Abstract 13678: Serum Hepatokine Selenoprotein P is Upregulated by Hepatic Hypoperfusion and Predicts Adverse Prognosis in Heart Failure Patients

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Tomofumi Misaka ◽  
Yasuhiro Ichijo ◽  
Akiomi YOSHIHISA ◽  
Yu Hotsuki ◽  
Watanabe Koichiro ◽  
...  
Keyword(s):  
Heart Failure ◽  
Peak Systolic Velocity ◽  
Shear Wave Elastography ◽  
Left Ventricular ◽  
Right Atrial ◽  
Enzyme Linked Immunosorbent Assay ◽  
Selenoprotein P ◽  
Abdominal Ultrasonography ◽  
Peripheral Tissues ◽  
Hepatic Congestion

Introduction: Cardiac and multiple organ network is involved in the pathophysiology of heart failure (HF). Hepatokines, which are produced and secreted from the liver, have regulatory functions in the peripheral tissues. However, the interaction between the heart and liver or clinical relevance of hepakokines in HF remains poorly understood. The present study aimed to elucidate the clinical significance of hepatokine selenoprotein P in HF. Methods and Results: We enrolled 250 participants including 171 hospitalized patients with HF and 79 control subjects. The serum concentration of selenoprotein P was measured by an enzyme-linked immunosorbent assay. We found that the serum selenoprotein P levels in HF patients were significantly higher than those in controls (14.8 ± 7.5 vs. 8.4 ± 4.6 mg/L, P<0.01). Next, the HF patients were categorized into 4 groups based on the hepatic hemodynamics assessed by abdominal-ultrasonography, which determined liver congestion by shear wave elastography (liver-SWE, >1.33 m/s) and liver hypoperfusion by peak systolic velocity of the celiac artery (celiac-PSV, <62.4 cm/s). Selenoprotein P levels were significantly upregulated in patients with liver hypoperfusion compared to patients with liver congestion ( Figure A ). Selenoprotein P was negatively correlated with celiac-PSV (P<0.01), cardiac output (P<0.01), and left ventricular stroke volume (P=0.03), whereas no correlations were observed between selenoprotein P and indices of congestion such as liver-SWE and right atrial pressure. Kaplan-Meier analysis demonstrated that a higher selenoprotein P group showed a lower event-free rate from re-hospitalization due to worsening HF ( Figure B ). Conclusion: Upregulation of liver-derived selenoprotein P was associated with hepatic hypoperfusion, not hepatic congestion, and related to the adverse prognosis in HF. Selenoprotein P may be a novel molecule involved in the cardio-hepatic interaction.

scholarly journals External assessment of the EUROMACS right-sided heart failure risk score

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Hirak Shah ◽  
Thomas Murray ◽  
Jessica Schultz ◽  
Ranjit John ◽  
Cindy M. Martin ◽  
...  
Keyword(s):  
Heart Failure ◽  
Right Ventricular ◽  
Risk Score ◽  
Pressure Ratio ◽  
Area Under The Curve ◽  
Left Ventricular ◽  
Right Atrial ◽  
Risk Scores ◽  
External Assessment ◽  
Failure Risk

AbstractThe EUROMACS Right-Sided Heart Failure Risk Score was developed to predict right ventricular failure (RVF) after left ventricular assist device (LVAD) placement. The predictive ability of the EUROMACS score has not been tested in other cohorts. We performed a single center analysis of a continuous-flow (CF) LVAD cohort (n = 254) where we calculated EUROMACS risk scores and assessed for right ventricular heart failure after LVAD implantation. Thirty-nine percent of patients (100/254) had post-operative RVF, of which 9% (23/254) required prolonged inotropic support and 5% (12/254) required RVAD placement. For patients who developed RVF after LVAD implantation, there was a 45% increase in the hazards of death on LVAD support (HR 1.45, 95% CI 0.98–2.2, p = 0.066). Two variables in the EUROMACS score (Hemoglobin and Right Atrial Pressure to Pulmonary Capillary Wedge Pressure ratio) were not predictive of RVF in our cohort. Overall, the EUROMACS score had poor external discrimination in our cohort with area under the curve of 58% (95% CI 52–66%). Further work is necessary to enhance our ability to predict RVF after LVAD implantation.

