Borlaug, BA

Abstract Background and Aims Decrease in pulmonary vascular resistance (PVR) during exercise confers favourable prognosis in biventricular physiology, but its role in Fontan circulation remains unknown. This study aimed to evaluate the prognostic value of PVR index (PVRI) response to exercise in adults post-Fontan palliation. Methods Retrospective cohort of 88 adults (age ≥18 years) post-Fontan undergoing exercise (supine cycling) cardiac catheterization. Patients were categorized into absence (n = 23) or presence (n = 65) of exercise-induced reduction in PVRI. The clinical endpoint was a composite of death or transplantation. Results Age at catheterization was 32.2 ± 8.8 years, and 45.5% were female. Resting and exercise PVRI were 1.9 ± 0.9 and 1.2 (interquartile range [IQR] 0.8–2.1) WU·m2, respectively. Clinical, biochemical and echocardiographic parameters were not associated with PVRI response to exercise. During a follow-up of 2.2 ± 1.4 (IQR 1.2–2.6) years, resting PVRI was not associated with the clinical endpoint (hazard ratio [HR] 0.95 per WU·m2, 95% confidence interval [CI] 0.52–1.74; P = 0.86), whereas exercise PVRI was (HR 2.15 per WU·m2, 95% CI 1.24–3.73; P = .007). Exercise PVRI remained predictive of outcomes after adjusting for exercise pulmonary artery wedge pressure (HR 2.08 per WU·m2, 95% CI 1.19–3.62; P = .01) or clinical risk factors individually. Two-year event-free survival was lower in the no PVRI reduction than in the reduction group (67% vs 95%; P < .001). Conclusions In adults post-Fontan, PVRI response to exercise is a robust predictor of clinical outcomes and offers additive prognostic information beyond resting invasive haemodynamic data and clinical risk factors, underscoring the importance of invasive exercise testing in this population.

Abstract Background Systemic arterial compliance and venous capacitance are typically impaired in patients with heart failure with preserved ejection fraction (HFpEF), contributing to hemodynamic congestion with stress. Sodium-glucose cotransporter-2 inhibitors (SGLT2i) reduce hemodynamic congestion and improve clinical outcomes in patients with HFpEF, but the mechanisms remain unclear. Purpose This study tested the hypothesis that SGLT2i dapagliflozin would improve systemic arterial compliance and venous capacitance during exercise in patients with HFpEF. Methods In this secondary analysis from the RCT trial, patients with HFpEF underwent invasive hemodynamic exercise testing at baseline and following treatment for 24 weeks with dapagliflozin or placebo. Patients were required to display pulmonary capillary wedge pressure (PCWP) ≥25 mmHg during exercise at the time of baseline evaluation. Radial artery pressure (BP) was measured continuously using a fluid-filled catheter with transformation to aortic pressure, central hemodynamics were measured using high-fidelity micromanometers, and stressed blood volume was estimated (eSBV) from hemodynamic indices fit to a comprehensive cardiovascular model. Results A total of 37 patients completed the study and were included in this analysis (21 dapagliflozin and 16 placebo). Patients were predominantly women (24/37, 65%) and older (mean age 67 years). There was no statistically significant effect of dapagliflozin on resting BP, but dapagliflozin reduced systolic BP during peak exercise (estimated treatment difference [ETD], -18.8 mmHg, 95% CI: -33.9 to -3.7, P=0.016) (Figure 1A). Dapagliflozin improved exertional total arterial compliance (TAC) index (ETD, 0.06 mL/mmHg/m2, 95% CI: 0.003 to 0.11, P=0.039) (Figure 1B) and aortic root characteristic impedance (ETD, -2.6 mmHg/ml*sec, 95% CI: -5.1 to -0.03, P=0.048) during peak exercise, with no significant effect on systemic vascular resistance. Dapagliflozin reduced eSBV at rest and during peak exercise (ETD, -292 mmHg, 95% CI: -530 to -53, P=0.018) (Figure 1C), and improved venous capacitance evidenced by a decline in ratio of eSBV to total blood volume (ETD, -7.3%, 95% CI -13.3 to -1.3, P=0.020). Each of these effects of dapagliflozin during peak exercise were also observed during matched 20W exercise intensity. Improvements in TAC index and eSBV were correlated with decreases in body weight, and reduction in systolic BP with treatment was correlated with the change in eSBV during exercise (r=0.40, P=0.019) (Figure 2A). Decreases in BP were correlated with reduction in PCWP during exercise (r=0.56, P<0.001) (Figure 2B). Conclusion In patients with HFpEF, treatment with dapagliflozin improved systemic arterial compliance and venous capacitance during exercise, while reducing aortic characteristic impedance, suggesting a reduction in arterial wall stiffness. These vascular effects may partially explain the clinical benefits with SGLT2i in HFpEF.

