scholarly journals The Impact of Endoscopic Stapler Selection on Bleeding at the Vascular Stump in Pulmonary Artery Transection

2020 ◽  
Vol Volume 13 ◽  
pp. 41-47 ◽  
Author(s):  
Yoshio Tsunezuka ◽  
Nobuhiro Tanaka ◽  
Hideki Fujimori
2021 ◽  
Vol 23 (1) ◽  
Author(s):  
Ryan J. Pewowaruk ◽  
Gregory P. Barton ◽  
Cody Johnson ◽  
J. Carter Ralphe ◽  
Christopher J. Francois ◽  
...  

Abstract Background Branch pulmonary artery (PA) stenosis (PAS) commonly occurs in patients with congenital heart disease (CHD). Prior studies have documented technical success and clinical outcomes of PA stent interventions for PAS but the impact of PA stent interventions on ventricular function is unknown. The objective of this study was to utilize 4D flow cardiovascular magnetic resonance (CMR) to better understand the impact of PAS and PA stenting on ventricular contraction and ventricular flow in a swine model of unilateral branch PA stenosis. Methods 18 swine (4 sham, 4 untreated left PAS, 10 PAS stent intervention) underwent right heart catheterization and CMR at 20 weeks age (55 kg). CMR included ventricular strain analysis and 4D flow CMR. Results 4D flow CMR measured inefficient right ventricular (RV) and left ventricular (LV) flow patterns in the PAS group (RV non-dimensional (n.d.) vorticity: sham 82 ± 47, PAS 120 ± 47; LV n.d. vorticity: sham 57 ± 5, PAS 78 ± 15 p < 0.01) despite the PAS group having normal heart rate, ejection fraction and end-diastolic volume. The intervention group demonstrated increased ejection fraction that resulted in more efficient ventricular flow compared to untreated PAS (RV n.d. vorticity: 59 ± 12 p < 0.01; LV n.d. vorticity: 41 ± 7 p < 0.001). Conclusion These results describe previously unknown consequences of PAS on ventricular function in an animal model of unilateral PA stenosis and show that PA stent interventions improve ventricular flow efficiency. This study also highlights the sensitivity of 4D flow CMR biomarkers to detect earlier ventricular dysfunction assisting in identification of patients who may benefit from PAS interventions.


2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Homeira Vafaei ◽  
Fahimeh Kaveh Baghbahadorani ◽  
Nasrin Asadi ◽  
Maryam Kasraeian ◽  
Azam Faraji ◽  
...  

Abstract Background Prenatal corticosteroid administration is known to be an effective strategy in improving fetal pulmonary maturity. This study aimed to evaluate the impact of maternal betamethasone administration on fetal pulmonary and other arteries Doppler velocity and the correlation between RDS development and Doppler indices results. Methods Fifty one singleton pregnancies between 26 and 34 gestational weeks with a diagnosis of preterm labor were included in the exposed group and received betamethasone. Fifty one uncomplicated pregnancies were included in the non-exposed group. Fetal pulmonary, umbilical and middle cerebral arteries Doppler parameters were evaluated before and 24 to 48 h after steroid administration in the exposed group and two times at same intervals in the non-exposed group. Maternal records were matched to neonatal charts if delivery happened, and demographic and outcome data were abstracted. Results When compared with the nonexposed group, fetuses treated with corticosteroids demonstrated significantly decreased umbilical artery Pulsatility index (PI) and significantly increased the middle cerebral artery PI, pulmonary artery Acceleration time (AT) and pulmonary artery AT/ET (Ejection time), while all other indices remained similar. We found significantly decreased pulmonary artery AT in the fetuses with respiratory distress syndrome (RDS) compared to those that did not. Conclusions The results of our study showed that maternal antenatal betamethasone administration caused significant changes in the fetus blood velocity waveforms and also affected the blood flow in the pulmonary artery which led to an increase in the pulmonary artery AT and AT/ET. Among those fetuses with RDS, we found a significant decrease in the pulmonary artery AT, but we did not observe any pulmonary artery AT/ET differences.


Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Maria Drakopoulou ◽  
Konstantinos Stathogiannis ◽  
Konstantinos Toutouzas ◽  
George Latsios ◽  
Andreas Synetos ◽  
...  

