Adaptive versus maladaptive cardiac remodelling in response to sustained β-adrenergic stimulation in a new ‘ISO on/off model’

On the one hand, sustained β-adrenergic stress is a hallmark of heart failure (HF) and exerts maladaptive cardiac remodelling. On the other hand, acute β-adrenergic stimulation maintains cardiac function under physiological stress. However, it is still incompletely understood to what extent the adaptive component of β-adrenergic signaling contributes to the maintenance of cardiac function during chronic β-adrenergic stress. We developed an experimental catecholamine-based protocol to distinguish adaptive from maladaptive effects. Mice were for 28 days infused with 30 mg/kg body weight/day isoproterenol (ISO) by subcutaneously implanted osmotic minipumps (‘ISO on’). In a second and third group, ISO infusion was stopped after 26 days and the mice were observed for additional two or seven days without further ISO infusion (‘ISO off short’, ‘ISO off long’). In this setup, ‘ISO on’ led to cardiac hypertrophy and slightly improved cardiac contractility. In stark contrast, ‘ISO off’ mice displayed progressive worsening of left ventricular ejection fraction that dropped down below 40%. While fetal and pathological gene expression (increase in Nppa, decrease in Myh6/Myh7 ratios, increase in Xirp2) was not induced in ‘ISO on’, it was activated in ‘ISO off’ mice. After ISO withdrawal, phosphorylation of phospholamban (PLN) at the protein kinase A (PKA) phosphorylation site Ser-16 dropped down to 20% as compared to only 50% at the Ca2+/Calmodulin-dependent kinase II (CaMKII) phosphorylation site Thr-17 in ‘ISO off’ mice. PKA-dependent cardioprotective production of the N-terminal proteolytic product of histone deacetylase 4 (HDAC4-NT) was reduced in ‘ISO off’ as compared to ‘ISO on’. Taken together, these data indicate that chronic ISO infusion induces besides maladaptive remodelling also adaptive PKA signalling to maintain cardiac function. The use of the ‘ISO on/off’ model will further enable the separation of the underlying adaptive from maladaptive components of β-adrenergic signalling and may help to better define and test therapeutic targets downstream of β-adrenergic receptors.

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Abstract 314: Loss of Sarcospan has a Deleterious Effect on Cardiac Function in Aged Mice

Circulation Research ◽

10.1161/res.115.suppl_1.314 ◽

2014 ◽

Vol 115 (suppl_1) ◽

Author(s):

Michelle S Parvatiyar ◽

Jamie L Marshall ◽

Maria C Jordan ◽

Reginald T Nguyen ◽

Kenneth P Roos ◽

...

Keyword(s):

