Higher Mean Pulmonary Artery Pressure Research Articles

Predictors of long intensive care need after lung transplantation.

While expected need for intensive care after lung transplantation (LTx) does not normally affect organ allocation, it would be useful to estimate whether intensive care capacity is limited. The aim of this study was to assess factors available before LTx to identify predictors of prolonged intensive care unit (ICU) length of stay (LOS) after LTx. All bilateral LTx recipients excluding re-transplantation and multi-organ transplantation at Oslo University Hospital from 2000 to 2013 were included (n=277). Predictive factors for ICU LOS were identified using pre- and perioperative variables. Univariate analyses showed that recipients with pulmonary arterial hypertension, young age, female gender, low body height, low pretransplant actual total lung capacity (aTLC), and recipients who received an oversized donor lung were at risk for long ICU LOS. Patients with emphysema had lower risk of long ICU LOS. In multivariate analyses, a lower aTLC (p<.001) and a higher mean pulmonary artery pressure (mPAP) (p=.004) predicted prolonged ICU LOS. We found that small recipient lung volume and high mPAP were predictors for prolonged ICU LOS. Our observations may be useful in planning use of resources in LTx, particularly in times of limited intensive care resources.

Abstract 14287: Iron Deficiency is Associated With More Severe Pulmonary Vascular Disease in Pulmonary Hypertension Due to Chronic Lung Disease

Background: Iron deficiency promotes pulmonary vascular remodeling in pre-clinical models, and is associated with worse outcomes in pulmonary arterial hypertension. However, the consequences of iron deficiency in patients with pulmonary hypertension due to chronic lung disease (Group 3 PH) are unexplored. Methods: We studied 122 consecutive Group 3 PH patients from the University of Minnesota Pulmonary Hypertension Repository. Serum soluble transferrin receptor (sTR) levels quantified iron deficiency. We evaluated the relationship between iron deficiency and pulmonary vascular disease, right ventricular (RV) function, exercise capacity, and survival. Results: The iron deficient group (&lt;4.8mg/L sTR) had significantly higher mean pulmonary arterial pressure (40±9 mmHg, n=59 vs. 44±13 mmHg, n=61; p =.02) and lower pulmonary arterial compliance (2.2±1.2 mL/mmHg, n=52 vs. 1.7±0.8 mL/mmHg, n=55; p =.01), but there was no difference in pulmonary vascular resistance. Moreover, there were trends for higher right atrial pressure (7±4 mmHg, n=58 vs. 9±6 mmHg, n=61; p =0.08) in iron deficient patients. However, iron deficiency did not significantly alter RV function by echocardiography, 6-minute walk distance, or survival. Conclusions: Iron deficiency in Group 3 PH is associated with worse pulmonary vascular disease. This suggests iron deficiency could contribute to pulmonary vascular disease in Group 3 PH, and future studies are needed to determine if iron replacement could be a therapy for this deadly type of PH.

Non-invasive vocal biomarker is associated with pulmonary hypertension

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

Pulmonary hemodaynamic in obesity

Abstract Background Higher prevalence of pulmonary hypertension exist in obesity subjects. Little known about pulmonary hemodynamics during exercise in obesity population. Purpose To assess and compare the response of pulmonary vascular resistance during exercise in obese subjects vs healthy controls. Methods Seventeen obesity subjects (gender: 25%men, age: 44±11 years, height: 1.7±0.1 m, weight: 111±17 kilogram, BMI: 38±4 kg/m2) were compared to twenty gender-, age-, height- and race-matched healthy control subjects (age: 46±12 years, height: 1.7±0.1 m, weight: 64±11 kilogram, BMI: 22±2 kg/m2). All subjects underwent an incremental exercise stress echocardiography with measurements of pulmonary artery pressure (PAP), cardiac output (CO), cardiac index (CI) and tricuspid annular plane systolic excursion (TAPSE) at rest and at increasing exercise intensities. Total pulmonary vascular resistance index (PVRi) was calculated as mean PAP/CI and right ventricular-arterial coupling as TAPSE/systolic PAP. Results The results are described in the table 1. Pulmonary hemodynamic was not different at rest between two groups, but lower at maximal exercise in obesity subjects. In obesity subjects, identical exercise level was associated with a higher mean PAP and PVRi, and a lower TAPSE/systolic PAP ratio. Conclusion While pulmonary hemodynamic seems preserved at rest in obesity patients, pulmonary vascular resistance is increased and right ventricular coupling is decreased, particularly at exercise. Funding Acknowledgement Type of funding source: None

Pulmonary hypertension in patients with interstitial pneumonia with autoimmune features.

