Pulmonary Artery Pressure In Patients Research Articles

Elevated Estimated Pulmonary Arterial Pressures in Patients with Chuvash Polycythemia.

Chuvash polycythemia is characterized by a homozygous 598C>T mutation in VHL and up regulation of HIF-1α during normoxia. Disorders of chronic hypoxia may be complicated by the development of pulmonary hypertension. Because of the up regulation of the hypoxic response in Chuvash polycythemia, we postulated that there may be a tendency to increased pulmonary artery pressures in this condition as well. To test this hypothesis, we analyzed results for Doppler echocardiography in 15 patients with Chuvash polycythemia and 15 Chuvash individuals without polycythemia. The tricuspid regurgitation velocity (TRV) allows estimation of pulmonary artery systolic pressure. A TRV of 2.5 m/sec or higher corresponds to a pulmonary artery systolic pressure of at least 35 mm Hg (normal up to 32 mm Hg), while a TRV of 3.0 m/sec or higher to a pressure of at least 46 mm Hg. The results are summarized in the Table.Pulmonary artery pressures as estimated by tricuspid regurgitation velocity (TRV) in Chuvash subjects with and without polycythemiaChuvash polycythemia (n = 15)Controls (n = 15)PAge in years; mean (SD)35 (17)35 (17)1.0Female sex in no. (%)8 (53%)8 (53%)1.0Hemoglobin in g/dL; mean (SD)16.7 (2.3)13.3 (1.2)<0.001TRV in m/sec; mean (SD)2.2 (0.6)1.4 (0.6)0.001TRV > 2.4 m/sec in no. (%)4 (27%)0 (0%)0.1Most of the patients with Chuvash polycythemia were receiving phlebotomy therapy and therefore many had hemoglobin concentrations in the upper normal range. Four of the patients with Chuvash polycythemia and none of the others had TRV ≥ 2.5 m/sec (range of 2.5 to 3.0), and mean TRVs were significantly higher in the patients with Chuvash polycythemia. Interestingly, the mean ± SD TRV in these 15 patients with Chuvash polycythemia was identical to the mean ± SD TRV that was recently reported in 195 American patients with sickle cell disease (Gladwin et al, NEJM 2004; 350:886), another hematological condition with a tendency to pulmonary hypertension. While the pulmonary arterial pressures detected so far in Chuvash polycythemia patients are lower than those in patients with primary pulmonary hypertension, our results suggest that pulmonary hypertension may be an unrecognized complication of Chuvash polycythemia.

Descriptive patterns of severe chronic pulmonary hypertension by chest radiography

To find chest roentgenographic (CXR) features to help differentiate two representative diseases with severe chronic pulmonary hypertension (PH). Thirty-six consecutive patients with chronic thromboembolic PH (CTEPH), 38 with primary PH (PPH), and 37 with left heart disease and PH. CXRs were reviewed about 6 features (left 2nd arc protrusion, right descending pulmonary artery diameter (rPAD), cardiothoracic ratio (CTR), right 2nd arc width, avascular area and pleural abnormality). Hemodynamic data and the degree of tricuspid regurgitation (TR) on echocardiography were compared with CXR findings. The diagnostic pattern of CTEPH was the presence of one of two findings, an avascular area or marked rPAD (>20mm) together with pleuritic change. The diagnostic pattern of PPH was one of the two features; without pleuritic abnormality, marked left 2nd arc protrusion (>10mm) or moderate left 2nd arc protrusion (5-10mm) with marked rPAD (<20mm). The sensitivity for the diagnosis of CTEPH among the three diseases was 78% and specificity was 92%. The sensitivity for the diagnosis of PPH was 45% and specificity was 88%. CTR and right 2nd arc width were related to the degree of TR in CTEPH and PPH. Characteristic roentgenographic findings can help differentiate two frequent diseases associated with chronic pulmonary hypertension and reflect the severity of disease.

Safety and hemodynamic effects of pulmonary angiography in patients with pulmonary hypertension: 10-year single-center experience.

