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

Circulation ◽  
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.

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

2014 ◽  
Vol 9 ◽  
pp. IMI.S13939 ◽  
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.

scholarly journals Corticotropin releasing hormone receptor 2 exacerbates chronic cardiac dysfunction

2017 ◽  
Vol 214 (7) ◽  
pp. 1877-1888 ◽  
Author(s):  
Takuma Tsuda ◽  
Mikito Takefuji ◽  
Nina Wettschureck ◽  
Kazuhiko Kotani ◽  
Ryota Morimoto ◽  
...  
Keyword(s):  
Heart Failure ◽  
Chronic Heart Failure ◽  
Cardiac Dysfunction ◽  
Hormone Receptor ◽  
Adenosine Monophosphate ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Corticotropin Releasing Hormone ◽  
Ventricular Ejection Fraction ◽  
Releasing Hormone

Heart failure occurs when the heart is unable to effectively pump blood and maintain tissue perfusion. Despite numerous therapeutic advancements over previous decades, the prognosis of patients with chronic heart failure remains poor, emphasizing the need to identify additional pathophysiological factors. Here, we show that corticotropin releasing hormone receptor 2 (Crhr2) is a G protein–coupled receptor highly expressed in cardiomyocytes and continuous infusion of the Crhr2 agonist, urocortin 2 (Ucn2), reduced left ventricular ejection fraction in mice. Moreover, plasma Ucn2 levels were 7.5-fold higher in patients with heart failure compared to those in healthy controls. Additionally, cardiomyocyte-specific deletion of Crhr2 protected mice from pressure overload-induced cardiac dysfunction. Mice treated with a Crhr2 antagonist lost maladaptive 3′-5′-cyclic adenosine monophosphate (cAMP)–dependent signaling and did not develop heart failure in response to overload. Collectively, our results indicate that constitutive Crhr2 activation causes cardiac dysfunction and suggests that Crhr2 blockade is a promising therapeutic strategy for patients with chronic heart failure.

scholarly journals Xinmailong Injection for Improvement of Cardiac Function in Patients with Heart Failure: A Systematic Review and Meta-Analysis

2020 ◽  
Vol 2020 ◽  
pp. 1-13
Author(s):  
Yuan-long Sun ◽  
Yi-ping Li ◽  
Ting-ting Qiang ◽  
Xiao-fen Ruan ◽  
Xiao-long Wang
Keyword(s):  
Heart Failure ◽  
Cardiac Function ◽  
Periplaneta Americana ◽  
Meta Analysis ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Cochrane Library ◽  
Ventricular Ejection Fraction ◽  
Patients With Heart Failure ◽  
Potential Factor

Background. Insect drugs have great potential for treating cardiovascular diseases. Xinmailong (XML) injection, a bioactive composite extracted from Periplaneta americana (a species of cockroach), was wildly used in treating heart failure in China. This meta-analysis aimed to assess the efficacy and safety of XML injection for the improvement of cardiac function in HF. Materials and Methods. Online literature search for relevant studies was performed using databases including PubMed, EMBASE, Cochrane Library, CNKI, and Wanfang. Left ventricular ejection fraction (LVEF), six-minute walk test (6MWT), and brain natriuretic peptide (BNP) were selected as target outcomes. The analysis was performed using Stata 12.0, and sources of heterogeneity were explored by subgroup analysis and metaregression. Results. 32 studies were included in this meta-analysis after meeting the inclusion/exclusion criteria. The results demonstrated that additional use of XML improved LVEF (WMD = 5.82, 95% CI: 5.52–7.13, P < 0.00001 ) and 6MWT (WMD = 51.48, 95% CI: 35.83–67.13, P < 0.00001 ) and reduced BNP (WMD = −172.84, 95% CI: −205.79 to −139.89, P < 0.00001 ). The results of subgroup analyses and metaregression suggested that XML injection has more cardiac function improvement for middle-aged HF patients than youth, and greater LVEF and 6MWT improvement were associated with higher average age. Conclusions. XML plus conventional treatment demonstrated a significant effect in reducing cardiac dysfunction in HF patients, and age is a potential factor of higher efficacy. Given the heterogeneity and bias of the included RCTs, large, prospective, rigorous trials are still needed.

