Low-dose erythropoietin improves cardiac function in experimental heart failure without increasing haematocrit

Immunosuppressive therapy is an established therapeutic option in patients suffering from multiple sclerosis (MS). In an open nonrandomized study we serially assessed cardiac function in 30 consecutive patients with MS before, during, and after mitoxantrone therapy. Mitoxantrone (12 mg/m2) was administered intravenously at 3-month intervals. Before each infusion, cardiac function was assessed by history taking, resting electrocardiogram, and echocardiography. Whereas no patient experienced clinical signs of heart failure, left ventricular pump function decreased continuously during mitoxantrone therapy and did not recover after cessation. The presented data suggest a dose-dependent and long-lasting toxic cardiac effect of low-dose mitoxantrone therapy in MS.

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A novel urotensin II receptor antagonist, KR-36996, improved cardiac function and attenuated cardiac hypertrophy in experimental heart failure

European Journal of Pharmacology ◽

10.1016/j.ejphar.2017.02.003 ◽

2017 ◽

Vol 799 ◽

pp. 94-102 ◽

Cited By ~ 13

Author(s):

Kwang-Seok Oh ◽

Jeong Hyun Lee ◽

Kyu Yang Yi ◽

Chae Jo Lim ◽

Byung Kil Park ◽

...

Keyword(s):

Heart Failure ◽

Cardiac Hypertrophy ◽

Cardiac Function ◽

Receptor Antagonist ◽

Urotensin Ii ◽

Experimental Heart Failure

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Low-Dose ^|^beta;-Blocker in Combination With Milrinone Safely Improves Cardiac Function and Eliminates Pulsus Alternans in Patients With Acute Decompensated Heart Failure

Circulation Journal ◽

10.1253/circj.cj-12-0033 ◽

2012 ◽

Vol 76 (7) ◽

pp. 1646-1653 ◽

Cited By ~ 24

Author(s):

Shigeki Kobayashi ◽

Takehisa Susa ◽

Takeo Tanaka ◽

Wakako Murakami ◽

Seiko Fukuta ◽

...

Keyword(s):

Heart Failure ◽

Cardiac Function ◽

Beta Blocker ◽

Low Dose ◽

Acute Decompensated Heart Failure ◽

Decompensated Heart Failure ◽

Pulsus Alternans

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An anti-chymase RNA aptamer improved cardiac function in experimental heart failure

Proceedings for Annual Meeting of The Japanese Pharmacological Society ◽

10.1254/jpssuppl.wcp2018.0_po2-3-18 ◽

2018 ◽

Vol WCP2018 (0) ◽

pp. PO2-3-18

Author(s):

Denan Jin ◽

Shinji Takai ◽

Yosuke Nonaka ◽

Satoko Yamazaki ◽

Masatoshi Fujiwara ◽

...

Keyword(s):

Heart Failure ◽

Cardiac Function ◽

Rna Aptamer ◽

Experimental Heart Failure

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Early Treatment with Hepatocyte Growth Factor Improves Cardiac Function in Experimental Heart Failure Induced by Myocardial Infarction

Journal of Pharmacology and Experimental Therapeutics ◽

10.1124/jpet.102.041772 ◽

2003 ◽

Vol 304 (2) ◽

pp. 654-660 ◽

Cited By ~ 23

Author(s):

Hongkui Jin ◽

Renhui Yang ◽

Wei Li ◽

Annie K. Ogasawara ◽

Ralph Schwall ◽

...

Keyword(s):

Myocardial Infarction ◽

Heart Failure ◽

Growth Factor ◽

Hepatocyte Growth Factor ◽

Cardiac Function ◽

Early Treatment ◽

Experimental Heart Failure ◽

Hepatocyte Growth

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Selective ETA receptor blockade prevents left ventricular remodeling and deterioration of cardiac function in experimental heart failure

Cardiovascular Research ◽

10.1016/s0008-6363(98)00159-x ◽

1998 ◽

Vol 39 (3) ◽

pp. 600-608 ◽

Cited By ~ 54

Author(s):

P Mulder

Keyword(s):

Heart Failure ◽

Cardiac Function ◽

Ventricular Remodeling ◽

Left Ventricular Remodeling ◽

Left Ventricular ◽

Receptor Blockade ◽

Experimental Heart Failure ◽

Eta Receptor

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Low-dose simvastatin improves survival and ventricular function via eNOS in congestive heart failure

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.00347.2006 ◽

2006 ◽

Vol 291 (6) ◽

pp. H2743-H2751 ◽

Cited By ~ 26

Author(s):

James J. M. Greer ◽

Aman K. Kakkar ◽

John W. Elrod ◽

Lewis J. Watson ◽

Steven P. Jones ◽

...

Keyword(s):

Heart Failure ◽

Congestive Heart Failure ◽

Cardiac Hypertrophy ◽

Cardiac Function ◽

Pulmonary Edema ◽

Murine Model ◽

Low Dose ◽

Simvastatin Treatment ◽

Simvastatin Therapy ◽

Vehicle Treatment

3-Hydroxy-3-methylglutaryl coenzyme A reductase inhibitors increase endothelial nitric oxide synthase (eNOS) activity by multiple mechanisms. We previously reported that genetic overexpression of eNOS improves survival and cardiac function in congestive heart failure (CHF). In the present study, we tested the hypothesis that low-dose treatment with an 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor exerts beneficial effects on survival and/or cardiac function in a murine model of CHF. Mice were subjected to permanent ligation of the left coronary artery and randomized to receive either saline vehicle or simvastatin (0.25 mg/kg) 2 h after myocardial infarction and daily (0.25 mg/kg) for 7 days, followed by 21 days of administration every other day for a total duration of 28 days. Myocardial infarct size was not reduced by simvastatin therapy ( P = not significant between groups). Simvastatin treatment did significantly ( P < 0.05) improve survival (45%) compared with vehicle treatment (25%). In addition, simvastatin treatment significantly improved ( P < 0.01) left ventricular function and significantly ( P < 0.01) abrogated cardiac hypertrophy and pulmonary edema compared with vehicle treatment. The protective effects of simvastatin were abrogated by delayed initiation of treatment or genetic ablation of eNOS. In conclusion, low-dose simvastatin therapy significantly improves survival and cardiac function and reduces both cardiac hypertrophy and pulmonary edema via an eNOS-dependent mechanism in a murine model of CHF.

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