Abstract 33: Prostaglandin E2 Reduces Cardiac Contractility via EP3 Receptor

2015 ◽  
Vol 117 (suppl_1) ◽  
Author(s):  
Xiaosong Gu ◽  
Jiang Xu ◽  
Xiao-Ping Yang ◽  
Edward Peterson ◽  
Pamela Harding
Keyword(s):  
Prostaglandin E2 ◽  
Cardiac Contractility ◽  
Peak Height ◽  
Left Ventricular ◽  
Reduced Ejection Fraction ◽  
Langendorff Preparation ◽  
Cell Contractility ◽  
Isolated Hearts ◽  
Developed Pressure ◽  
Ep3 Receptor

Prostaglandin E2 (PGE2) EP receptors EP3 and EP4 are present in the heart and signal via decreased and increased cAMP production, respectively. Previously we reported that cardiomyocyte-specific EP4 KO mice develop a phenotype of dilated cardiomyopathy with reduced ejection fraction. We thus hypothesized that PGE2 decreases contractility via EP3. To test this hypothesis, the effects of PGE2 and the EP1/EP3 agonist sulprostone (sulp) were examined in the mouse langendorff preparation and in adult mouse cardiomyocytes (AVM) using the IonOptix cell contractility system. Isolated hearts of 18-20 wk old male C57Bl/6 mice were mounted and equilibrated for 10 min, then perfused with PGE2 (10 -6 mol/l) or sulp (10 -6 mol/l) for 30 min. Values at the end of equilibration were set to 100%. Compared to vehicle, PGE2 decreased +dp/dt (77.8±3% vs 96.7±3%, p<0.01) and left ventricular developed pressure, LVDP (77.2±2% vs 96.8±3%, p<0.001). Sulp decreased +dp/dt (75.9±2% vs 96.7±3%, p<0.001), -dp/dt (72.2±1% vs 85.7±1%, p<0.01) and LVDP (70.9±1% vs 96.8±3%, p<0.001). The effects of both PGE2 and sulp were reversed by the EP3 antagonist, L789,106 (10 -6 mol/l). Myocyte contractility was evaluated on the IonOptix system with pacing at 1Hz. Treatment with PGE2 (10 -9 M) for 10 min reduced contractility as measured by peak height (3.69 ± 0.48% for vehicle vs 2.00 ± 0.22% for PGE2, p < 0.05 ), departure velocity (-171.9 ± 22.9 um/sec for vehicle vs -106.3± 12.5 um/sec for PGE2, p < 0.05) and return velocity (87.7 ± 16.3 um/sec for vehicle vs 36.7 ± 6.6 um/sec for PGE2, p < 0.05) with similar effects noted for sulp. Sulp reduced change in peak height (4.79 ± 1.15% for vehicle vs 1.81 ± 0.37% for sulp, p < 0.05), departure velocity (-169.1 ± 35.8 um/sec for vehicle vs -59.4 ± 10.3 um/sec for sulp, p < 0.05) and return velocity (86.5 ± 23.8 um/sec for vehicle vs 16.9 ± 14.7 um/sec for sulp, p < 0.05). We then examined the acute effects of PGE2 and sulp on expression of phosphorylated phospholamban (PLN) and SERCA using Western blot. Treatment of AVM for 15min with either PGE2 or sulp decreased expression of phosphorylated PLN corrected to total PLN, by 67% and 43%. SERCA2a expression was unaffected. In conclusion, PGE2 and sulp reduce contractility via the EP3 receptor through effects on PLN.

Oxygen delivery and myocardial function in rabbit hearts perfused with cell-free hemoglobin

1992 ◽  
Vol 72 (2) ◽  
pp. 476-483 ◽  
Author(s):  
V. W. MacDonald ◽  
R. M. Winslow
Keyword(s):  
Oxygen Uptake ◽  
Myocardial Function ◽  
Oxygen Affinity ◽  
Left Ventricular ◽  
Rate Of Change ◽  
Free Hemoglobin ◽  
Langendorff Preparation ◽  
Oxygen Gradients ◽  
Developed Pressure ◽  
Krebs Henseleit Buffer