Abstract 18902: Adaptive Servo-ventilation is More Effective in Dilated Cardiomyopathy Patients than Ischemic Cardiomyopathy Patients and Heart Failure with Preserved Ejection Fraction Patients

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Tatsunori Ikeda ◽  
Manabu Fujimoto ◽  
Masakazu Yamamoto ◽  
Kazuyasu Okeie ◽  
Hisayoshi Murai ◽  
...  
Keyword(s):  
Heart Failure ◽  
Ejection Fraction ◽  
Cardiac Function ◽  
Dilated Cardiomyopathy ◽  
Ischemic Cardiomyopathy ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Preserved Ejection Fraction ◽  
Ventricular Ejection Fraction ◽  
Adaptive Servo Ventilation

Introduction: Central sleep apnea (CSA) is a common complication in heart failure patients (HF) and closely associated with poor prognosis. Adaptive servo-ventilation (ASV) is a new treatment for HF with CSA. Some study indicated ASV might improve cardiac function and its prognosis. However, there was little discussion by each background disease. Methods and Results: We examined 64 HF with CSA patients (involving 15 dilated cardiomyopathy (DCM) patients, 27 ischemic cardiomyopathy (ICM) patients, and 22 heart failure with preserved ejection fraction (HFpEF) patients) treated with ASV who had not been admitted to the hospital due to worsening HF in the 6 months before initiating ASV therapy. During 1 and 6 months observation, apnia-hypopnea index and brain natriuretic peptide were decreased significantly than baseline in all groups. There was similar in left ventricular ejection fraction in ICM and HFpEF groups during observation, however, in DCM group, there was significantly improved (29.3 +/- 14.3 to 36.5 +/- 12.4, and to 40.5 +/- 14.9%, P<0.01 compared with baseline). And left ventricular end systolic diameter was significantly shortened (53.7 +/- 11.1 to 30.4 +/- 11.5, and to 47.6 +/- 12.0 mm, P<0.01 compared with baseline), in spite of left ventricular end diastolic diameter was not changed. Conclusions: These results indicate that ASV is more effective in DCM patient with modifying hemodynamics and cardiac function than ICM and HFpEF patients.

scholarly journals A Meta-Analysis of the Therapeutic Effects of Glucagon-Like Peptide-1 Agonist in Heart Failure

2012 ◽  
Vol 2012 ◽  
pp. 1-7 ◽  
Author(s):  
Mohammed Munaf ◽  
Pierpaolo Pellicori ◽  
Victoria Allgar ◽  
Kenneth Wong
Keyword(s):  
Heart Failure ◽  
Ejection Fraction ◽  
Cardiac Function ◽  
Animal Studies ◽  
Meta Analysis ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Therapeutic Effects ◽  
Significant Heterogeneity ◽  
Ventricular Ejection Fraction

We conducted a meta-analysis of the existing literature of the therapeutic effects of using GLP-1 agonists to improve the metabolism of the failing heart. Animal studies showed significant improvement in markers of cardiac function, such as left ventricular ejection fraction (LVEF), with regular GLP-1 agonist infusions. In clinical trials, the potential effects of GLP-1 agonists in improving cardiac function were modest: LVEF improved by 4.4% compared to placebo (95% C.I 1.36–7.44, ). However, BNP levels were not significantly altered by GLP-1 agonists in heart failure. In two trials, a modest increase in heart rate by up to 7 beats per minute was noted, but meta-analysis demonstrated this was not significant statistically. The small number of studies plus variation in the concentration and length of the regime between the trials would limit our conclusions, even though statistically, heterogeneity chi-squared tests did not reveal any significant heterogeneity in the endpoints tested. Moreover, studies in non-diabetics with heart failure yielded conflicting results. In conclusion, the use of GLP-1 agonists has at best a modest effect on ejection fraction improvement in heart failure, but there was no significant improvement in BNP levels in the meta-analysis.

scholarly journals Lingguizhugan decoction attenuates doxorubicin-induced heart failure in rats by improving TT-SR microstructural remodeling