Pulmonary hypertension in interstitial lung diseases is associated with increased mortality and hospitalizations and reduced exercise capacity. Interstitial pneumonia with autoimmune features (IPAF) is a recently described interstitial lung disease. The characteristics of pulmonary hypertension in IPAF patients are unknown. We sought to characterize patients with IPAF based on their echocardiographic probability of pulmonary hypertension and compare patients with and without pulmonary hypertension identified by right heart catheterization. We conducted a retrospective study of patients seen in the interstitial lung disease clinic from 2015 to 2018. Forty-seven patients with IPAF were identified. Patients were classified into low, intermediate and high echocardiographic pulmonary hypertension probabilities. A sub-group analysis of patients with pulmonary hypertension and without pulmonary hypertension (IPAF-PH vs. IPAF-no PH) identified by right heart catheterization was also performed. Linear regression analysis was performed to study the association between 6-min-walk-distance (6MWD) and pulmonary vascular resistance (PVR) while adjusting for age and body mass index. Right ventricular hypertrophy (>5 mm), right ventricular enlargement (>41 mm) and right ventricular systolic dysfunction defined as fractional area change% ≤35 was present in 76%, 24%, and 39% of patients, respectively. Pulmonary hypertension was identified in 12.7% of patients. IPAF-PH patients had higher mean pulmonary artery pressure and lower cardiac output compared to the IPAF-no PH group (34 mmHg vs. 19 mmHg, p = 0.002 and 4.0 vs. 5.7 L/min, p = 0.023, respectively). Lower 6MWD was associated with higher PVR on regression analysis (p = 0.002). Pulmonologists should be aware that a significant number of IPAF patients may develop pulmonary hypertension. Reduced 6MWD may suggest the presence of pulmonary hypertension in IPAF patients.

PREVALENCE AND CLINICAL IMPLICATIONS OF PULMONARY ARTERY ANEURYSMS IN PATIENTS WITH PULMONARY HYPERTENSION

SESSION TITLE: Pulmonary Vascular Disease Posters SESSION TYPE: Original Investigation Posters PRESENTED ON: October 18-21, 2020 PURPOSE: Pulmonary artery aneurysm (PAA) is defined as a main pulmonary artery (PA) diameter greater than 40 mm. Pulmonary arterial hypertension (PAH) is one of the conditions most commonly associated with the development of PAA but it is still uncertain which factors contribute to the development of PAA in PAH patients. We sought to identify the prevalence of PAA in PAH patients and to determine prognostic implications of PAA identification. METHODS: Data collection of patients in the Pulmonary Hypertension clinic at Keck Medical Center from January 2010 to January 2020 was conducted. Patient demographics and PAH etiology information was collected. Additional data regarding functional status, as determined by NYHA class and 6 MWD, and hemodynamics per RHC and TTE measurements was collected. Patients were described as having Pulmonary Artery Aneurysms if their CT report noted a main PA size greater than or equal to 40 mm. RESULTS: A total of 473 patients were identified in the cohort of patients being treated in the PH clinic. Of these patients, 331 had a CT chest completed throughout their course. 68 patients were noted to have PAA during their follow-up period. The average main PA size at time of initial CT was 42.5 mm in the PAA group and 32.1 mm in the non-PAA group. Patients with PAA were noted to have a lower average age compared to non-PAA patients (46.49 years vs 50.92 years). Among PAA patients, the most common etiologies of PAH were idiopathic and congenital heart disease (CHD) (24.53% and 22.64% respectively). PAA patients had significantly higher rates of moderate to severe RV dysfunction (39.06% vs 20.48%) and RV dilation (73.44% vs 52.57%) on their initial TTE. Patients with PAA were also noted to have a significantly higher mean pulmonary artery pressure at time of their first RHC (53.27 mmHg vs 41.11 mmHg). In addition, patients with PAA were noted to have significantly higher PVR with a mean PVR of 8.39 wood units in the PAA group vs. 5.60 wood units in the non-PAA group. No significant difference on these parameters was present between PAA and non-PAA patients on most recent testing. CONCLUSIONS: Patients with PAA were noted to be younger and were predominantly patients with idiopathic PAH and CHD. Those with PAA identified had more hemodynamically significant disease on presentation as evidenced by higher mPAP and PVR in addition to higher rates of moderate to severe RV dysfunction and dilation. On repeat RHC and TTE, there was no significant difference between mPAP, PVR or rates of moderate to severe RV dysfunction suggesting potential increased responsiveness to treatment among patients with PAA. CLINICAL IMPLICATIONS: The presence of PAA may serve as a prognostic and diagnostic marker in patients with PAH. Importantly, it may indicate patients have had more longstanding disease and may signify an increased responsiveness to treatment as suggested by improved hemodynamics on RHC and TTE. DISCLOSURES: No relevant relationships by Tiffany Chang, source=Web Response No relevant relationships by Lucas Cruz, source=Web Response No relevant relationships by Jared Geibig, source=Web Response No relevant relationships by Moses Koo, source=Web Response No relevant relationships by Ashil Panchal, source=Web Response Speaker/Speaker's Bureau relationship with Actelion, United therapeutic, and Bayer Please note: $20001 - $100000 Added 05/30/2020 by Bassam Yaghmour, source=Web Response, value=Honoraria

