90 Table 1 Demographics, clinical characteristics and outcomes of patients with primary PH compared with secondary PH Abstract 90 Figure 1 Kaplan-Meier Survival Curves of Primary PH (Blue) and Secondary PH (Green) over 15-Years Abstracts Heart 2019;105(Suppl 6):A1–A193 A75 on S etem er 6, 2023 by gest. P rocted by coright. httpeart.bm jcom / H ert: frst pulished as 10.113artjnl-2019-B C S 88 on 26 M ay 219. D ow nladed fom OPCS-4 coding to identify patients with different diagnoses. In this study, primary PH was identified with an ICD-10 code of I270 (specific) and secondary PH included all other codes relating to PH. Results Of our PH cohort, 1688 patients had primary PH (58.3%) and 1207 patients had secondary PH (41.7%). Table 1 shows the differences in selected clinical characteristics between both groups as well as crude mortality rates, readmissions and length of hospital stay. Kaplan-Meier curves for long-term survival are shown in figure 1. Cox-regression was performed for survival and found lower adjusted mortality with secondary PH compared to primary PH (adjusted HR 0.87, 95% CI [0.78–0.98], p=0.018). Conclusion Date from the UK-ACALM ‘big data’ registry confirms poor long-term prognosis with both primary and secondary PH over a 15-year follow-up. Surprisingly, one in three patients will have died by 5-years. Improved survival was observed in secondary PH compared to primary PH possibly reflecting the treatment of reversible causes of secondary PH. Further studies are required to understand survival differences in this complex population, where therapies continue to evolve. Conflict of Interest Nil 91 THE RELATION BETWEEN THYROID DYSFUNCTION AND MORTALITY IN PATIENTS WITH CHRONIC HEART FAILURE Nathan Samuel*, Joseph Cuthbert, Oliver Brown, Syed Kazmi, John GF Cleland, Alan Rigby, Andrew Clark. Hull York Medical School; Department of Academic Cardiology, Hull York Medical School; Robertson Centre for Biostatistics 10.1136/heartjnl-2019-BCS.89 Introduction Thyroid dysfunction is common in patients with chronic heart failure (CHF), but there is conflicting Abstract 91 Table 1 Demographics, clinical characteristics and pharmacological treatment of patients with heart failure according to thyroid status91 Table 1 Demographics, clinical characteristics and pharmacological treatment of patients with heart failure according to thyroid status *Included 12 patients with overt hypothyroidism (TSH>4.7mU/l, fT4<7.8pmol/l), of whom 2 patients were on thyroxine replacement. †Included 43 patients with overt hyperthyroidism (TSH<0.35, fT4>21.0pmol/l), of whom 5 patients were on thyroxine replacement. M, missing; TSH, thyroid stimulating hormone; fT4, serum free thyroxine level; N, number of patients; NT-proBNP, N-terminal prohormone of brain natriuretic peptide; BMI, body mass index; AF, Atrial Fibrillation; SBP, systolic blood pressure; DBP, diastolic blood pressure; NYHA, New York Heart Association classification; LVSD, left ventricular systolic dysfunction; IHD, ischaemic heart disease; DM, diabetes mellitus; COPD, chronic obstructive pulmonary disease; ACEi, angiotensin converting enzyme inhibitor; ARB, angiotensin II receptor blocker; β-Blocker, beta blocker; MRA, mineralocorticoid receptor antagonist; Hb, haemoglobin; N/A, not applicable. Abstracts A76 Heart 2019;105(Suppl 6):A1–A193 on S etem er 6, 2023 by gest. P rocted by coright. httpeart.bm jcom / H ert: frst pulished as 10.113artjnl-2019-B C S 88 on 26 M ay 219. D ow nladed fom

BACKGROUND: Primary graft dysfunction (PGD) represents ischemia-reperfusion injury in the lung allograft, and elevated left ventricular end-diastolic pressure (LVEDP) may contribute to capillary leak. We tested whether pre-transplant LVEDP or pulmonary capillary wedge pressure (mPCWP) are related to PGD risk. We hypothesized that elevated LVEDP and mPCWP would increase PGD risk. METHODS: We reviewed adult double lung transplant recipients at the University of Alberta Hospital from 2004 to 2016 with pre-transplant LVEDP measurements. The primary outcome was Grade 3 PGD at 48 to 72 hours post-transplant. We used regression analysis to assess the association between LVEDP and mPCWP with Grade 3 PGD risk, as well as agreement between these measurements. RESULTS: Three hundred thirty double lung transplant recipients were included in the study, and 63 (19%) developed Grade 3 PGD at 48 or 72 hours. Mean LVEDP was 16 +/- 7 mm Hg in the Grade 3 PGD group and 12 +/- 5 mm Hg in the non-PGD group (p < 0.0001). LVEDP >15 mm Hg was associated with an adjusted odds ratio (OR) of 3.83 (95% confidence interval [CI] 1.90 to 7.73, p < 0.0001), whereas mPCWP >15 mm Hg showed similar findings (adjusted OR 4.25 [1.83 to 9.86], p = 0.0008). Correlation and agreement between LVEDP and mPCWP were fair. CONCLUSIONS: Elevated pre-transplant LVEDP increases the risk of severe PGD after lung transplant, as does elevated mPCWP. These measurements appear to be complementary as markers of prospective PGD risk. (C) 2019 International Society for Heart and Lung Transplantation. All rights reserved.