2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Xueping Li ◽  
Guangmin Xu ◽  
Shujun Wei ◽  
Baocheng Zhang ◽  
Huan Yao ◽  
...  
Keyword(s):  
Heart Failure ◽  
Left Ventricular Ejection Fraction ◽  
Ejection Fraction ◽  
Cardiac Dysfunction ◽  
Left Ventricular ◽  
The Body ◽  
Ventricular Ejection ◽  
Left Ventricular Ejection ◽  
Heart Weight ◽  
Ventricular Ejection Fraction

Abstract Background Lingguizhugan decoction (LGZG), an ancient Chinese herbal formula, has been used to treat cardiovascular diseases in eastern Asia. We investigated whether LGZG has protective activity and the mechanism underlying its effect in an animal model of heart failure (HF). Methods A rat model of HF was established by administering eight intraperitoneal injections of doxorubicin (DOX) (cumulative dose of 16 mg/kg) over a 4-week period. Subsequently, LGZG at 5, 10, and 15 mL/kg/d was administered to the rats intragastrically once daily for 4 weeks. The body weight, heart weight index (HWI), heart weight/tibia length ratio (HW/TL), and serum BNP level were investigated to assess the effect of LGZG on HF. Echocardiography was performed to investigate cardiac function, and H&E staining to visualize myocardial morphology. Myocardial ultrastructure and T-tubule-sarcoplasmic reticulum (TT-SR) junctions were observed by transmission electron microscopy. The JP-2 protein level was determined by Western blotting. The mRNA level of CACNA1S and RyR2 and the microRNA-24 (miR-24) level were assayed by quantitative RT-PCR. Results Four weeks after DOX treatment, rats developed cardiac damage and exhibited a significantly increased BNP level compared with the control rats (169.6 ± 29.6 pg/mL versus 80.1 ± 9.8 pg/mL, P < 0.001). Conversely, LGZG, especially at the highest dose, markedly reduced the BNP level (93.8 ± 17.9 pg/mL, P < 0.001). Rats treated with DOX developed cardiac dysfunction, characterized by a strong decrease in left ventricular ejection fraction compared with the control (58.5 ± 8.7% versus 88.7 ± 4.0%; P < 0.001). Digoxin and LGZG improved cardiac dysfunction (79.6 ± 6.1%, 69.2 ± 2.5%, respectively) and preserved the left ventricular ejection fraction (77.9 ± 5.1, and 80.5 ± 4.9, respectively, P < 0.01). LGZG also improved the LVEDD, LVESD, and FS and eliminated ventricular hypertrophy, as indicated by decreased HWI and HW/TL ratio. LGZG attenuated morphological abnormalities and mitochondrial damage in the myocardium. In addition, a high dose of LGZG significantly downregulated the expression of miR-24 compared with that in DOX-treated rats (fold change 1.4 versus 3.4, P < 0.001), but upregulated the expression of JP-2 and antagonized DOX-induced T-tubule TT-SR microstructural remodeling. These activities improved periodic Ca2+ transients and cell contraction, which may underly the beneficial effect of LGZG on HF. Conclusions LGZG exerted beneficial effects on DOX-induced HF in rats, which were mediated in part by improved TT-SR microstructural remodeling.

FUNCTIONAL RESILIENCE OF C57BL/6J MOUSE HEART TO DIETARY FAT OVERLOAD

2021 ◽  
Author(s):  
Satya Murthy Tadinada ◽  
Eric T. Weatherford ◽  
Greg V. Collins ◽  
Gourav Bhardwaj ◽  
Jesse Cochran ◽  
...  
Keyword(s):  
Cardiac Function ◽  
Diabetic Cardiomyopathy ◽  
Cardiac Dysfunction ◽  
High Fat Diet ◽  
Saturated Fat ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Mouse Heart ◽  
High Fat ◽  
Ventricular Ejection Fraction