Cardiac Function ◽

Immune Cell ◽

Expression Profiles ◽

Weight Ratio ◽

Left Ventricular ◽

Calcium Handling ◽

Left Ventricular Ejection ◽

Adrenergic Stimulation ◽

Cardiac Sarcolemma ◽

Ventricular Ejection Fraction

Sarcospan (SSPN) has been shown to have an important role in stabilizing sarcolemmal dystrophin- and utrophin-glycoprotein adhesion complexes. Loss of sarcolemmal integrity leads to immune cell infiltration and inappropriate exchange of cellular contents with the extracellular milieu. Our laboratory has shown SSPN loss destabilizes skeletal muscle adhesion and reduces sarcolemmal dystrophin localization, whereas its complete loss due to mutation underlies development of Duchenne muscular dystrophy (DMD). Loss of dystrophin leads to cardiac dysfunction and early mortality in DMD patients. The role of SSPN in the heart is unknown. We present immunofluorescence data revealing reduction of dystrophin and the sarcoglycans with a coordinate increase of β1D integrin levels at the SSPN-null cardiac sarcolemma relative to WT. Also, SSPN loss decreases cardiac P-Akt levels, disrupting signaling promoting compensatory physiological hypertrophy. These studies suggest a fundamental role for SSPN in cardiac maintenance and function, since left ventricular mass increases with age and upon isoproterenol administration (0.8 mg/day for two wks). Aged SSPN-null mice developed hypertrophy, evidenced as increased heart/body weight ratio and left ventricular wall dimension. The SSPN-null mice lacked the characteristic initial rise in cardiac output, left ventricular ejection fraction (LvEF %), induced by chronic β-adrenergic stimulation. Functionally, aged SSPN-null hearts had an increased E/A ratio indicating restrictive ventricular filling and decreased fractional shortening F/S (%) upon isoproterenol administration. Aged untreated SSPN-null hearts had increased fibrosis compared to aged WT controls, however isoproterenol treated SSPN-null hearts displayed exacerbated fibrotic response compared to WT. To assess whether SSPN-null hearts have altered gene expression profiles during progression of pathogenesis, qRT-PCR will be utilized to measure differences in expression of fetal gene and calcium-handling proteins. In summary, we have found that SSPN has an important role in maintaining cardiac function, its loss exacerbates the hypertrophic response and localization of stabilizing adhesion complexes at the cardiac muscle sarcolemma.

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A Randomized Controlled Trial to Study the Effect of Yoga Therapy on Cardiac Function and N Terminal Pro BNP in Heart Failure

Integrative Medicine Insights ◽

10.4137/imi.s13939 ◽

2014 ◽

Vol 9 ◽

pp. IMI.S13939 ◽

Cited By ~ 12

Author(s):

Bandi Hari Krishna ◽

Pravati Pal ◽

G. K. Pal ◽

J. Balachander ◽

E. Jayasettiaseelon ◽

...

Keyword(s):

Heart Failure ◽

Cardiac Function ◽

Medical Therapy ◽

Left Ventricular ◽

Left Ventricular Ejection ◽

Control Group ◽

Tei Index ◽

Ventricular Ejection Fraction ◽

Yoga Therapy ◽

Standard Medical Therapy

Aims The purpose of this study was to evaluate whether yoga training in addition to standard medical therapy can improve cardiac function and reduce N terminal pro B-type natriuretic peptide (NT pro BNP) in heart failure (HF). Methods 130 patients were recruited and randomized into two groups: Control Group (CG) ( n = 65), Yoga Group (YG). In YG, 44 patients and in CG, 48 patients completed the study. Cardiac function using left ventricular ejection fraction (LVEF), myocardial performance index (Tei index), and NT pro BNP, a biomarker of HF, was assessed at baseline and after 12 weeks. Result Improvement in LVEF, Tei index, and NT pro BNP were statistically significant in both the groups. Furthermore, when the changes in before and after 12 weeks were in percentage, LVEF increased 36.88% in the YG and 16.9% in the CG, Tei index was reduced 27.87% in the YG and 2.79% in the CG, NT pro BNP was reduced 63.75% in the YG and 10.77% in the CG. The between group comparisons from pre to post 12 weeks were significant for YG improvements (LVEF, P < 0.01, Tei index, P < 0.01, NT pro BNP, P < 0.01). Conclusion These results indicate that the addition of yoga therapy to standard medical therapy for HF patients has a markedly better effect on cardiac function and reduced myocardial stress measured using NT pro BNP in patients with stable HF.

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Abstract 1213: Cardiac Overexpression of Epac1 in Transgenic Mice Protects Heart from Lipopolysaccharide-induced Cardiac Dysfunction and Inhibits JAK-STAT Pathway

Circulation ◽

10.1161/circ.116.suppl_16.ii_246-b ◽

2007 ◽

Vol 116 (suppl_16) ◽

Author(s):

Satoshi Okumura ◽

Yunzhe Bai ◽

Meihua Jin ◽

Sayaka Suzuki ◽

Akiko Kuwae ◽

...

