scholarly journals Usefulness of right ventricular isovolumic relaxation time in predicting systolic pulmonary artery pressure

2008 ◽  
Vol 9 (4) ◽  
pp. 547-554 ◽  
Author(s):  
N. Brechot ◽  
L. Gambotti ◽  
S. Lafitte ◽  
R. Roudaut
Keyword(s):  
Relaxation Time ◽  
Pulmonary Artery ◽  
Right Ventricular ◽  
Pulmonary Artery Pressure ◽  
Systolic Pulmonary Artery Pressure ◽  
Isovolumic Relaxation Time ◽  
Artery Pressure ◽  
Isovolumic Relaxation

Abstract 19195: Pulmonary Artery Pulsatility Index Predicts Right Ventricular Failure Following LVAD Surgery

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Kevin J Morine ◽  
Michael S Kiernan ◽  
Duc T Pham ◽  
David Denofrio ◽  
Navin K Kapur
Keyword(s):  
Pulmonary Artery ◽  
Right Ventricular ◽  
Pulmonary Artery Pressure ◽  
Pulsatility Index ◽  
Right Ventricular Failure ◽  
Right Atrial ◽  
Systolic Pulmonary Artery Pressure ◽  
Stroke Work ◽  
Ventricular Failure ◽  
Artery Pressure

Introduction: Identification of pre-operative right ventricular dysfunction may improve patient selection for isolated LVAD surgery. The pulmonary artery pulsatility index (PaPi) is a recently described hemodynamic metric. We evaluated baseline PaPi as a predictor of post-operative right ventricular failure (RVF) following LVAD surgery. Methods: We conducted a retrospective review of 132 consecutive LVAD implantations at our hospital. Demographic, clinical, hemodynamic and echocardiographic data were evaluated for their association with the development of RVF. RVF was defined as need for RVAD or inotrope dependence for greater than 14 days. PaPi was calculated as [(systolic pulmonary artery pressure-diastolic pulmonary artery pressure)/right atrial (RA) pressure]. Univariate analysis was performed to identify baseline predictors of RVF. Multivariate logistic regression was used to adjust for baseline RA pressure. Results: RVF occurred in 31 of 132 patients (23%); all cases were due to prolonged inotropes. PaPi was lower among patients with RVF compared to those without (no RVF: mean 2.75± SD1.17 vs RVF: 1.38±0.46, P<0.0001). RA pressure, RA to pulmonary capillary wedge pressure ratio (RA/PCWP) and RV stroke work index (RVSWI) were also associated with RVF. Previously identified markers of RV function including mean pulmonary artery pressure and qualitative RV dysfunction by 2D echo were not associated with RVF. Comparison of the area under the curve from receiver operator characteristic curve analysis demonstrated that a PaPi<1.85 was most predictive of RVF (Figure). PaPi remained an independent predictor of RVF after adjusting for RA pressure in a multivariate model. Conclusions: PaPi is a routinely available and easily calculated hemodynamic variable associated with RVF following LVAD surgery superior to established markers. Further evaluation of PaPi as part of a risk prediction model to guide clinical decision making may be warranted.

Abstract 16599: Impaired Right Ventricular Contractile Reserve During Exercise in Endurance Athletes With Right Ventricular Arrhythmias

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Guido Claessen ◽  
Andre La Gerche ◽  
Jens-Uwe Voigt ◽  
Steven Dymarkowski ◽  
Luc Van Hees ◽  
...  
Keyword(s):  
Pulmonary Artery ◽  
Right Ventricular ◽  
Pulmonary Artery Pressure ◽  
Ventricular Arrhythmias ◽  
Systolic Pressure ◽  
Endurance Athletes ◽  
Contractile Reserve ◽  
Systolic Pulmonary Artery Pressure ◽  
Exercise Echocardiography ◽  
Artery Pressure