Right Ventricular Arterial Elastance is Associated with Prognostic Value in one Year Mortality Following Left Ventricular Assist Device Placement

Background In patients with end-stage heart failure (HF), acute right heart failure (RHF) after left ventricular assist device (LVAD) implantation is known to be a source of significant morbidity and mortality. Previous data identified RV pulsatility load using pulmonary arterial compliance as a marker for 6-month mortality in LVAD patients. We aimed to test whether the right ventricular arterial elastance (RVEa) was associated with increased risk of 1 year mortality after LVAD implantation. Hypothesis Patients with higher RVEa at preimplantation have a higher risk of dying at 1 year. Methods We retrospectively identified 381 patients with complete pre-implant hemodynamics obtained Results The majority of patients (65%) had RVEa≥1 (Fig. 1). When comparing baseline demographics, those with RVEa ≥1 were younger, had a lower proportion of hypertension, coronary artery disease, and more likely to be on inotropes pre-implantation. Those with RVEa ≥1 had lower SV, and pulmonary artery pressure index; and higher mean pulmonary artery pressure, pulmonary wedge capillary pressure and transpulmonary gradient. Multivariate survival analysis adjusted for heart rate, BMI, age, and gender demonstrated the only independent predictor of mortality was RVEa ≥1 (hazard ratio 1.80, [95% CI 1.07 - 3.05], p= 0.028). Conclusions Our multi-institutional study demonstrates that higher RVEa is associated with increased 1 year mortality post-VAD implantation. These data may be generalizable to other academic institutions and warrants further investigation in larger cohorts.

Prevalence and clinical features of bone morphogenetic protein receptor type 2 mutation in Korean idiopathic pulmonary arterial hypertension patients: The PILGRIM explorative cohort.

BackgroundPulmonary arterial hypertension (PAH) is a progressive chronic disease with poor outcomes. One reason for poor prognosis is the lack of understanding regarding individual variability in response to treatment. Idiopathic PAH (IPAH) patients with bone morphogenetic protein receptor type 2 (BMPR2) mutations have distinct phenotypes that are crucial for individualized therapy but evidence regarding their prevalence and clinical features in the Korean population is lacking. Therefore, the present study aimed to screen Korean IPAH patients for BMPR2 mutations and analyze their clinical phenotypes.MethodsWe enrolled 73 unrelated IPAH patients for BMPR2 mutation screening between March 2010 to November 2015 from 11 hospitals in Korea. Thirty-three lineal family members from 6 families of BMPR2 mutation carriers were also screened.ResultsAmong 73 patients, 16 (22%) had BMPR2 mutations. Mutation carriers were younger (27 vs. 47 years; p = 0.02) and had a higher mean pulmonary arterial pressure (mPAP) than non-carriers (64 vs. 51 mmHg; p<0.05). Of the 16 individuals with mutations, 5 deletion, 2 splice-site, 6 nonsense, and 3 missense mutations were found, among which, 9 were newly identified mutation types. Patients less than 30 years old had more BMPR2 mutations (44 vs. 14%; p = 0.04) and a higher mPAP (64 vs. 50 mmHg; p = 0.04) compared with those equaled to or over 30 years old. There were no differences in hemodynamic profiles or the proportion of BMPR2 mutation carriers between groups according to sex.ConclusionThe prevalence of BMPR2 mutations in Korean IPAH patients was 22%. Mutation carriers were younger and had a poorer hemodynamic profile compared with the non-carriers.Clinical trial registrationClinicaltrials.gov NCT01054105

Plasma irisin levels are associated with hemodynamic and clinical outcome in idiopathic pulmonary arterial hypertension patients.