Molecular mechanisms underlying cardiac dysfunction and subsequent heart failure in diabetic cardiomyopathy are incompletely understood. Initially we intended to test the role of GRK2, a potential mediator of cardiac dysfunction in diabetic cardiomyopathy, but found that control animals on HFD did not develop cardiomyopathy. Cardiac function was preserved in both wildtype and GRK2 knockout animals fed high fat diet as indicated by preserved left ventricular ejection fraction (LVEF) although heart mass was increased. The absence of cardiac dysfunction led us to rigorously evaluate the utility of diet-induced obesity to model diabetic cardiomyopathy in mice. Using pure C57BL/6J animals and various diets formulated with different sources of fat- lard (32% saturated fat, 68% unsaturated fat) or hydrogenated coconut oil (95% saturated fat), we consistently observed left ventricular hypertrophy, preserved LVEF and preserved contractility measured by invasive hemodynamics in animals fed high fat diet. Gene expression patterns that characterize pathological hypertrophy were not induced but a modest induction of various collagen isoforms and matrix metalloproteinases were observed in heart with high fat diet feeding. PPARa-target genes that enhance lipid utilization such as Pdk4, CD36, AcadL and Cpt1b were induced, but mitochondrial energetics were not impaired. These results suggest while long-term fat feeding in mice induces cardiac hypertrophy and increases cardiac fatty acid metabolism, it may not be sufficient to activate pathological hypertrophic mechanisms that impair cardiac function or induce cardiac fibrosis. Thus, additional factors that are currently not understood may contribute to the cardiac abnormalities previously reported by many groups.

Anthracycline-related cardiotoxicity: epidemiology, surveillance, prophylaxis, management, and prognosis

2018 ◽  
Author(s):  
Daniela Cardinale ◽  
Carlo Maria Cipolla
Keyword(s):  
Heart Failure ◽  
Cardiac Dysfunction ◽  
Cell Injury ◽  
Clinical Effectiveness ◽  
Angiotensin Converting Enzyme Inhibitors ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Current Standard ◽  
Converting Enzyme Inhibitors ◽  
Ventricular Ejection Fraction

Anthracycline-induced cardiotoxicity is of considerable concern, as it may compromise the clinical effectiveness of treatment, affecting both quality of life and overall survival in cancer patients, independently of the oncological prognosis. It is probable that anthracycline-induced cardiotoxicity is a unique and continuous phenomenon starting with myocardial cell injury, followed by progressive left ventricular ejection fraction (LVEF) decline that, if disregarded and not treated progressively leads to overt heart failure. The main strategy for minimizing anthracycline-induced cardiotoxicity is early detection of high-risk patients and prompt prophylactic treatment. According to the current standard for monitoring cardiac function, cardiotoxicity is usually detected only when a functional impairment has already occurred, precluding any chance of its prevention. At present, anthracycline-induced cardiotoxicity can be detected at a preclinical phase, very much before the occurrence of heart failure symptoms, and before the LVEF drops by measurement of cardiospecific biochemical markers or by Doppler myocardial and deformation imaging. The role of troponins in identifying subclinical cardiotoxicity and treatment with angiotensin-converting enzyme inhibitors, in order to prevent LVEF reduction is an effective strategy that has emerged in the last 15 years. If cardiac dysfunction has already occurred, partial or complete LVEF recovery may still be achieved if cardiac dysfunction is detected early after the end of chemotherapy and heart failure treatment is promptly initiated.

P3554CMR Fast-SENC intramyocardial LV & RV segmental strain helps manage cardioprotective therapy in patients exhibiting cardiotoxicity during cancer treatment

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
H Steen ◽  
M Montenbruck ◽  
P Wuelfing ◽  
S Esch ◽  
A K Schwarz ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Heart Failure ◽  
Cardiac Function ◽  
Cancer Treatment ◽  
Cancer Patients ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Ventricular Ejection Fraction ◽  
The Impact

