Abstract 14978: Heart Failure Patient Adherence and Decreased Perception of Illness During Remote Hemodynamic Monitoring

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Lisa D Rathman ◽  
Samuel F Sears ◽  
Robert C Capodilupo ◽  
Robert C Bourge ◽  
Akshay S Desai ◽  
...  
Keyword(s):  
Heart Failure ◽  
Hemodynamic Monitoring ◽  
Time Course ◽  
Diastolic Pressure ◽  
Patient Adherence ◽  
Illness Perception ◽  
Pressure Data ◽  
Measurement Interval ◽  
Pulmonary Pressure ◽  
Sense Of Security

Introduction: Effective management of ambulatory heart failure (HF) requires active patient (pt) participation. In telemonitoring of weights and symptoms, pt adherence to transmission is often halved within 6 months (M). Although ambulatory pulmonary pressure-guided management decreases hospitalizations and improves quality of life, the time course of pt perception of illness and sense of security in relation to monitoring frequency is not known. Hypothesis: Pts will perceive decreased impact of their HF during pulmonary pressure-guided management, which may contribute to their engagement in transmission of ambulatory PAP. Methods: The post-approval study for the implanted PA sensor was amended to include serial measurements of pt reported outcomes, (PRO, n=143), including the Brief Illness Perception Questionnaire (BIPQ). Treatment was adjusted to a target PA diastolic pressure 8 to 20 mmHg and adherence to transmitting pressure data from home was collected. Results: In the PRO cohort, mean age was 68 years, 58% were male, and 55% with HFpEF. Negative illness perception (BIPQ) decreased during each measurement interval. Pts reported improvement in symptoms, sense of security, sense of control and less impact of illness on their emotions at each time point, equally with HFpEF or HFrEF. In this cohort pt adherence to transmitting pressures was high throughout 24 M, Fig.1. Perception of illness was most favorable at 2 years, at which time there was a slight decline in transmission frequency. Conclusions: Pt perception of HF was positively impacted during ambulatory hemodynamic monitoring including improvement in symptoms, less emotional effect of illness, improved sense of security and control over their HF throughout follow-up. This was associated with high-level pt adherence to pressure data transmission. The optimal level of chronic monitoring for stable pts to maintain clinical benefit while minimizing disease awareness beyond 2 years is still unknown.

Dynamic changes in conduction velocity and gap junction properties during development of pacing-induced heart failure

2007 ◽  
Vol 293 (2) ◽  
pp. H1223-H1230 ◽  
Author(s):  
Fadi G. Akar ◽  
Robert D. Nass ◽  
Samuel Hahn ◽  
Eugenio Cingolani ◽  
Manish Shah ◽  
...  
Keyword(s):  
Heart Failure ◽  
Conduction Velocity ◽  
Connexin 43 ◽  
Time Course ◽  
Diastolic Pressure ◽  
Left Ventricular ◽  
Early Event ◽  
Mechanical Function ◽  
Dynamic Changes ◽  
End Stage

End-stage heart failure (HF) is characterized by changes in conduction velocity (CV) that predispose to arrhythmias. Here, we investigate the time course of conduction changes with respect to alterations in connexin 43 (Cx43) properties and mechanical function during the development of HF. We perform high-resolution optical mapping in arterially perfused myocardial preparations from dogs subjected to 0, 3, 7, 14, and 21 days of rapid pacing to produce variable degrees of remodeling. CV is compared with an index of mechanical function [left ventricular end-diastolic pressure (LVEDP)] and with dynamic changes in the expression, distribution, and phosphorylation of Cx43. In contrast to repolarization, CV was preserved during early stages of remodeling (3 and 7 days) and significantly reduced at later stages, which were associated with marked increases in LVEDP. Measurements of differentially phosphorylated Cx43 isoforms revealed early, sustained downregulation of pan-Cx43 that preceded changes in CV and LVEDP, a gradual rise in a dephosphorylated Cx43 isoform to over twofold baseline levels in end-stage HF, and a late abrupt increase in pan-Cx43, but not dephosphorylated Cx43, lateralization. These data demonstrate that 1) CV slowing occurs only at advanced stages of remodeling, 2) total reduction of pan-Cx43 is an early event that precedes mechanical dysfunction and CV slowing, 3) changes in Cx43 phosphorylation are more closely associated with the onset of HF, and 4) Cx43 lateralization is a late event that coincides with marked CV reduction. These data reveal a novel paradigm of remodeling based on the timing of conduction abnormalities relative to changes in Cx43 isoforms and mechanical dysfunction.

