Resolution of acute coronary venous hypertension and its impact on myocardial edema and left ventricular function
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abstract
Acute myocardial edema (AME) attributable to coronary venous hypertension (CVH) compromises left ventricular (LV) function by unknown mechanisms. We postulated that, the time-course of LV recovery accompanying AME resolution may facilitate elucidation of these mechanisms. In anesthetized dogs, AME was induced by inflating a Swan-Ganz catheter balloon in the coronary sinus. LV pressure-volume loops (PVL) were generated by micromanometry and sonomicrometry and we used preload recruitable stroke work (PRSW) to assess LV contractility. Myorardial water content (MWC) was determined from duplicate biopsies. After instrumentation, baseline LV PVL and biopsies were obtained. The Swan-Ganz balloon was then maximally inflated for 180 min followed by deflation and recovery for 180 min. Zero and 30-min baseline PRSW and LV MWC were not different (paired t test, P > 0.05). LV MWC increased significantly with CVH (repeated measures ANOVA, P < 0.05) but returned toward baseline at 180 min of recovery. PRSW was decreased at 180 min of CVH and returned to baseline concurrent with edema resolution. We conclude that MWC and the functional compromise attributable to AME may normalize within 180 min of CVH discontinuation. These data suggest that visroelastic effects may primarily contribute to edema-induced ventricular dysfunction, and that acute disruption of interstitial matrix components, if present, has little effect on LV contractility.
