ASSOCIATION BETWEEN HEMODYNAMIC PARAMETERS AND THE DEGENERATION OF SUSTAINED VENTRICULAR TACHYCARDIAS INTO VENTRICULAR-FIBRILLATION IN RATS

A. HAGENDORFF, C. VAHLHAUS, W. JUNG, C. MARTIN, G. HEUSCH AND B. LUDER ITZ. Association Between Hemodynamic Parameters and the Degeneration o f Sustained Ventricular Tachycardias into Ventricular Fibrillation in Rats. Journal of Molecular and Cellular Cardiology (1997) 29, 3091-310 3. Sustained ventricular tachycardias (VT) often degenerate into ventr icular fibrillation (VF). In the present study, the impact of VT on me an arterial blood pressure (MAP), myocardial blood now (MBF), and myoc ardial oxygen consumption (MVO2) was assessed. In addition, the degene ration of sustained VT into VF was analysed with respect to MAP. MBF w as measured in 48 anesthetized rats with colored microspheres; arteria l catecholamine levels were measured by HPLC in 16 additional rats dur ing control conditions and VT. MBF (4.66 +/- 1.29 ml/g/min; mean +/- S .D.) did not change with the onset of VT (5.37 +/- 1.92 ml/g/min, N.S. ). Epinephrine (0.22 +/- 0.13 ng/ml) and norepinephrine (0.37 +/- 0.12 ng/ml) increased during VT (3.55 +/- 2.68 ng/ml, P<0.01; 0.88 +/- 0.4 4 ng/ml, P<0.05), respectively. VF was more frequent when MAP remained normal (MAP>80 mmHg: 26%) than with hypotension (MAP<80 mmHg: 2%, P<0 .05). Mechanical failure was observed in 10% of rats with severe hypot ension (MAP<60 mmHg), and 2% with moderate hypotension (MAP 60-80 mmHg ). The endo-epicardial MBF ratio in the VF group was significantly low er than that in the non-VF group (0.94 +/- 0.17 v 1.11 +/- 0.24, P<0.0 5). Conclusions: severe hypotension predisposes to the occurrence of a cute mechanical failure during VT; moderate hypotension during VT, how ever, serves as a protective mechanism against VF in structurally norm al hearts. Subendocardial hypoperfusion in the presence of an increase d energy demand during VT is suggested to be responsible for the initi ation of VF. (C) 1997 Academic Press Limited.