scholarly journals Respiratory-related heart rate variability in progressive experimental heart failure

2005 ◽  
Vol 289 (4) ◽  
pp. H1729-H1735 ◽  
Author(s):  
Sophie Motte ◽  
Myrielle Mathieu ◽  
Serge Brimioulle ◽  
Anne Pensis ◽  
Lynn Ray ◽  
...  
Keyword(s):  
Heart Failure ◽  
Heart Rate ◽  
Heart Rate Variability ◽  
Spectral Analysis ◽  
Left Ventricular ◽  
Right Atrial ◽  
Left Ventricular Ejection ◽  
Total Power ◽  
Progressive Heart Failure ◽  
Atrial Natriuretic

Heart failure is associated with autonomic imbalance, and this can be evaluated by a spectral analysis of heart rate variability. However, the time course of low-frequency (LF) and high-frequency (HF) heart rate variability changes, and their functional correlates during progression of the disease are not exactly known. Progressive heart failure was induced in 16 beagle dogs over a 7-wk period by rapid ventricular pacing. Spectral analysis of heart rate variability and respiration, echocardiography, hemodynamic measurements, plasma atrial natriuretic factor, and norepinephrine was obtained at baseline and every week, 30 min after pacing interruption. Progressive heart failure increased heart rate (from 91 ± 4 to 136 ± 5 beats/min; P < 0.001) and decreased absolute and normalized (percentage of total power) HF variability from week 1 and 2, respectively ( P < 0.01). Absolute LF variability did not change during the study until it disappeared in two dogs at week 7 ( P < 0.05). Normalized LF variability increased in moderate heart failure ( P < 0.01), leading to an increased LF-to-HF ratio ( P < 0.05), but decreased in severe heart failure ( P < 0.044; week 7 vs. week 5). Stepwise regression analysis revealed that among heart rate variables, absolute HF variability was closely associated with wedge pressure, right atrial and pulmonary arterial pressure, left ventricular ejection fraction and volume, ratio of maximal velocity of early (E) and atrial (A) mitral flow waves, left atrial diameter, plasma norepinephrine, and atrial natriuretic peptide (0.45 < r < 0.65, all P < 0.001). In tachycardia-induced heart failure, absolute HF heart rate variability is a more reliable indicator of cardiac dysfunction and neurohumoral activation than LF heart rate variability.

Abstract 13304: Liver Dispersion Predicts Adverse Outcomes in Patients With Heart Failure

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Yu Hotsuki ◽  
Akiomi Yoshihisa ◽  
Koichiro Watanabe ◽  
Yu Sato ◽  
Yusuke Kimishima ◽  
...  
Keyword(s):  
Heart Failure ◽  
Cardiac Death ◽  
Cardiac Event ◽  
Liver Stiffness ◽  
Adverse Outcomes ◽  
Right Atrial ◽  
Gamma Glutamyl Transferase ◽  
Abdominal Ultrasonography ◽  
Patients With Heart Failure ◽  
Glutamyl Transferase

Background: It has been recently reported that liver stiffness assessed by transient elastography reflects right atrial pressure (RAP), and is associated with worse outcome in patients with heart failure (HF). However, the relationship between liver dispersion (LD, a novel indicator of liver viscosity) determined by abdominal ultrasonography and RAP, and prognostic impacts of LD on HF patients have not been fully examined. We aimed to clarify associations of LD with parameters of liver functional test (LFT) and right-heart catheterization (RHC), and cardiac event such as cardiac death and worsening HF in patients with HF. Methods and Results: We performed abdominal ultrasonography, LFT, RHC, and followed up cardiac events including cardiac death and unplanned hospitalization due to HF in patients with HF (n=157). We examined associations of LD with parameters of LFT and RHC. There were significant correlations between LD and circulating levels of gamma-glutamyl transferase (R=0.197, P=0.018), cholinesterase (R=-0.301, P=0.001), and 7S domain of collagen type IV (P4NP 7S, a marker of fibrosis, R=0.334, P<0.001), but not with RAP (R=0.067, P=0.514) or cardiac index (R=-0.038, P=0.667). During the follow up period (median 305 days), 6 cardiac deaths and 18 unplanned hospitalization due to HF occurred. In the Kaplan-Meier analysis ( Figure ), cardiac event rate was significantly higher in the high LD group (LD ≥10.0 (m/s)/kHz, n=79) than in the low LD group (LD < 10.0 (m/s)/kHz, n=78; log-rank, P=0.007). In the multivariable Cox proportional hazard analysis, high LD was found to be an independent predictor of cardiac event (hazard ratio 3.274, 95% confidence interval 1.203-8.912, P=0.020). Conclusions: LD assessed by abdominal ultrasonography reflects liver fibrosis rather than liver congestion, and is associated with adverse prognosis in HF patients.