Isolated rabbit hearts were perfused with Krebs-Henseleit buffer that contained 1.5 g/dl hemoglobin Ao [HbAo; PO2 at which half-saturation of hemoglobin occurs = 12 Torr], human hemoglobin cross-linked between alpha-chains with bis(3,5-dibromosalicyl)fumarate (alpha alpha-Hb; PO2 at which half-saturation of hemoglobin occurs = 30 Torr), or fatty acid-free bovine serum albumin (BSA). Myocardial performance and oxygen uptake were determined at different aortic PO2's [arterial PO2 (PaO2)] by use of an isovolumic Langendorff preparation. Function and oxygen uptake were comparable among the three different groups of hearts at an average mean PaO2 of 557 Torr. As PaO2 decreased, myocardial function was preserved better in hearts perfused with hemoglobin than in hearts perfused with Krebs-Henseleit buffer alone or with BSA. Hearts perfused with either HbAo or alpha alpha-Hb exhibited similar 10% decreases in left ventricular developed pressure and rate of change in left ventricular developed pressure at PaO2 of 141 Torr compared with a 58% decrease with BSA. However, corresponding venous PO2's were lower with HbAo (20 Torr) than with alpha alpha-Hb (35 Torr), and oxygen uptake decreased by 36% with HbAo but remained constant with alpha alpha-Hb. These data suggest that although myocardial function can be sustained over a fairly broad range of hemoglobin oxygen affinities, tissue oxygen gradients and myocardial oxygen uptake are maintained better by cell-free hemoglobin with an oxygen affinity in the normal physiological range.

Adenosine antagonism decreases metabolic but not functional recovery from ischemia

1991 ◽  
Vol 260 (1) ◽  
pp. H193-H200 ◽  
Author(s):  
D. A. Angello ◽  
J. P. Headrick ◽  
N. M. Coddington ◽  
R. M. Berne
Keyword(s):  
Functional Recovery ◽  
Left Ventricular ◽  
Low Flow ◽  
Ischemia And Reperfusion ◽  
Constant Flow ◽  
Hemodynamic Parameters ◽  
Isolated Hearts ◽  
Rat Hearts ◽  
Adenosine Antagonism ◽  
Developed Pressure

The effect of adenosine receptor antagonism on function and metabolism was examined in isolated hearts during low flow ischemia and reperfusion. Isovolumic rat hearts perfused at constant flow were subjected to 30 min of ischemia followed by 30 min of reperfusion. Infusion of vehicle or 10 microM 8-phenyltheophylline (8-PT) was initiated 10 min before ischemia and maintained throughout reperfusion. 8-PT infusion had no significant effects on hemodynamic parameters or metabolism preischemia. During ischemia, left ventricular developed pressure declined to approximately 15% of preischemic values in control and 8-PT hearts, and ATP and PCr decreased to approximately 73 and 60% of preischemic values. Inorganic phosphate (Pi) increased to 353 = 41 and 424 +/- 53% of preischemic values in control and 8-PT hearts, respectively. After reperfusion, function recovered to greater than 95% of preischemic levels in control and 8-PT hearts. Unlike control hearts, recovery of metabolites was significantly different during reperfusion in 8-PT hearts (P less than 0.05); ATP, phosphocreatine, and Pi recovered to 82 +/- 8, 71 +/- 8, and 281 +/- 27% of preischemic values, respectively. Venous purine washout was significantly greater (P less than 0.05) during reperfusion in 8-PT hearts (327 +/- 113 nmol) than in control hearts (127 +/- 28 nmol). Blockade of adenosine receptors appears to adversely affect metabolic but not functional recovery in the ischemic-reperfused myocardium.

Cardioprotection in chronically hypoxic rabbits persists on exposure to normoxia: role of NOS and KATP channels

2005 ◽  
Vol 288 (1) ◽  
pp. H62-H68 ◽  
Author(s):  
Colleen M. Fitzpatrick ◽  
Yang Shi ◽  
William C. Hutchins ◽  
Jidong Su ◽  
Garrett J. Gross ◽  
...  
Keyword(s):  
Myocardial Ischemia ◽  
Chronic Hypoxia ◽  
Katp Channels ◽  
Left Ventricular ◽  
Adaptation To Hypoxia ◽  
Isolated Hearts ◽  
Percent Recovery ◽  
Subsequent Exposure ◽  
Developed Pressure ◽  
Oxide Synthase