Objective: Severe aortic stenosis leads to increased pulmonary arterial systolic pressure. A controversy still remains regarding the impact of persistent pulmonary hypertension (PHT) on prognosis of patients undergoing transcatheter aortic valve implantation (TAVI). We sought to investigate the impact of persistent PHT on 2-year all-cause mortality of patients with severe aortic stenosis following TAVI. Methods: Patients with severe and symptomatic aortic stenosis (effective orifice area [EOA]≤1 cm 2 ) who were scheduled for TAVI with a self-expanding valve at our institution were prospectively enrolled. Prospectively collected echocardiographic data before and after TAVI were retrospectively analyzed in all patients. Pulmonary artery systolic pressure was estimated as the sum of the right ventricular to the right atrial gradient during systole and the right atrial pressure. PHT following TAVI was classified as absent if <35 mmHg and persistent if ≥35 mmHg. Primary clinical end-point was 2-year all-cause mortality defined according to the criteria proposed by the Valve Academic Research Consortium-2. Results: Hundred and forty patients (mean age: 82±9 years) were included in the study. The primary clinical end point occurred in 17 patients (12%) during a median follow-up period of 2 years. Mean pulmonary artery systolic pressure was reduced in all patients following TAVI (45±9 versus 41±6 mmHg, p<0.01). Mortality rate was higher in patients with persistent PHT compared to patients with normal pulmonary artery systolic pressure following TAVI (26% versus 14 %, p<0.01). Patients that reached the primary clinical end point had a higher post procedural mean systolic pulmonary pressure (43±9 versus 39±6 mmHg, p=0.02). In multivariate regression analysis, persistence of PHT (OR: 2.51, 95% CI: 1.109-7.224, p=0.01) was an independent predictor of long-term mortality. Conclusions: The persistence of pulmonary hypertension after TAVI is associated with long term mortality. Identifying the population that will clearly benefit from TAVI is still need to be validated by larger trials.


2021 ◽  
Vol 8 ◽  
Author(s):  
Vanessa Martínez ◽  
María Sanz-de la Garza ◽  
Blanca Domenech-Ximenos ◽  
César Fernández ◽  
Ana García-Alvarez ◽  
...  

Background: The cardiac response to endurance exercise has been studied previously, and recent reports have described the extension of this remodeling to the pulmonary vasculature. However, these reports have focused primarily on land-based sports and few data are available on exercise-induced cardio-pulmonary adaptation in swimming. Nor has the impact of sex on this exercise-induced cardio-pulmonary remodeling been studied in depth. The main aim of our study was to evaluate cardiac and pulmonary circulation remodeling in endurance swimmers. Among the secondary objectives, we evaluate the impact of sex and endurance sport discipline on this cardio-pulmonary remodeling promoted by exercise training.Methods:Resting cardiovascular magnetic resonance imaging was performed in 30 healthy well-trained endurance swimmers (83.3% male) and in 19 terrestrial endurance athletes (79% male) to assess biventricular dimensions and function. Pulmonary artery dimensions and flow as well as estimates of pulmonary vascular resistance (PVR) were also evaluated.Results:In relation to the reference parameters for the non-athletic population, male endurance swimmers had larger biventricular and pulmonary artery size (7.4 ± 1.0 vs. 5.9 ± 1.1 cm2, p &lt; 0.001) with lower biventricular ejection fraction (EF) (left ventricular (LV) EF: 58 ± 4.4 vs. 67 ± 4.5 %, p &lt; 0.001; right ventricular (RV) EF: 60 ± 4 vs. 66 ± 6 %, p &lt; 0.001), LV end-diastolic volume (EDV): 106 ± 11 vs. 80 ± 9 ml/m2, p &lt; 0.001; RV EDV: 101 ± 14 vs. 83 ± 12 ml/m2, p &lt; 0.001). Significantly larger LV volume and lower LV EF were also observed in female swimmers (LV EF: 60 ± 5.3 vs. 67 ± 4.6 %, p = 0.003; LV EDV: 90 ± 17.6 vs. 75± 8.7 ml/m2, p = 0.002). Compared to terrestrial endurance athletes, swimmers showed increased LV indexed mass (75.0 ± 12.8 vs. 61.5 ± 10.0 g/m2, p &lt; 0.001). The two groups of endurance athletes had similar pulmonary artery remodeling.Conclusions: Cardiac response to endurance swimming training implies an adaptation of both ventricular and pulmonary vasculature, as in the case of terrestrial endurance athletes. Cardio-pulmonary remodeling seems to be less extensive in female than in male swimmers.