scholarly journals The Role of Cardiac T-Cadherin in the Indicating Heart Failure Severity of Patients with Non-Ischemic Dilated Cardiomyopathy

Medicina ◽  
2020 ◽  
Vol 56 (1) ◽  
pp. 27
Author(s):  
Vaida Baltrūnienė ◽  
Ieva Rinkūnaitė ◽  
Julius Bogomolovas ◽  
Daiva Bironaitė ◽  
Ieva Kažukauskienė ◽  
...  
Keyword(s):  
Heart Failure ◽  
Dilated Cardiomyopathy ◽  
Experimental Studies ◽  
Left Ventricular ◽  
Human Myocardium ◽  
Enzyme Linked Immunosorbent Assay ◽  
Cox Regression Analysis ◽  
Non Ischemic Dilated Cardiomyopathy ◽  
The Mean

Background and objectives: T-cadherin (T-cad) is one of the adiponectin receptors abundantly expressed in the heart and blood vessels. Experimental studies show that T-cad sequesters adiponectin in cardiovascular tissues and is critical for adiponectin-mediated cardio-protection. However, there are no data connecting cardiac T-cad levels with human chronic heart failure (HF). The aim of this study was to assess whether myocardial T-cad concentration is associated with chronic HF severity and whether the T-cad levels in human heart tissue might predict outcomes in patients with non-ischemic dilated cardiomyopathy (NI-DCM). Materials and Methods: 29 patients with chronic NI-DCM and advanced HF were enrolled. Patients underwent regular laboratory investigations, echocardiography, coronary angiography, and right heart catheterization. TNF-α and IL6 in serum were detected by enzyme-linked immunosorbent assay (ELISA). Additionally, endomyocardial biopsies were obtained, and the levels of T-cad were assessed by ELISA and CD3, CD45Ro, CD68, and CD4- immunohistochemically. Mean pulmonary capillary wedge pressure (PCWP) was used as a marker of HF severity, subdividing patients into two groups: mean PCWP > 19 mmHg vs. mean PCWP < 19 mmHg. Patients were followed-up for 5 years. The study outcome was composite: left ventricular assist device implantation, heart transplantation, or death from cardiovascular causes. Results: T-cad shows an inverse correlation with the mean PCWP (rho = −0.397, p = 0.037). There is a tendency towards a lower T-cad concentration in patients with more severe HF, as indicated by the mean PCWP > 19 mmHg compared to those with mean PCWP ≤ 19 mmHg (p = 0.058). Cardiac T-cad levels correlate negatively with myocardial CD3 cell count (rho = −0.423, p = 0.028). Conclusions: Univariate Cox regression analysis did not prove T-cad to be an outcome predictor (HR = 1, p = 0.349). However, decreased T-cad levels in human myocardium can be an additional indicator of HF severity. T-cad in human myocardium has an anti-inflammatory role. More studies are needed to extend the role of T-cad in the outcome prediction of patients with NI-DCM.

scholarly journals Plasma IL-37 Elevated in Patients with Chronic Heart Failure and Predicted Major Adverse Cardiac Events: A 1-Year Follow-Up Study

