0378 : Time course of cardiac dysfunction in experimental acute decompensation of chronic heart failure

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• 作者：Marianne Lachaux ; Nicolas Peschanski ; Najah Harouki ; Jean-Paul Henry ; Lionel Nicol ; Ebba Brakenhielm ; Antoine Ouvrard-Pascaud ; Vincent Richard ; Chrsitian Thuillez ; Paul Mulder ; ^{paul.mulder@univ-rouen.fr" class="auth_mail" title="E-mail the corresponding author}
• 刊名：Archives of Cardiovascular Diseases Supplements
• 出版年：2016
• 出版时间：April 2016
• 年：2016
• 卷：8
• 期：3
• 页码：236
• 全文大小：47 K

文摘

Exacerbation of chronic heart failure (HF), better known as acute decompensated HF, is characterized by a rapid further decrease of an already HF-related impaired cardiac function, which despite medical treatment only partially recovers. However, no representative experimental model of acute decompensated HF exists, limiting pre-clinical evaluation of emerging therapies and mechanistic understanding.

Objective

We evaluated the time course of cardiac dysfunction of acute decompensation in rats with chronic HF.

Methods

Three months after coronary artery ligation resulting in established chronic HF, rats received 2.5 ml tap water (control) or 1.8 g/kg NaCl (dissolved in 2.5 ml tap water) provoking acute decompensation. Cardiac output (echocardiography), LV tissue perfusion (MRI) and coronary endothelial function (Mulvany) were assessed 1 and 13 days after NaCl loading.

Results

One day after NaCl loading, the HF-related impairment of cardiac output was already aggravated (sham: 145±2 ml/min; HF: 125±3 ml/min; p<0.05 vs. sham; HF+Salt: 105±3 ml/min; p<0.05 vs. HF), associated with further reductions of myocardial perfusion (sham: 8.50±0.19 ml/min/g; HF: 6.01±0.19 ml/min/g; p<0.05 vs. sham; HF+Salt: 4.41±0.23 ml/min/g; p<0.05 vs. HF) and Ach-induced relaxation (% of preconstriction at the concentration of 10-4 M Ach) of coronary arteries (sham: 97±1%; HF: 55±1%; p<0.05 vs. sham; HF+Salt: 27±5%; p<0.05 vs. HF). Thirdteen days after NaCl loading, cardiac output partially recovered (117±5 ml/min), myocardial perfusion (4.51±.0.23 ml/min/g) and coronary relaxation (28±1%) remained reduced.

Conclusion

Our data show that in rats with HF, NaCl loading provokes immediately a further aggravation of cardiac and coronary dysfunctions. Moreover, the aggravation is sustained and only partially recovery over-time. This rat model allows the evaluation cardiac systolic and diastolic function of emerging therapies for humans with acute decompensation of chronic HF.

The author hereby declares no conflict of interest