Irisin has been considered to reflect oxidative stress. This study aimed to show whether plasma irisin levels are correlated with hemodynamic dysfunction and predict the clinical outcome of patients with idiopathic pulmonary arterial hypertension (IPAH). A total of 68 adult IPAH patients were prospectively recruited in the present study. Plasma irisin levels were measured by the ELISA method in enrolled IPAH patients. Baseline clinical characteristics, and hemodynamic and clinical outcome were compared according to different plasma irisin levels. IPAH patients were divided into high irisin group (irisin ≥ 7.3μg/ml) and low irisin group (irisin < 7.3μg/ml) according to median values of irisin levels. Total plasma cholesterol levels (P = 0.027) and low-density lipoprotein cholesterol (LDL-C) levels (P = 0.042) were higher in high irisin group and were positively correlated with plasma irisin levels. IPAH patients in low irisin group had a significantly higher mean pulmonary artery pressure (mPAP, P = 0.047), systolic pulmonary artery pressure (sPAP, P = 0.022), systolic right-ventricular pressure (sRVP, P = 0.007), mean right atrial pressure (mRAP, P = 0.043), and systolic right atrial pressure (sRAP, P = 0.020). mRAP, sRAP, and diastolic right atrial pressure (dRAP) were negatively correlated with plasma irisin levels. Low irisin group predicts adverse hemodynamic status and poor free of event survival rate (P = 0.030, log-rank test). Multivariate analysis indicates plasma irisin levels to be an independent predictor of prognosis in IPAH patients after adjusting for related covariates (HR 0.786; 95% CI 0.584, 0.957; P = 0.038). Plasma irisin levels may serve as a novel biomarker in IPAH patients for hemodynamic severity assessment and clinical outcome evaluation.

Pulmonary Vasodilator Therapy in Children with Single Ventricle Physiology: Effects on Saturation and Pulmonary Arterial Pressure

In children with single ventricle physiology, increased pulmonary vascular resistance may impede surgical progression or result in failing single ventricle physiology. The use of pulmonary vasodilators has been suggested as a potential therapy. However, knowledge on indication, dosage, and effect is limited. A retrospective case notes review of all (n = 36) children with single ventricle physiology, treated with pulmonary vasodilators by the UK Pulmonary Hypertension Service for Children 2004–2017. Therapy was initiated in Stage 1 (n = 12), Glenn (n = 8), or TCPC (n = 16). Treatment indications were high mean pulmonary arterial pressure, cyanosis, reduced exercise tolerance, protein-losing enteropathy, ascites, or plastic bronchitis. Average dose of sildenafil was 2.0 mg/kg/day and bosentan was 3.3 mg/kg/day. 56% had combination therapy. Therapy was associated with a reduction of the mean pulmonary arterial pressure from 19 to 14 mmHg (n = 17, p < 0.01). Initial therapy with one or two vasodilators was associated with an increase in the mean saturation from 80 to 85%, (n = 16, p < 0.01). Adding a second vasodilator did not give significant additional effect. 5 of 12 patients progressed from Stage 1 to Glenn, Kawashima, or TCPC, and 2 of 8 from Glenn to TCPC during a mean follow-up time of 4.7 years (0–12.8). Bosentan was discontinued in 57% and sildenafil in 14% of treated patients and saturations remained stable. Pulmonary vasodilator therapy was well tolerated and associated with improvements in saturation and mean pulmonary arterial pressure in children with single ventricle physiology. It appears safe to discontinue when no clear benefit is observed.

Involvement of overweight and lipid metabolism in the development of pulmonary hypertension under conditions of chronic intermittent hypoxia.

