Pulmonary Vascular Bed In Patients Research Articles

Reconstruction of the pulmonary vascular bed at the stages of hemodynamic correction in patients with functionally single ventricle

The OBJECTIVE was to study the prevalence and nature of congenital and acquired anatomical features of the pulmonary vascular bed in patients with single ventricle and to evaluate their impact on staged hemodynamic correction.METHODS AND MATERIALS. The study was a retrospective cohort study based on the study of the experience of surgical treatment of patients with a single ventricle from 2005 to 2022. 208 patients, 95 females and 113 males met the inclusion criteria. Depending on the type of the first stage of correction, all patients were divided into three groups: 1 – patients after the Norwood operation (n=84), 2 – patients after the isolated systemic-to-pulmonary shunts (n=74), 3 – patients after pulmonary artery band or those who did not need the first stage of surgical treatment (n=50).RESULTS. From all patients who survived the Stage-I (158 patients), 47 (30 %) patients underwent 72 reconstructive interventions on the pulmonary arteries: 8 % – before Stage-II, 46 % – at Stage-II, 17 % – between stages II and III, 11 % – at Stage-III and 18 % – after Stage-III. When comparing freedom from stenosis of the pulmonary arteries, statistically significant differences were found between groups of patients (p=0.005), with the least freedom from stenosis in group 1 (after the Norwood operation) and the greatest freedom from stenosis in group 3 (after pulmonary artery band or without first stage of correction).CONCLUSIONS. Patients with a functionally single ventricle are at risk of developing pulmonary artery stenosis throughout the entire period of staged hemodynamic correction and after its completion. The identified narrowing needs immediate correction, since a long-term existing narrowing can lead to hypoplasia of the pulmonary vascular bed and become an obstacle to the timely Fontan completion. More extensive use of tomographic imaging techniques is recommended in order to fully assess the degree of narrowing.

The pulmonary vascular bed in patients with functionally univentricular physiology and a Fontan circulation.

Fontan palliation represents one of the most remarkable surgical advances in the management of individuals born with functionally univentricular physiology. The operation secures adult survival for all but a few with unfavourable anatomy and/or physiology. Inherent to the physiology is passive transpulmonary blood flow, which produces a vulnerability to adequate filling of the systemic ventricle at rest and during exertion. Similarly, the upstream effects of passive flow in the lungs are venous congestion and venous hypertension, especially marked during physical activity. The pulmonary vascular bed has emerged as a defining character on the stage of Fontan circulatory behaviour and clinical outcomes. Its pharmacologic regulation and anatomic rehabilitation therefore seem important strategic therapeutic targets. This review seeks to delineate the important aspects of pulmonary artery development and maturation in functionally univentricular physiology patients, pulmonary artery biology, pulmonary vascular reserve with exercise, and pulmonary artery morphologic and pharmacologic rehabilitation.

Leads dislodged into the pulmonary vascular bed in patients with cardiac implantable electronic devices.

IntroductionSpontaneous lead dislodgement into the pulmonary circulation is a rare complication of permanent pacing with unproven harmfulness and an indication of controversial class for transvenous lead extraction (TLE).AimTo assess TLE safety in patients with leads dislodged into the pulmonary artery.Material and methodsA retrospective analysis of a 9-year-old database of transvenous lead extraction procedures comprising 1767 TLEs was carried out, including a group of 19 (1.1%) patients with leads dislodged into the pulmonary artery (LDPA).ResultsUnder univariate analysis the factors that increased the likelihood of the presence of an electrode in the pulmonary artery were mean lead dwelling time (increase of risk by 9% per year), total number of leads in the heart before TLE (increase of risk by 66% for one lead) and the number of abandoned leads (increase of risk by 119%). The presence of LDPA was associated with frequent occurrence of intracardiac lead abrasion (increase by 316%) and isolated lead-related infective endocarditis (LRIE) (increase by 500%). There were no statistically significant differences in clinical (p = 0.3), procedural (p = 0.94) or radiological (p = 0.31) success rates in compared (LDPA and non-LDPA) groups. Long-term mortality after TLE was comparable in both groups.ConclusionsAs the effectiveness and safety of TLE in patients with LDPA are comparable to those in standard TLE procedures, in our opinion, such patients should be considered TLE candidates.

Can platelet indices predict obstruction level of pulmonary vascular bed in patients with acute pulmonary embolism?