We sought to examine the incidence of complications and change in pulmonary artery pressure in patients with pulmonary hypertension who were undergoing pulmonary angiography. A retrospective review was performed for all patients who underwent pulmonary angiography over a 10-year period at a single institution. Patients with moderate pulmonary hypertension (pulmonary artery pressure, 30-59 mm Hg) and severe pulmonary hypertension (pulmonary artery pressure, >/= 60 mm Hg) served as the study population. Demographic data, clinical indication, pre- and postcontrast pulmonary artery pressure measurements, type of pulmonary hypertension, contrast agent volume, complications, and American Society of Anesthesiologists (ASA) classification were recorded for all patients and compared. Two hundred two of 612 patients who underwent pulmonary angiography had pulmonary hypertension. Moderate pulmonary hypertension was present in 155 patients (77%) and severe pulmonary hypertension, in 47 patients (23%). Three (2.0%) of four complications were fatal. The complication rate was higher in patients with severe pulmonary hypertension compared with patients with moderate pulmonary hypertension but not statistically significant (6.3% vs 0.6%, p = 0.63). Patients with complications had a higher mean ASA score than those without complications (4.0 vs 3.0, p = 0.03). Patients with lung transplants had the greatest increase in pulmonary artery pressure after pulmonary angiography compared with all other clinical indications (16.75 +/- 12.97 mm Hg vs 5.46 +/- 6.86 mm Hg, p = 0.003). The complication rate of pulmonary angiography in patients with pulmonary hypertension is low. However, in severely ill patients with acute pulmonary hypertension, pulmonary angiography should be undertaken with extreme caution.

Should thrombolytic therapy be used in patients with pulmonary embolism?

More than thirty years have passed since streptokinase was first shown to dissolve pulmonary arterial thrombi and normalize pulmonary artery pressure in patients with acute pulmonary embolism (PE). Following the initial observations, a number of controlled clinical trials confirmed that treatment with streptokinase, urokinase or alteplase recombinant tissue plasminogen activator is superior to heparin alone in improving angiographic and hemodynamic parameters in these patients. At present, there is consensus that patients with massive PE presenting with overt right ventricular failure (clinical instability and cardiogenic shock) should promptly be treated with thrombolytic agents, since they are at a particularly high risk for death or life-threatening complications during the acute phase. At the other end of the clinical spectrum, thrombolysis for PE is not indicated in the absence of right ventricular dysfunction. In fact, the prognosis of patients with small pulmonary emboli (not affecting pulmonary artery pressure and right ventricular afterload), is excellent and, as a result, the bleeding risks of thrombolysis may outweigh the potential benefits of this treatment. Currently, the thrombolysis debate focuses on patients with submassive PE, i.e. those who present with signs of subclinical, impending right heart failure. Recently, a number of clinical studies demonstrated that these patients are also at risk for an adverse clinical outcome. Besides the established prognostic value of echocardiography, evidence is now accumulating that cardiac troponins and, possibly, pro-brain natriuretic peptide levels also may permit an early, reliable risk stratification of patients with PE and particularly help identify submassive PE in the presence of apparent clinical stability. Recently, the Management Strategies and Prognosis of Pulmonary Embolism-3 trial examined the effects of thrombolysis on the prognosis of patients with acute submassive PE. The study patients were randomly assigned to receive alteplase (100 mg over 2 hours) or placebo with concomitant heparin anticoagulation. Although in-hospital mortality was low in both the alteplase and the heparin-only group, this study showed for the first time that early treatment with alteplase can improve the clinical course of patients with acute submassive PE, and particularly reduce the need for emergency escalation of treatment. Importantly, no fatal or cerebral bleeding episodes were observed in the alteplase group. This fact indicates that use of thrombolysis in PE can be safe in patients who have no contraindications to this type of treatment. Based on these data, the indications for thrombolysis can be extended to include patients presenting with submassive PE.