Hypoxia from birth increases resistance to myocardial ischemia in infant rabbits. We hypothesized that increased cardioprotection in hearts chronically hypoxic from birth persists following development in a normoxic environment and involves increased activation of nitric oxide synthase (NOS) and ATP-dependent K (KATP) channels. Resistance to myocardial ischemia was determined in rabbits raised from birth to 10 days of age in a normoxic (FiO2 = 0.21) or hypoxic (FiO2 = 0.12) environment and subsequently exposed to normoxia for up to 60 days of age. Isolated hearts ( n = 8/group) were subjected to 30 min of global ischemia followed by 35 min of reperfusion. At 10 days of age, resistance to myocardial ischemia (percent recovery postischemic recovery left ventricular developed pressure) was higher in chronically hypoxic hearts (68 ± 4%) than normoxic controls (43 ± 4%). At 10 days of age, NG-nitro-l-arginine methyl ester (200 μM) and glibenclamide (3 μM) abolished the cardioprotective effects of chronic hypoxia (45 ± 4% and 46 ± 5%, respectively) but had no effect on normoxic hearts. At 30 days of age resistance to ischemia in normoxic hearts declined (36 ± 5%). However, in hearts subjected to chronic hypoxia from birth to 10 days and then exposed to normoxia until 30 days of age, resistance to ischemia persisted (63 ± 4%). l-NAME or glibenclamide abolished cardioprotection in previously hypoxic hearts (37 ± 4% and 39 ± 5%, respectively) but had no effect on normoxic hearts. Increased cardioprotection was lost by 60 days. We conclude that cardioprotection conferred by adaptation to hypoxia from birth persists on subsequent exposure to normoxia and is associated with enhanced NOS activity and activation of KATP channels.

scholarly journals 164 Effect of cardiac contractility modulation therapy on myocardial work in patients with heart failure with reduced ejection fraction

2021 ◽  
Vol 23 (Supplement_G) ◽  
Author(s):  
Daniele Masarone ◽  
Stefano De Vivo ◽  
Vittoria Errigo ◽  
Antonio D’ Onofrio ◽  
Giuliano D’Alterio ◽  
...  
Keyword(s):  
Heart Failure ◽  
Ejection Fraction ◽  
Cardiac Contractility ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Cardiac Contractility Modulation ◽  
Reduced Ejection Fraction ◽  
Constructive Work ◽  
Global Work ◽  
The Impact

Abstract Aims Cardiac contractility modulation therapy (CCMT) has been shown to reduce hospitalizations and to improve quality of life in heart failure patients with reduced ejection fraction (HFrEF) who remain symptomatic despite disease-modifying therapies. Strain imaging derived myocardial work (MW) is an emerging tool for evaluating left ventricular mechanics by incorporating systolic deformation and afterload burden in the analysis. To evaluate prospectively the impact of CCMT in HFrEF patients on MW derived parameters in relation to standard echocardiographic indices. Methods and results We recruited 12 HFrEF patients with indications to CCMT according to current clinical practice. A comprehensive echo-Doppler evaluation, including speckle tracking derived assessment of global longitudinal strain (GLS), was performed before and after three months from the CCM device implantation. Parameters of MW such as global work index (GWI), global constructive work (GCW) global wasted work (GWW), and global work efficiency (GWE) were calculated according to standardized procedures. Median values (interquartile range) were compared for all those parameters from baseline and 3-month follow-up with Wilcoxon Rank Sum test for continuous variables. At three months from CCM implant an improvement of LVEF [from 32% (27–34) to 36% (29–39), P &lt; 0.05], GLS [from 7.4% (6.2–11.2) to 9.9% (7.5–9.4), P &lt; 0.05], GWI [from 461 mmHg (372–613) to 589 mmHg (413–696), P &lt; 0.05], GCW [from 800 mmHg (620–930) to 970 mmHg (644–1009), P = 0.236], and GWE [from 73% (65–78) to 85% (78–87), P &lt; 0.05] was observed, with a consistent reduction of GWW [from 161 mmHg (148–227) to 125 mmHg (101–188), P &lt; 0.05]. We also found a positive correlation between the magnitude of LVEF improvement and the baseline values of GCW (r = 0.727, P = 0.011). Conclusions At 3 months, CCMT significantly improves standard and advanced left ventricular systolic function indices. This improvement is due to the increase of constructive work and a reduction of wasted work. In addition, the increase of left ventricular ejection fraction can be predicted by the global constructive work levels at baseline.