Abstract Funding Acknowledgements Type of funding sources: None. Background. Recent evidence shows epicardial adipose tissue (EAT) acts as a paracrine organ and may directly alter myocardial function by exerting mechanical compression. Purpose. We evaluated EAT thickness through transthoracic echocardiography and investigated its relationship with cardiopulmonary fitness and cardiovascular haemodynamics at rest and during exercise in a population of heart failure (HF) patients with reduced (HFrEF) and preserved (HFpEF) ejection fraction. Methods. We prospectively enrolled 393 consecutive HF outpatients (205 HFrEF, 188 HFpEF) who had been referred to our hospital due to dyspnoea and/or effort intolerance, together with 44 healthy controls. We performed a resting state-of-the-art echocardiographic evaluation, followed by combined cardiopulmonary-echocardiography exercise stress. Results. EAT thickness was higher in HFpEF (median 8 mm, interquartile range [IQR] 4–12 mm) and progressively reduced in controls (median 5 mm, IQR 3–7 mm; p < 0.0001) and HFrEF (median 3 mm, IQR 2–6 mm). In HFpEF, EAT thickness was inversely correlated with peak oxygen consumption (VO2) and peripheral oxygen extraction (AVO2diff), while a direct association was observed for the same parameters in HFrEF (Figure 1). Furthermore, EAT independently predicted peak VO2 and AVO2diff in HFrEF and HFpEF regardless of body mass index and waist circumference. These relationships were direct in HFrEF (standard regression coefficient [SRC] for peak VO2: 0.18, p = 0.02; SRC for peak AVO2diff: 0.17, p = 0.03) and indirect in HFpEF (SRC for peak VO2: -0.33, p < 0.0001; SRC for peak AVO2diff: -0.25, p < 0.0001). As there are no definite cut-off values to define increased EAT, patients were divided based on the median EAT value (5 mm) of the overall population. Thinner EAT (≤5 mm) was associated with worse LV systolic dysfunction (peak average S’) and remodeling (3D LV mass index) in HFrEF. In HFpEF, on the other hand, increased EAT (>5 mm) was related to worse right ventricular systolic dysfunction (3D right ventricular ejection fraction) and more severe left atrio-ventricular (left atrium reservoir strain/left ventricle global longitudinal strain) and right ventriculo-arterial (tricuspid annular plane systolic excursion/systolic pulmonary artery pressure) coupling (Figure 2). Conclusion. In HFpEF, increased EAT thickness is associated with a worse hemodynamic profile and functional capacity. Conversely, in HFrEF, EAT thinning portends more advanced LV dysfunction and impaired cardiopulmonary fitness. Abstract Figure 1 Abstract Figure 2

Abstract Funding Acknowledgements Type of funding sources: None. Background. Recent evidence shows that increased epicardial adipose tissue (EAT) thickness is associated with metabolic syndrome, microvascular dysfunction and enhanced pericardial restraint. Purpose. We measured echocardiography-derived EAT thickness in a population of heart failure (HF) patients with reduced (HFrEF) and preserved (HFpEF) ejection fraction to examine the relationship between EAT and prognosis at clinical follow-up. Methods. We prospectively enrolled 393 consecutive HF outpatients (205 HFrEF, 188 HFpEF) who had been referred to our hospital due to dyspnoea and/or effort intolerance. We performed a resting clinical and biohumoral evaluation, followed by combined cardiopulmonary-echocardiography exercise stress. We considered a composite endpoint of cardiovascular death and HF-related hospitalization during follow-up. Results. Patients with HFpEF displayed greater EAT thickness (median 8 mm, interquartile range [IQR] 4–12 mm) than HFrEF (median 3 mm, IQR 2–6 mm; p < 0.0001). During a median follow-up of 20.9 months (IQR 15-25 months), 34 cardiovascular deaths and 146 HF hospitalizations were reported, with no significant differences between the two HF phenotypes. EAT was shown to predict adverse events independently from body mass index, waist circumference and other well-established prognostic markers in HF (such as NT-proBNP and peak oxygen consumption). The risk of adverse events increased with increasing EAT thickness in HFpEF and with EAT thinning in HFrEF. Kaplan-Meier analyses for the composite endpoint showed that in HFpEF, the survival probability was significantly lower in patients with thicker EAT than those with thinner EAT. In HFrEF, conversely, patients with increased EAT thickness had a higher survival probability than those with reduced EAT thickness (Figure 1). Conclusion. EAT accumulation is increased in HFpEF compared to HFrEF and carries different prognostic meanings in the two subsets. In HFpEF, EAT thickening portends adverse outcomes, which may be due to the secretion of pro-inflammatory and pro-atherogenic adipokines and increased mechanical restraint. In HFrEF, EAT thinning is associated with a worse prognosis, probably reflecting a more advanced catabolic state (e.g., cardiac cachexia). Larger studies are needed to determine whether or not EAT has a causal role in influencing progression and survival in the different HF phenotypes. Abstract Figure 1

Abstract Background Increased epicardial adipose tissue (EAT) thickness correlates with metabolic syndrome, insulin resistance, microvascular dysfunction and enhanced pericardial restraint. Purpose We measured echocardiographic EAT thickness in heart failure (HF) patients with reduced (HFrEF) or preserved (HFpEF) ejection fraction to determine whether EAT could bear prognostic significance at clinical follow-up. Methods We prospectively enrolled 393 consecutive HF outpatients (205 HFrEF, 188 HFpEF) referred to our hospital due to dyspnoea and/or effort intolerance. We performed a resting clinical and biohumoral evaluation, followed by combined cardiopulmonary-echocardiography exercise stress. A composite of cardiovascular death and HF-related hospitalization was chosen as endpoint during follow-up. Results Patients with HFpEF displayed higher EAT thickness (median 8 mm, interquartile range [IQR] 4–12 mm) than HFrEF (median 3 mm, IQR 2–6 mm; p<0.0001). During a median follow-up of 20.9 months (IQR 15–25 months), we reported 34 cardiovascular deaths and 146 HF hospitalizations, with no significant differences between the two HF subsets. EAT predicted adverse events independently from body mass index and well-established markers of poor prognosis (e.g., NT-proBNP, peak oxygen consumption). The risk of adverse events increased with increasing EAT thickness in HFpEF and with EAT thinning in HFrEF. Kaplan-Meier analyses for the composite endpoint showed that in HFpEF, the survival probability was significantly lower in patients with thicker EAT than those with thinner EAT. In HFrEF, conversely, patients with thicker EAT had a higher survival probability than those with reduced EAT thickness (Figure 1). Conclusion EAT accumulation is more marked in HFpEF than HFrEF and carries different prognostic meanings in the two subsets. In HFpEF, EAT thickening portends adverse outcome, which may be due to increased mechanical restraint and secretion of pro-inflammatory and pro-atherogenic adipokines. In HFrEF, greater EAT thickness seems to have a protective role, while EAT thinning is associated with a worse prognosis, likely reflecting a catabolic state (i.e. cardiac cachexia). Larger studies will clarify whether EAT is a bystander or an active player in the different HF phenotypes. Funding Acknowledgement Type of funding sources: None. Figure 1