scholarly journals Role of diastolic properties in the transition to failure in a mouse model of the cardiac dilatation

2006 ◽  
Vol 291 (6) ◽  
pp. H2971-H2979 ◽  
Author(s):  
Peter N. Costandi ◽  
Lawrence R. Frank ◽  
Andrew D. McCulloch ◽  
Jeffrey H. Omens
Keyword(s):  
Heart Failure ◽  
Time Course ◽  
Diastolic Pressure ◽  
Systolic Function ◽  
Genetically Engineered ◽  
Hypertrophic Growth ◽  
Physiological Characterization ◽  
First Derivative ◽  
Stress Strain Relation ◽  
Developed Pressure

Although the physiological states of hypertrophic remodeling and congestive heart failure have been intensively studied, less is known about the transition from one to the other. The use of genetically engineered murine models of heart failure has proven valuable in characterizing the progression of remodeling and its ultimate decompensation to failure. Mice deficient in the cytoskeletal muscle LIM-only protein (MLP) are known to present with a clinical picture of dilated cardiomyopathy and transition to failure as adults. Longitudinal high-field magnetic resonance (MR) cardiac imaging provided a time course of remodeling where an improvement in ejection fraction and stroke volume (15- vs. 31-wk MLP−/− mice; P < 0.0001) was temporally concurrent with an abrupt phase of end-diastolic chamber dilatation. Hemodynamic analysis conducted throughout that dilatation phase showed improved ratio of maximum first derivative of pressure to end-diastolic pressure (dP/d tmax/EDP; 15- vs. 31-wk MLP−/− mice; P < 0.0005), ratio of minimum first derivative of pressure to EDP (dP/d tmin/EDP; 15- vs. 31-wk MLP−/− mice; P < 0.003), and developed pressure (15- vs. 31-wk MLP−/− mice; P < 0.0001) levels in the MLP−/− mice. Computational modeling techniques were used to estimate the EDP volume relationship, revealing that although MLP hearts possess a stiffer stress-strain relation, chamber compliance increased as a function of dilatation. This detailed physiological characterization during a phase of rapid anatomical remodeling suggests that systolic function in the MLP−/− mice may temporarily improve as a result of alterations in chamber compliance, which are mediated by dilatation. In turn, a balance may exist between exploiting the Frank-Starling mechanism and altering chamber compliance that maintains function in the absence of hypertrophic growth. Though initially compensatory, this process may exhaust itself and consequently transition to a maladaptive course.

Estimation of Left Ventricular Wall Stiffness by Analysis of Late Diastolic Pressure Components

2011 ◽  
Author(s):  
Casandra L. Niebel ◽  
Kelley C. Stewart ◽  
Takahiro Ohara ◽  
John J. Charonko ◽  
Pavlos P. Vlachos ◽  
...  
Keyword(s):  
Heart Failure ◽  
Left Ventricle ◽  
Diastolic Dysfunction ◽  
Diastolic Pressure ◽  
Left Ventricular Diastolic Dysfunction ◽  
Left Ventricular ◽  
Ventricular Wall ◽  
Ventricular Relaxation ◽  
Wall Stiffness ◽  
Ventricular Diastolic Dysfunction

Left ventricular diastolic dysfunction (LVDD) is any abnormality in the filling of the left ventricle and is conventionally evaluated by analysis of the relaxation driven phase, or early diastole. LVDD has been shown to be a precursor to heart failure and the diagnosis and treatment for diastolic failure is less understood than for systolic failure. Diastole consists of two filling waves, early and late and is primarily dependent on ventricular relaxation and wall stiffness.

