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“So I have Pulmonary Hypertension after all?”: Characterization and outcomes of patients with the new haemodynamic definition of pulmonary hypertension
Session:
Posters - F. Valvular, Myocardial, Pericardial, Pulmonary, Congenital Heart Disease
Speaker:
João Grade Santos
Congress:
CPC 2021
Topic:
F. Valvular, Myocardial, Pericardial, Pulmonary, Congenital Heart Disease
Theme:
21. Pulmonary Circulation, Pulmonary Embolism, Right Heart Failure
Subtheme:
21.2 Pulmonary Circulation, Pulmonary Embolism, Right Heart Failure – Epidemiology, Prognosis, Outcome
Session Type:
Posters
FP Number:
---
Authors:
João Grade Santos; Ana Rita Pereira; Mariana Martinho; Barbara Ferreira; Alexandra Briosa; Ana Marques; Sofia Alegria; Filipa Ferreira; Rita Calé; Sofia Almeida; Hélder Pereira
Abstract
<p><span style="font-size:11pt"><span style="background-color:white"><span style="font-family:Calibri,sans-serif"><strong><span style="background-color:white"><span style="color:#222222">Introduction:</span></span></strong> <span style="background-color:white"><span style="color:black">Since the 1st World Health Organization Symposium on Pulmonary Hypertension, Pulmonary hypertension (PH) was defined by a mean pulmonary arterial pressure (mPAP) =25 mmHg. During the 6th World Symposium on Pulmonary Hypertension the haemodynamic definition of PH was revised, lowering the threshold from =25 mmHg to >20 mmHg.</span></span></span></span></span></p> <p><span style="font-size:11pt"><span style="background-color:white"><span style="font-family:Calibri,sans-serif"><strong><span style="background-color:white"><span style="color:#222222">Purpose:</span></span></strong><span style="background-color:white"><span style="color:#222222"> Our aim was to assess the characteristics and outcomes of the patients who had a new haemodynamic diagnosis of PH</span></span><span style="background-color:white"><span style="color:black">.</span></span></span></span></span></p> <p><span style="font-size:11pt"><span style="background-color:white"><span style="font-family:Calibri,sans-serif"><strong><span style="background-color:white"><span style="color:#222222">Methods</span></span></strong><span style="background-color:white"><span style="color:#222222">: We performed a 9 year retrospective analysis of all patients undergoing RHC for suspicion of pulmonary hypertension and had a </span></span><span style="background-color:white"><span style="color:black">mPAP >20 mmHg and < 25mmhg with increased pulmonary vascular resistance (defined by =3 Wood units), without vasodilator therapy or additional therapy, in a </span></span><span style="background-color:white"><span style="color:#222222">single expert centre. Medical records were analysed for demographic and procedural data.</span></span></span></span></span></p> <p><span style="font-size:11pt"><span style="background-color:white"><span style="font-family:Calibri,sans-serif"><strong><span style="background-color:white"><span style="color:#222222">Results</span></span></strong><span style="background-color:white"><span style="color:#222222">: Of the 321 patients assessed and submitted to RHC, 24 patients fulfilled all inclusion criteria and were analysed. The mean age was 60 </span></span><span style="color:black">± 13 at time of RHC with a female preponderance (74%). All patients where referred due to echocardiographic suspicion of PH. 34,8% were asymptomatic; 43,5% were in New York Heart Association (NYHA) class II; 21,7% were in NYHA class III.</span></span></span></span></p> <p><span style="font-size:11pt"><span style="background-color:white"><span style="font-family:Calibri,sans-serif"><span style="color:black">As for the clinical classification, 26% were group I; 8,7% group II; 17,4% group III; 30,4% group IV and 17,4% multifactorial; </span></span></span></span></p> <p><span style="font-size:11pt"><span style="background-color:white"><span style="font-family:Calibri,sans-serif"><span style="color:black">With an average follow up of 3,8 ± 2,4 years only 3 patients (13%) had right ventricle disfunction, 1 episode (4%) of admission due to cardiovascular cause and no documented cardiovascular deaths (with 5 patients, 21%, with a non-cardiovascular/undisclosed death).</span></span></span></span></p> <p><span style="font-size:11pt"><span style="background-color:white"><span style="font-family:Calibri,sans-serif"><span style="color:black">Only 4 (17%) patients had a repetition of RHC, 1 was performed after thromboendoarterectomy and documented normalization of haemodynamic parameters, 1 had no PH and 2 progressed to the classic definition of PH, 1 patient in group 2 latter submitted to heart transplant and 1 patient in group 3 who was not eligible for vasodilator therapy, without events in the follow up.</span></span></span></span></p> <p><span style="font-size:11pt"><span style="background-color:white"><span style="font-family:Calibri,sans-serif"><strong><span style="background-color:white"><span style="color:#222222">Conclusions</span></span></strong><span style="background-color:white"><span style="color:#222222">: The patients who constitute the new haemodynamic definition of PH, with</span></span><span style="background-color:white"><span style="color:black"> mPAP >20 mmHg and < 25mmhg, </span></span><span style="background-color:white"><span style="color:#222222">may constitute a low risk sub-group of patients, only requiring follow up in a dedicated center without prompt initiation of therapy.</span></span></span></span></span></p>
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