scholarly journals Velvet Antler Ameliorates Cardiac Function by Restoring Sarcoplasmic Reticulum Ca2+-ATPase Activity in Rats With Heart Failure After Myocardial Infarction

2021 ◽  
Vol 12 ◽  
Author(s):  
Haoyue Shi ◽  
Tianzi Zhao ◽  
Yanjun Li ◽  
Xiang Xiao ◽  
Jiayun Wu ◽  
...  
Keyword(s):  
Heart Failure ◽  
Cardiac Function ◽  
Protein Expression ◽  
Ischemia Reperfusion ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Histopathological Analysis ◽  
Mrna Levels ◽  
Ventricular Ejection Fraction ◽  
Velvet Antler

Objective: Velvet antler (VA; cornu cervi pantotrichum), a well-known traditional Chinese medicine, has been shown to exert cardioprotective effects. The purpose of this study was to investigate the effect of VA on heart failure (HF) caused by ischemia-reperfusion, and explore its possible mechanism from the regulation of sarcoplasmic/endoplasmic reticulum Ca2+-ATPase 2 alpha (SERCA2a).Methods: A rat model of HF was established by ligating the left anterior descending coronary artery of male Sprague–Dawley rats (n = 88). One week after surgery, VA (200, 400, or 800 mg/[kg day−1]) or enalapril (1 mg/[kg day−1]) was administered daily for the next 4 weeks. Heart function was detected by echocardiography and histopathological analysis. The serum BNP level was measured by ELISA, and the expression of SERCA2a, PLB, PLB-Ser16, and PKA was determined by western blotting. SERCA2a and PLB mRNA levels were determined by real-time quantitative PCR.Results: Compared with the sham group, cardiac function in the HF group, including the serum BNP level, heart mass index, myocardial collagen deposition, and left ventricular ejection fraction, was markedly reduced; however, these changes could be reversed by VA treatment. In addition, VA (200 mg/[kg·d−1]) inhibited the decrease of SERCA2a and PLB mRNA levels and SERCA2a, PLB, PLB-Ser16, and PKA protein expression and restored the activity of SERCA2a and PKA. Enalapril affected only PLB protein expression.Conclusion: VA can improve myocardial fibrosis and ventricular remodeling in rats, thereby helping to restore cardiac function. The underlying mechanism may be related to the upregulation of the expression and activation of PKA and PLB and the restoration of the expression and activity of SERCA2a.

Metformin improves cardiac function in a nondiabetic rat model of post-MI heart failure

2011 ◽  
Vol 301 (2) ◽  
pp. H459-H468 ◽  
Author(s):  
Meimei Yin ◽  
Iwan C. C. van der Horst ◽  
Joost P. van Melle ◽  
Cheng Qian ◽  
Wiek H. van Gilst ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Cardiac Function ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Oral Glucose ◽  
Mrna Levels ◽  
Ventricular Ejection Fraction ◽  
Glucose Levels ◽  
First Choice

Metformin is the first choice drug for the treatment of patients with diabetes, but its use is debated in patients with advanced cardiorenal disease. Epidemiological data suggest that metformin may reduce cardiac events, in patients both with and without heart failure. Experimental evidence suggests that metformin reduces cardiac ischemia-reperfusion injury. It is unknown whether metformin improves cardiac function (remodeling) in a long-term post-MI remodeling model. We therefore studied male, nondiabetic, Sprague-Dawley rats that were subjected to either myocardial infarction (MI) or sham operation. Animals were randomly allocated to treatment with normal water or metformin-containing water (250 mg·kg−1·day−1). At baseline, 6 wk, and 12 wk, metabolic parameters were analyzed and oral glucose tolerance tests (OGTT) were performed. Echocardiography and hemodynamic parameters were assessed 12 wk after MI. In the MI model, infarct size was significantly smaller after 12-wk metformin treatment (29.6 ± 3.2 vs. 38.0 ± 2.2%, P < 0.05). Moreover, metformin resulted in less left ventricular dilatation (6.0 ± 0.4 vs. 7.6 ± 0.6 mm, P < 0.05) and preservation of left ventricular ejection fraction (65.8 ± 3.7% vs. 48.6 ± 5.6%, P < 0.05) compared with MI control. The improved cardiac function was associated with decreased atrial natriuretic peptide mRNA levels in the metformin-treated group (50% reduction compared with MI, P < 0.05). Insulin resistance did not occur during cardiac remodeling (as indicated by normal OGTT) and fasting glucose levels and the pattern of the OGTT were not affected by metformin. Molecular analyses suggested that altered AMP kinase phosphorylation status and low insulin levels mediate the salutary effects of metformin. Altogether our results indicate that metformin may have potential to attenuate heart failure development after myocardial infarction, in the absence of diabetes and independent of systemic glucose levels.