Background Both primary and secondary pulmonary hypertension (PH) are independently associated with morbidity and mortality. Compared to primary PH, the underlying pathology in secondary PH remains diverse as seen in the WHO classification. As such, variation in long-term outcomes remains unclear. We examined the differences in clinical characteristics and long-term mortality between primary and secondary PH using the United Kingdom (UK) Algorithm for Co-morbidity, Associations, Length of stay and Mortality (ACALM) Registry. Methods Out of 1,816,230 patients admitted to several hospitals in Northern England from January 2000 to July 2014 (15-year follow-up), 2895 patients with PH were identified using the UK ACALM study protocol. ACALM utilizes a ‘big data’ approach to amalgamate multiple datasets and ICD-10/OPCS-4 coding to identify patients with different diagnoses. In this study, primary PH was identified with an ICD-10 code of I270 (specific) and secondary PH included all other codes relating to PH. Results Of our PH cohort, 1688 patients had primary PH (58.3%) and 1207 patients had secondary PH (41.7%). Table 1 shows the differences in selected clinical characteristics between both groups as well as crude mortality rates, readmissions and length of hospital stay. Kaplan-Meier curves for long-term survival are shown in figure 1. Cox-regression was performed for survival and found lower adjusted mortality with secondary PH compared to primary PH (adjusted HR 0.87, 95% CI [0.78–0.98], p=0.018). Conclusion Date from the UK-ACALM ‘big data’ registry confirms poor long-term prognosis with both primary and secondary PH over a 15-year follow-up. Surprisingly, one in three patients will have died by 5-years. Improved survival was observed in secondary PH compared to primary PH possibly reflecting the treatment of reversible causes of secondary PH. Further studies are required to understand survival differences in this complex population, where therapies continue to evolve. Conflict of Interest Nil

We hypothesized that an automated speech- recognition-inspired classification algorithm could differentiate between the heart sounds in subjects with and without pulmonary hypertension (PH) and outperform physicians. Heart sounds, electrocardiograms, and mean pulmonary artery pressures (mPAp) were recorded simultaneously. Heart sound recordings were digitized to train and test speech-recognition-inspired classification algorithms. We used mel-frequency cepstral coefficients to extract features from the heart sounds. Gaussian-mixture models classified the features as PH (mPAp ≥ 25 mmHg) or normal (mPAp < 25 mmHg). Physicians blinded to patient data listened to the same heart sound recordings and attempted a diagnosis. We studied 164 subjects: 86 with mPAp ≥ 25 mmHg (mPAp 41 ± 12 mmHg) and 78 with mPAp < 25 mmHg (mPAp 17 ± 5 mmHg) (p < 0.005). The correct diagnostic rate of the automated speech-recognition-inspired algorithm was 74% compared to 56% by physicians (p = 0.005). The false positive rate for the algorithm was 34% versus 50% (p = 0.04) for clinicians. The false negative rate for the algorithm was 23% and 68% (p = 0.0002) for physicians. We developed an automated speech-recognition-inspired classification algorithm for the acoustic diagnosis of PH that outperforms physicians that could be used to screen for PH and encourage earlier specialist referral.

Renal dysfunction is common in heart failure. However, the understanding of renal hemodynamics in combined heart kidney failure is limited and assessed by surrogate measures. Renal hemodynamics studied in experimental animals (rats, mice, dogs) has revealed that autoregulation of renal blood flow (RBF) is established by myogenic response (MR) and tubuloglomerular feedback (TGF). However, this data has not been available in humans. In this pilot study, we measured flow velocity and renal artery diameter to assess RBF in humans allowing a more direct analysis of MR and TGF characteristics. We assessed RBF at 50 Hz using a Doppler-based flow velocity measurement by introducing a FloWire (Volcano) into the renal artery of 8 human subjects who were undergoing cardiac catheterization. RBF was derived from Doppler velocities over 5-10 minutes and renal artery diameter. Renal artery pressure (RAP) was measured in the abdominal aorta at the root of the renal artery. Seven subjects displayed variations in RAP allowing assessment of MR and TGF by time series analysis. RBF remained stable despite variations in RAP in some (but not all) of the patients, consistent with autoregulatory behaviour (see example). MR and TGF signatures could be identified in the Gain, Coherence and Phase plots. The use of this newly developed method to assess autoregulation efficiency established by MR revealed good efficiency among half of the individuals. This approach makes it possible to investigate RBF dynamics, MR, TGF and efficiency of autoregulation in humans. Further studies are being undertaken to refine the analytical methodology for human samples and to compare patients with and without heart failure with respect to RBF dynamics. In the future, this methodology may provide a more physiologic parameter to assess diagnosis, prognosis and therapeutics in patients with heart or circulatory failure. Grant support from Univ of Alberta Hospital Foundation.