There is growing evidence that exposure to hypoxia, regardless of the source, elicits several metabolic responses in individuals. These responses are constitutive and are usually observed under hypoxia but vary according to the type of exposure. The aim of this review was to describe the involvement of obesity and lipid metabolism in the development of high-altitude pulmonary hypertension and in the development of acute mountain sickness under chronic intermittent hypoxia. Overweight or obesity, which are common in individuals with long-term chronic intermittent hypoxia exposure (high-altitude miners, shift workers, and soldiers), are thought to play a major role in the development of acute mountain sickness and high-altitude pulmonary hypertension. This association may be rooted in the interactions between obesity-related metabolic and physical alterations, such as increased waist circumference and neck circumference, among others, which lead to critical ventilation impairments; these impairments aggravate hypoxemia at high altitude, thereby triggering high-altitude diseases. Overweight and obesity are strongly associated with higher mean pulmonary artery pressure in the context of long-term chronic intermittent hypoxia. Remarkably, de novo synthesis of triglycerides by the sterol regulatory element-binding protein-1c pathway has been demonstrated, mainly due to the upregulation of stearoyl-CoA desaturase-1, which is also associated with the same outcomes. Therefore, overweight, obesity, and other metabolic conditions may hinder proper acclimatization. The involved mechanisms include respiratory impairment, alteration of the nitric oxide pathways, inflammatory status, reactive oxygen species imbalance, and other metabolic changes; however, further studies are required.

Corrected QT Interval in Severe Aortic Stenosis: Clinical and Hemodynamic Correlates and Prognostic Impact

BackgroundThe role of the electrocardiogram for risk stratification in patients with severe aortic stenosis is not established. We assessed the hemodynamic correlates and the prognostic value of the corrected QT interval (QTc) in patients with severe aortic stenosis undergoing aortic valve replacement. MethodsThe QT interval was measured in a 12-lead electrocardiogram in 485 patients (age 74 ± 10 years, 57% male) with severe aortic stenosis (indexed aortic valve area 0.41 ± 0.13 cm2/m2, left ventricular ejection fraction 58 ± 12%) the day prior to cardiac catheterization. Prolonged QTc was defined as QTc >450 ms in men and QTc >470 ms in women. The outcome parameter was all-cause mortality. ResultsPatients with prolonged QTc (n = 100; 77 men, 23 women) had similar indexed aortic valve area but larger left ventricular and left atrial size, lower left ventricular ejection fraction, more severe mitral regurgitation, lower cardiac index, and higher mean pulmonary artery pressure, mean pulmonary artery wedge pressure, and pulmonary vascular resistance, as compared with patients with normal QTc (n = 385). After a median follow-up of 3.7 years (interquartile range, 2.6-5.2) after surgical (n = 349) or transcatheter (n = 136) aortic valve replacement, patients with prolonged QTc had higher mortality than those with normal QTc (hazard ratio 2.81 [95% confidence interval, 1.51-5.20]; P < .001). Prolonged QTc was an independent predictor of death along with more severe mitral regurgitation and higher pulmonary vascular resistance. ConclusionsIn patients with severe aortic stenosis, prolonged QTc is a marker of an advanced disease stage associated with an adverse hemodynamic profile and increased long-term mortality after aortic valve replacement.

Obstructive sleep apnea and pulmonary hypertension: a bidirectional relationship.

Citation:Mesarwi O, Malhotra A. Obstructive sleep apnea and pulmonary hypertension: a bidirectional relationship. J Clin Sleep Med. 2020;16(8):1223–1224.

Continuous real-time monitoring of pulmonary arterial pressure using a tip deflecting microcatheter in an infant with pulmonary arterial hypertension

We present the case of a 3-month-old boy with pulmonary arterial hypertension after corrective repair of total anomalous pulmonary venous connection. The patient developed severe pulmonary arterial hypertension with a high mean pulmonary arterial pressure of 45 mmHg. We performed continuous monitoring of pulmonary arterial pressure using a tip deflecting microcatheter in the intensive care unit. We successfully managed this patient based on real-time pulmonary arterial pressure measurements. Continuous real-time monitoring of pulmonary arterial pressure using this microcatheter enables individualized targeted therapy for infants with pulmonary arterial hypertension.

Acute vasodilator testing following Fontan palliation: an opportunity to guide precision care?