Abstract 264: Nitrite Therapy Ameliorates Myocardial Injury via H2S and Nuclear Factor-Erythroid 2-Related Factor 2 (Nrf2)-Dependent Signaling in Chronic Heart Failure

2015 ◽  
Vol 117 (suppl_1) ◽  
Author(s):  
Kazi N Islam ◽  
Erminia Donnarumma ◽  
Shashi Bhushan ◽  
David J Lefer
Keyword(s):  
Heart Failure ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Left Ventricular ◽  
Antioxidant Defenses ◽  
Left Ventricular Ejection ◽  
Related Factor ◽  
Mrna Levels ◽  
Ventricular Ejection Fraction ◽  
Nrf2 Activation

Background: Nitric oxide (NO) and hydrogen sulfide (H 2 S) are reduced in congestive heart failure. Recent studies suggest cross-talk between NO and H 2 S signaling. We previously reported that sodium nitrite (NaNO 2 ) significantly ameliorates myocardial ischemia-reperfusion injury and heart failure. Nrf2 regulates the expression of antioxidant protein genes and is upregulated by H 2 S. We examined the effects of NaNO 2 therapy on endogenous H 2 S bioavailability and Nrf2 activation in mice subjected to ischemia-induced heart failure. Materials and Methods: Mice underwent 60 min. of left coronary artery occlusion and 4 weeks (WKS) of reperfusion. NaNO 2 (165 μg/kg) or saline vehicle (VEH) was administered at reperfusion and then in drinking water (100 mg/L) for 4 wks. Left ventricular ejection fraction (LVEF) was determined at baseline and 4 wks of reperfusion. Myocardial tissue was collected and analyzed for oxidative stress status and respective gene/protein levels. Results: NaNO 2 therapy preserved LVEF (47 ± 4% vs. 32 ± 4%, p < 0.01) and LV diastolic and systolic dimensions (LVEDD/LVESD; 4.0/3.1 mm vs. 4.5/3.9 mm, p < 0.05) at 4 wks. MDA and protein carbonyl contents were significantly reduced in NaNO 2 treated mice as compared to VEH. NaNO 2 markedly increased expression of CuZn-superoxide dismutase and catalase at 4 wks. Furthermore, NaNO 2 increased mRNA levels of H 2 S producing enzymes and H 2 S bioavailabilty. Cardiac Nrf2 activation was also observed with NaNO 2 therapy. Conclusions: Our results demonstrate that NaNO 2 therapy significantly improves left ventricular function via by increasing H 2 S bioavailability, activation of Nrf2, and increased antioxidant defenses.1

Abstract 17053: Cardiac AKAP12 Signalosome Overexpression Exacerbation of Heart Failure and Cardiac Calcium Handling

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Hanan Qasim ◽  
Bradley K McConnell
Keyword(s):  
Heart Failure ◽  
Protein Expression ◽  
Left Ventricular ◽  
Cardiac Contraction ◽  
Calcium Handling ◽  
Left Ventricular Ejection ◽  
Mrna Levels ◽  
Control Groups ◽  
Ventricular Ejection Fraction ◽  
Males And Females

Introduction: Heart failure (HF) is responsible for 1 out of 8 deaths per year in the U.S.A. and is the major cause of death globally. Calcium cycling is crucial for proper signaling processes and efficient cardiac contraction. In failing hearts, remodeled calcium handling contributes to cardiac dysfunction. Previously we reported enhanced cardiac function in mice lacking a functional A-Kinase Anchoring Protein 12 (AKAP12). In this study, we aim to investigate the role of AKAP12 overexpression (oxAKAP12) on heart failure progression through assessing Sarco/Endoplasmic Reticulum Ca2+-ATPase (SERCA2) and its regulatory protein Phospholamban (PLN). Hypothesis: Cardiac AKAP12 overexpression potentiates HF development through its action on SERCA2. Methods: HF was developed in WT and oxAKAP12-Tg mice of 8-10 weeks old males and females, through chronic Isoproterenol (ISO) administration (60 mg/kg/day for 14-days). Left ventricular homogenates were used for gene expression analysis. Furthermore, AKAP12 was transiently overexpressed in AC16 cells (human cardiomyocytes cell line), to assess protein expression levels upon treatment with 100 nM of ISO for 12-hrs. Results: Cardiac oxAKAP12 in both males and females reduced left ventricular ejection fraction (EF) by 14.5±2.5% and fractional shortening (FS) by 22.7±2.0% after 14-days of chronic ISO treatment when compared to control groups. Both RNA sequencing and RTqPCR analysis showed a significant reduction of SERCA2 and PLN mRNA levels, respectively, in left ventricular homogenates of male (53.5±2.0%, 39.0±2.5%) and female (50.0±2.5%, 45.0±2.0%) groups overexpressing AKAP12 treated with ISO (14-days) compared to control groups (p<0.005). In AC16 cells overexpressing AKAP12 and treated with ISO, SERCA2 protein expression was reduced by 37% (p=0.0413) while PLN protein expression was not significantly reduced compared to control groups. Conclusions: Cardiac oxAKAP12 negatively influences systolic function in both male and female mice, potentially through affecting calcium handling, which will be assessed in future experiments by evaluating calcium transients and sarcomere shortening in isolated primary cardiomyocytes from oxAKAP12 and control mice.

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.

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

2016 ◽  
Vol 2016 ◽  
pp. 1-8 ◽  
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.

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.

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.

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