Abstract Background Epicardial adipose tissue (EAT) acts as a paracrine organ and could exert direct mechanical compression on the myocardium. Purpose We investigated the impact of echocardiographic EAT thickness on metabolic profile and cardiovascular hemodynamics at rest and during exercise in heart failure (HF) patients with reduced (HFrEF) and preserved (HFpEF) ejection fraction Methods We prospectively enrolled 393 consecutive HF outpatients (205 HFrEF, 188 HFpEF) referred to the our hospital due to dyspnoea and/or effort intolerance. We performed a resting clinical and biohumoral evaluation, followed by combined cardiopulmonary-echocardiography exercise stress. The protocol also included 44 healthy controls. Results Patients with HFpEF displayed the greatest EAT thickness (median 8 mm, interquartile range [IQR] 4–12 mm), while those with HFrEF had thinner EAT (median 3 mm, IQR 2–6 mm) than controls (median 5 mm, IQR 3–7 mm; p<0.0001). In HFrEF, EAT thickness was inversely associated with natriuretic peptides, Troponin T, and C-reactive protein levels. In HFpEF, it was directly correlated with Troponin-T and C-reactive protein levels. EAT thickness was inversely correlated with peak oxygen consumption (VO2) and peripheral oxygen extraction (AVO2diff) in HFpEF, while a direct association was observed in HFrEF (Fig 1). EAT resulted in an independent predictor of peak VO2 and AVO2diff in HFrEF and HFpEF regardless of body mass index, but the relationships were direct in HFrEF (standard regression coefficient [SRC] for peak VO2: 0.18, p=0.02; SRC for peak AVO2diff: 0.17, p=0.03) and indirect in HFpEF (SRC for peak VO2: −0.33, p<0.0001; SRC for peak AVO2diff: −0.25, p<0.0001). The analysis of cardiac mechanics revealed that thinner EAT was associated with worse left ventricle systolic dysfunction (average S') and remodeling (3D left ventricle mass) in HFrEF. In HFpEF, increased EAT was related to more severe left atrio-ventricular (left atrium reservoir strain/left ventricle global longitudinal strain) and right ventriculo-arterial (tricuspid annular plane systolic excursion/systolic pulmonary artery pressure) coupling (Figure 2). Conclusion In HFpEF, EAT accumulation is associated with worse hemodynamic and metabolic profile. In HFrEF, conversely, EAT thinning portends more severe LV dysfunction and impaired global functional capacity. Funding Acknowledgement Type of funding sources: None. Figure 1Figure 2

Abstract Funding Acknowledgements Type of funding sources: None. Aims. Combined cardiopulmonary exercise test (CPET) and exercise stress echocardiography (ESE) provides a non-invasive tool to study cardiopulmonary pathophysiology. We analyzed how cardiac functional reserve during exercise relates to peak oxygen consumption (VO2). Methods and Results. We performed a symptom-limited graded ramp bicycle CPET-ESE in 30 healthy controls and 357 patients: 113 at risk of developing heart failure (American College of Cardiology/American Heart Association HF Stages A-B) and 244 in HF Stage C with preserved (HFpEF, n = 101) or reduced ejection fraction (HFrEF, n = 143). Peak VO2 significantly decreased from controls to Stage A-B and Stage C (Table 1). A multivariable regression model to predict peak VO2 revealed peak left ventricular systolic annulus tissue velocity (S"), peak