Pulmonary vasodilators improve the functional capacity of some patients with pulmonary arterial hypertension. However, pulmonary vasodilators frequently fail to improve unequivocal endpoints of efficacy in patients with lower pulmonary arterial pressures who have been palliated with a Fontan procedure. Haemodynamic measurements and the results of acute vasodilator testing in a subset of patients were reviewed to determine whether some patients acutely respond more favourably to sildenafil and might be candidates for precision care with a phosphodiesterase V inhibitor long term. Heart catheterisation was performed in 11 patients with a Fontan procedure. Haemodynamic measurements were performed before and after treatment with intravenous sildenafil (mean 0.14, range 0.05-0.20 mg/kg). Results (mean±standard deviation) were compared by paired and unpaired t-tests to identify statistically significant changes. Sildenafil was acutely associated with changes in mean pulmonary arterial pressure, transpulmonary gradient, indexed blood flow, and indexed vascular resistance. Changes in mean pulmonary arterial pressure were greater for patients with a mean pulmonary arterial pressure greater than 14mmHg compared to patients with a lower mean pulmonary arterial pressure. Changes in transpulmonary gradient were greater for patients with a transpulmonary gradient greater than 5mmHg compared to patients with a lower transpulmonary gradient. Sildenafil acutely decreases mean pulmonary arterial pressure and transpulmonary gradient and causes greater acute changes in patients with higher mean pulmonary arterial pressures and transpulmonary gradients. Haemodynamic measurements and vasodilator testing might help to guide precision care following Fontan palliation.

Non-invasive vocal biomarker is associated with pulmonary hypertension.

Emerging data suggest that noninvasive voice biomarker analysis is associated with coronary artery disease. We recently showed that a vocal biomarker was associated with hospitalization and heart failure in patients with heart failure. We evaluate the association between a vocal biomarker and invasively measured indices of pulmonary hypertension (PH). Patients were referred for an invasive cardiac hemodynamic study between January 2017 and December 2018, and had their voices recorded on three separate occasions to their smartphone prior to each study. A pre-established vocal biomarker was determined based on each individual recording. The intra-class correlation co-efficient between the separate voice recording biomarker values for each individual participant was 0.829 (95% CI 0.740-0.889) implying very good agreement between values. Thus, the mean biomarker was calculated for each patient. Patients were divided into two groups: high pulmonary arterial pressure (PAP) defined as ≥ 35 mmHg (moderate or greater PH), versus lower PAP. Eighty three patients, mean age 61.6 ± 15.1 years, 37 (44.6%) male, were included. Patients with a high mean PAP (≥ 35 mmHg) had on average significantly higher values of the mean voice biomarker compared to those with a lower mean PAP (0.74 ± 0.85 vs. 0.40 ± 0.88 p = 0.046). Multivariate logistic regression showed that an increase in the mean voice biomarker by 1 unit was associated with a high PAP, odds ratio 2.31, 95% CI 1.05-5.07, p = 0.038. This study shows a relationship between a noninvasive vocal biomarker and an invasively derived hemodynamic index related to PH obtained during clinically indicated cardiac catheterization. These results may have important practical clinical implications for telemedicine and remote monitoring of patients with heart failure and PH.

Hemodynamic profile of patients with severe aortic valve stenosis and atrial fibrillation versus sinus rhythm

BackgroundIn patients with severe aortic stenosis (AS), atrial fibrillation (AF) is associated with increased long-term mortality after aortic valve replacement (AVR), which may be due to unfavorable hemodynamics in AF. We aimed to analyze the hemodynamic profile of patients with severe AS and AF versus sinus rhythm (SR). MethodsWe performed cardiac catheterization in 486 patients (age 74 ± 10 years, 58% males) with severe AS [indexed aortic valve area 0.41 ± 0.13 cm2, left ventricular ejection fraction 58 ± 12%]: 50 patients had AF, and 436 patients had SR. All patients underwent surgical (n = 350) or transcatheter (n = 136) AVR. ResultsDespite similar indexed aortic valve area (0.41 ± 0.11 vs. 0.41 ± 0.12 cm2/m2; p = 0.45) patients with AF had lower left ventricular ejection fraction, larger left atrial size, lower tricuspid annular plane systolic excursion, higher mean pulmonary artery pressure (34 ± 13 vs. 24 ± 9 mmHg), mean pulmonary artery wedge pressure (mPAWP; 22 ± 8 vs. 15 ± 7 mmHg), and pulmonary vascular resistance (2.8 ± 1.9 vs. 2.0 ± 1.3 Wood units) and lower stroke volume index (26 ± 9 vs. 37 ± 10 ml/m2) than patients with SR (p < 0.05 for all). Patients with AF and SR had a different mPAWP-left ventricular end-diastolic pressure (LVEDP) relationship with higher mPAWP in AF and higher LVEDP in SR. After a median follow-up of 49 (interquartile range, 35–64) months post-AVR patients with AF (p = 0.05) and patients with a larger difference between mPAWP and LVEDP (p = 0.005) had higher mortality. ConclusionsPatients with severe AS and concomitant AF have a distinct and significantly worse hemodynamic profile compared to patients with SR associated with worse clinical outcome.