Serum Soluble Fas in Patients with Schistosomal Cor pulmonale

Background: Schistosomal cor pulmonale is considered an important pathological condition in endemic areas. Few recent studies have reported the role of apoptosis in pulmonary hypertension. Objectives: The aim of this study was to assess serum levels of soluble Fas (sFas), an inhibitor of apoptosis, in patients with schistosomal cor pulmonale as compared to patients with cor pulmonale due to chronic obstructive pulmonary disease (COPD) and normal subjects. Methods: Serum sFas was assessed in 15 men with schistosomal cor pulmonale (age 32 ± 10 years), 15 men with chronic cor pulmonale secondary to COPD and 20 healthy men, matched for age. Results: Serum levels of sFas were significantly higher in patients with schistosomal cor pulmonale (74 ± 80 U/ml) than in patients with cor pulmonale due to COPD (15 ± 10 U/ml) and normal subjects (19 ± 11 U/ml, p < 0.001 in both). In patients with schistosomal cor pulmonale, sFas was significantly higher in patients with mean pulmonary artery pressure >30 mm Hg as compared to patients with pressure ≤30 mm Hg (109 ± 97 vs. 34 ± 20 U/ml, p = 0.01). There was a significant correlation between serum sFas and the mean pulmonary artery pressure in patients with bilharzial cor pulmonale (r = 0.4, p < 0.01), but not in patients with COPD (r = 0.1, p = NS). Conclusions: Serum sFas levels are elevated in patients with schistosomal cor pulmonale and they are related to the severity of pulmonary hypertension. These findings suggest a role of apoptosis in schistosomal cor pulmonale.

Sildenafil in patients with cardiovascular disease

Cardiologists are seeing increasing numbers of patients with erectile dysfunction (ED), which frequently coexists with cardiovascular disease. The pharmacologic profile of the new class of phosphodiesterase (PDE) inhibitors—specifically PDE5 inhibitors—and their potential effects on hemodynamic variables have therefore become significant factors in therapeutic decision making. Most of the published data linking PDE5 inhibitor effects and cardiovascular disease relate to sildenafil, although ≥2 new agents are in various stages of development and clinical trials. Sildenafil and other PDE5 inhibitors act on vascular smooth muscle, predominantly in the corpus cavernosum. PDE5 is not found in cardiomyocytes, and no effect of PDE5 inhibition on cardiac contractility has been demonstrated. On the basis of a safety database comprising thousands of men with ED, sildenafil has demonstrated minimal adverse effects in men with stable ischemia, hypertension, and/or severe coronary artery disease. Sildenafil has modest effects on hemodynamic variables and has been shown to increase coronary artery flow reserve. Alone or combined with ≥1 antihypertensive medication, sildenafil did not increase the incidence of adverse events or hypotensive episodes. Sildenafil-associated decreases in systolic and diastolic blood pressure, the result of its vasodilator activity, have been modest. Sildenafil has decreased both elevated pulmonary vascular resistance and elevated pulmonary artery pressures in patients with pulmonary vascular disease. Beneficial changes in hemodynamics have been observed with the use of sildenafil in patients with congestive heart failure with underlying ischemic and other dilated cardiomyopathies. No association between sildenafil and increased cardiovascular morbidity or mortality has emerged in analyses of clinical trial data.

Pulmonary venous wedge pressures accurately predict pulmonary arterial pressures in children with single ventricle physiology.

We investigated the relationship between pulmonary venous wedge and pulmonary arterial pressures in patients with single ventricle physiology. This relationship has been studied in other cardiac conditions but not in this unique group of patients. We made 60 paired measurements from one or both lungs in 40 patients, and divided the patients into three groups. Group 1 consisted of patients whose pulmonary blood supply was via an aortopulmonary shunt (n = 14), group 2 included patients with a bi-directional Glenn anastomosis (n = 20), and group 3 included patients with a pulmonary arterial band (n = 6). Venous wedge pressure estimated arterial pressure within 3 mmHg in 59 of 60 paired measurements. Plots of the difference between pulmonary artery and pulmonary venous wedge pressures versus the mean showed excellent correlation, with a mean difference of approximately 1 for group 1 (mean difference, -0.15 +/- 1.3 mmHg) and group 2 (mean difference, 0.52 +/- 1.12 mmHg). The relationship was poor in group 3 (mean difference, -2.00 +/- 4.80 mmHg) but was much better with the exclusion of the one outlying patient in whom pulmonary venous wedge pressure significantly overestimated pulmonary arterial pressure (mean difference, -0.33 +/- 2.07 mmHg). We conclude that pulmonary venous wedge pressure accurately estimates pulmonary arterial pressure in patients palliated for single ventricle physiology, but care must be taken in patients with a pulmonary arterial band.

Upper extremity peripheral venous pressure measurements accurately reflect pulmonary artery pressures in patients with cavopulmonary or Fontan connections.