TAPSE/PAPs (tricuspid annular plane systolic excursion/systolic pulmonary artery pressure) and low-load left atrial reservoir strain/E/e’ were independent predictors, in addition to peak heart rate, stroke volume and workload (adjusted R²=0.76, p < 0.0001). The model was successfully tested in subjects with atrial fibrillation (n = 49), and with (n = 224) and without (n = 163) beta-blockers (all p < 0.01). Peak S’ showed the highest accuracy in predicting peak VO2 < 10 mL/kg/min (cut-point ≤ 7.5 cm/s; AUC = 0.92, p < 0.0001) and peak VO2 > 20 mL/kg/min (cut-point > 12.5 cm/s; AUC = 0.84, p < 0.0001) in comparison to the other cardiac variables of the model (p < 0.05). Conclusions. A model incorporating different measures of cardiac mechanics is strongly related to peak aerobic capacity and may help in identifying different causes of effort intolerance from HF Stage A to C. Table 1 Variable Overall population (n = 387) Controls (n = 30) Stage A-B (n = 113) Stage C-HFpEF (n = 101) Stage c-HFrEF (n = 143) p-value Age, years 68.9 ± 11.1 67.1 ± 10.6 67.7 ± 10.4 70.5 ± 10.1 68.5 ± 11 0.1 Male, n (%) 247 (64) 18 (60) 70 (62) 57 (56) 102 (71) 0.1 VO2 @peak, mL/min/kg 15.7 (12.1-19.6) 23 (21.7- 29.7) 18 (15.4- 20.7)* 13.6 (11.8- 16.8)*† 14.2 (10.7- 17.5)*† <0.0001 Workload @peak, W 90 (65-120) 130 (115-195) 110 (84-130)* 70 (55-100)*† 80 (60-110)*† <0.0001 Heart rate @peak, bpm 123 ± 22 142 ± 12 130 ± 20* 115 ± 17*† 119 ± 23*† <0.0001 Stroke volume @peak, mL 83 (71-99) 98 (85-114) 86 (76-107) 83 (74-97)* 75 (63-95)*† <0.0001 Average S" @peak, cm/s 11.2 ± 3.8 17.1 ± 3.9 13.3 ± 2.9* 10.6 ± 2.5*† 8.7 ± 2.7*†‡ <0.0001 TAPSE/PAPs @peak, mm/mmHg 0.75 (0.46-0.97) 1.05 (0.93- 1.16) 0.81 (0.52- 0.91)* 0.52 (0.38- 0.83)*† 0.58 (0.41- 0.89)*† <0.0001 Left atrial reservoir strain/E/e" @low-load, % 2.25 (1.17-5.04) 6.23 (4.45-6.77) 4.34 (3.89- 5.58)* 2.23 (1.31- 2.86)*† 1.91 (1.07-2.44)*†‡ <0.0001 * p < 0.01 vs Controls; † p < 0.01 vs Stage A-B; ‡ p < 0.01 vs Stage C-HFpEF. PAPs systolic pulmonary artery pressure; TAPSE: tricuspid annular plane systolic excursion; VO2: oxygen consumption. Abstract Figure 1

Abstract Funding Acknowledgements Type of funding sources: None. Aims. We tested the prognostic role of a risk score including bio-humoral evaluation, cardiopulmonary-echocardiographic stress (CPET-ESE) and lung ultrasound, in patients with heart failure (HF) with reduced and preserved ejection fraction (HFrEF and HFpEF), and subjects at risk of developing HF (American College of Cardiology/American Heart Association Stages A and B). Methods and results. We evaluated 318 subjects: 94 in Stages A-B, 194 in Stage C (85 HFpEF and 109 HFrEF), and 30 age and sex-matched controls (Stage 0). During a median follow-up of 18.5 months, we reported 40 urgent HF visits, 31 HF hospitalisations and 10 cardiovascular deaths. Cox proportional-hazards regression for predicting adverse events identified five independent predictors and each was assigned a number of points proportional to its regression coefficient: Δstress-rest B-lines >10 (3 points), peak oxygen consumption <16 mL/kg/min (2 points), minute ventilation/carbon dioxide production slope ≥36 (2 points), peak systolic pulmonary artery pressure ≥50 mmHg (1 point) and resting N-terminal pro-brain natriuretic peptide (NT-proBNP) >900 pg/mL (1 point). We defined three risk categories: low-risk (<3 points), intermediate-risk (3-6 points), and high-risk (>6 points). The event-free survival probability for these three groups were 93%, 52% and 20%, respectively. Hazard Ratio was 4.55 for each risk category upgrade (95% confidence