Computed tomography pulmonary arterial obstruction index ratio (CTPAOIR) is related with the severity of pulmonary embolism (PE). Platelet indices including mean platelet volume (MPV), platelet distribution width (PDW) are reported to be increased in acute PE. In this study, we aimed to evaluate the relationship between CTPAOIR and platelet indices and the utility of these parameters in the determination of PE severity. We retrospectively analysed the demographic data, clinical probability scores, laboratory data and echocardiographic findings of 63 acute PE patients who were diagnosed by pulmonary arterial computed tomography angiography. The hospital records of 38 (60.3%) male and 25 (39.7%) female patients with acute PE and 29 (58%) male and 21 (42%) female healthy control were evaluated (P = 0.803). The mean value of MPV, PDW levels, platelet counts and red cell distribution width levels were higher in PE groups than in control subjects (P < 0.05). Massive PE was present in 33.3% of PE patients. There were statistically significant differences in terms of hospital length of stay (HLS), mean value of MPV, CTPAOIR and systolic pulmonary arterial pressure (sPAP) in addition to systolic arterial pressure between massive and submassive PE patients (P < 0.05 for all). CTPAOIR was positively correlated with HLS, clinical probability scores, D-Dimer level, MPV, PDW levels and sPAP. Platelet indices, MPV and PDW, can be used for the determination of disease severity, and lead to therapeutic strategies for PE patients.

Noninvasive assessment of acute cardiopulmonary effects of an oral single dose of sildenafil in patients with idiopathic pulmonary hypertension

We aimed to assess the acute cardiopulmonary effects of a 100-mg oral single dose of sildenafil in patients with idiopathic pulmonary hypertension (IPAH) using a well-validated but less-used noninvasive echocardiographic method for the measurement of both systolic and diastolic pulmonary artery pressure (PAP), by tricuspid regurgitation (TR) velocity curve analysis. We studied 12 consecutive patients with IPAH (10 patients with New York Heart Association functional class III, and 2 patients with functional class II). A 100-mg oral single dose of sildenafil was added to previous medications of all patients and its immediate effects were evaluated 1, 5, and 12 h after treatment. Using paired analysis, administration of a 100-mg oral single dose of sildenafil led to a significant reduction in mean PAP and a remarkable increase in pulmonary acceleration time (PAT) 1 h after treatment (P = 0.000; 95% confidence interval [CI] 18.99-26.00 and P = 0.005; 95% CI -12.89 to -2.95, respectively). In addition, although the right heart dimensions (right atrium and right ventricle) showed a trend toward improvement, the differences were not statistically significant (P = 0.13 and P = 0.08, respectively). Our results demonstrated that Doppler examination of TR alone can be easily used for the estimate of systolic and diastolic PAP in patients with IPAH. This study also shows that sildenafil is the only drug given orally that can evaluate the vasodilatory capacity of the pulmonary vascular bed in patients with IPAH, with promising effects on mPAP and PAT in these patients.

Evaluación de la tolerancia al ejercicio en pacientes con schistosomiasis crónica sin evidencias clínicas de compromiso cardiopulmonar tratados con praziquantel

The purpose of this study was to evaluate whether a progressive cycle ergometer test (PCET) can detect minimal functional abnormalities that might indicate compromise of the pulmonary vascular bed in patients treated with praziquantel for chronic schistosomiasis who have no clinical signs of cardiopulmonary impairment. We studied 9 patients (whose mean (SD) age was 38 (18) years and 10 control subjects aged 32 (14) years. Both groups were evaluated by spirometry and a PCET to determine maximum oxygen consumption, heart rate, minute ventilation and gas exchange. Echocardiograms were used to rule out the presence of associated heart disease. Lung function was similar among patients and controls. Slight decreases in maximum oxygen consumption and heart rate reserve were observed with effort during the PCET, with normal respiratory response. No echocardiographic abnormalities that might indicate the presence of pulmonary vascular occlusive disease were observed. The results showed that the resting lung function is normal in these patients. However, there was a slight decrease in exercise tolerance, probably related to physical detraining. The data obtained during exercise indicated that pulmonary vascular occlusive disease is unlikely in these patients. Abnormalities may appear in later stages of the disease or in patients who do not receive early medical treatment.

