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- W2790147213 abstract "In recent years, an increasing body of evidence has emerged postulating that rightventricular (RV) - pulmonary artery (PA) ventriculoarterial coupling may offer insightinto the transition from RV adaptation to RV maladaptation in different cardiopulmonarydisorders and heart failure. RV-PA ventriculoarterial coupling is a matching betweenRV contractility (Ees – End-Systolic Elastance) and afterload (Ea – Effective ArterialElastance). While ventriculoarterial coupling has been extensively described in the LVand used to determine optimal conditions for the efficient transfer to blood from theventricle into the aorta, it remains unclear whether this relationship can be translated tothe thinner walled RV that pumps at lower pressures against a more compliantpulmonary vascular system. Therefore, the pressure-volume (PV)-loop studies in thisthesis were undertaken to assess whether ventriculoarterial uncoupling due topressure overload or sub-optimal contractility contributed to further RV diastolicdysfunction.An in-vivo porcine model of RV-PA ventriculoarterial coupling was developed to defineoptimal conditions. This animal model was used to provide insights into two clinicalpatient groups that have RV dysfunction due to: i) long-term RV pressure overload inpatients with a clinical diagnosis of chronic thromboembolic disease (CTED) /pulmonary hypertension (CTEPH); and ii) aortic valve stenosis transmitted byventricular interdependence and septal wall reconfiguration in patients treated withtranscatheter aortic valve implantation (TAVI).The animal model determined an ventriculoarterial coupling ratio at maximal strokework (Ees/Eamax sw = 0.68±0.23) threshold, below which cardiac output and RV strokework fell. In the first clinical study this threshold was used to reclassify 25% of a cohortof patients with CTED or CTEPH. Two patients with CTED were identified with anEesEa below 0.68 suggesting occult RV dysfunction whilst three patients with CTEPHdemonstrated Ees/Ea≥0.68 suggesting residual RV energetic reserve. In the secondclinical study ventricular interdependence phenomena caused septal reconfigurationand increased RV volumes after valve deployment, due to the reduction in LVafterload. However, the rapid pacing (RP) protocol used to stabilise the aortic valveduring deployment also caused RP-induced ischemia and stunning. This resulted in thereduction of Ees and led to Ees/Ea uncoupling and further diastolic dysfunction.This work has demonstrated that: Low Ees/Ea aligns with features of RV maladaptationin CTED. Characterization of Ees/Ea in CTED may allow for better identification ofoccult RV dysfunction in patients with otherwise normal pulmonary hemodynamics; anda reduction in Ees following TAVI correlates with increased RV diastolic dysfunction,due to RP-induced ischemia and stunning." @default.
- W2790147213 created "2018-03-29" @default.
- W2790147213 creator A5054731445 @default.
- W2790147213 date "2017-01-01" @default.
- W2790147213 modified "2023-09-27" @default.
- W2790147213 title "Optimising RV-PA ventriculoarterial-coupling to improve RV diastolic function in patients with cardiopulmonary disorders" @default.
- W2790147213 hasPublicationYear "2017" @default.
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