Abstract 1082: Cytoskeletal Protein 4.1R Affects Repolarisation And Regulates Calcium Handling In The Heart

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Cesare M Terracciano ◽  
Nadia Sohrabi ◽  
Urszula Siedlecka ◽  
Mark A Stagg ◽  
Gopal K Soppa ◽  
...  
Keyword(s):  
Mechanical Stability ◽  
Amplitude Ratio ◽  
Cardiac Contractility ◽  
Adaptor Proteins ◽  
Left Ventricular ◽  
Calcium Handling ◽  
Macromolecular Complex ◽  
Human Heart Failure ◽  
Cell Contractility ◽  
Protein 4.1R

The 4.1 proteins are a family of multifunctional adaptor proteins that organise signalling/transport/cell adhesion molecules. They are capable of interaction with the spectrin-actin network thereby conferring mechanical stability to the cell membrane, with several ion transporters associated to this macromolecular complex. Protein 4.1R is expressed in the heart and upregulated in deteriorating human heart failure. However, no data exists on the roles of protein 4.1R in myocardial regulation and function. In particular, it is unknown whether this protein can influence cardiac contractility and/or electrophysiology. 4.1R-deficient mice (KO) were studied using echocardiography and ECG monitoring with radiotelemetry. Left ventricular dimensions were increased in KO mice (LV diameter - Dia (cm): WT = 0.43 ± 0.01 [6] (mean ± SEM [n]); KO = 0.49 ± 0.01 [6]; p < 0.01) - Sys cm): WT = 0.29 ± 0.01 [6]; KO = 0.34 ± 0.02 [6]; p < 0.05) with no changes in ejection fraction and fractional shortening. ECG analysis revealed reduced heart rate (RR interval (ms): WT = 113±5 [6]; KO = 139 ± 601 [6]; p < 0.01) accompanied by prolonged QT interval (corrected (ms): WT = 46 ± 2 [6]; KO = 52 ± 1 [6]; p < 0.05). The action potential duration (APD) measured in isolated ventricular myocytes was prolonged in KO (APD 90% at 1Hz (ms) WT = 146 ± 20 [21]; KO = 231 ± 29 [28]; p < 0.05). Ca transients, elicited by 1Hz field-stimulation and measured using the fluorescent indicator indo-1, were larger (amplitude (ratio units r.u.): WT = 0.07 ± 0.006 [22]; KO = 0.1 ± 0.006 [33]; p<0.05) and slower to decay in the KO group (time to 50% decline (ms): WT = 78 ± 3 [22]; KO = 91 ± 3 [33]; p < 0.05). This was associated with increased SR Ca content, (20 mM caffeine-induced indo-1 transient amplitude (r.u.): WT = 0.09 ± 0.01 [7]; KO = 0.13 ± 0.01 [16]; p < 0.05) and increased frequency of Ca sparks, measured by confocal microscopy using Fluo-4 (sparks/100μm/s. WT = 0.52 ± 0.08 [111]; KO = 1.21 ± 0.14 [124]; p < 0.001). We conclude that protein 4.1 R affects repolarisation of cardiac myocytes. This may have a role in bringing about QT prolongation in KO mice. The prolonged APD, together with effects on Ca handling proteins, may alter Ca regulation and cell contractility. The specific mechanisms controlling these effects are under investigation.

Growth hormone reverses age-related cardiac myofilament dysfunction in rats

2001 ◽  
Vol 281 (2) ◽  
pp. H915-H922 ◽  
Author(s):  
Thomas Wannenburg ◽  
Amir S. Khan ◽  
David C. Sane ◽  
Mark C. Willingham ◽  
Tony Faucette ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Cardiac Contractility ◽  
Left Ventricular ◽  
Force Generation ◽  
Brown Norway ◽  
Isolated Hearts ◽  
Gh Replacement ◽  
Age Related ◽  
Cardiac Myofilament ◽  
Lv Volume

We tested the hypotheses that aging is associated with a reduction in overall cardiac contractility and myofilament force generation that could be reversed with growth hormone (GH) replacement. Three groups of male Brown-Norway rats were studied: young (YSAL: 8 mo old, n = 13), old (OSAL: 28 mo old, n = 13), and old GH-treated (OGH: 28 mo old, n = 12; 300 μg bovine GH, twice a day for 30 days). The left ventricular (LV) pressure-volume relation was derived in isolated hearts, after which isolated trabecular muscles from these hearts were permeabilized and maximal myofilament force generation (Fmax) was measured. LV developed pressures at a LV volume of 0.3 ml were significantly depressed with age: 84 ± 6 vs. 71 ± 6 mmHg (YSAL vs. OSAL, respectively, P= 0.001) and not restored by GH (69 ± 4 mmHg). Fmaxwas reduced in the aged hearts: 47.5 ± 3.12 vs. 35.9 ± 3.03 mN/mm2 (YSAL vs. OSAL, respectively, P = 0.014) but was restored with GH replacement to 46.7 ± 3.12 mN/mm2 (OSALvs. OGH, P = 0.021). Our results suggest that cellular myofilament contractility is reduced with aging and restored with GH replacement.