Plasma endothelin-1 levels in patients with left-to-right shunt with or without pulmonary hypertension

The aim of this study was to evaluate the role of endothelin-1 (ET-1) in pathophysiology of pulmonary hypertension (PH) secondary to congenital heart disease with left-to-right shunt. Twenty-three children (12 male, 11 female) aged 0.58–13 years were enrolled the study. Blood samples were drawn from superior vena cava, right atrium, right ventricle, pulmonary artery and pulmonary wedge or pulmonary vein during cardiac catheterization. Plasma ET-1 levels were assayed by ELISA. Patients were divided into two groups according to the presence or absence of PH. Plasma ET-1 levels of the study group were compared to the peripheral venous and arterial ET-1 levels of 11 healthy infants and children (aged 0.75–13 years). Plasma ET-1 levels in patients with left-to-right shunt were found significantly higher than those of controls. However, plasma ET-1 levels were similar between the two groups of the patients. Pulmonary venous ET-1 levels were higher than the levels of superior vena cava, this suggested an increased production of ET-1 in pulmonary vascular bed in patients with PH. No correlations were found between plasma ET-1 levels and pulmonary arterial pressure, pulmonary vascular resistance and pulmonary blood flow in the patients. Plasma ET-1 levels of the patients with left-to-right shunt were increased independently from pulmonary arterial pressure and pulmonary vascular resistance. This increase was related to the production of ET-1 in pulmonary vascular bed in patients with PH. ET-1 could not be found to be directly related to the development of PH in the patients with left-to-right shunt.

Relation between endothelin-1 spillover in the lungs and pulmonary vascular resistance in patients with chronic heart failure

Objectives. The aim of this study was to clarify the origin of plasma endothelin-1 and to determine the relation between pulmonary vascular resistance and endothelin-1 secretion in the pulmonary circulation in patients with chronic congestive heart failure.Background. Plasma levels of endothelin-1, a potent endothelium-derived vasoconstrictor peptide, are increased in congestive heart failure, but the source has not been clarified. Recent studies have indicated a relation between endothelin-1 and pulmonary hypertension. We therefore evaluated the contribution of endothelin-1 secretion in the pulmonary circulation to the regulation of pulmonary vascular resistance in patients with chronic heart failure.Methods. A comparison was made of the plasma levels of endothelin-1 between the main pulmonary artery and the pulmonary capillary wedge region, as well as between the femoral artery and the femoral vein in 62 patients with chronic heart failure. Stepwise multivariate regression analysis was used to detect independent predictors of pulmonary vascular resistance among the various vasoconstrictor hormones in these patients.Results. There was no significant difference in plasma endothelin-1 levels between the femoral artery and vein. In contrast, plasma endothelin-1 increased significantly from the main pulmonary artery to the pulmonary capillary wedge region ([mean ± SEM] 3.1 ± 0.23 vs. 4.6 ± 0.36 pg/ml, p < 0.01), and the increase was related to the severity of heart failure. Among the various vasoconstrictor factors, such as plasma active renin concentration, plasma angiotensin II, plasma norepinephrine, femoral venous plasma endothelin-1 and pulmonary endothelin-1 spillover, only endothelin-1 spillover in the lungs showed an independent and significant correlation with pulmonary vascular resistance (r = 0.82, p < 0.001).Conclusions. The main source of circulating endothelin-1 is not the peripheral vascular bed but the pulmonary vascular bed in patients with chronic heart failure. In addition, endothelin-1 secretion in the lungs may regulate the pulmonary vascular resistance in patients with chronic heart failure. These findings are consistent with a significant role for endogenous endothelin-1 in the pathophysiology of heart failure, espscially in the pulmonary circulation.

Growth and development of the pulmonary vascular bed in patients with tetralogy of Fallot with or without pulmonary atresia.

Growth and development of the pulmonary vascular bed in patients with tetralogy of Fallot with or without pulmonary atresia.

Studies on mitral stenosis by analog computer analysis of radiocardiograms. Changes in cardiac output and the distribution of circulating blood.

