cause of mortality and morbidity. Forty-four percent of patients would not have gotten intravenous (IV) thrombolysis due to contraindications or delay. Catheter-directed thrombolysis with fragmentation has been shown to improve short-term and long-term outcomes in acute high-risk patients of pulmonary embolism. Methodology: Patients presented de nova with massive pulmonary embolism or with subacute pulmonary embolism. Some presented with failed thrombolysis from other centers. Results: Our experience from these patients shows that a policy of mechanical thrombus breakdown with a 5F multipurpose or pigtail catheter followed by a urokinase infusion can achieve satisfactory results. Fifty patients with acute were treated with thrombolysis with or without mechanical breakdown. There was 96% event-free survival. With subacute PE, using a mechanical breakdown plus IV thrombolysis, there was fall in pulmonary arterial pressures (PAPs) with 100% 6-month event-free survival. In seven patients with failed thrombolysis, this strategy leads to fall in PAPs and 100% survival at 2 years. Conclusions: Various catheter-based techniques are available which can be used in combination with thrombolysis to achieve good results. Surgery should be considered if the catheter-based techniques fail.

Pathophysiology and treatment of high-altitude pulmonary vascular disease.

It is estimated that >140 million people live above 2500 m in various regions of the world.1 There are many challenges to living at high altitude, but chronic exposure to alveolar hypoxia is prominent among them. Inspired Po2 falls from ≈150 mm Hg at sea level to ≈100 mm Hg at 3000 m and 43 mm Hg on the summit of Everest (8400 m).2,3 The body responds by hyperventilating, increasing resting heart rate, and stimulating red cell production in an attempt to maintain the oxygen content of arterial blood at or above sea level values.2 However, hypoxic pulmonary vasoconstriction (HPV) and vascular remodeling, together with increased erythropoiesis, place an increased pressure load on the right ventricle (RV). How well healthy humans adapt to hypoxia depends on their rate of ascent to altitude, the severity and duration of their exposure, and their genetic background. ### Pulmonary Vascular Response to Hypoxia For most mammals, including humans, a rise in pulmonary artery pressure (PAP) is an early and inevitable consequence of ascent to high altitude. Resting mean PAP increases along a parabolic curve from 15 mm Hg at 2000 m to ≈30 mm Hg at 4500 m.4 The exceptions and interindividual variation in the magnitude of response offer a natural experiment that might provide insight into fundamental underlying mechanisms ( vide infra ). The initial rise in PAP on exposure to hypoxia is attributed to HPV. With chronic hypoxia, other mechanisms that likely drive vascular remodeling soon contribute to the elevated pressure (Figure 1A). After 2 or 3 weeks of hypoxia, there is little response to rebreathing 100% oxygen, indicating a structural resistance to pulmonary blood flow rather than one based solely on increased vasomotor tone.6 A fall in PAP on re-exposure to a normal oxygen environment is evident in rats monitored by telemetry over days …

Abstract 19492: Novel Assessment of Pulmonary and Systemic Pressures During Treadmill Testing via Implantable Telemetry in a Rat Model of Pulmonary Arterial Hypertension

