Pulmonary transit time as a marker of diastolic dysfunction in Takotsubo.

Author(s):  
Riccardo Cau
1968 ◽  
Vol 07 (02) ◽  
pp. 125-129
Author(s):  
J. Měštan ◽  
V. Aschenbrenner ◽  
A. Michaljanič

SummaryIn patients with acquired and congenital valvular heart disease correlations of the parameters of the radiocardiographic curve (filling time of the right heart, minimal pulmonary transit time, peak-to-peak pulmonary transit time, and the so-called filling time of the left heart) with the mean pulmonary artery pressure and the mean pulmonary “capillary” pressure were studied. Further, a regression equation was determined by means of which the mean pulmonary “capillary” pressure can be predicted.


2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
L Houard ◽  
H Langet ◽  
S Militaru ◽  
M F Rousseau ◽  
A C Pouleur ◽  
...  

Abstract Background Assessment of congestion and cardiac function has been shown to have both therapeutic and prognostic implication for the management of patient with CHF. Pulmonary transit time (PTT) assessed by cMR is a novel parameter, which reflects not only hemodynamic congestion but also LV and RV function. Purpose We sought to explore the prognostic value of the pulmonary transit time assessed in seconds (PTT) and in beats (PTB) and the pulmonary blood volume indexed (PBVi) above conventional well-known risk factors including cMR-RVEF and estimated pulmonary artery pressure (eSPAP) in predicting outcomes. PBVi is defined by the product of PTB and the stroke volume indexed to body surface area. Methods 401 patients in sinus rhythm with a LVEF <35% (age 61±13 years; 25% female) underwent a cMR and an echocardiography. Patients were followed for a primary endpoint of overall mortality. Results Average cMR-LVEF was 23±7%, cMR-RVEF was 43±15%, average estimated systolic pulmonary pressure (eSPAP) was 33±12mmH, average PTT was 11±6s, PTB 8.9±5.6 bpm and average PBVi 305.5±254.9ml/m2. After a median follow-up of 6 years, 182 reached the primary endpoint. In univariate cox regression, age, ischemic cardiomyopathy, hypertension, diabetes, NYHA class III-IV, eSPAP >40mmHg, E/A ratio, e/e'ratio, cMR-RVEF, LV scar, PTT, PTB, PBVi, GFR, beta blockers and diuretics were associated with overall mortality. For the multivariate analysis, a baseline model was created where age, ischemic etiology, NYHA functional class III-IV, eSPAP >40 mmHg, beta-blockers and cMR-RVEF were found to be significantly and independently associated with the primary endpoint. PTT (X2 to improve = 5.3, HR: 1.03; 95% CI: [1.01; 1.06]; P=0.015), PTB (X2 to improve = 11.8, HR: 1.06; 95% CI: [1.03; 1.09]; P<0.001) and PBVi (X2 to improve = 7.7, HR: 1.08; 95% CI: [1.03; 1.14]; P=0.002) showed a significantly additional prognostic value over the baseline model (p<0.001). Conclusion Pulmonary transit time and pulmonary blood volume provide higher prognostic information over well-known risk factors including cMR-RVEF and eSPAP with high power to stratify prognosis in HF-rEF and might be promising tools to identify patients at higher risk among HF patients. Acknowledgement/Funding Fond National de recherche scientifique (FNRS)


2012 ◽  
Vol 73 (2) ◽  
pp. 194-201 ◽  
Author(s):  
Serena Crosara ◽  
Ingrid Ljungvall ◽  
Marco L. Margiocco ◽  
Jens Häggström ◽  
Alberto Tarducci ◽  
...  

2018 ◽  
Vol 38 (11) ◽  
pp. 1974-1981 ◽  
Author(s):  
He Zhao ◽  
Jiaywei Tsauo ◽  
Xiaowu Zhang ◽  
Huaiyuan Ma ◽  
Ningna Weng ◽  
...  

2021 ◽  
Vol 22 (Supplement_2) ◽  
Author(s):  
A Seraphim ◽  
K Knott ◽  
K Menacho ◽  
J Augusto ◽  
R Davies ◽  
...  