Pulmonary pressure, telemedicine, and heart failure therapy

The Lancet ◽  
2016 ◽  
Vol 387 (10017) ◽  
pp. 408-410 ◽  
Author(s):  
Nikolaos Dagres ◽  
Gerhard Hindricks
Keyword(s):  
Heart Failure ◽  
Heart Failure Therapy ◽  
Pulmonary Pressure

Importance of antioxidant and antiapoptotic effects of β-receptor blockers in heart failure therapy

2004 ◽  
Vol 287 (3) ◽  
pp. H1003-H1012 ◽  
Author(s):  
Keisuke Kawai ◽  
Fuzhong Qin ◽  
Junya Shite ◽  
Weike Mao ◽  
Shuji Fukuoka ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Heart Failure ◽  
Ventricular Remodeling ◽  
Diastolic Pressure ◽  
Cardiac Pacing ◽  
Left Ventricular ◽  
Beneficial Effects ◽  
Myocyte Apoptosis ◽  
Adrenergic Blocking ◽  
Fractional Shortening

The present study was carried out to determine whether beneficial effects of carvedilol in congestive heart failure (CHF) are mediated via its β-adrenergic blocking, antioxidant, and/or α-adrenergic blocking action. Rabbits with heart failure induced by rapid cardiac pacing were randomized to receive subcutaneous carvedilol, metoprolol, propranolol plus doxazosin, or placebo pellets for 8 wk and compared with sham-operated rabbits without pacing. We found rapid cardiac pacing produced clinical heart failure, left ventricular dilation, and decline of left ventricular fractional shortening. This was associated with an increase in left ventricular end-diastolic pressure, decrease in left ventricular first derivative of left ventricular pressure, and myocyte hypertrophy. Tissue oxidative stress measured by GSH/GSSG was increased in the heart with increased oxidation product of mitochondrial DNA, 8-oxo-7,8-dihydro-2′-deoxyguanosine, increase of Bax, decrease of Bcl-2, and increase of apoptotic myocytes as measured by anti-single-stranded DNA monoclonal antibody. Administration of carvedilol and metoprolol, which had no effect in sham animals, attenuated cardiac ventricular remodeling, cardiac hypertrophy, oxidative stress, and myocyte apoptosis in CHF. In contrast, propranolol plus doxazosin, which has less antioxidant effects, produced smaller effects on left ventricular function and myocyte apoptosis. In all animals, GSH/GSSG correlated significantly with changes of left ventricular end-diastolic dimension ( r = −0.678, P < 0.0001), fractional shortening ( r = 0.706, P < 0.0001), and apoptotic myocytes ( r = −0.473, P = 0.0001). Thus our findings suggest antioxidant and antiapoptotic actions of carvedilol and metoprolol are important determinants of clinical beneficial effects of β-receptors in the treatment of CHF.

Abstract 131: C-kit+ Cells Generated From Failed Heart Do Not Improve Failed Heart Function

2013 ◽  
Vol 113 (suppl_1) ◽  
Author(s):  
Liudmila Zakharova ◽  
Hikmet Nural ◽  
James R Nimlos ◽  
Snjezana Popovic ◽  
Lorraine Feehery ◽  
...  
Keyword(s):  
Heart Failure ◽  
Left Ventricle ◽  
Diastolic Pressure ◽  
Heart Function ◽  
Smooth Muscle Actin ◽  
Functional Improvement ◽  
Gene Expressions ◽  
Coronary Vein ◽  
Mesenchymal Transition

A pilot clinical study using autologous c-Kit+ cells showed improvement in cardiac functions in congestive heart failure (CHF), however, it is unclear if c-Kit+ cells isolated from CHF hearts are equally as potent as cells from controls. To test the potency of CHF c-Kit+ cells, myocardial infarction (MI) was created by permanent ligation of the left anterior descending coronary artery. Six weeks after MI, animals with left ventricle end-diastolic pressure (LVEDP) ≥20 mmHg and scar size ≥30% of left ventricle (LV) were designated as CHF rats. We found that CHF atrial explants generated less c-Kit+ cells compared to shams (15.7% vs. 11% sham vs. CHF). CHF c-Kit+ cells exhibited elevated levels of epicardial to mesenchymal transition markers, including Snail (2.5 fold) and Pai1 (3 fold), while the expression level of epithelial marker, E-cadherin was 3 fold lower in CHF c-Kit+ cells. Moreover, CHF c-Kit+ cells exhibited reduced gene expressions of pluripotency markers; 2.1 fold decrease in Nanog and 4.5 fold decrease in Sox 2 compared to sham cells. To evaluate the potency of the c-Kit+ cells, 1 x 10 6 cells isolated from CHFs or shams were delivered to 3 weeks post-MI CHF hearts. Cells were pre-labeled with GFP to enable their tracing in vivo and delivered to the infarcted myocardium via left coronary vein by a retrograde coronary sinus cell infusion (RCI). RCI delivery resulted in a cell distribution of LV (30%), right atrium (30%) and right ventricle (20%), while only 10% of cells were found in a left atrium. Three weeks after cells delivery, rats transplanted with sham c-Kit+ cells showed improved LVEDP (29.4 ± 6 vs. 11.7 ± 3.5 mmHg, CHF vs. CHF+ sham c-Kit+ cells) and a rise in peak rate of pressure (dPdt max) (3988 ± 520 vs. 5333 ± 597 mmHg/s). In contrast, no functional improvement was detected in rats transplanted with CHF c-Kit+ cells. Histological analysis demonstrated that transplanted c-Kit+/GFP+ cells were mostly incorporated into blood vessels and co-localized with endothelial marker vWf, and α-smooth muscle actin. Our results showed that left coronary vein is an efficient route for c-Kit+ cell delivery and that c-Kit+ cells isolated from CHF rats are less potent when transplanted in chronic heart failure rat model compared to those isolated from control.