2017 ◽  
Vol 2017 ◽  
pp. 1-6 ◽  
Author(s):  
Xiling Shou ◽  
Jing Lin ◽  
Cui Xie ◽  
Yi Wang ◽  
Chaofeng Sun
Keyword(s):  
Heart Failure ◽  
Chronic Heart Failure ◽  
Cox Regression ◽  
Left Ventricular ◽  
Major Adverse Cardiac Events ◽  
Left Ventricular Ejection ◽  
Enzyme Linked Immunosorbent Assay ◽  
Cardiac Events ◽  
Cox Regression Analysis ◽  
Adverse Cardiac Events

A great number of basic and clinical studies have demonstrated that inflammatory cytokines play an important role in the development and progression of chronic heart failure (CHF). However, there is limited information about the role of novel cytokine interleukin-37 (IL-37) in heart failure. We measured plasma IL-37 levels by enzyme-linked immunosorbent assay (ELISA) in 158 patients with chronic heart failure and 30 control subjects. Our results showed that plasma IL-37 levels were significantly elevated in patients with CHF compared with healthy controls (143.73 ± 26.83 pg/ml versus 45.2 ± 11.56 pg/ml,P<0.001). Furthermore, plasma IL-37 levels were positively correlated with hs-CRP, hs-TnT, and NT-proBNP and negatively correlated with left ventricular ejection function (LVEF). 11 patients died of cardiovascular cause, and 27 HF patients were rehospitalized for worsening HF within 12 months. Multivariate Cox regression analysis showed that plasma IL-37 is an independent predictor of major adverse cardiac events (MACE). Furthermore, CHF patients with >99 pg/ml plasma IL-37 had significantly higher incidences of MACE within 12 months. Our data suggest that plasma IL-37 may play a role in the pathogenesis of CHF and may be a novel predictor of poor prognosis in HF patients.

Factors involved in delaying the rise in peripheral resistance in developing heart failure

1994 ◽  
Vol 267 (1) ◽  
pp. H211-H216 ◽  
Author(s):  
K. Kiuchi ◽  
R. P. Shannon ◽  
N. Sato ◽  
M. Bigaud ◽  
C. Lajoie ◽  
...  
Keyword(s):  
Heart Failure ◽  
Diastolic Pressure ◽  
Peripheral Resistance ◽  
Left Ventricular ◽  
Right Atrial ◽  
Plasma Norepinephrine ◽  
Peripheral Vascular ◽  
Vascular Control ◽  
Developing Heart

The development of heart failure (HF) on peripheral vascular control was studied in 10 conscious dogs with measurements of cardiac output (CO) and left ventricular (LV), arterial, and right atrial pressures. At 3 wk after pacing-induced HF, CO was not decreased from 2.5 +/- 0.2 l/min, whereas LV dP/dt fell (from 2,858 +/- 71 to 1,409 +/- 69 mmHg/s) and LV end-diastolic pressure increased (from 4.8 +/- 0.4 to 27.3 +/- 1.1 mmHg) (P < 0.05). At 4–7 wk after pacing, CO was significantly decreased (to 1.6 +/- 0.1 l/min; P < 0.05), but total peripheral resistance (TPR) did not rise, despite increases in plasma norepinephrine and renin activity (P < 0.05). In the presence of ganglionic blockade, TPR was still not increased in HF. In vitro studies in isolated femoral artery segments demonstrated reduced intrinsic tone (0.028 +/- 0.007 g/mg; P < 0.05) as compared with vessels from sham-operated controls (0.124 +/- 0.023 g/mg), whereas the intracellular calcium level was not altered in HF. Thus, during the development of HF, severe contractile dysfunction precedes the fall in CO, which, in turn, precedes the rise in TPR. The delayed rise in TPR appears to involve a reduction in intrinsic peripheral vascular tone, despite neurohumoral activation.

scholarly journals Left ventricular longitudinal systolic dysfunction is associated with right atrial dyssynchrony in heart failure with preserved ejection fraction