Introduction: Ventricular arrhythmias in endurance athletes (EAs) frequently originate from a mildly dysfunctional right ventricle (RV). We evaluated whether RV dysfunction in EAs with ventricular arrhythmias of RV origin (EA-VAs) becomes more apparent during exercise than at rest. Methods: Ten healthy EAs, 7 healthy non-athletes (NAs) and 17 EA-VAs (8 with ICD) first underwent cardiopulmonary exercise testing to determine maximal power (Pmax). Then, exercise echocardiography was performed at 25%, 50% and 66% of Pmax to measure the RV end-systolic pressure-area ratio (ESPAR), a surrogate of RV contractility, which was calculated as systolic pulmonary artery pressure/RV end-systolic area. Finally, all subjects without ICD underwent cardiac MRI during supine bicycle exercise at similar workloads with simultaneous invasive pulmonary artery pressure measurement to determine the RV end-systolic pressure-volume ratio (SP/ESV). Results: At rest, RV ESPAR was similar in EA-VAs relative to NAs (P=0.1), although slightly lower than in NAs (P=0.02). During exercise, EA-VAs had an impaired increase in RV ESPAR compared to both EAs and NAs (interaction P<0.0001; Figure 1A). Also the slopes of RV ESPAR to absolute workload (in Watts) were lower in EA-VAs than in EAs and NAs (P<0.0001) and correlated highly with the slopes of RV SP/ESV to workload obtained by MRI and invasive pressure measures (R=0.75; P<0.0001). Figure 1B shows that resting and peak exercise RV ESPAR cutoffs of 1.4 and 3.9 mmHg/cm 2 had a sensitivity of 77% and 79% and specificity of 80% and 100%, respectively, to identify EA-VAs. Conclusion: EA-VAs have impaired RV contractility which is evident during exercise but hardly at rest. This strengthens the association between RV arrhythmias and functional impairment. Our data suggest that exercise echocardiography is sufficiently accurate to determine RV contractile reserve in a non-invasive manner and may assist in risk stratification of RV remodeling in EAs.

P1479Deterioration in right ventricular strain precedes occurrence of pulmonary hypertension in patients with preclinical diastolic disfunction

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
A L Chilingaryan ◽  
L G Tunyan ◽  
K G Adamyan
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Artery ◽  
Right Ventricular ◽  
Pulmonary Artery Pressure ◽  
Longitudinal Strain ◽  
Independent Predictor ◽  
Volume Index ◽  
Systolic Pulmonary Artery Pressure ◽  
Free Wall ◽  
Artery Pressure

Abstract Preclinical diastolic disfunction (PDD) often progresses to heart failure and distinct clinical predictors for this transformation are yet to be defined. Since deterioration of longitudinal strain (LS) can occur before the changes of more conventional parameters, we assumed that right ventricular free wall longitudinal strain (RVLS) might start deteriorating before the pulmonary hypertension can be established. Methods We followed up 243 patients (143 female) 67±9 years with PDD for 3 years. All patients had an impaired relaxation or pseudo normal transmitral patterns and E/e' 8–13 at rest, normal NT-proBNP values, and systolic pulmonary artery pressure (sPAP) ≤30 mm Hg. PDD was diagnosed by stress echocardiography (SE) if E/e' ≥13, transmittal E wave deceleration time reduction >50ms, systolic pulmonary artery pressure (sPAP) <30 mmHg, and patients remained asymptomatic during SE. RVLS as average of RV free wall 3 segments values, left atrial peak reservoir LS (LALS) as average of two LA basal segments in four chamber view and left ventricular peak systolic global LS (LVGLS) were measured by speckle tracking (ST). ST and SE was performed with 6 months intervals. 35 healthy subject served as controls. Results Patients with PDD had higher RVLS, LVGLS, and lower LALS compared with controls (RVLS –23.2±4.2% vs –27.3±5.1%, p<0.001; LVGLS –17.8±5.2% vs –21.9±2.8%, p<0.001; LALS 39.7±3.7% vs 44.1±4.9%, p<0.002). 76 (31.3%) patients developed sPAP increase >30 mmHg at rest or SE during follow up of which 34 (44.7%) had dyspnea. Patients with increased sPAP had higher RVLS and lower LALS values at baseline compared with the rest of PDD patients without significant differences in other parameters (RVLS –17.9±2.8% vs –24.8±3.6%, p<0.002; LALS 37.7±2.3% vs 41.5±3.6%, p<0.003; LVGLS –17.4±4.8% vs –18.2±5.1%, p>0.05). Both LALS and RVLS correlated with LA end diastolic volume index (LALS r=0.51, p<0.01; RVLS r=0.54, p<0.01). Additionally RVLS was an independent predictor of sPAP rise (OR=2.7; 95% CI=2.43–6.92; p<0.01). Conclusion RVLS is an independent predictor of sPAP increase in patients with PDD.