interval [CI], 3.44-5.93). The area-under-curve for the scoring system to predict events was 0.92 (95% CI 0.88-0.96). Conclusion. A multiparametric risk score including indices of exercise-induced pulmonary congestion, markers of cardiopulmonary dysfunction and NT-proBNP identifies patients at increased risk for HF events across the HF spectrum. Table 1 Variable EPYC score EPYC score <3 (low risk) n = 217 EPYC score 3-6 (intermediate risk) n = 70 EPYC score >6 (high risk) n = 31 p-value (between risk categories) Event-free (n = 244) 0 (0 - 2) 210 (97) 32 (46) 2 (6) <0.0001 With events (n = 74) 6 (4 - 9) 7 (3) 38 (54) 29 (94) <0.0001 p-value (event-free vs with events) <0.0001 <0.0001 <0.0001 <0.0001 Stage 0-Controls (n = 30) 0 (0 - 1) 30 0 0 <0.0001 Stages A-B (n = 94) 1 (0 - 2) 85 (45) 6 (9) 3 (10) <0.0001 Stage C-HFpEF (n = 85) 3 (1 - 6)*† 46 (25) 29 (41) 10 (32) <0.0001 Stage C-HFrEF (n = 109) 4 (2 - 7)*† 56 (30) 35 (50) 18 (58) <0.0001 p-value (between HF Stages) <0.0001 <0.0001 <0.0001 <0.0001 Values are mean ± standard deviation, n (%), or median [25th quartile, 75th quartile]. * p < 0.01 vs Stage 0-Controls; † p < 0.01 vs Stages A-B. Abstract Figure 1

Abstract Background The HFA-PEFF algorithm has been recently developed and is recommended by the European Society of Cardiology to make a diagnosis of heart failure with preserved ejection fraction (HFpEF). Based on functional echocardiography criteria, morphological criteria, and natriuretic peptide levels, a score from 1 to 6 is obtained with higher scores indicating a higher probability of HFpEF. Purpose This study investigates the prognostic value of the HFA-PEFF score in HFpEF patients hospitalised for decompensation. Methods This retrospective cohort study includes consecutive patients with HFpEF, admitted to Mayo Clinic Rochester between 2010–2015 and requiring treatment with intravenous loop diuretics for congestion. The HFA-PEFF score was calculated for all patients with echocardiography data available within 1 year and natriuretic peptide levels obtained upon admission. The study population was subsequently stratified according to HFA-PEFF score ≤4 (n=79), =5 (n=93), or =6 (n=271). Incidence rates of recurrent heart failure admissions per 100 patient-years of follow-up, time to all-cause mortality, and mortality causes were compared among strata. Results In 443 patients with HFpEF (78±12 years; 60% women), higher HFA-PEFF score was associated with older age, female gender, higher systolic blood pressure, and worse renal function. Heart failure readmission rates were higher in patients with HFA-PEFF score =5 [46.0 (38.5–53.5)] or HFA-PEFF score =6 [45.0 (40.1–49.8)] versus HFA-PEFF score ≤4 [28.9 (22.7–35.0); P-value<0.001 for differences; see upper panel figure]. Increasing HFA-PEFF score was associated with a shorter median survival (P-value<0.001), which was 65 months (36–89 months) in HFA-PEFF score ≤4, 45 months (26–59 months) in HFA-PEFF score =5, and 28 months (22–42 months) in HFA-PEFF score =6 (see lower panel figure). The proportions of deaths directly related to heart failure were comparable among HFA-PEFF strata (49% versus 49% versus 52%, respectively; P-value=0.903), as was the contribution of cardiovascular death (60% versus 57% versus 63%, respectively; P-value=0.662). Overall, few differences in patterns of mortality causes were observed among strata. There was a lower contribution of primary respiratory disease (mainly chronic obstructive pulmonary disease) to mortality in patients with a higher HFA-PEFF score (26% versus 19% versus 6%, respectively; P-value<0.001). Conclusions Higher HFA-PEFF score in hospitalized patients with HFpEF is associated with increased risk of subsequent heart failure readmissions and all-cause mortality, which includes both heart failure specific and non-heart failure mortality. Heart failure readmissions & mortality Funding Acknowledgement Type of funding source: Foundation. Main funding source(s): Belgian American Educational Foundation (B.A.E.F.); Special Research Fund (BOF) of Hasselt University (Hasselt, Belgium)