Abstract P237: Is Ischemia/Reperfusion an Efficient Method for Producing Heart Failure in Rats?

Hypertension ◽  
2016 ◽  
Vol 68 (suppl_1) ◽  
Author(s):  
Ana Carolina M Omoto ◽  
Fábio N Gava ◽  
Mauro de Oliveira ◽  
Carlos A Silva ◽  
Rubens Fazan ◽  
...  
Keyword(s):  
Heart Failure ◽  
Diastolic Pressure ◽  
Histopathological Examination ◽  
Ischemia Reperfusion ◽  
Mitral Annulus ◽  
Mortality Rates ◽  
Tissue Doppler ◽  
Left Ventricular ◽  
Coronary Artery Ligation ◽  
Artery Ligation

Myocardium infarction (MI) elicited by coronary artery ligation (CAL) is commonly used to induce chronic heart failure (HF) in rats. However, CAL shows high mortality rates. Given that ischemia-reperfusion (IR) may cause the development of HF, this approach may be useful for obtaining a model of HF with low mortality rates. Therefore, it was compared the model of CAL vs. IR in rats, evaluating the mortality and cardiac morphological and functional aspects. The IR consisted of 30 minutes of cardiac ischemia. Wistar rats were assigned into three groups: CAL: n=18; IR: n=7; SHAM (fictitious IR): n=7. After four weeks of CAL, the subjects were evaluated by echocardiography and ventriculography as well. The statistical analysis consisted of ANOVA combined with Tukey’s posthoc test (p<0.05). There were no deaths in the IR and SHAM groups, whereas in the CAL group the mortality rate was 33.33% (6 out of 18). In the CAL group echocardiography showed increased left ventricular (LV) cavity during systole (8.3 ± 1mm) and diastole (10.5 ± 1mm); decreased LV free wall during systole (1.4 ± 0.5 mm); increased left atrium/aorta (2.3 ± 0.4) ratio. These changes were not significant in IR (4.8 ± 0.5mm, 7.6 ± 0.6mm, 2.6 ± 0.3 mm, 1.6 ± 0.2) and SHAM (4.6 ± 0.6 mm, 7.7 ± 0.8mm, 2.8 ± 0.4mm, 1.5 ± 0.2) groups. There was also the reduction in the ejection fraction in the CAL group (41 ± 12 %) when compared with IR (65 ± 9%) and SHAM (69 ± 7%) groups. The tissue Doppler analysis from the lateral mitral annulus showed reduction in E′ in CAL (-29 ± 8 mm/s) and IR (-31± 9 mm/s) groups when compared with the SHAM (-48 ± 11 mm/s) group. The ventriculography in the CAL group showed smaller maximum dP/dt (6519 ± 1062) and greater end-diastolic pressure (33 ± 8 mmHg) when compared with IR (8716 ± 756 mmHg/s; 9 ± 9 mmHg) and SHAM (7989 ± 1230 mmHg/s; 9 ± 7 mmHg) groups. The CAL group presented transmural infarct size of 40% of the left ventricular wall, measured under histopathological examination. In conclusion, IR for 30 minutes caused only small changes in LV diastolic function, assessed by tissue Doppler; however, the IR was not effective for promoting HF, as observed with CAL. Thus, it is possible that prolonged IR is necessary for promoting significant HF in rats.

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