scholarly journals P834 Pulmonary arterial hypertension in patients with direct-acting antiviral medications for hepatitis C virus infection - a prospective observational cohort study

2020 ◽  
Vol 21 (Supplement_1) ◽  
Author(s):  
D Schild ◽  
G J Hellige ◽  
R J Piso ◽  
N Arenja
Keyword(s):  
Hepatitis C ◽  
Pulmonary Artery ◽  
Right Ventricular ◽  
Pulmonary Artery Pressure ◽  
Left Ventricular ◽  
Hcv Infection ◽  
P Value ◽  
Systolic Pulmonary Artery Pressure ◽  
Artery Pressure ◽  
Direct Acting Antiviral

Abstract Funding Acknowledgements Kantonsspital Olten, Switzerland Background In patients with chronic hepatitis C virus (HCV) infection, a higher risk for pulmonary artery hypertension (PAH) has been described after interferon (IFN) therapy. With the development of direct-acting antiviral (DAA) agents, vast improvements have been made in tolerance and less complications of HCV treatment. However, except of a few case reports, to date no clinical study about the evidence of PAH in patients with DAA medication for HCV infection has been published. We hypothesized that in patients, who receive DAA medication for HCV-infection, the systolic pulmonary artery pressure (sPAP) will not change significantly during and after competition of the therapy and there may be a lower post treatment risk for PAH within the population. Methods We prospectively enrolled patients who underwent treatment with DAA for chronic HCV infection. The patients received a transthoracic echocardiography (TTE) for the measurement of the pulmonary artery pressure before, during (8 weeks after starting the medication) and 8 weeks after completion of the HCV medication for evaluation of sPAP (figure 1). The whole treatment period took 8-12 weeks. Results Between June 2016 and October 2018, 33 patients completed the study protocol. In mean, the patient’s age was 50.1 ± 1.4 years and 30% of the population were female. Three patients (9 %) were HCV and human immunodeficiency virus (HIV) coinfected. The patients received different treatment regimens, according to hepatitis C genotype and co-medication. The left ventricular systolic and diastolic function were normal in all patients before treatment was started (left ventricular ejection fraction 60.7% [59.7 – 61.7%], E/A 1.18 [1.0 – 1.37]). The following table depicts the right ventricular parameter before the DAA therapy was started, 8 weeks after therapy start, and 8 weeks after therapy was completed. The analysis showed no significant difference between the sPAP in all three groups (25.9 ± 1.2 mmHg vs. 26.0 ± 1.3 mmHg vs.26.9 ± 1.1 mmHg, p-value 0.37, see figure). Conclusion DAA-therapy in chronic HCV infected patients is not associated with PAH in a follow-up of 2 months after the treatment was completed. Echocardiography Data Echocardiography data Before DAA medication was started 8 weeks after DAA-therapy 8 weeks after completion of DAA-therapy p-Value Right ventricular fractional area change (FAC), % 49.1 ± 1.4 51.7 ± 1.0 51.8 ± 1.1 0.09 Tricuspid Annular Plane Systolic Excursion (TAPSE), mm 25.2 ± 1.1 25.8 ± 0.7 24.3 ± 0.5 0.4 Right ventricular/right atrial gradient, mmHg 19.9 ± 1.0 20.5 ± 0.9 21.0 ± 0.8 0.24 Systolic pulmonary artery pressure (sPAP), mmHg 25.9 ± 1.2 26.0 ± 1.3 26.9 ± 1.1 0.37 Abstract P834 Figure. Multiple variable graph of sPAP

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