Abstract
The phosphodiesterase inhibitors (amrinone, milrinone and enoximone) can cause major improvement in the performance of the failing heart without increasing myocardial oxygen consumption. This appears to be the result of a reduction in left ventricular systolic wall stress due to peripheral arteriolar vasodilatation, which offsets the increase in myocardial oxygen consumption that would otherwise result from an enhanced inotropic state. In comparison, catecholamine agents such as dobutamine, given at doses that achieve the same level of inotropic enhancement or improved left ventricular performance, produce less associated arteriolar vasodilatation and a significant (approximately 30%) increase in myocardial oxygen consumption. This difference between the phosphodiesterase inhibitors and the conventional catecholamine agents may be of clinical importance in patients with limited coronary flow reserve due to severe congestive heart failure.
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