Left ventricular response to sustained volume overload from chronic aortic valve regurgitation in rats
- PMID: 12751134
- DOI: 10.1054/jcaf.2003.17
Left ventricular response to sustained volume overload from chronic aortic valve regurgitation in rats
Abstract
Objectives: Aortic regurgitation (AR) induces left ventricular (LV) eccentric hypertrophy in response to chronic volume overload. Patients suffering from this disease often remain asymptomatic for decades before progressive LV dysfunction develops silently. Because of this slow evolution, large clinical trials with long-term follow-up on subjects with chronic AR are hard to perform. To overcome this problem, animal models have been developed in the past but results were very heterogeneous.
Methods: Helped by echocardiography, we refined a known technique to induce homogeneous degrees of severe AR in Wistar-Kyoto rats. The effects on LV function without treatment and with nifedipine (25 mg/kg daily) (a drug currently recommended in humans with chronic AR) were evaluated by echocardiography.
Results: Over 6 months, nontreated animals developed progressive LV dilatation and eccentric hypertrophy, characteristic of chronic LV volume overload. The animals also developed progressive LV systolic dysfunction, mimicking closely the evolution of the disease in humans. Abnormal filling parameters were also detected in the majority of animals. Systolic and diastolic abnormalities were prevented but only partially in the group treated with nifedipine.
Conclusion: This model can be used to study chronic AR and LV dysfunction associated with the disease. Nifedipine seems to protect the LV against chronic volume overload but only partially. Treatment strategies currently used in humans deserve further investigation.
Similar articles
-
Comparative study of vasodilators in an animal model of chronic volume overload caused by severe aortic regurgitation.Circ Heart Fail. 2009 Jan;2(1):25-32. doi: 10.1161/CIRCHEARTFAILURE.108.801548. Circ Heart Fail. 2009. PMID: 19808312
-
Angiotensin-converting enzyme inhibitor captopril prevents volume overload cardiomyopathy in experimental chronic aortic valve regurgitation.Can J Physiol Pharmacol. 2004 Mar;82(3):191-9. doi: 10.1139/y04-005. Can J Physiol Pharmacol. 2004. PMID: 15052285
-
Fenofibrate reduces cardiac remodeling and improves cardiac function in a rat model of severe left ventricle volume overload.Life Sci. 2013 Jan 17;92(1):26-34. doi: 10.1016/j.lfs.2012.10.022. Epub 2012 Nov 7. Life Sci. 2013. PMID: 23142240
-
[The best of valvular heart disease in 2006].Arch Mal Coeur Vaiss. 2007 Jan;100 Spec No 1:19-28. Arch Mal Coeur Vaiss. 2007. PMID: 17405561 Review. French.
-
The relationship of left ventricular geometry and hypertrophy to left ventricular function in valvular heart disease.J Heart Valve Dis. 1995 Oct;4 Suppl 2:S132-8; discussion S138-9. J Heart Valve Dis. 1995. PMID: 8563989 Review.
Cited by
-
Sex differences in the evolution of left ventricle remodeling in rats with severe volume overload.BMC Cardiovasc Disord. 2020 Feb 3;20(1):51. doi: 10.1186/s12872-020-01360-0. BMC Cardiovasc Disord. 2020. PMID: 32013884 Free PMC article.
-
Female rats with severe left ventricle volume overload exhibit more cardiac hypertrophy but fewer myocardial transcriptional changes than males.Sci Rep. 2017 Apr 7;7(1):729. doi: 10.1038/s41598-017-00855-9. Sci Rep. 2017. PMID: 28389667 Free PMC article.
-
Surgical and physiological challenges in the development of left and right heart failure in rat models.Heart Fail Rev. 2019 Sep;24(5):759-777. doi: 10.1007/s10741-019-09783-4. Heart Fail Rev. 2019. PMID: 30903356 Free PMC article. Review.
-
Testosterone deficiency reduces cardiac hypertrophy in a rat model of severe volume overload.Physiol Rep. 2019 May;7(9):e14088. doi: 10.14814/phy2.14088. Physiol Rep. 2019. PMID: 31054220 Free PMC article.
-
Effects of the cardiac myosin activator Omecamtiv-mecarbil on severe chronic aortic regurgitation in Wistar rats.BMC Cardiovasc Disord. 2018 May 21;18(1):99. doi: 10.1186/s12872-018-0831-3. BMC Cardiovasc Disord. 2018. PMID: 29783950 Free PMC article.
Publication types
MeSH terms
Substances
LinkOut - more resources
Full Text Sources
Research Materials
Miscellaneous