Hemodynamic Effects of Concomitant Mitral Valve Surgery and Left Ventricular Assist Device Implantation.

There are conflicting data regarding whether concomitant mitral valve surgery (MVS) at left ventricular assist device (LVAD) implantation is beneficial. This study aimed to assess the hemodynamic effects of concomitant MVS. Of all 73 enrolled patients, 44 patients had undergone concomitant MVS and 29 patients had not. Before LVAD implantation, MVS group had higher pulmonary capillary wedge pressure (p = 0.04). After LVAD implantation, MVS group had higher mean pulmonary artery pressure and cardiac output (CO). During the hemodynamic ramp study, MVS group had steeper CO slopes (0.18 [0.13 0.28] vs. 0.15 [0.08, 0.20] L/min/step; p = 0.04) at incremental LVAD speed and achieved a higher CO at the optimized set speed (5.5 [4.7, 6.9] vs. 4.9 [4.0, 5.7] L/min; p = 0.03). One-year freedom from death or heart failure readmission was statistically comparable between the two groups (61% vs. 80%, p = 0.20). Thus far, after LVAD implantation and concomitant MVS, patients had increased pulmonary hypertension, despite having higher CO and a better response of CO at incremental LVAD speed. The implication of hemodynamic features after concomitant MVS on clinical outcomes warrants further investigation.

POST OPERATIVE INHALED NITRIC OXIDE USE AND EARLY OUTCOMES AFTER FONTAN SURGERY COMPLETION

Prolonged length of hospital stay (PLOS) is associated with higher mortality and complications after cardiac surgery. One of the risk factors of PLOS after Fontan is high mean pulmonary artery pressure. Inhaled nitric oxide (iNO) is a potent pulmonary vasodilator frequently used in the perioperative

Impact of concurrent right ventricular myocardial infarction on outcomes among patients with left ventricular myocardial infarction

To compare in-hospital outcomes between left ventricular myocardial infarction (LVMI) patients with and without right ventricular myocardial infarction (RVMI). Patients with acute ST-segment elevation MI (STEMI) undergoing primary percutaneous coronary intervention (PCI) were enrolled and divided into LVMI with and without RVMI groups. Between-group differences and in-hospital outcomes were compared. Compared to patients without RVMI, patients with RVMI were more likely to be male, have higher body mass index, serum levels of C-reactive protein (8.9 ± 2.4 vs 6.2 ± 2.1 mg/dL), B-type natriuretic peptide (1295 ± 340 vs 872 ± 166 pg/mL) and cardiac troponin-I (8.6 ± 2.9 vs 5.2 ± 2.1 ng/mL), and have diabetes (36.3% vs 3.4%) and dyslipidemia (53.4% vs 48.1%). Patients with RVMI had lower left and right ventricular ejection fraction (50.5 ± 5.6% vs 53.4 ± 3.8% and 33.6 ± 2.9% vs 45.7 ± 2.0%), but had higher mean pulmonary artery pressure (30.6 ± 3.3 vs 23.8 ± 3.1 mm Hg). Compared to patients without RVMI, patients with RVMI had higher odds of in-hospital all-cause mortality (4.1% vs 1.0%) and new onset acute heart failure (3.4% vs 1.0%). After adjusted for confounding factors, LVMI with RVMI remained independently associated with composite outcomes, with odds ratio 1.66 (95% confidence interval 1.39–2.04). Compared to isolated LVMI patients, those with concomitant RVMI have higher odds of in-hospital complications, particularly all-cause mortality and new onset acute heart failure.