Acute aortocaval fistula: role of low perfusion pressure and subendocardial remodeling on left ventricular function

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.

Increased myocardial stiffness due to cardiac titin isoform switching in a mouse model of volume overload limits eccentric remodeling

“…2D). The decreased in collagen content observed in ACF mice is consistent with that found by others[3-5, 7, 8] and is thought to be a result of increased expression and activation of matrix metalloproteinases (MMPs)[8, 10, 30-32]. …”

Myocardial interaction of apixaban after experimental acute volume overload

“…Net cardiac remodeling of the ventricles and septum are interdependent during AVO. 13 In this model, acute volume overload leads to a sudden backflow of blood to the right side of the heart that compresses the septum towards the left side of the heart. 8 Compensating mechanisms associated with the onset of acute cardiac failure include intramyocardial artery ischemia along with ventricular cellular swelling.…”

Aortocaval fistula presenting as Type 2 acute myocardial infarction in a patient with severe arteriopathy

“…[ 10 ] Animal studies have shown low systemic blood pressure and elevated LV end-diastolic pressure in the setting of ACF. [ 11 ] The resulting shunt to the low-pressure caval system reduces coronary driving pressures during diastole, precipitating LV systolic and diastolic dysfunction. [ 11 ] In other animal models, subendocardial fibrosis was seen in the infarcted and noninfarcted myocardium as a result of low coronary driving pressure.…”

“…[ 11 ] The resulting shunt to the low-pressure caval system reduces coronary driving pressures during diastole, precipitating LV systolic and diastolic dysfunction. [ 11 ] In other animal models, subendocardial fibrosis was seen in the infarcted and noninfarcted myocardium as a result of low coronary driving pressure. [ 12 ] The presence of LV hypertrophy and mild coronary artery disease could aggravate the ischemic myocardial state precipitated by ACF.…”