2007 ◽  
Vol 292 (5) ◽  
pp. L1202-L1210 ◽  
Author(s):  
Shen Zhang ◽  
Hemal H. Patel ◽  
Fiona Murray ◽  
Carmelle V. Remillard ◽  
Christian Schach ◽  
...  

Pulmonary vascular remodeling due to overgrowth of pulmonary artery smooth muscle cells (PASMC) is a major cause for the elevated vascular resistance in patients with idiopathic pulmonary arterial hypertension (IPAH). Increased cytosolic Ca2+ concentration, resulting from enhanced capacitative Ca2+ entry (CCE) and upregulated transient receptor potential (TRP) channel expression, is involved in stimulating PASMC proliferation. The current study was designed to determine the impact of cAMP, a second messenger that we hypothesized would blunt aspects of PASMC activity, as a possible contributor to IPAH pathophysiology. Short-term (30 min) pretreatment with forskolin (FSK; 10 μM), a direct activator of adenylyl cyclase, in combination with the cyclic nucleotide phosphodiesterase inhibitor isobutylmethylxanthine (IBMX; 200 μM), attenuated CCE in PASMC from normal subjects, patients without pulmonary hypertension (NPH), and patients with IPAH. The FSK-mediated CCE inhibition was independent of protein kinase A (PKA), because the PKA inhibitor H89 negligibly affected the decrease in CCE produced by cAMP. By contrast, longer (4 h) treatment with FSK (with IBMX) attenuated CCE in normal and NPH PASMC but enhanced CCE in IPAH PASMC. This enhancement of CCE was abolished by PKA inhibition and associated with an upregulation of TRPC3. In addition, cAMP increased TRPC1 mRNA expression in IPAH (but not in normal or NPH) PASMC, an effect blunted by H89. Furthermore, iloprost, a prostacyclin analog that increases cAMP, downregulated TRPC3 expression in IPAH PASMC and FSK-mediated cAMP increase inhibited IPAH PASMC proliferation. Although a rapid rise in cellular cAMP decreases CCE by a PKA-independent mechanism, sustained cAMP increase inhibits CCE in normal and NPH PASMC but increases CCE via a PKA-dependent pathway in IPAH PASMC. The divergent effect of cAMP on CCE parallels effects on TRPC expression. The results suggest that the combined use of a PKA inhibitor and cAMP-elevating drugs may provide a novel approach for treatment of IPAH.


2018 ◽  
Vol 8 (2) ◽  
pp. 204589401877305 ◽  
Author(s):  
Batool AbuHalimeh ◽  
Milind Y. Desai ◽  
Adriano R. Tonelli

The diagnosis of pulmonary hypertension (PH) requires a right heart catheterization (RHC) that reveals a mean pulmonary artery pressure ≥ 25 mmHg. The pulmonary artery catheter traverse the right atrium and ventricle on its way to the pulmonary artery. The presence of abnormal right heart structures, i.e. thrombus, vegetation, benign or malignant cardiac lesions, can lead to complications during this procedure. On the other hand, avoidance of RHC delays the diagnosis and treatment of PH, an approach that might be associated with worse outcomes. This paper discusses the impact of right heart lesions on the diagnosis of PH and suggests an approach on how to manage this association.


Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Fusako Sera ◽  
Tomohito Ohtani ◽  
kei nakamoto ◽  
Shungo Hikoso ◽  
Daisaku Nakatani ◽  
...  