Keyword(s):

Heart Failure ◽

Cyclic Amp ◽

Transgenic Mice ◽

Cardiac Function ◽

Proinflammatory Cytokines ◽

Cardiac Dysfunction ◽

Left Ventricular ◽

Left Ventricular Ejection ◽

Ventricular Ejection Fraction ◽

Stat Pathway

The sympathetic nervous system and proinflammatory cytokines are believed to play independent roles in the pathophysiology of heart failure. However, the recent identification of Epac (exchange protein activated by cyclic AMP), a new cyclic AMP-binding protein that directly activates Rap1, have implicated that there may be a potential cross talk between the sympathetic and cytokine signals. In order to examine the role of Epac in cytokine signal to regulate cardiac function, we have generated transgenic mice expressing the human Epac1 gene under the control of alpha-cardiac myosin heavy chain promoter (Epac1-TG), and examined their response in lipopolysaccharide (LPS)-induced cardiac dysfunction, a well established model for sepsis-induced cardiac dysfunction. Sepsis-induced cardiac dysfunction results from the production of proinflammatory cytokines. At baseline, left ventricular ejection fraction (LVEF) was similar (TG vs. NTG, 67±1.7 vs. 69±2.1%, n =7–9). The degree of cardiac hypertrophy (LV(mg)/tibia(mm)) was also similar at 3 months old (TG vs. NTG 4.0±0.1 vs. 4.2±0.1, n =5–6), but it became slightly but significantly greater in Epac1-TG at 5 month old (TG vs. NTG 4.9±0.1 vs. 4.4±0.1, p< 0.05, n =5–7). LPS (5mg/kg) elicited a significant and robust reduction of LVEF in both Epac1-TG and NTG, but the magnitude of this decrease was much less in Epac1-TG at 6 hr after injection (TG vs. NTG 48±2.4 vs. 57±1.8%, p< 0.01, n =6–9). At 24 hr after injection, cardiac function was restored to the baseline in both Epac1-TG and NTG. We also examined the activation of JAK-STAT pathway at 24 hr after injection. The tyrosine phosphorylation of STAT1 (Tyr701) and STAT3 (Tyr705) in LV, which is an indicator of STAT activation, was reduced to a greater degree in Epac1-TG by 31±8.8% ( p< 0.05, n =4) and 29±5.9% ( p< 0.05, n =7), respectively, relative to that in NTG. Taken together, Epac1 protects the heart from the cytokine-induced cardiac dysfunction, at least in part, through the inhibition of the JAK-STAT pathway, suggesting the beneficial role played by sympathetic signal to antagonize proinflammatory cytokine signal in heart failure.

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Effects of Exercise on Cardiac Function Outcomes in Women Receiving Anthracycline or Trastuzumab Treatment for Breast Cancer: A Systematic Review and Meta-Analysis

Applied Sciences ◽

10.3390/app11188336 ◽

2021 ◽

Vol 11 (18) ◽

pp. 8336

Author(s):

Pedro Antunes ◽

Dulce Esteves ◽

Célia Nunes ◽

Anabela Amarelo ◽

José Fonseca-Moutinho ◽

...

Keyword(s):