After the bidirectional cavopulmonary or Fontan operation, the physiologic consequence is passive flow of the systemic venous return to the pulmonary arteries. Knowledge of pulmonary artery pressure (PA) is valuable in the management of these patients, and obtaining this information without the need for a central line or cardiac catheterization would be advantageous. The aim of this study was to evaluate the correlation between upper extremity peripheral venous (PV) pressures and PA or superior vena cava (SVC) pressures in patients who have undergone cavopulmonary or Fontan connections. During cardiac catheterization, 19 patients with complex cyanotic heart disease who had undergone a cavopulmonary shunt or Fontan procedure were studied. Simultaneous pressure measurements were obtained from the peripheral intravenous line placed prior to the procedure and the SVC or PA. The mean pressures were compared. The mean PV pressure was 17.5 +/- 5.6 mmHg. The mean SVC or PA pressure was 16.1 +/- 5.4 mmHg. The mean difference was 1.5 +/- 1.5 mmHg ( p < 0.001). The correlation coefficient PV to SVC or PA pressure was 0.97 ( p < 0.001). PV pressure measurements taken from an upper extremity accurately reflect PA pressures in patients who have undergone a cavopulmonary shunt or Fontan procedure.

Management of pulmonary hypertension: physiological and pharmacological considerations for anesthesiologists.

For decades the pulmonary circulation was not considered as important as the systemic (“greater”) circulation. However, pulmonary hypertension can arise because of many diseases of the heart and lung. Therefore, increasing efforts in research have been undertaken leading to a profound increase in un

Significance of pulmonary artery pressure in emphysema patients with mild-to-moderate hypoxemia

The guidelines of the Global Initiative for Chronic Obstructive Lung Disease (GOLD) do not recommend the measurement of pulmonary artery pressure in patients with chronic obstructive pulmonary disease (COPD). This is on the basis that the mean pulmonary artery pressure (mPAP) does not provide more clinical information than measurement of the oxygen tension in arterial blood ( PaO 2). The mPAP correlates well with PaO 2 in emphysema patients with severe hypoxemia ( PaO 2⩽7.3 kPa (55 mmHg)). However, the occurrence and significance of mPAP is unclear in patients without severe hypoxemia ( PaO 2>7.3 kPa (55 mmHg)). In order to evaluate the usefulness of measurement of mPAP in emphysema patients without severe hypoxemia, we performed right heart catheterization and investigated the pulmonary hemodynamics of 53 patients without severe hypoxemia. In addition, we identified long-term prognostic factors with a mean follow-up term of 77 months after right heart catheterization. Seventeen of 27 patients with mild-to-moderate hypoxemia exhibited pulmonary hypertension (mPAP⩾2.7 kPa (20 mmHg)) and the classification according to severity in GOLD exhibited a greater correlation to mPAP than PaO 2. Moreover, only mPAP was found to be a significant prognostic factor according to multivariate proportional hazards analysis ( P=0.01). We conclude that mPAP is more informative about the severity of emphysema than PaO 2 in patients with mild-to-moderate hypoxemia.

Does the myocardial performance index affect pulmonary artery pressure in patients with mitral stenosis? A tissue Doppler imaging study.

The relation between systolic pulmonary artery pressure (PAP) and mitral stenosis (MS) has been poorly understood. Although the mitral valve area (MVA) is an important factor affecting the PAP, there is a wide spectrum of the PAP in patients with MS despite a similar MVA. So, we analyzed whether the left and right ventricular myocardial performance index (MPI) correlated with the PAP. Two-dimensional Doppler echocardiography was performed in 46 patients with MS. The left atrial diameter, mean mitral gradient, and MVA were measured. The PAP was derived from the tricuspid regurgitant jet velocity. The ejection time (ET), isovolumetric relaxation time (IRT), and contraction time (ICT) were measured on annulus of interventricular septum, lateral, inferior and anterior wall of left ventricle, and right ventricle free wall from apical two- and four-chamber views in patients with MS and 40 age-matched healthy patients by tissue Doppler imaging (TDI). Then the MPI was calculated as (IRT + ICT)/ET for both left and right ventricle. The correlation of PAP with MVA, mean mitral gradient, left atrial diameter, and left and right ventricular MPI was evaluated. MVA and PAP were measured as 1.57 +/- 0.39 cm2 (0.8-2.5 cm2)and 42 +/- 16 mmHg, respectively. It was determined that the MPI increased in patients with MS(0.59 +/- 0.1 vs 0.48 +/- 0.07, P < 0.001). It was also demonstrated that the MVA, left atrial diameter, mean diastolic gradient, and left ventricular MPI were correlated with PAP(r =-0.39 [P = 0.007], r = 0.43 [P = 0.003], r = 0.58 [P < 0.001], and r = 0.65 [P < 0.001], respectively). In multivariate analysis, although the PAP correlated with mean diastolic gradient and MPI (r = 0.39 [P = 0.013], and r = 0.48 [P < 0.001]), it did not correlate with left atrial diameter and MVA. The PAP also correlated with right ventricular MPI(r = 0.63 [P < 0.001]). This study demonstrates that the left ventricular MPI obtained by TDI is an important marker of PAP, and right ventricular MPI correlates with the PAP in patients with MS.