Phosphorylated compounds and function in isolated hearts: a 31P-NMR study

1991 ◽  
Vol 260 (1) ◽  
pp. H110-H117
Author(s):  
J. Aussedat ◽  
A. Ray ◽  
S. Lortet ◽  
H. Reutenauer ◽  
S. Grably ◽  
...  
Keyword(s):  
Work Load ◽  
Creatine Phosphate ◽  
Myocardial Cell ◽  
Left Ventricular ◽  
Mitochondrial Activity ◽  
Isolated Hearts ◽  
Nmr Study ◽  
Phosphorylated Compounds ◽  
Developed Pressure ◽  
And Function

The potential role of phosphorylated compounds in the control of myocardial cell respiration was investigated by means of 31P-nuclear magnetic resonance (NMR) spectroscopy. Isolated isovolumic rat hearts, perfused with a 9 mM glucose, 2 mM pyruvate medium at a constant beating rate (6 Hz) and temperature (37 degrees C), were subjected to changes in work load by varying the calcium concentration ([Ca2+]) in the perfusion fluid from 0.5 to 1.0, 1.5, or 2.0 mM. Each change in left ventricular developed pressure (LVDP) induced by the [Ca2+] change was accompanied by alterations in the inorganic phosphate-to-creatine phosphate ratio ([Pi]/[PCr]), with the ATP level remaining constant. The relationship between [Pi]/[PCr] and LVDP followed a Michaelis-Menten pattern with an apparent Michaelis constant (Km) of 0.09 and a maximal LVDP of 91 mmHg. This Km corresponded to intracellular concentrations of 1.2 mM for Pi and 13.0 mM for PCr. The calculated [ADP] and phosphorylation potential corresponding to these values were 44 microM and 151,000 M-1, respectively. All these values are close to those estimated under in situ physiological conditions. These results support the assumption that in the rat heart, as in skeletal muscle, mitochondrial activity could be controlled by changes in phosphorylated compound concentrations under normoxic conditions.

Abstract 419: Stim1 is Associated With Calcium Microdomains That are Required for Myofilament Remodeling and Signaling During Cardiac Hypertrophy

2015 ◽  
Vol 117 (suppl_1) ◽  
Author(s):  
Cory Parks ◽  
Ryan D Sullivan ◽  
Salvatore Mancarella
Keyword(s):  
Cardiac Hypertrophy ◽  
Heart Function ◽  
Cardiac Contractility ◽  
Pressure Overload ◽  
Left Ventricular ◽  
Neonatal Rat ◽  
Excitable Cells ◽  
Rat Cardiomyocytes ◽  
Cell Contractility

Stromal Interaction Protein 1 (STIM1) is the intracellular component of the store operated calcium channels. It is a ubiquitous Ca2+ sensor, prevalently located in the sarcoplasmic reticulum. In non-excitable cells, STIM1 is a key element in the generation of Ca2+signals that lead to gene expression and cell proliferation. A growing body of literature now suggests that STIM1 is important for normal heart function and plays a key role in the development of pathological cardiac hypertrophy. However, the precise mechanisms involving STIM1 and the Ca2+ signaling in excitable cells are not clearly established. We show that in neonatal rat cardiomyocytes, the spatial properties of STIM1-dependent Ca2+ signals determine restricted Ca2+ microdomains that regulate myofilaments remodeling and spatially segregated activation of pro-hypertrophic factors. Indeed, in vivo data obtained from an inducible cardiac restricted STIM1 knockout mouse, exhibited left ventricular dilatation associated with reduced cardiac contractility, which was corroborated by impaired single cell contractility. Furthermore, mice lacking STIM1 showed less adverse structural remodeling in response to pathological pressure overload-induced cardiac hypertrophy (transverse aortic constriction, TAC). We further show that the Ca2+ pool associated with STIM1 is the ON switch for extracellular signal-regulated kinase (ERK1/2)-mediated cytoplasm to nucleus signaling. These results highlight how STIM1-dependent Ca2+ microdomains have a major impact on intracellular Ca2+ homeostasis, cytoskeletal remodeling, signaling and cardiac function, even when excitation-contraction coupling is present.