Objectives: 1) To determine if pulmonary arterial pressures (PAP) may be measured simultaneously with systemic blood pressures (BP) during exercise testing in laboratory rats using implantable telemetry; and 2) To determine the relationship of exercise intensity to acute PAP exercise responses over the course of PAH development. Methods: A specialized implantable transmitter (Data Sciences International); via telemetry following thoracotomy with right ventricular (RV) and abdominal aortic catheter positioning, respectively enabled simultaneous systolic, diastolic and mean PAP and BP recordings. Following recovery, an incremental treadmill test measured maximal aerobic capacity (VO 2 max) via analysis of expired gases. Steady state exercise testing was then performed for 3 different submaximal relative intensities: 50, 75, and 90% VO 2 max. Pressures were recorded during each test, as well as pre- and post- exercise. At 2.5 weeks following monocrotaline (MCT, 40 mg/kg) administration (mild PH) and 7 weeks post-MCT (advanced PH), VO 2 max and steady-state exercise tests were repeated. Results: Compared to pre-MCT, at 2.5 weeks post-MCT systolic PAP increased from 25 to 41 mmHg at rest; from 105 to 117 mmHg at peak exercise; and from 40 to 58 mmHg, 46 to 65 mmHg, and 55 to 75 mmHg during running at 50, 75, and 90% VO 2 max, respectively. At 7 weeks post-MCT, PAP further increased at rest (to 59 mmHg), and during steady state running (to 69, 70, and 73 mmHg, at 50, 75, and 90% VO 2 max, respectively). During recovery from steady state exercise, the fall in PAP occurred more rapidly post-MCT, bringing PAP to even lower than resting from 10 min to 2h into recovery. Conclusions: Using implantable telemetry we have accomplished dual pressure recordings during serial exercise tests before and after PAH induction. The rise in PAP relative to exercise intensity is steeper in PAH but is accompanied by a post-exercise window of normalized PAP, which may be attributed to pronounced acute pulmonary endothelial activation. Future work will investigate how these acute effects translate to wall stress and RV remodeling with chronic exercise training and may allow for optimized exercise prescription for patients affected with PAH.

IS-017 Pulmonary Vascular Resistance In The Preterm Infant–From Physiological To Pathological

<h3></h3> Serial cardiac ultrasound has given us a window on circulatory transition, both normal and abnormal. Preterm birth is not physiological so physiology has to be assessed in well term babies. Pulmonary blood flow increases with the first breath as resistance falls and these balance each other so that the fall in pulmonary artery pressure (PAP) over the first 4–6 h of life is modest. So, early on, well babies will have PAPs close to systemic pressures confounding early assessment for pulmonary hypertension. The ‘pulmonary ischaemia’ model of RDS originated from early studies when RDS was a different disease. PAP will fall more slowly in preterm babies ventilated with RDS but, in most preterm babies, PAP is below systemic BP even in the early hours after birth. Thus the impact is too much blood in the pulmonary circulation due, not pulmonary ischaemia from high vascular resistance and blood bypassing the lungs. There are exceptions to the above, particularly babies with severe RDS, congenital pneumonia or those born after prolonged oligohydramnios, in whom raised PAP is a consistent finding. Oligohydramnios babies are not common, so have been a difficult group to study systematically but several case series have described this as well as the responsiveness of this group to iNO. There seems to be sub-clinical persistent raised pulmonary vascular resistance in many babies with chronic lung disease. The significance of this is uncertain but in the most severe cases, pulmonary hypertension can be an important component of the disease.

The Effect of Parenteral Lipid Emulsions on Pulmonary Hemodynamics and Eicosanoid Metabolites in Preterm Infants

Soy-based intravenous fat emulsion (IVFE) is known to cause a rise in pulmonary artery pressure in the preterm infant, thought to be mediated through eicosanoid metabolites of linoleic acid. We compared the effect of soy-based IVFE and an olive-oil-based IVFE containing less than half the content of linoleic acid on pulmonary artery pressure and eicosanoid metabolites in preterm infants receiving parenteral nutrition. In this pilot study at a regional neonatal intensive care unit (ICU), infants received either a soy-based or olive-oil-based IVFE as part of an otherwise identical feeding protocol. Pulmonary artery pressure and urinary thromboxane B2 and prostaglandin F1 alpha were measured at baseline and maximum lipid infusion. There was a greater fall in pulmonary artery pressure in the olive-oil-based IVFE group compared with the soy-based IVFE group. A decrease in urine thromboxane/prostaglandin F1 alpha ratio was seen only in the olive-oil-based IVFE group. In the parenterally fed preterm infant, an olive-oil-based IVFE may have a beneficial effect on pulmonary artery pressure when compared with soy-based IVFE. Effects on pulmonary vascular tone are likely to be mediated through alterations in eicosanoid metabolism. A randomized trial is warranted to compare the effects of different lipid emulsions.

“Global myocardial ischaemia after PDA ligation” – An anomaly with duct dependant coronary circulation?!