Thirty-three patients with pure mitral stenosis were studied by radiocardiography and cardiac catheterization to assess changes in blood flow and the distribution of circulating blood. Radiocardiograms were analyzed by Kuwahara's model using an analog computer. The volumes of the right heart, lung, left heart and the rest of the whole circulatory system were obtained, as well as the cardiac output and the circulating blood volume (BV). Stroke index (SI) showed a tendency to decrease with diminished mitral valve area (MVA). In the presence of atrial fibrillation SI was 28% smaller than that of patients with sinus rhythm. The contribution of atrial contraction to the flow was inferred to be larger than in the normal hemodynamic state. A rough linear correlation was found between mean right heart volume (RHV) and mean pulmonary arterial pressure (PAm) (r=+0.69). The relationship between RHV and MVA was smaller than 1 cm2. Increase in mean left heart volume (LHV) was found but was not so prominent as that in RHV. The ratio of RHV to LHV showed a good linear correlation with PAm (r=+0.81). Significant increase in pulmonary blood volume (PBV) was found. Multiple regression analysis revealed that in the group with lower pulmonary arteriolar resistance (PAR < 250 dynes·sec·cm-5) the major determinants of PBV were BV and mean intravascular pressure (Pi). In the group with higher PAR (PAR&ges;250) determinants were BV and PAR, while Pi was not important. These findings suggest a decreased distensibility of the pulmonary vascular bed in patients with pulmonary hypertension. The present study revealed that severe mitral stenosis with pulmonary hypertension is associated with decreased pulmonary vascular distensibility, and that the sustained pressure load on the right ventricle leads to dilatation of the right chambers of the heart and to right ventricular failure.

The pulmonary vascular bed in patients with complete transposition of the great arteries.

Histological material obtained at autopsy from 35 patients over three months of age with complete transposition of the great arteries (TGA) was examined. Two of six patients less than a year of age with an intact ventricular septum and closed ductus arteriosus were found to have pulmonary vascular changes of at least grade 3 severity; in addition, two of seven patients with a large ventricular septal defect in this age group showed changes of similar severity. The reported low incidence of marked pulmonary vascular changes in patients with only an interatrial communication dying during the first year of life would appear to be due in part to the high proportion of cases less than three months old in whom there was not sufficient time for such changes to develop. Although the incidence is not as high as that found beyond a year of age, it is sufficiently high to influence the management of infants beyond three months of age. Hemodynamic studies were performed following atrial baffle repair in 34 patients. All but one of the 16 patients operated upon prior to two years of age had a pulmonary arteriolar resistance (Rpa) less than 3 units M2 at the time of review, including three with a large communication at ventricular or great vessel level who underwent surgery before two months of age. Repair at an older age did not preclude a low Rpa on follow-up, but in 11 of the 18 patients who were two or more years of age at the time of repair it was greater than 3 units M2. None of these latter patients had a large ventricular septal defect or patent ductus arteriosus. Comparison of postoperative hemodynamic data with autopsy studies would suggest that advanced pulmonary vascular disease is associated with earlier death among patients with complete transposition of the great arteries.

Vasomotor tone in the pulmonary vascular bed in patients with left-to-right shunts.

Vasomotor tone in the pulmonary vascular bed in patients with left-to-right shunts.

The Labile Properties of the Pulmonary Vascular Bed in Patients with Pulmonary Emphysema.

s1 May 1961The Labile Properties of the Pulmonary Vascular Bed in Patients with Pulmonary Emphysema.R. H. Behnke, M.D., (Assoc.), J. F. Williams Jr., M.D., D. H. White, M.D.R. H. Behnke, M.D., (Assoc.)Search for more papers by this author, J. F. Williams Jr., M.D.Search for more papers by this author, D. H. White, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-54-5-1059_1 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptThe factors which produce pulmonary hypertension in patients with pulmonary emphysema are poorly understood. The present study was undertaken in such patients to determine whether this vascular bed functions as a fixed rigid system or is labile as shown by pharmacologic alteration of its tone.Patients with pulmonary emphysema, established by clinical and laboratory tests, who were free of congestive heart failure, were studied at rest and with steady-state exercise prior to and during infusion of acetylcholine (2 to 8 mg./min.) and isoproterenol (.005 to .010 mg./min.) with determination of wedge, pulmonary, and systemic arterial pressures and cardiac output (CO).... This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Indianapolis, Ind. (CI) PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 May 1961Volume 54, Issue 5Page: 1059-1059KeywordsAcetylcholineBlood pressureCardiac outputClinical laboratoriesEmphysemaExerciseHeart failureIsoproterenolLaboratory testsPulmonary hypertension ePublished: 1 December 2008 Issue Published: 1 May 1961 PDF downloadLoading ...