Relation of pulmonary venous wedge pressures to pulmonary artery pressures in patients with single ventricle physiology

Accurate assessment of pulmonary artery pressures (PAP) is important in determining the indication for Fontan procedure in patients with single ventricle physiology. However, it is sometimes difficult to measure PAP directly. Pulmonary vein wedge pressure (PVWP) may be used as an alternative to PAP in such cases. Several studies have demonstrated that PVWP correlates with PAP 1 Rao S. Sissman N.J. The relationship of pulmonary venous wedge to pulmonary arterial pressures. Circulation. 1971; 44: 565-574 Crossref PubMed Scopus (13) Google Scholar , 2 Hawker R.E. Celermajor J.M. Comparison of pulmonary artery and pulmonary venous pressures in congenital heart disease. Br Heart J. 1973; 35: 386-391 Crossref PubMed Google Scholar , 3 Waldman J.D. LaCorte M. Dick M. John S.A. Miettinen O.S. LaFarge C.G. The pulmonary venous wedge pressure in pulmonary artery hypertension. Cathet Cardiovasc Diagn. 1977; 3: 231-239 Crossref PubMed Scopus (8) Google Scholar , 4 Chern M.S. Yeh S.J. Lin F.C. Wu D. Hung J.S. Estimation of pulmonary artery pressure from pulmonary vein wedge pressure. Cathet Cardiovasc Diagn. 1994; 31: 277-282 Crossref PubMed Scopus (6) Google Scholar since a technique of catheterization for obtaining PVWP was introduced by Hellems et al. 5 Hellems H.K. Haynes F.W. Dexter L. Kinney T.D. Pulmonary capillary pressure in animals estimated by venous and arterial catheterization. Am J Physiol. 1948; 155: 98-105 PubMed Google Scholar However, these studies were based on patients with simple heart disease, and little is known about patients with complex heart disease. Accurate measurements of PAP and pulmonary vascular resistance (Rp) are critical in the selection of patients with complex heart disease for the Fontan procedure. If PVWP is used as an alternative to PAP, a small difference between PAP and PVWP could produce a big difference in the Rp, resulting in misinterpretation in determining the indication for the Fontan procedure. Thus, it is necessary to know not only the correlation between PVWP and PAP, but also to know how closely PVWP estimates PAP in patients with single ventricle physiology. The purpose of this report was to evaluate how accurately PVWP estimates PAP and to assess the relation focusing on the clinical use of PVWP as an alternative to PAP in patients who are being evaluated as Fontan candidates.

Relationship between ECG findings and pulmonary artery pressure in patients with acute massive pulmonary thromboembolism.

Pulmonary thromboembolism (PTE) is associated with various electrocardiogram (ECG) abnormalities, but the utility of evaluating the severity of PTE based on ECG abnormalities alone has not been investigated in Japanese patients previously. The purpose of this study was to examine the relationship between ECG abnormalities and the mean pulmonary artery pressure (MPAP) in patients with acute massive PTE (AMPTE). ECG examination of 21 patients, who were diagnosed with AMPTE by pulmonary arteriography, found that S(1)Q(3)T (3) was the most frequently observed abnormality (in 67% of the patients), followed by negative T (62%), clockwise rotation (57%), and ST elevation (48%). When these patients were divided into 2 groups based on the level of MPAP, 8 of the 11 ECG findings, which were associated with PTE in a previous report, were more frequently observed in Group H (MPAP >/=40 mmHg) than in Group L (MPAP <40 mmHg). MPAP correlated significantly with the total number of ECG abnormalities (r=0.82, p<0.001). In particular, at least 5 ECG abnormalities were noted in patients with MPAP >/=45 mmHg. These results suggested that the total number of ECG abnormalities in patients with AMPTE can be used to evaluate the severity of APTE, including PAP level.