Breast Cancer ◽

Systematic Review ◽

Cardiac Function ◽

Meta Analysis ◽

Left Ventricular ◽

Left Ventricular Ejection ◽

Cochrane Library ◽

Circulating Biomarkers ◽

Ventricular Ejection Fraction ◽

Secondary Outcomes

Background: we conducted a systematic review and meta-analysis of randomized controlled trials (RCTs) to evaluate the efficacy of exercise training on cardiac function and circulating biomarkers outcomes among women with breast cancer (BC) receiving anthracycline or trastuzumab-containing therapy. Methods: PubMed, EMBASE, Cochrane Library, Web of Science and Scopus were searched. The primary outcome was change on left ventricular ejection fraction (LVEF). Secondary outcomes included diastolic function, strain imaging and circulating biomarkers. Results: Four RCTs were included, of those three were conducted during anthracycline and one during trastuzumab, involving 161 patients. All trials provided absolute change in LVEF (%) after a short to medium-term of treatment exposure (≤6 months). Pooled data revealed no differences in LVEF in the exercise group versus control [mean difference (MD): 2.07%; 95% CI: −0.17 to 4.34]. Similar results were observed by pooling data from the three RCTs conducted during anthracycline. Data from trials that implemented interventions with ≥36 exercise sessions (n = 3) showed a significant effect in preventing LVEF decline favoring the exercise (MD: 3.25%; 95% CI: 1.20 to 5.31). No significant changes were observed on secondary outcomes. Conclusions: exercise appears to have a beneficial effect in mitigating LVEF decline and this effect was significant for interventions with ≥36 exercise sessions.

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Positive impact of cardiac contractile modulation on myocardial contractility and left ventricular synchronization in a patient with a left ventricular noncompaction

Siberian Medical Journal ◽

10.29001/2073-8552-2020-35-2-157-162 ◽

2020 ◽

Vol 35 (2) ◽

pp. 157-162

Author(s):

I. A. Ryabov ◽

I. N. Mamchur ◽

T. Yu. Chichkova ◽

S. E. Mamchur ◽

I. N. Sizova ◽

...

Keyword(s):

Heart Failure ◽

Myocardial Contractility ◽

Positive Impact ◽

Cardiac Contractility ◽

Left Ventricular ◽

Left Ventricular Ejection ◽

Ventricular Ejection Fraction ◽

Cardiac Contractile ◽

Heart Failure Questionnaire

The article provides a clinical case of a 58-year-old man with the fi rst clinical manifestation of chronic heart failure in the presence of a signifi cant decrease in the left ventricular ejection fraction. Left ventricular non-compaction cardiomyopathy was diagnosed by echocardiography. After 12 months, a cardiac contractility modulation device was implanted to the patient in the presence of disease progression despite optimal medical therapy. We assessed the course of disease, quality of life, exercise tolerance, and myocardial contractility of the patient before and six months after surgery. The methods of assessment were collection of patient complaints, physical examination, electrocardiography (ECG), fi lling out the Minnesota Living with Heart Failure Questionnaire (MLHFQ), sixminute walk test, spiroergometry, and echocardiography.

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87Effects of the chymase inhibitor fulacimstat on adverse cardiac remodelling after acute myocardial infarction - Results of the CHIARA MIA 2 trial

European Heart Journal ◽

10.1093/eurheartj/ehz747.0017 ◽

2019 ◽

Vol 40 (Supplement_1) ◽

Author(s):

H D Duengen ◽

R J Kim ◽

D Zahger ◽

K Orvin ◽

D Admon ◽

...

Keyword(s):