scholarly journals Propylthiouracil-induced hypothyroidism is associated with increased tolerance of the isolated rat heart to ischaemia-reperfusion

2003 ◽  
Vol 178 (3) ◽  
pp. 427-435 ◽  
Author(s):  
C Pantos ◽  
V Malliopoulou ◽  
I Mourouzis ◽  
K Sfakianoudis ◽  
S Tzeis ◽  
...  
Keyword(s):  
Left Ventricular ◽  
Isolated Rat Heart ◽  
Isolated Hearts ◽  
Global Ischaemia ◽  
Basal Expression ◽  
Kinase C ◽  
Ischaemia Reperfusion ◽  
Protein Kinase C Epsilon ◽  
Developed Pressure ◽  
Jnk Activation

The present study investigated the response of the hypothyroid heart to ischaemia-reperfusion. Hypothyroidism was induced in Wistar rats by oral administration of propylthiouracil (0.05%) for 3 weeks (HYPO rats), while normal animals (NORM) served as controls. Isolated hearts from NORM and HYPO animals were perfused in Langendorff mode and subjected to zero-flow global ischaemia followed by reperfusion (I/R). Post-ischaemic recovery of left ventricular developed pressure was expressed as % of the initial value (LVDP%). Basal expression of protein kinase C epsilon (PKCepsilon) and PKCdelta and phosphorylation of p46 and p54 c-jun NH(2)-terminal kinases (JNKs) in response to I/R were assessed by Western blotting. LVDP% was found to be significantly higher in HYPO hearts than in NORM. At baseline, PKCepsilon expression was 1.4-fold more in HYPO than in NORM hearts, P<0.05, while PKCdelta was not changed. Furthermore, basal phospho-p54 and -p46 JNK levels were 2.2- and 2.6-fold more in HYPO than in NORM hearts, P<0.05. In response to I/R, in NORM hearts, phospho-p54 and -p46 JNK levels were 5.5- and 6.0-fold more as compared with the baseline values, P<0.05, while they were not significantly altered in HYPO hearts. HYPO hearts seem to display a phenotype of cardioprotection against ischaemia-reperfusion and this is associated with basal PKCepsilon overexpression and attenuated JNK activation after I/R.

scholarly journals Cardiac contractility modulation therapy in elderly patients with chronic heart failure: results of the 12-month follow-up

2021 ◽  
Vol 28 (2) ◽  
pp. 5-10
Author(s):  
I. A. Chugunov ◽  
K. V. Davtyan ◽  
A. H. Topchyan ◽  
N. A. Mironova ◽  
E. M. Gupalo
Keyword(s):  
Heart Failure ◽  
Elderly Patients ◽  
Nyha Class ◽  
Cardiac Contractility ◽  
Signs And Symptoms ◽  
Left Ventricular ◽  
Additional Treatment ◽  
Cardiac Contractility Modulation ◽  
Reduced Ejection Fraction

Aim. This study aimed to evaluate the efficacy and safety of cardiac contractility modulation (CCM) therapy in elderly patients with heart failure with reduced ejection fraction (HFrEF).Methods. Sixteen patients older than 65 years old (median age 70 years) undergoing CCM Optimizer (Impulse Dynamics) device implantation due to HFrEF (NYHA class II - 9 (56%), III - 4 (25%), IV - 3 (19%)) were enrolled in this two-center observational study. Before implantation 6-minute walk test (6MWT), transthoracic echocardiography (TTE) was performed on all patients, and NTproBNP levels were assessed. The follow-up duration was 12 months with 2, 6, 12-month follow-up visits. Control 6MWT, TTE and NTproBNP tests were performed at 6-month and 12-month follow-up visits.Results. Two patients died during follow-up due to HF decompensation. The remaining patients showed a significant improvement in 6MWT (350 m vs 402.5 m, p=0,01). We also noted a tendency towards the left ventricular EF improvement (33% vs 40%, p=0,2) and lower values of NTproBNP levels (1112 pg/ml vs 527 pg/ml, p=0,19).Conclusion. CCM therapy is a safe and efficient additional treatment option to manage elderly patients with HFrEF for reducing signs and symptoms of HF.

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