A 5 month old infant presented to referring hospital with respiratory distress and growth faltering. Growth faltering investigations included an echocardiogram which showed large PDA with left to right shunt, mild to moderate mitral regurgitation, dilated left atrium and left ventricle. She was referred to our cardiac surgical centre for duct ligation. She underwent PDA ligation and developed ventricular fibrillation post operatively. The infant was defibrillated and converted to sinus rhythm. An ECG showed features of global ischaemia. Trans-thoracic echocardiogram revealed an Anomalous Left Coronary Artery from Pulmonary Artery (ALCAPA). The anomalous coronary artery was reimplanted into the aortic root. She made a good recovery post-operatively after three day intensive care. Clinical features of ALCAPA are generally due to myocardial ischaemia secondary to low pressure coronary circulation and poorly oxygenated blood1. In our patient, the presence of a large PDA prevented fall in pulmonary artery pressure and maintained the antegrade blood flow to the left coronary artery until it was ligated. ALCAPA is a rare cardiac anomaly occurring in one of 300 000 live births1. It is usually an isolated anomaly, but rarely be associated with other left to right shunts1–3. ALCAPA should be considered when ischaemia follows an acute reduction in pulmonary artery pressure. Previous reports have described fatal outcomes after ligation of a PDA in patients with undiagnosed ALCAPA2,3. Our case once again emphasises the importance of demonstrating the coronary artery anatomy in all patients before surgical closure of left to right shunt lesions.

Home-made fenestrated amplatzer occluder for atrial septal defect and pulmonary arterial hypertension

We report the management of a patient with secundum atrial septal defect (ASD) and severe pulmonary hypertension. A 65-year-old male with recently diagnosed atrial septal defect was referred to our centre for decompensated right heart failure with rest and exercise induced dispnea and severe pulmonary hypertension. Right heart catheterization confirmed a mean pulmonary pressure of about 55 mmHg and a Qp/Qs of 2.7. An occlusion test with a compliant large balloon demonstrated partial fall of pulmonary arterial pressure. The implantation of a home-made fenestrated Amplatzer ASD Occluder (ASO) was planned in order to decrease left-to-right shunt and promote further decrease of pulmonary arterial pressure in the long-term. Thus, by means of mechanical intracardiac echocardiography study with a 9F 9 MHz UltraIce catheter (Boston Scientific Corp.), we selected a 34 mm ASO for implantation. Four millimeter fenestration was made inflating a 4 mm non-compliant coronary balloon throughout the waist of the ASO, which was successfully implanted under intracardiac echocardiography. After six months, a decrease of pulmonary arterial pressure to 24 mmHg and full compensated right heart failure was observed on transthoracic echocardiography and clinical examination. This case suggests that transcatheter closure with home-made fenestrated ASD in elderly patients with severe pulmonary hypertension is feasible.

Inhaled Nitroglycerin Versus Inhaled Milrinone in Children with Congenital Heart Disease Suffering from Pulmonary Artery Hypertension

The aim of the present study was to compare the acute effects of inhaled milrinone and inhaled nitroglycerin on pulmonary and systemic hemodynamics in children with acyanotic congenital heart disease (left-to-right shunt) and pulmonary artery hypertension. Randomized clinical trial. Catheterization laboratory of a tertiary care hospital. Thirty-five children below the age of 12 years who were suffering from acyanotic congenital heart disease with left-to-right intracardiac shunt and pulmonary artery hypertension (mean PA pressure > 30 mmHg). Right-heart catheterization was done using an end-hole balloon wedge pressure catheter. Baseline pulmonary and systemic hemodynamic parameters were recorded for all patients while breathing room air. All patients then underwent pulmonary vasodilator testing with 100% oxygen. Following this, patients were randomized into two groups and received either inhaled milrinone (group M, n = 18) or inhaled nitroglycerin (group N, n = 17) in a 50% air-oxygen mixture. Oximetry data were used to calculate systemic and pulmonary cardiac output based on Fick's principle. Systolic, diastolic, and mean pulmonary artery pressures decreased significantly in both the groups after drug nebulization, while there were no significant changes in systemic pressures. The percentage decrease from baseline in systolic (5.2% v 8.6%, p = 0.43), diastolic (19.5% v 16.8%, p = 0.19) and mean (14.9% v14.5%, p = 0.29) pulmonary artery pressures were comparable in both groups. The pulmonary vascular resistance index (PVRI) decreased from 9.0 ± 3.9 to 2.9 ± 1.7 Wood Units (WU)/m(2) in group M (p < 0.001) and from 8.6 ± 3.8 to 3.2 ± 3.3 WU/m(2) in group N (p < 0.001). The fall in pulmonary artery pressures after drug nebulization in both groups was comparable to the fall seen with 100% oxygen. Both milrinone and nitroglycerin when given via the inhaled route significantly decrease systolic, diastolic and mean pulmonary artery pressures as well as PVRI without significant effects on systemic hemodynamics. Both the drugs given via inhaled route therefore can offer a good therapeutic choice and can help decrease the high inspired oxygen concentrations needed to treat pulmonary artery hypertensive episodes in perioperative settings.