Myocardial Infarction ◽

Cardiac Mri ◽

Left Ventricular ◽

Cardiac Remodelling ◽

Left Ventricular Ejection ◽

Controlled Study ◽

P Value ◽

Tissue Remodelling ◽

Ventricular Ejection Fraction ◽

Chymase Inhibitor

Abstract Introduction Adverse cardiac remodelling represents the most important risk factor for the development of heart failure (HF) after myocardial infarction (MI). Chymase is a protease that generates locally pro-fibrotic factors such as angiotensin II, TGFβ, and matrixmetallproteases that contribute to tissue remodelling. Purpose This phase IIa study examined the effects of the chymase inhibitor fulacimstat on functional parameters of adverse cardiac remodelling after acute MI. Methods A double-blind, multinational, randomized, placebo-controlled study was performed in patients after first STEMI who were treated with primary percutaneous coronary intervention within 24h of symptom onset. To enrich for patients at risk of adverse remodelling, main inclusion criteria were a left-ventricular ejection fraction (LVEF)≤45% and an infarct size>10% on day 5 to 9 post MI as measured by cardiac MRI. On day 6 to 12 post MI, patients were randomized to treatment with either 25 mg fulacimstat (n=54) or placebo (n=53) twice daily on top of standard of care. The changes in LVEF, LVEDVI, and LVESVI from baseline to 6 months of treatment were analyzed by a central blinded cardiac MRI core laboratory. Results Fulacimstat was safe and well tolerated, 64.8% of patients treated with fulacimstat and 75.5% of patients treated with placebo reported treatment emergent adverse events. Fulacimstat achieved exposures that were approximately 10-fold higher than those predicted to be required for minimal therapeutic activity. After six months of treatment, there were no effects of fulacimstat compared to placebo on the changes in LVEF, LVEDVI, and LVESVI (see Table). Analysis of primary efficacy parameters Parameter Placebo Fulacimstat p-value LVEF (%) baseline 37.2±6.1 39.1±5.5 0.15 6 months 41.2±8.4 42.6±8.4 0.45 delta 4.0±5.0 3.5±5.4 0.69 LVEDVI (mL/m2) baseline 80.0±17.1 77.4±18.2 0.51 6 months 85.1±19.1 84.7±23.4 0.94 delta 5.1±18.9 7.3±13.3 0.54 LVESVI (mL/m2) baseline 50.5±13.0 47.3±12.3 0.26 6 months 51.1±16.9 49.6±18.1 0.71 delta 0.6±14.8 2.3±11.2 0.56 Data are given as mean ± standard deviation. Conclusion Fulacimstat was safe and well tolerated in patients with left-ventricular dysfunction (LVD) after first STEMI but had no effect on adverse cardiac remodelling in the experimental setting of this study. Acknowledgement/Funding The study was funded by its sponsor BAYER AG

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Transplantation of Endothelial Progenitor Cells in the Treatment of Coronary Artery Microembolism in Rats

Cell Transplantation ◽

10.1177/0963689720912688 ◽

2020 ◽

Vol 29 ◽

pp. 096368972091268

Author(s):

Yajun Xue ◽

Boda Zhou ◽

Jian Wu ◽

Guobin Miao ◽

Kun Li ◽

...

Keyword(s):

Growth Factor ◽

Cardiac Function ◽

Progenitor Cells ◽

Endothelial Progenitor Cells ◽

Low Dose ◽

Left Ventricular ◽

Left Ventricular Ejection ◽

High Dose ◽

Endothelial Progenitor ◽

Ventricular Ejection Fraction

As the impairment of myocardial microenvironments due to coronary microembolization (CME) compromises the treatment effect of percutaneous coronary intervention and leads to adverse prognosis, we hypothesized that endothelial progenitor cells (EPCs) transplantation could improve cardiac function in the condition of CME. Low- (2 × 105) and high- (2 × 106) dose rat bone marrow-derived EPCs were transplanted in a model of CME. To develop a CME model, rats were injected with autologous micro-blood-clots into the left ventricle. Echocardiograph was examined before and 1, 7, and 28 days after EPC transplantation; serum cardiac troponin I (cTNI), von Willebrand factor (vWF), and cardiac microRNA expression were examined one day after EPCs transplantation. Heart morphology and vascular endothelial growth factor (VEGF), vWF, and basic fibroblast growth factor (bFGF) expression were examined one day after EPC transplantation. After 10 days of culture inductions, BM-EPCs have high purity as confirmed by flow cytometry. Cardiac function reflected by left ventricular ejection fraction significantly decreased after CME treatment and rescued by low-dose EPC. Compared to the sham group, cTNI and vWF serum levels increased significantly after CME treatment and rescued by low-dose EPC and high-dose EPC. Low-dose EPC treatment decreased myocardial necrosis and fibrosis and elevated cardiac expression of VEGF and vWF, while decreasing the cardiac expression of bFGF. Low-dose EPC treatment significantly suppressed cardiac expression of microRNA-19a but significantly enhanced microRNA-21, microRNA-214, and microRNA-486-3p expression. In conclusion, our results indicate that low-dose EPC transplantation may play a proangiogenic, antifibroblast, antifibrosis, and antinecrosis role and enhance cardiac function in a rat model of CME through a microRNA-related pathway.

