Surgical Acute Volume-Overload Impacts Early on Myocardium - An Experimental Study

Acute volume-overload (AVO) predisposes to cardiac failure. Global cardiac injury may ensue after acute right-sided distension of the heart due to AVO. We experimentally investigated whether surgical AVO impacts early on the myocardium and some markers of injury.

Thirty-four syngeneic Fisher rats underwent surgical abdominal aortocaval fistula to induce AVO. The hearts were procured for regional and quantitative histology after one and three days. Gene expressions for atrial natriuretic peptide (ANP), matrix metalloprotease 9 (MMP9), transforming growth factor β (TGFβ) and YKL40 were investigated for myocardial injury.

The relative number of ischemic intramyocardial arteries were abundant in the septum of the hearts with AVO compared with controls at day 1 and 3 [0.16 ± 0.02 vs. 0.02 ± 0.01, point score unit (PSU), p = 0.002 and 0.14 ± 0.02 vs. 0.02 ± 0.01, PSU, p = 0.009, respectively] followed by similar changes in the left ventricle at day 3 (0.11 ± 0.02 vs. 0.04 ± 0.01, PSU, p = 0.007). Indicating early myocardial injury, ANP (p = 0.019) was increased in AVO hearts as compared with controls at day 1, as expected. More interestingly, MMP9 (p = 0.003 and p = 0.006), TGFβ (p = 0.002 and p = 0.004) and YKL40 (p = 0.001 and p = 0.003) expressions were significantly increased at day 1 and 3, along with macrophage infiltration into the myocardium supporting the role of factors produced by alternatively activated macrophages in the pathogenesis of AVO-induced pathophysiology in the heart.

Surgical AVO induces an early ischemic myocardial response observed in the intramyocardial arteries. Early expression of key parameters of cardiac remodeling suggest for the onset of early cardiac failure after AVO.