Abstract Funding Acknowledgements Type of funding sources: Foundation. Main funding source(s): British Heart Foundation Clinical Research Training Fellowship Background Pulmonary transit time (PTT) is a quantitative biomarker of cardiopulmonary status. Rest PTT was previously shown to predict outcomes in specific disease models, but clinical adoption is hindered but challenges in data acquisition. Whether evaluation of PTT during stress encodes incremental prognostic information has not been previously investigated as scale. Objectives To compare the prognostic value of stress and rest PTT derived from a fully automated, in-line method of estimation using perfusion CMR, in a large patient cohort. Methods A retrospective two-center study of patients referred clinically for adenosine stress myocardial perfusion assessment using CMR. Analysis of right and left ventricular cavity arterial input function curves from first pass perfusion was performed automatically, allowing the in-line estimation of both rest and stress PTT. Association with major adverse cardiovascular events (MACE) was evaluated. MACE was defined as a composite outcome of myocardial infarction, stroke, heart failure admission and ventricular tachycardia or appropriate ICD treatment (including ICD shock and/or anti-tachycardia pacing). Results 985 patients (67% male, median age 62 years (IQR 52,71)) were included, with median left ventricular ejection fraction (LVEF) of 62% (IQR 54-69). Median stress PTT was shorter than rest PTT 6.2 (IQR 5.1, 7.7) seconds versus 7.7 (IQR, 6.4, 9.2) seconds. Stress and rest PTT were highly correlated (r = 0.69; p &lt; 0.001). Stress PTT also correlated with LVEF (r=-0.37), stress MBF (r=-0.31), LVEDVi (r = 0.24), LA area index (r = 0.32) (p &lt; 0.001 for all). Over a median follow-up period of 28.6 (IQR, 22.6 35,7) months, MACE occurred in 61 (6.2%) patients. After adjusting for prognostic factors, both rest and stress PTT, independently predicted MACE, but not all-cause mortality. For every 1xSD (2.39s) increase in rest PTT the adjusted hazard ratio (HR) for MACE was 1.43 (95% CI 1.10-1.85, p = 0.007). The hazard ratio for one standard deviation (2.64s) increase in stress PTT was 1.34 (95% CI 1.048-1.723; p = 0.020) after adjusting for age, LVEF, hypertension, diabetes, sex and presence of LGE Conclusions In this 2-center study of 985 patients, we deploy a fully automated method of PTT estimation using perfusion mapping with CMR and show that both stress and rest PTT are independently associated with adverse cardiovascular outcomes. In this patient cohort, there is no clear incremental prognostic value of stress PTT, over its evaluation during rest. Figure 1. Stress and Rest Pulmonary Transit Time estimation using myocardial perfusion CMR Figure 2. Event-free survival curves for major adverse cardiovascular events (Heart failure hospitalization, myocardial infarction, stroke and ventricular tachycardia/ICD treatment) according to mean rest PTT (8.05seconds) and mean stress PTT (6.7seconds). Log-rank for both p &lt; 0.05


1977 ◽  
Vol 232 (4) ◽  
pp. E382-E387 ◽  
Author(s):  
L. Z. Bito ◽  
R. A. Baroody ◽  
Mary E. Reitz

Inhibitors of prostaglandin (PG) transport (probenecid, indomethacin, or bromcresol green) were found to eliminate the difference between the pulmonary transit time of 3H and 14C when [3H]PGF2alpha and E114C]sucrose were injected as a single intra-arterial bolus into the isolated perfused rat lung. Similar results were obtained with PGE1. The transit time of [3H]PGA1 was not significantly different from that of [14C]sucrose even in the absence of an inhibitor. These inhibitors increased the amount of [3H]PGF2alpha or [3H]PGE1 and decreased the amount of [3H]PG metabolites found in the venous effluent: these agents also inhibited the pulmonary metabolism of continously infused, nonradioactive PGF2alpha. One of the three inhibitors, bromcresol green, was shown not to be an effective inhibitor of PG metabolism in cell-free preparations of rat lung homogenates. These results indicated that under normal conditions, PG's are rapidly transported into intracellular compartment(s) where they are metabolized. Inhibition of this transport process prevents rapid access of PG's to the cytoplasmic enzymes and therefore inhibits pulmonary PG metabolism. This implies that inhibitors of PG transport, including anti-inflammatory organic acids, and some PG antagonists, metabolites, and analogues, can be expected to inhibit the pulmonary metabolism of PG's and thus could potentiate the systemic effects endogenous or exogenous PG's.


2017 ◽  
Vol 122 (3) ◽  
pp. 460-469 ◽  
Author(s):  
Melissa M. Bouwsema ◽  
Vincent Tedjasaputra ◽  
Michael K. Stickland

Previous work suggests that women may exhibit a greater respiratory limitation in exercise compared with height-matched men. Diffusion capacity (DlCO) increases with incremental exercise, and the smaller lungs of women may limit membrane diffusing capacity (Dm) and pulmonary capillary blood volume (Vc) in response to the increased oxygen demand. We hypothesized that women would have lower DlCO, DlCO relative to cardiac output (DlCO/Q̇), Dm, Vc, and pulmonary transit time, secondary to lower Vc at peak exercise. Sixteen women (112 ± 12% predicted relative V̇o2peak) and sixteen men (118 ± 22% predicted relative V̇o2peak) were matched for height and weight. Hemoglobin-corrected diffusing capacity (DlCO), Vc, and Dm were determined via the multiple-[Formula: see text] DlCO technique at rest and during incremental exercise up to 90% of V̇o2peak. Both groups increased DlCO, Vc, and Dm with exercise intensity, but women had 20% lower DlCO ( P < 0.001), 18% lower Vc ( P = 0.002), and 22% lower Dm ( P < 0.001) compared with men across all workloads, and neither group exhibited a plateau in Vc. When expressed relative to alveolar volume (Va), the between-sex difference was eliminated. The drop in DlCO/Q̇ was proportionally less in women than men, and mean pulmonary transit time did not drop below 0.3 s in either group. Women demonstrate consistently lower DlCO, Vc, and Dm compared with height-matched men during exercise; however, these differences disappear with correction for lung size. These results suggest that after differences in lung volume are accounted for there is no intrinsic sex difference in the DlCO, Vc, or Dm response to exercise. NEW & NOTEWORTHY Women demonstrate lower diffusing capacity-to-cardiac output ratio (DlCO/Q̇), pulmonary capillary blood volume (Vc), and membrane diffusing capacity (Dm) compared with height-matched men during exercise. However, these differences disappear after correction for lung size. The drop in DlCO/Q̇ was proportionally less in women, and pulmonary transit time did not drop below 0.3 s in either group. After differences in lung volume are accounted for, there is no intrinsic sex difference in DlCO, Vc, or Dm response to exercise.


Author(s):  
Charlotte Summers ◽  
Jessica White ◽  
Nanak Singh ◽  
Iain Mackenzie ◽  
Andrew Johnston ◽  
...  

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