A model of isolated autologously hemoperfused porcine slaughterhouse lungs

Models of isolated and perfused lungs study pathophysiological phenomena of the airways, but are limited by restricted resemblance to the human situation, non-physiological perfusates or the need for the use of high numbers of laboratory animals. The present model was established to address these difficulties. Aim of the current study was the establishment of an animal model that uses slaughterhouse animals and closely resembles physiological conditions found in humans. We used a model of hemoperfused isolated porcine slaughterhouse lungs using autologous blood, metabolically controlled via a dialysis system. Over a period of 135 minutes positive inspiratory pressure, pulmonary arterial pressure, pulmonary vein oxygen partial pressure and lung weight were assessed. Stable organ function was maintained over 135 minutes with an amount of 2,500-3,000 ml perfusate without fall in pulmonary arterial pressure. During the time the positive inspiratory pressure and lung weight increased, while pulmonary vein oxygen partial pressure decreased. The present model of isolated hemoperfused slaughterhouse lungs displays a useful new and economic approach to evaluate pulmonary function and toxicity of different substances on an organ level. As a major economic advantage in comparison to models using laboratory animals, the current model might be run using blood and organs obtained from slaughterhouse animals.

Toward understanding response to cardiac resynchronization therapy: left ventricular dyssynchrony is only one of multiple mechanisms

To date, most published echocardiographic methods have assessed left ventricular (LV) dyssynchrony (DYS) alone as a predictor for response to cardiac resynchronization therapy (CRT). We hypothesized that the response is instead dictated by multiple correctable factors. A total of 161 patients (66 +/- 10 years, EF 24 +/- 6%, QRS > 120 ms) were investigated pre- and post-CRT (median of 6 months). Reduction in NYHA Class >/=1 or LV reverse remodelling (end-systolic volume reduction >/= 10%) defined response. Four different pathological mechanisms were identified. Group1: LVDYS characterized by a pre-ejection septal flash (SF) (87 patients, 54%). Elimination of SF (77 of 87 patients) resulted in reverse remodelling in 100%. Group 2: short-AV delay (21 patients, 13%) resolution (19 of 21 patients) resulted in reverse remodelling in 16 of 19. Group 3: long-AV delay (16 patients, 10%) resolution (14 of 16 patients) resulted in NYHA Class reduction >/=1 in 11 with reverse remodelling in five patients. Group 4: exaggerated LV-RV interaction (15 patients, 9%) reduced post-CRT. All responded clinically with fall in pulmonary artery pressure (P = 0.003) but did not volume respond. Group 5: patients with none of the above correctable mechanisms (22 patients, 14%). None responded to CRT. CRT response is dictated by correction of multiple independent mechanisms of which LVDYS is only one. Long-axis DYS measurements alone failed to detect 40% of responders.

