scholarly journals Sildenafil ameliorates left ventricular T-tubule remodeling in a pressure overload-induced murine heart failure model

2016 ◽  
Vol 37 (4) ◽  
pp. 473-482 ◽  
Author(s):  
Chun-kai Huang ◽  
Bi-yi Chen ◽  
Ang Guo ◽  
Rong Chen ◽  
Yan-qi Zhu ◽  
...  
Keyword(s):  
Heart Failure ◽  
Pressure Overload ◽  
Left Ventricular ◽  
Failure Model ◽  
Heart Failure Model

Abstract 563: Cardiac TIGAR Reduces Myocardial Energetics and Cardiac Functionin the Pressure Overload Heart Failure Model

2019 ◽  
Vol 125 (Suppl_1) ◽  
Author(s):  
Yoshifumi Okawa ◽  
Atsushi Hoshino ◽  
Tomoya Kitani ◽  
Ryoetsu Yamanaka ◽  
Daichi Hato ◽  
...  
Keyword(s):  
Heart Failure ◽  
Pressure Overload ◽  
Failure Model ◽  
Myocardial Energetics ◽  
Heart Failure Model

scholarly journals A Juvenile Murine Heart Failure Model of Pressure Overload

2010 ◽  
Vol 32 (2) ◽  
pp. 145-153 ◽  
Author(s):  
Kristopher M. Cumbermack ◽  
Jun Cheng ◽  
Yibing Nong ◽  
William T. Mahle ◽  
Ronald W. Joyner ◽  
...  
Keyword(s):  
Heart Failure ◽  
Pressure Overload ◽  
Failure Model ◽  
Heart Failure Model

scholarly journals Synthesis of new azaindeno-acetonitrile derivative with inotropic activity against heart failure model

2019 ◽  
Vol 9 (6) ◽  
pp. 4598-4604
Keyword(s):  
Heart Failure ◽  
Biological Activity ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Failure Model ◽  
Inotropic Activity ◽  
Inotropic Drugs ◽  
Heart Failure Model ◽  
Steroid Derivative

Several steroid derivatives have prepared as inotropic drugs; however, there are few reports on azaindeno-steroid derivatives with inotropic activity. The objective of this investigation was to prepare some azaindeno-acetonitrile derivatives (compounds 3 to 7) to evaluate their biological activity on left ventricular pressure. The first step was achieved by preparation of azaindeno-steroid derivatives using reactions of etherification and addition. The second stage involves the evaluation of biological activity from azaindeno-steroid derivatives on left ventricular pressure in a heart failure model using either estrone or an enone-steroid derivative (compound 2) as controls. The results showed that only compound 6 increases left ventricular pressure compared with estrone, compounds 2-5 and 6. In conclusion, the positive inotropic effect exerted by compound 6 depends on the functional groups involved in its chemical structure.

Abstract 134: Influence of Predictive Modeling in Implementing Optimal Heart Failure Therapy in Inpatient setting

2014 ◽  
Vol 7 (suppl_1) ◽  
Author(s):  
Hari Prasad ◽  
Gujan Choudhary ◽  
Ali Fahad ◽  
Dwight Stapleton
Keyword(s):  
Heart Failure ◽  
Medical Therapy ◽  
Systolic Heart Failure ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Failure Model ◽  
Heart Failure Therapy ◽  
Device Therapy ◽  
Predictive Tool ◽  
Heart Failure Model

Background: A gap remains between evidence-based guidelines in the treatment of heart failure and current pharmacologic and device therapy. The Seattle Heart Failure Model is an accurate predictive tool that allows the clinician to quantitatively assess the influence of pharmacologic and device therapy on heart failure that has been validated in outpatient setting. We attempt to use the Seattle Heart Failure Model in optimizing the heart failure therapy. Methods: We examined 405 patients’ charts who were admitted with a diagnosis of acute systolic heart failure or acute on chronic systolic heart failure with left ventricular ejection fraction ≤ 40%. Twenty-one data elements were entered into the Seattle Heart Failure Model to create a survival estimate before and after implementation of interventions known to be beneficial, both pharmacologic (addition of ACE/ARB, statin, β-blocker, aldosterone blocker) and device-based (consideration for AICD, BiV pacer, BiV ICD). Results: The mean age of the population examined was 77 ± 9 years. The cohort was comprised of 72 % males, mean weight 89 ± 22.5kg, with NYHA class 2.4 ± 0.6 symptoms. Ischemic etiology was identified in 86% with a mean left ventricular EF of 29.8 ± 9 %. Laboratory data included mean Hgb 10.1 ±1.5g/dL with 15 ± 8% lymphocytes, mean total cholesterol of 176 ± 42mg/dL and mean sodium of 133 ± 3.5mmol/L. The one year all-cause mortality rates were 19.5 % reflecting advanced heart failure population. In the 405 patients examined, we were able to alter therapy (medical or device) in 86%. This included advancement of medical therapy in 56%, consideration for device referral in 11%, or both (medical therapy and device referral) in 19 %. This augmentation of therapy resulted in an increase in estimated mean life expectancy from 6.6 years to 9.6 years (p < 0.001). Conclusion: Use of the Seattle Heart Failure Model significantly helps in intensification of heart failure therapy when applied at time of discharge or in first follow up visit post discharge.

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