Comparison of pulmonary venous flow velocities and left ventricular diastolic and ejection time in patients with moderate mitral and aortic stenosis. Pulmonary venous flow velocities in mitral and aortic stenosis.

Doppler pulmonary venous flow velocities (PVFV) pattern are useful parameters in assessing the left ventricular diastolic functions. Both mitral stenosis (MS) and aortic stenosis (AS) lead to diastolic dysfunction. We compared PVFV and left ventricular diastolic and ejection time (ET) in patients with moderate MS and AS. Forty-three patients with moderate MS (group 1), 65 patients with moderate AS (group 2), and 33 healthy subjects as controls (group 3) were included in this study. After obtaining standard measurements echocardiographically, diastolic period (DP), ET, the ratio of the DP to the ET (DP/ET), isovolumetric contraction time (ICT), isovolumetric relaxation time (IRT), peak systolic flow velocity (PS), peak antegrade diastolic flow velocity (PD), peak reversal flow velocity at atrial contraction (PRA), the ratio of the peak systolic to the diastolic flow velocity (PS/PD), deceleration time of the antegrade diastolic flow (PDDT), and pressure half time of the peak antegrade diastolic flow velocity (PDPHT) were measured. Mitral valve area (MVA), aortic valve area (AVA), systolic pulmonary artery pressure (PAP), peak and mean gradients were calculated with standard formulas. In univariate analysis, MVA was correlated with PDPHT and PDDT (r = -0.41; p < 0.01, r = -0.36; p < 0.05, respectively), also it was correlated with DP/ET (r = -0.57; p < 0.001). Mitral peak and mean diastolic gradient were correlated with PS/PD (r = -0.43; p < 0.01, r = -0.36; p < 0.05, respectively) and DP/ET (r = 0.51; p < 0.01, r = 0.46; p < 0.01, respectively). AVA was only correlated with DP/ET (r = 0.38; p < 0.05). Aortic peak and mean systolic gradient were correlated with PS/PD (r = -0.29; p < 0.05, r = -0.27; p < 0.05, respectively) and DP/ET (r = -0.38; p < 0.01, r = -0.40; p < 0.01, respectively). In the same analysis, PAP in patients in group 1 and 2 was correlated with PS/PD (r = -0.42; p < 0.01 and r = -0.40; p < 0.01, respectively) and also it was correlated with PD (r = 0.37; p < 0.05 and r = 0.27; p < 0.05, respectively) in both groups. Moderate MS and AS similarly affect the PVFV, and PS/PD correlates with hemodynamics similarly both in MS and AS. Nevertheless, PDDT and PDPHT correlate with solely MVA. IRT higher in AS than MS, though DP/ET and ICT higher in MS than AS, and DP/ET relates with the severity of both MS and AS.

Le sildenafil (Viagra®), 5 ans après : données actuelles en pathologie cardiovasculaire

Sildenafil is an inhibitor of phosphodiesterase 5, which has important vasodilatory properties. Though sildenafil provokes a decrease in systemic arterial pressure, its safety has been confirmed in large series of patients on several kinds of anti-hypertensive therapy. Likewise, post-marketing surveys, in the US or United Kingdom, have recorded a number of cardio-vascular deaths following sildenafil administration which was lower than expected, provided the contra-indication with the concomitant use of nitrates is observed. In patients with known or suspected coronary artery disease, sildenafil does not modify the tolerance or results of echocardiographic exercise testing. However, sildenafil does increase coronary flow reserve, both in narrowed or normal coronary arteries, with no sign of a “steal” phenomenon. Because of its capacity to retard the degradation of cGMP, by the inhibition of phosphodiesterase 5, the effect of sildenafil in primary pulmonary hypertension has been evaluated in several studies: acutely, sildenafil decreases pulmonary artery pressure, either alone or in combination with inhaled iloprost or NO. On the same line, sildenafil decreases hypoxia-induced pulmonary hypertension in normal volunteers. These findings, together with reports of long-term improvement in symptoms and levels of pulmonary artery pressure in patients with primary pulmonary hypertension, will warrant further trials to document its potential role in this otherwise severe disease.