Counterpoint: Chronic Hypoxia-induced Pulmonary Hypertension does not Lead to Loss of Pulmonary Vasculature

Exposure of native sea level dwellers to chronic hypoxia due to migration to high altitude leads to the development of increased pulmonary vascular resistance causing pulmonary hypertension. In some susceptible individuals this progressively worsens causing right ventricular failure and ultimately

Combination Therapy With Oral Sildenafil and Beraprost for Pulmonary Arterial Hypertension Associated With CREST Syndrome

Pulmonary arterial hypertension (PAH) is commonly associated with CREST (Calcinosis, Raynaud phenomenon, Esophageal motility disorders, Sclerodactyly, and Telangiectasia) syndrome. Sildenafil, an oral phosphodiesterase type-5 inhibitor, may offer benefits in the pharmacological management of PAH. However, little is known about the long-term hemodynamic effects of sildenafil, and the potential role of sildenafil in long-term combination with beraprost, an oral prostacyclin analogue, remains unclear. We therefore examined the hemodynamic effect of oral sildenafil alone and when coadministered with beraprost in a patient with PAH associated with CREST syndrome. Traces of the acute hemodynamic effects of beraprost (20 microg) disappeared after 2 hours. In contrast, the acute hemodynamic effects of sildenafil (50 mg) produced a greater reduction in PAP (31%) and PVR (40%), and these effects also disappeared after 5 hours. After 1 month of combination therapy of sildenafil (25 mg) twice daily and beraprost (20 microg) 3 times daily, the fall in pulmonary artery pressure and pulmonary vascular resistance was sustained (31% in both). Furthermore, the patient had significantly improved her 3-minute walk test and NYHA function class without significant adverse effects at the reported doses. The findings indicate that oral sildenafil is a potent pulmonary vasodilator that appears to act synergistically with oral beraprost to cause sustained pulmonary vasodilatation in a patient with PAH associated with CREST syndrome.

Inhaled iloprost as a bridge to transplant in advanced pulmonary fibrosis and secondary pulmonary hypertension

The development of secondary pulmonary hypertension is a poor prognostic factor in patients with pulmonary fibrosis. An acute challenge of inhaled iloprost, a chemically stable derivative of prostacyclin, has previously been shown to cause selective pulmonary vasodilatation in secondary pulmonary hypertension. We assessed its short-term efficacy in patients with advanced pulmonary fibrosis and secondary pulmonary hypertension as a bridge to transplantation. We studied seven patients (4 with UIP, and 3 with advanced sarcoidosis) all in New York Heart Association functional class IV. Iloprost was nebulized using a Schill multisonic nebulizer, and administered 3 hourly in increasing daily doses to a maintenance of 90mcg/day. The effects of inhaled iloprost were assessed by echocardiography, shuttle walk test and right heart catheterization (n 2). Inhalation of iloprost was well tolerated, and administered for a mean (SEM) of 2.4 (0.9) months. Two of 4 UIP patients and 1 of 2 sarcoid patients died during the follow up. There was a fall in pulmonary artery pressure, 73mmHg (19) before iloprost, versus 40mmHg (9) after iloprost therapy (p 0.26). There was a non significant improvement in pulmonary artery pressure when assessed by echo, 60mmHg (8) before versus 48mmHg (7) after iloprost therapy (p 0.28). Shuttle walk distance improved, but not significantly, 86m (34) before, versus 104m (48) after iloprost therapy (p 0.77). Inhaled iloprost therapy with terminal pulmonary fibrosis may only benefit selected (sarcoid) patients.

Randomised controlled trial of postnatal sodium supplementation in infants of 25–30 weeks gestational age: effects on cardiopulmonary adaptation

BACKGROUNDIt has previously been shown that, in preterm babies, routine sodium supplementation from 24 hours after birth is associated with increased risk of oxygen dependency and persistent expansion of the...

Hemodynamic effects of basal and stimulated release of endogenous nitric oxide in isolated human lungs.