Abstract Background Heart failure (HF) is a debilitating disease and is associated with significant morbidity and mortality, and costs to health care systems. Monitoring the impact of therapy remotely holds the potential to reduce HF-related hospitalizations, improve quality of life, and optimize the use of the limited resources. Voice signal is an emerging non-invasive biomarker that has been associated with a number of disease states. We previously identified a significant relationship between specific vocal biomarkers and coronary artery disease, and recently extended these observations by showing that a pre-specified voice biomarker was associated with increased mortality and re-hospitalization in patients with HF. Purpose In the current study, we evaluated the association between a vocal biomarker derived from voice signal analysis and invasively measured indices of pulmonary hypertension (PH). We hypothesized that the pre-specified voice biomarker might be associated with hemodynamic indices reflective of PH that are known to be linked to HF-severity, and that predict outcomes such as HF-related hospitalization and death. Methods The study population included patients referred for an invasive cardiac hemodynamic study between January 2017 and December 2018. Subjects had their voice signal recorded to their smartphone on three separate occasions prior to the cardiac study. A pre-established numeric vocal biomarker was derived from each recording, and the mean vocal biomarker calculated for each patient. Patients were a priori divided into two groups: those with high pulmonary arterial pressure (PAP) defined as ≥35 mmHg consistent with moderate or greater PH, versus those with a lower PAP. Results Eighty three patients, mean age 61.6±15.1 years, 37 (44.6%) male, were included in the study. The intraclass correlation coefficient for the vocal biomarker in all patients was 0.83 implying very good agreement between values. Patients with a high mean PAP (≥35 mmHg) had significantly higher values of the voice biomarker compared to those with a lower mean PAP (0.74±0.85 vs. 0.43±0.86, p=0.008). Patients with a high pulmonary vascular resistance (PVR) defined as a PVR ≥1.7 Wood Units had significantly higher values of the voice biomarker compared to those with a lower PVR (0.62±0.83 vs. 0.33±0.90, p=0.026). Multivariable logistic regression showed that an increase in the voice biomarker by 1 unit was significantly associated with a high PAP, odds ratio (OR) 2.31, 95% CI 1.05–5.07, p=0.038, and with borderline significance with a high PVR, OR 2.14, 95% CI 0.94–4.87, p=0.07. Conclusion The current study shows a relationship between a noninvasive vocal biomarker derived from voice signal analysis and invasively derived hemodynamic indices related to PH obtained during cardiac catheterization. These results may have important and practical clinical implications for telemedicine and remote monitoring of patients with HF and PH. Funding Acknowledgement Type of funding source: Private grant(s) and/or Sponsorship. Main funding source(s): Mayo Foundation; Beyond Verbal Communications