ArticleInternational journal of experimental pathology2013
Acute aortocaval fistula: role of low perfusion pressure and subendocardial remodeling on left ventricular function.
Article in International journal of experimental pathology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 7 citations in OpenAlex.
- Myocardial interaction of apixaban after experimental acute volume overload.The Journal of international medical research · 2022Article
- Early reversibility of histological changes after experimental acute cardiac volume-overload.American journal of cardiovascular disease · 2022Article
- Monoamine oxidase A inhibition protects the myocardium after experimental acute volume overload.Anatolian journal of cardiology · 2019Article
- Aortocaval Fistula Presenting as Type 2 Acute Myocardial Infarction in a Patient with Severe Arteriopathy.Indian journal of critical care medicine : peer-reviewed, official publication of Indian Society of Critical Care Medicine · 2018Article
- Surgical Acute Volume-Overload Impacts Early on Myocardium - An Experimental Study.Acta Cardiologica Sinica · 2017Article
- Increased myocardial stiffness due to cardiac titin isoform switching in a mouse model of volume overload limits eccentric remodeling.Journal of molecular and cellular cardiology · 2015Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The experimental model of aortocaval fistula is a useful model of cardiac hypertrophy in response to volume overload. In the present study it has been used to investigate the pathologic subendocardial remodeling associated with the development of heart failure during the early phases (day 1, 3, and 7) following volume overload. Compared with sham treated rats, aortocaval fistula rats showed lower systemic blood pressure and higher left ventricular end-diastolic pressure This resulted in lower coronary driving pressure and left ventricular systolic and diastolic dysfunction. Signs of myocyte necrosis, leukocyte cell infiltration, fibroplasia and collagen deposition appeared sequentially in the subendocardium where remodeling was more prominent than in the non-subendocardium. Accordingly, increased levels of TNF-alpha, IL-1 beta, and IL-6, and enhanced MMP-2 activity were all found in the subendocardium of rats with coronary driving pressure ≤ 60 mmHg. The coronary driving pressure was inversely correlated with MMP-2 activity in subendocardium in all time-points studied, and blood flow in this region showed positive correlation with systolic and diastolic function at day 7. Thus the predominant subendocardial remodeling that occurs in response to low myocardial perfusion pressure during the acute phases of aortocaval fistula contributes to early left ventricular dysfunction.
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