Inhaled alternatives to nitric oxide.

should decrease pulmonary artery pressure (PAP) and pulmonary vascular resistance (PVR), without affecting systemic arterial pressure (SAP), and potentially improve oxygenation by redistributing pulmonary blood flow to ventilated areas of lung. INO (INO Therapeutics Inc., Clinton NJ) possesses these properties and has gained approval from the Food and Drug Administration (FDA) for the care of neonates with acute lung injury and pulmonary hypertension (PH), and widespread clinical acceptance (but not FDA approval) for adults with PH with or without lung injury. Delivered as a gas, INO is preferentially distributed to the ventilated areas of the lung, where it produces relaxation of pulmonary vascular smooth muscle via activation of guanylate cyclase and the conversion of guanosine-5-triphosphate to cyclic guanosine monophosphate. 1 Absorbed INO is rapidly inactivated by hemoglobin, thereby preventing systemic effects and confining its vasodilator properties to the pulmonary circulation. 1 The search for inhaled selective pulmonary vasodilators was an active area of research, particularly in Europe and Australia, before the widespread publicity and testing of INO in the early 1990s. However, research on this subject appears to have declined inversely with the growing acceptance and use of INO. Until FDA approval had been granted, INO had been supplied free of charge in the United States on an investigational-drug basis. However, after FDA approval, the cost of treatment with INO became very expensive. This prompted a search at our institution for alternative agents to INO. The purpose of this article is to review the published experience concerning alternative inhaled vasodilators and, when possible, compare their reported efficacy with that of INO.

Is the use of modified Bernoulli equation valid in estimating pulmonary artery pressures in patients with severely dilated tricuspid annulus?

Is the use of modified Bernoulli equation valid in estimating pulmonary artery pressures in patients with severely dilated tricuspid annulus?

Effects of nesiritide (B-type natriuretic peptide) on pulmonary artery pressures in patients with acute decompensated congestive heart failure

Effects of nesiritide (B-type natriuretic peptide) on pulmonary artery pressures in patients with acute decompensated congestive heart failure

Plasma Markers of Endothelial Dysfunction in Pulmonary Hypertension

To evaluate and to correlate endothelial cell dysfunction, using recently available plasma markers, with the magnitude of pulmonary artery pressure in patients with severe pulmonary hypertension (PH). Selected plasma markers of endothelial cell dysfunction were studied: nitric oxide (NO), thrombomodulin, tissue factor pathway inhibitor, and soluble endothelium, leukocyte, and platelet selectins (sE-, sL-, sP-selectins, respectively). Padova University Hospital and Department of Pathology and Pharmacology, Loyola University of Chicago, Chicago, IL. Fifteen patients had severe PH (four men and 11 women; mean age, 49.7 +/- 2.9 years: seven patients had primary pulmonary hypertension [PPH] and eight patients had secondary pulmonary hypertension [SPH]), and 20 patients were healthy control subjects. In patients with PH, sP- and sE-selectins were elevated, whereas sL-selectin was lower in comparison with the selectin levels in control subjects. However, the differences between patients with PH and control subjects were significant only for sL-selectin (p < 0.0001) and sE-selectin (p < 0.03). The NO level was significantly lower in patients with PH compared with the NO level in control subjects (p < 0.01). No difference in tissue factor pathway inhibitor level was noted between control subjects and patients with PH. Only a weak correlation was found between thrombomodulin plasma levels and magnitude of systolic pulmonary artery pressure (r = -0.528, p < 0.05). Our data are in keeping with the evidence for significant endothelial cell dysfunction in patients with PH and the need for chronic anticoagulation believed to increase survival in these patients. In addition, these data seem to suggest a need for newer agents that are able to increase the antithrombotic endothelial function.

Independent and additive prognostic value of right ventricular systolic function and pulmonary artery pressure in patients with chronic heart failure

Independent and additive prognostic value of right ventricular systolic function and pulmonary artery pressure in patients with chronic heart failure