2016 ◽  
Vol 35 (4) ◽  
pp. 207-214 ◽  
Author(s):  
Ibadete Bytyçi ◽  
Edmond Haliti ◽  
Gëzim Berisha ◽  
Arbërie Tishukaj ◽  
Faik Shatri ◽  
...  
Keyword(s):  
Heart Failure ◽  
Ejection Fraction ◽  
Systolic Dysfunction ◽  
Left Ventricular ◽  
Right Atrial ◽  
Preserved Ejection Fraction

The Effect of Left Ventricular Assist Device Therapy in Patients with Heart Failure and Mixed Pulmonary Hypertension

2017 ◽  
Vol 40 (2) ◽  
pp. 67-73 ◽  
Author(s):  
Hoong S. Lim ◽  
Neil Howell ◽  
Aaron Ranasinghe
Keyword(s):  
Heart Failure ◽  
Heart Rate ◽  
Pulmonary Hypertension ◽  
Left Ventricular ◽  
Ventricular Assist Devices ◽  
Right Atrial ◽  
Pulmonary Hemodynamics ◽  
Ventricular Assist ◽  
Significant Difference ◽  
Left Ventricular Assist

Background Diastolic pressure gradient (DPG) of ≥7 mmHg has been proposed to distinguish mixed pulmonary hypertension from isolated post-capillary pulmonary hypertension in heart failure (HF). We evaluated the changes in pulmonary hemodynamics with left ventricular assist devices (LVADs) in patients with DPG of ≥7 or <7 mmHg, and effects on peak oxygen uptake (VO2) in patients with advanced HF. Methods Pre- and post-LVAD implant pulmonary hemodynamics (including right atrial (RA) pressures, DPG, pulmonary vascular resistance (PVR), pulmonary capacitance (PCap) and cardiac output), echocardiography, cardiopulmonary exercise test were measured in 38 consecutive patients. Results Ten of 38 patients had baseline DPG ≥7 mmHg. There were no significant difference in baseline characteristics, peak VO2 and ventilation slope, but PVR were higher, and PCap lower in patients with DPG ≥7 mmHg. Pulmonary artery pressures improved in all patients, but PVR and DPG remained higher and PCap lower in patients with baseline DPG ≥7 mmHg after a median follow-up of 181 (IQR 153–193) days. Peak VO2 increased and ventilation slope reduced post-LVAD, and these improvements were comparable between groups. Only RA pressure reduction and exercise increase in heart rate were significant predictors of peak VO2 increase on multivariate analysis. Conclusions Baseline DPG of ≥7 mmHg compared to DPG <7 mmHg have persistently lower PCap and higher PVR post-LVAD, but the increase in peak VO2 was comparable despite these residual pulmonary vascular abnormalities. The improvement in peak VO2 was related to reduction in right atrial pressure and exercise increase in heart rate.

Adverse effects of atrioventricular synchronous right ventricular pacing on left ventricular sympathetic activity, efficiency, and hemodynamic status

2006 ◽  
Vol 291 (5) ◽  
pp. H2377-H2379 ◽  
Author(s):  
Abdul Al-Hesayen ◽  
John D. Parker
Keyword(s):  
Heart Failure ◽  
Right Ventricular ◽  
Sympathetic Activity ◽  
Left Ventricular ◽  
Right Atrial ◽  
Lv Function ◽  
Atrial Pacing ◽  
Ventricular Pacing ◽  
Rv Pacing ◽  
Norepinephrine Spillover

Right ventricular (RV) pacing is now recognized to play a role in the development of heart failure in patients with and without underlying left ventricular (LV) dysfunction. We used the cardiac norepinephrine spillover method to test the hypothesis that RV pacing is associated with cardiac sympathetic activation. We studied 8 patients with normal LV function using temporary right atrial and ventricular pacing wires. All measurements were carried out during a fixed atrial pacing rate. The radiotracer norepinephrine spillover technique was employed to measure total body and cardiac sympathetic activity while changes in LV performance were evaluated with a high-fidelity manometer catheter. Atrioventricular synchronous RV pacing, compared with atrial pacing alone, was associated with a 65% increase in cardiac norepinephrine spillover, an increase in LV end-diastolic pressure, and a reduction in myocardial efficiency. These responses may play a role in the development of heart failure and poor outcomes that are associated with chronic RV pacing.

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