Abstract Background Cardiotoxicity during cancer treatment has become an acknowledged problem of chemotherapy medications and radiation therapy. Limitations of biomarkers and imaging tests such as echocardiography left ventricular ejection fraction (LVEF) hinder early detection of cardiotoxicity and proactive cardioprotective therapy. Once the heart is unable to compensate for subclinical dysfunction, systemic damage and remodeling occurs increasing the potential for heart failure. Fast-SENC segmental intramyocardial strain (fSENC) is a unique cardiac magnetic resonance imaging (CMR) test that regionally detects subclinical intramyocardial dysfunction in 1 heartbeat. This study evaluates the ability of fSENC to detect subclinical cardiotoxicity and manage cardioprotective therapy in cancer patients. Methods This single center, prospective Prefect Study was used to evaluate cardiotoxicity and the impact of cardioprotective therapy in Breast Cancer and Lymphoma patients (NCT03543228). fSENC was acquired with a 1.5T MRI and processed with the MyoStrain software to quantify intramyocardial strain. Segmental strain was measured in three short axis scans (basal, midventricular & apical) with 16LV/6RV longitudinal segments & three long axis scans (2-, 3-, 4-chamber) with 21LV/5RV circumferential segments. fSENC CMR was performed before chemotherapy, during and after anthracycline/taxan therapy, at 1 year follow-up, and as needed in between designated follow-up periods. Cardioprotective therapy was offered to patients meeting the definition of cardiotoxicity by the ESC Guidelines on Cardiotoxicity and/or ESMO Clinical Practice Guidelines or those observing a substantial decline in cardiac function. Comparisons were made with paired t-Test with a 95% confidence interval. Results Two hundred eight (208) CMRs were performed in fifty-two (52) patients (44 female). Patients had an average (± stdev) age of 53 (15) yrs, BMI of 26 (5) kg/m2; 77% had breast cancer, 23% had Lymphoma. fSENC CMRs required 11 (2) min total exam time. Figure 1 shows bar graphs of the % of normal LV myocardium (e.g. % LV MyoStrain Segments <−17%) at baseline and sequential follow-ups for patients without cardiotoxicity and with cardiotoxicity requiring cardioprotective therapy. Patients observing cardiotoxicity had a statistically significant decline in cardiac function measured by segmental fSENC (p=0.0002) which resolved after cardioprotective therapy. Figure 1 Conclusion Segmental fSENC intramyocardial strain detects subclinical cardiotoxicity during chemotherapy and impact of cardioprotective therapy. The ability to serve as a surrogate safety endpoint for chemotherapy or other pharmacological agents, and aid management of cardiotoxicity by serving as a surrogate efficacy endpoint for cardioprotection agents, dosage, and patient compliance may help physicians detect subclinical cardiac dysfunction, and proactively manage cancer patients to avoid early or late heart failure.

scholarly journals The power of optimal medical therapy using angiotensin receptor-neprilysin inhibitor in acute decompensated heart failure, sparing a critical patient open-heart surgery with a device therapy: a case report

2020 ◽  
Author(s):  
Fady Gerges ◽  
Austin Komaranchath ◽  
Faiz Al Bakshy ◽  
Abdallah Almaghraby
Keyword(s):  
Heart Failure ◽  
Case Report ◽  
Coronary Artery ◽  
Ejection Fraction ◽  
Cardiac Function ◽  
Acute Decompensated Heart Failure ◽  
Decompensated Heart Failure ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Ventricular Ejection Fraction

Abstract Background Timely use of Sacubitril/Valsartan has the potential to significantly improve cardiac function and dramatically reduce secondary mitral regurgitation (MR) severity even in patients presenting with acute decompensated heart failure (HF), not only in compensated chronic HF patients. The outstanding impact of echocardiography is obvious in monitoring improvement of cardiac function and MR severity in patients with HF with reduced ejection fraction (HFrEF). Case summary We report a relevant case of an elderly patient who presented with acute decompensated HF and severe MR. He was symptomatic despite being on maximally tolerated doses of ACEI, beta-blockers, and diuretics. Left ventricular ejection fraction (LVEF) improved from 15% to 35% 2 weeks following initiation of Sacubitril/Valsartan during second HF hospitalization. There was a dramatic improvement of patient’s symptoms from New York Heart Association (NYHA) Class IV to NYHA I. N-terminal pro B-type natriuretic peptide reduced from 9000 pg/mL to 800 pg/mL. Coronary angiography depicted three-vessel coronary artery disease. The patient was advised to undergo coronary artery bypass graft surgery with mitral valve repair, then followed by implantation of a cardiac resynchronization therapy-defibrillator device (CRT-D) if no LV function improvement is observed after revascularization. The electrocardiogram showed Q waves in inferior leads with QRSd ≥ 125 ms, hence a good candidate for CRT. Following an elective percutaneous coronary intervention, LVEF further improved to 50%. The patient became asymptomatic with preserved LVEF on follow-up for 18 months later. Discussion This case report documents the swift echocardiographic and symptom improvement in a decompensated end-stage HF patient when Sacubitril/Valsartan initiated during acute setting.

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