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P370Added value changes in signal sonr in patients with = <30% left ventricular ejection fraction

EP Europace ◽

10.1093/europace/euaa162.023 ◽

2020 ◽

Vol 22 (Supplement_1) ◽

Author(s):

J J Garcia Guerrero ◽

J Fernandez De La Concha Castaneda ◽

A Chacon Pinero ◽

J Garcia Fernandez ◽

I Fernandez Lozano ◽

...

Keyword(s):

Ejection Fraction ◽

Hospital Admission ◽

Dilated Cardiomyopathy ◽

Interim Analysis ◽

Cardiac Contractility ◽

Inverse Correlation ◽

Left Ventricular ◽

Left Ventricular Ejection ◽

Ventricular Ejection Fraction ◽

Lv Ejection Fraction

Abstract Abstract/Introduction Decompensated congestive heart failure (CHF) is a main and increasing health problem worldwide, which leads to patients’ bad outcomes and high money expenditure. Direct relationship between Brain Natriuretic Peptides (NT-proBNP) increasing levels and adverse clinical outcomes have been demonstrated in patients with CHF. SonR signal sensor, a micro-accelerometer embedded in the tip of the atrial lead in patients implanted with devices, picks up cardiac muscle vibration. Its amplitude is a surrogate for cardiac contractility, which is found to be further reduced in patients with decompensated CHF. Purpose We sought to find a significant inverse correlation between SonR signal and NT-proBNP levels, in order to use SonR as a surrogate of NT-proBNP to anticipate worsening CHF leading to hospital admission. Methods AVCs SONR trial is a pilot, prospective, observational, multicentre study, in which patients with dilated cardiomyopathy, any aetiology, LV ejection fraction ≤ 30%, at least one recent (< 1 year) hospital admission due to CHF, and implanted with CRT-D devices (used as dual-chamber, no left ventricular (LV) lead implanted) with SonR sensor feature, were enrolled. During a year, NT-proBNP and SonR values were obtained every month, and both levels compared (Pearson’s test) Results This an interim analysis of our data, 18 months after the first patient was enrolled. Twenty two patients and 116 data pairs were analysed. Most patients were men (91%) and had ischemic dilated cardiomyopathy (59%). Mean age was 61 (range 34-82) and mean LV ejection fraction was 27% (range 15-30). The mean Pearson’s correlation coefficient of the NT-proBNP values and the SonR signal was r = - 0.36 (95% CI -0.51 to -0.19), p < 0.00006 (Figure) Conclusions The interim analysis of this study shows an inverse and very significant relationship between SonR signal and NT-proBNP values. This suggests SonR signal might be used as predictor of worsening CHF. Abstract Figure

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Left ventricular function following adjuvant chemotherapy for breast cancer: The NCIC CTG MA5 experience

Journal of Clinical Oncology ◽

10.1200/jco.2006.24.18_suppl.522 ◽

2006 ◽

Vol 24 (18_suppl) ◽

pp. 522-522 ◽

Cited By ~ 2

Author(s):

L. E. Shepherd ◽

W. Parulekar ◽

K. I. Pritchard ◽

M. Trudeau ◽

N. Paul ◽

...