Introduction: The proposed revision of hemodynamic definition of pulmonary hypertension (PH) adopts a lower threshold of mean pulmonary artery pressure (mPAP) > 20 mmHg. In addition, pulmonary vascular resistance (PVR) ≥ 3 Wood units (WU) is included as the definition of pre-capillary component of PH. Heart failure (HF) with preserved ejection fraction (HFpEF) can develop pre-capillary PH as well as post-capillary PH. We aimed to investigate the impact of the proposed definition of PH on clinical diagnosis of PH associated with HFpEF. Methods: From the PURSUIT-HFpEF (Prospective Multicenter Observational Study of Patients with Heart Failure with Preserved Ejection Fraction) registry, 225 patients who were hospitalized with HF and underwent right heart catheterization were categorized according to the current guidelines and the proposed definition of PH: non-PH, isolated post-capillary PH (Ipc-PH), pre-capillary PH, and combined pre- and post-capillary PH (Cpc-PH). In the proposed definition, patients with mPAP > 20 mmHg, PVR < 3 WU, and pulmonary artery wedge pressure ≤ 15 mmHg do not meet criteria for any of the above categories and are categorized as “unclassified PH”. Results: Prevalence of PH was significantly increased in the proposed definition compared to that in the current definition (51% vs 29%, p<0.0001), with a doubled frequency of pre-capillary PH (Fig A). Furthermore, 24 patients (11%) were diagnosed as unclassified PH and accounted for 22% of those with PH by the proposed definition. Among the PH categories in the proposed definition, Cpc-PH category was significantly relevant for worse prognosis at 1 year after discharge in patients with HFpEF (p=0.03 vs non-PH by log-rank test with Bonferroni's correction) (Fig 2). Conclusions: The new definition of PH resulted in a remarkable increase of prevalence of PH in HFpEF with a quite a few patients with unclassified PH and doubled frequency of pre-capillary PH.


2019 ◽  
Vol 43 (4) ◽  
pp. 177-183
Author(s):  
Shi-Min Yuan

Abstract Interleukin (IL)-6 is a pleiotropic cytokine, playing an important role in various pathological conditions, such as inflammatory, infectious, and neoplastic disorders. The casual relationship between IL-6 levels and development of pulmonary artery hypertension (PAH) has been elusive. Based on comprehensive retrieval of pertinent literature of recent two decades, this article aims to give an overview of the impact of IL-6 on PAH development in view of both clinical and experimental aspects. Results showed that IL-6 was overexpressed in all types of PAH in both human and animal models. The elevated IL-6 levels were closely related to right ventricular (RV) dysfunction and predicted poor prognosis and mortality of PAH patients. Several IL-6-regulated signaling pathways including transforming growth factor (TGF)-β/bone morphogenetic protein signaling pathway are involved in PAH development. IL-6 antagonizing agents are effective in ameliorating the symptoms and improving the RV function of PAH patients.


2019 ◽  
Vol 9 (3) ◽  
pp. 204589401987716
Author(s):  
Maria F. Zorzi ◽  
Emmanuelle Cancelli ◽  
Marco Rusca ◽  
Matthias Kirsch ◽  
Patrick Yerly ◽  
...  

The aim of this study was to evaluate the pathophysiological role and the prognostic significance of pulmonary artery compliance (CPA), a measure of right ventricular pulsatile afterload, in cardiogenic shock. We retrospectively included 91 consecutive patients with cardiogenic shock due to primary left ventricular failure, monitored with a pulmonary artery catheter within the first 24 h. CPA was calculated as the ratio of stroke volume to pulmonary artery pulse pressure, and we determined whether CPA predicted mortality and whether it performed better than other pulmonary hemodynamic variables. The overall in-hospital mortality in our cohort was 27%. Survivors and nonsurvivors had comparable left ventricular ejection fraction, systolic, diastolic and mean pulmonary artery pressure, transpulmonary gradient, diastolic pressure gradient, and pulmonary vascular resistance at 24 h. In contrast, CPA was the only pulmonary artery variable significantly associated with mortality in univariate and multivariate analyses. Mortality increased from 4.5% at the highest quartile of CPA (3.6–6.5 mL/mmHg) to 43.5% at the lowest quartile (0.7–1.7 mL/mmHg). In 64 patients with a PAC inserted immediately upon admission, we calculated the trend of CPA between admission and 24 h. This trend was positive in survivors (+0.8 ± 1.3 ml/mmHg) but negative in nonsurvivors (−0.1 ± 1.0 mL/mmHg). The lower CPA in nonsurvivors was associated with more severe right ventricular systolic dysfunction. In conclusion, a reduced compliance of the pulmonary artery promotes right ventricular dysfunction and is independently associated with mortality in cardiogenic shock. Future studies should evaluate the impact on pulmonary arterial compliance and right ventricular afterload of therapies used in cardiogenic shock.


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