Background-We compared the hemodynamic responses to inhibition or stimulation of endothelial nitric oxide (NO) release of isolated explanted lungs from transplantation recipients with pulmonary hypertension and in normotensive unallocated donor lungs. Methods and Results-Lungs from 10 patients with severe pulmonary hypertension (SPH) and from 16 patients with severe chronic obstructive lung disease (COLD) were studied. Fourteen normotensive lungs were studied as controls. The lungs were perfused at a constant flow. In protocol 1 N(G)-nitro-L-arginine methyl ester caused a similar rise in baseline pulmonary artery pressure (PAP) that was similar in SPH (+17.1+/-4.2 mm Hg; n=5), COLD (+15.5+/-4.8 mm Hg; n=8), and control lungs (+14.5+/-1.5 mm Hg; n=7). Arterial occlusion demonstrated that most of the changes with N(G)-nitro-L-arginine methyl ester were precapillary. The response to sodium nitroprusside (10(-8) to 10(-4) mol/L) was similar in all groups. In protocol 2, the lungs were preconstricted, and acetylcholine (10(-9) to 10(-5) mol/L) caused a lesser fall in PAP in both COLD and SPH lungs compared with control (-41.9+/-8.6%, -55. 7+/-7.6%, and -73.2+/-2.5%, respectively; P<0.05), whereas sodium nitroprusside (10(-5) mol/L) decreased PAP to initial levels in all lungs. Conclusions-Stimulated release of NO is impaired in arteries of lungs with plexogenic or hypoxemic pulmonary hypertension. In contrast, basal release of NO appears to be maintained.

Haemodynamic effects of altering arterial oxygen saturation in preterm infants with respiratory failure

AIMSTo examine the haemodynamic effects of brief alteration in arterial oxygenation in preterm infants with respiratory failure.METHODSEighteen preterm infants with respiratory failure, aged 9–76 hours, underwent detailed Doppler echocardiographic assessment...

Angiotensin-converting enzyme (ACE) inhibitors revert abnormal right ventricular filling in patients with restrictive left ventricular disease

Objectives. Our aim was to determine mechanisms underlying abnormalities of right ventricular (RV) diastolic function seen in heart failure.Background. It is not clear whether these right-sided abnormalities are due to primary RV disease or are secondary to restrictive physiology on the left side of the heart. The latter regresses with angiotensin-converting enzyme inhibition (ACE-I).Methods. Transthoracic echo-Doppler measurements of left- and right-ventricular function in 17 patients with systolic left ventricular (LV) disease and restrictive filling before and 3 weeks after the institution of ACE-I were compared with those in 21 controls.Results. Before ACE-I, LV filling was restrictive, with isovolumic relaxation time short and transmitral E wave acceleration and deceleration rates increased (p < 0.001). Right ventricular long axis amplitude and rates of change were all reduced (p < 0.001), the onset of transtricuspid Doppler was delayed by 160 ms after the pulmonary second sound versus 40 ms in normals (p < 0.001) and overall RV filling time reduced to 59% of total diastole. Right ventricular relaxation was very incoordinate and peak E wave velocity was reduced. Peak RV to right atrial (RA) pressure drop, estimated from tricuspid regurgitation, was 45 ± 6 mm Hg, and peak pulmonary stroke distance was 40% lower than normal (p < 0.001). With ACE-I, LV isovolumic relaxation time lengthened, E wave acceleration and deceleration rates decreased and RV to RA pressure drop fell to 30 ± 5 mm Hg (p < 0.001) versus pre-ACE-I. Right ventricular long axis dynamics did not change, but tricuspid flow started 85 ms earlier to occupy 85% of total diastole; E wave amplitude increased but acceleration and deceleration rates were unaltered. Values of long axis systolic and diastolic measurements did not change. Peak pulmonary artery velocity increased (p < 0.01).Conclusions. Abnormalities of RV filling in patients with heart failure normalize with ACE-I as restrictive filling regresses on the left. This was not due to altered right ventricular relaxation or to a fall in pulmonary artery pressure or tricuspid pressure gradient, but appears to reflect direct ventricular interaction during early diastole.

Doppler assessment of pulmonary artery pressure in neonates at risk of chronic lung disease

AIMTo evaluate the pulmonary artery pressure (PAP) change in very low birthweight (VLBW) infants at risk of chronic lung disease (CLD).METHODSThe time to peak velocity:right ventricular ejection time (TPV:RVET) ratio...