Keyword(s):

Breast Cancer ◽

Cardiac Function ◽

Left Ventricular ◽

Left Ventricular Ejection ◽

Cancer Society ◽

Ventricular Ejection Fraction ◽

Adjuvant Breast Cancer ◽

Changes Over Time ◽

To Receive

522 Background: Cardiac toxicity associated with anthracylines and more recently herceptin used in adjuvant breast cancer treatment is well recognized. Little is known about long term cardiac function as measured by left ventricular ejection fraction (LVEF) in patients post therapy. We analyzed the database of a randomized Phase 3 NCIC CTG study to assess changes over time in LVEF. Methods: Between 1989–1993, 710 pre/perimenopausal patients with node positive breast cancer were allocated to receive CEF (cyclophosphamide (C) 75 mg/m2 po d 1–14, epirubicin (E) 60 mg/m2 IV and fluorouracil (F) 500mg/m2 IV d1,d8) or CMF (C 100mg/m2 po d1–14, methotrexate (M) 40mg/m2 and F 600mg/m2 IV d1,8) given every 28 days for 6 cycles. The 10 year relapse-free survival was 52% (CEF) vs 45% (CMF), HR 1.31; stratified log rank, P=.007 (JCO, 2005,23;5166). LVEF was measured on both arms at baseline, months 6, 12, 36, and 60. Results: Compliance was good with measurements available on 100% of women at baseline, and 39% and 40% of patients at 60 months on the CEF and CMF arms respectively. Changes in LVEF from baseline are shown in the table . Conclusion: Changes in cardiac function as measured by a decrease in LVEF are not infrequent in patients after adjuvant therapy, even in the absence of anthracyclines. At 60 months, decreases of >10% were seen in up to 25% of patients receiving epirubicin administered at a cumulative dose of 720mg/m2 and in up to 10% of patients receiving CMF on whom measurements were available. The clinical significance of these findings needs to be assessed. Acknowledgements: This study was supported by funding from the Canadian Cancer Society through the National Cancer Institute of Canada and Pfizer Inc. [Table: see text] [Table: see text]

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Ginsenoside Rg3 Improves Cardiac Function after Myocardial Ischemia/Reperfusion via Attenuating Apoptosis and Inflammation

Evidence-based Complementary and Alternative Medicine ◽

10.1155/2016/6967853 ◽

2016 ◽

Vol 2016 ◽

pp. 1-8 ◽

Cited By ~ 23

Author(s):

Li-ping Zhang ◽

Yi-chuan Jiang ◽

Xiao-feng Yu ◽

Hua-li Xu ◽

Min Li ◽

...

Keyword(s):

Myocardial Ischemia ◽

Cardiac Function ◽

Caspase 3 ◽

Ischemia Reperfusion ◽

Left Ventricular ◽

Left Ventricular Ejection ◽

Ginsenoside Rg3 ◽

Ventricular Ejection Fraction ◽

Function Impairment ◽

Myocardial Ischemia Reperfusion

Objectives. Ginsenoside Rg3 is one of the ginsenosides which are the main constituents isolated from Panax ginseng. Previous study demonstrated that ginsenoside Rg3 had a protective effect against myocardial ischemia/reperfusion- (I/R-) induced injury. Objective. This study was designed to evaluate the effect of ginsenoside Rg3 on cardiac function impairment induced by myocardial I/R in rats. Methods. Sprague-Dawley rats were subjected to myocardial I/R. Echocardiographic and hemodynamic parameters and histopathological examination were carried out. The expressions of P53, Bcl-2, Bax, and cleaved caspase-3 and the levels of TNF-α and IL-1β in the left ventricles were measured. Results. Ginsenoside Rg3 increased a left ventricular fractional shortening and left ventricular ejection fraction. Treatment with ginsenoside Rg3 also alleviated increases of left ventricular end diastolic pressure and decreases of left ventricular systolic pressure and ±dp/dt in myocardial I/R-rats. Ginsenoside Rg3 decreased apoptosis cells through inhibiting the activation of caspase-3. Ginsenoside Rg3 also caused significant reductions of the contents of TNF-α and IL-1β in left ventricles of myocardial I/R-rats. Conclusion. The findings suggested that ginsenoside Rg3 possessed the effect of improving myocardial I/R-induced cardiac function impairment and that the mechanism of pharmacological action of ginsenoside Rg3 was related to its properties of antiapoptosis and anti-inflammation.

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